The invention related to prodrug substituted benzoxazoles as estrogenic agents BACKGROUND OF THE INVENTION This invention relates to prodrug derivatives of substituted beazuxazoies, which are useful as estrogenic agents. The pleiotropic effects of estrogens in mammalian tissues have been well documented, and it is now appreciated that estrogens affect many organ systems [Mendelsohn and Karas, New England Journal of Medicine 340:1801-1811 (1999), Epperson, et al., Psychosomatic Medicine 61:676-697 (1999), Crandall, Journal of Womens Health & Gender Based Medicine 8:1155-1166 (1999), Monk and Brodaty, Dementia & Geriatric Cognitive Disorders 11:1-10 (2000), Hum and Macrae, Journal of Cerebral Blood Flow & Metabolism 20:631-652 (2000), Calvin, Maturitas 34:195- 210 (2000), Finking, etal., Zeitschrift furKardiologie 89: 442-453 (2000), Brincat, Maturitas 35:107-117 (2000), AAzzawi, Postgraduate Medical Journal 77:292-304 (2001)]. Estrogens can exert effects on tissues in several ways, and the most well characterized mechanism of action is their interaction with estrogen receptors leading to alterations in gene transcription. Estrogen receptors are ligand-activated transcription factors and belong to the nuclear hormone receptor superfamily. Other members of this family include the progesterone, androgen, glucocorticoid and mineralocorticoid receptors. Upon binding ligand, these receptors dimerize and can activate gene transcription either by directly binding to specific sequences on DNA (known as response elements) or by interacting with other transcription factors (such as AP1), which in turn bind directly to specific DNA sequences [Moggs and Orphanides, EMBO Reports 2:775-781 (2001), Hall, et al., Journal of Biological Chemistry 276: 36869-36872 (2001), McDonnell, Principles Of Molecular Regulation 351-361 (2000)]. A class of coregulatory proteins also can interact with the ligandbound receptor and further modulate its transcriptional activity [McKenna, et al., Endocrine Reviews 20:321-344 (1999)]. It has also been shown that estrogen receptors can suppress NFicB-rhediated transcription in both a ligand-dependent and independent manner [Quaedackers, et al., Endocrinology 142:1156-1166 (2001), Bhat, et al., Journal of Steroid Biochemistry & Molecular Biology 67:233-240 (1998), Pelzer, et al., Biochemical & Biophysical Research Communications 286:1153-7 (2001)]. Estrogen receptors can also be activated by phosphorylation. This phosphoryfation is mediated by growth factors such as EGF and causes changes in gene transcription in the absence of ligand [Moggs and Orphanides, EMBO Reports 2: 775-781 (2001), Hall, et al., Journal of Biological Chemistry 276: 36869-36872 A less well-characterized means by which estrogens can affect cells is through a so-called membrane receptor. The existence of such a receptor is controversial, but it has been well documented that estrogens can elicit very rapid non-genomic responses from cells. The molecular entity responsible for transducing these effects has not been definitively isolated, but there is evidence to suggest it is at least related to the nuclear forms of the estrogen receptors [Levin, Journal of Applied Physiology 91:1860-1867 (2001), Levin, Trends in Endocrinology & Metabolism 10:374-377 (1999)]. Two estrogen receptors have been discovered to date. The first estrogen receptor was cloned about 15 years ago and is now referred to as ERa [Green, et al., Nature 320:134-9 (1986)]. The second form of the estrogen receptor was found comparatively recently and is called ERp [Kuiper, et al., Proceedings of the National Academy of Sciences of the United States of America 93:5925-5930 (1996)]. Early work on ERP focused on defining its affinity for a variety of ligands and indeed, some differences with ERa were seen. The tissue distribution of ERp has been well mapped in the rodent and it is not coincident with ERa. Tissues such as the mouse and rat uterus express predominantly ERa, whereas the mouse and rat lung express predominantly ERp [Couse, etal., Endocrinology 138:4613-4621 (1997), Kuiper, et al., Endocrinology 138:863-870 (1997)]. Even within the same organ, the distribution of ERa and ERp can be compartmentalized. For example, in the mouse ovary, ERp is highly expressed in the granulosa cells and ERa is restricted to the thecal and stromal cells [Sar and Welsch, Endocrinology 140:963-971 (1999), Frtzpatrick, etal., Endocrinology 140:2581-2591 (1999)]. However, there are examples where the receptors are coexpressed and there is evidence from in vitro studies that ERa and ERp can form heterodimers [Cowley, et al,, Journal of Biological Chemistry 272:19858-19862 (1997)]. A large number of compounds have been described that either mimic or block the activity of 17p-estradiol. Compounds having roughly the same biological effects as 17p-estradiol, the most potent endogenous estrogen, are referred to as estrogen receptor agonists. Those which, when given in combination with 17p-estradiol, block its effects are called estrogen receptor antagonists. In reality, there is a continuum between estrogen receptor agonist and estrogen receptor antagonist activity and indeed, some compounds behave as estrogen receptor agonists in some tissues and estrogen receptor antagonists in others. These compounds with mixed activity are called selective estrogen receptor modulators (SERMS) and are therapeutically useful agents (e.g. EVISTA) [McDonnell, Journal of the Society for Gynecologic Investigation 7: S10-S15 (2000), Goldstein, et al., Human Reproduction Update 6:212-224 (2000)]. The precise reason why the same compound can have cell-specific effects has not been elucidated, but the differences in receptor conformation and/or in the milieu of coregulatory proteins have been suggested. It has been known for some time that estrogen receptors adopt different conformations when binding ligands. However, the consequence and subtlety of these changes has been only recently revealed.. The three dimensional structures of ERa and ERp have been solved by co-crystallization with various ligands and clearly show the repositioning of helix 12 in the presence of an estrogen receptor antagonist, which sterically hinders the protein sequences required for receptor-coregulatory protein interaction [Pike, et al., Embo 18:4608-4618 (1999), Shiau, et al., Cell 95: 927-937 (1998)]. In addition, the technique of phage display has been used to identify peptides that interact with estrogen receptors in the presence of different ligands [Paige, et al., Proceedings of the National Academy of Sciences of the United States of America 96:3999-4004 (1999)]. For example, a peptide was identified that distinguished between ERa bound to the full estrogen receptor agonists, 17JJestradiol and diethylstilbesterol. A different peptide was shown to distinguish between clomiphene bound to ERa and ERp. These data indicate that each ligand potentially places the receptor in a unique and unpredictable conformation that is likely to have distinct biological activities. As mentioned above, estrogens affect a panoply of biological processes. In addition, where gender differences have been described (e.g., disease frequencies, responses to challenge, etc.), it is possible that the explanation involves the difference in estrogen levels between males and females. Compounds having estrogenic activity are disclosed in U.S. Patent Application Ser. No. 10/309,699 filed December 4, 2002, now US Patent No. 6794403, and in WO 03/050095, which are incorporated herein by reference in their entireties. DESCRIPTION OF THE INVENTION This invention provides estrogenic compounds of formula I, having the structure: Qi and Q2 are independently H, a sugar residue or S(O)rOH, provided that Qt and Q2 are not both H; t is 0,1 or 2; R.J is hydrogen, hydroxyl, halogen, alkyl of 1-6 carbon atoms, trifluoroalkyl of 1-6 carbon atoms, cyctoalkyl of 3-8 carbon atoms, alkoxy of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, thioalkyl of 1-6 carbon atoms, sulfoxoalkyl of 1-6 carbon atoms, sulfonoalkyl of 1-6 carbon atoms, aryl of 6- 10 carbon atoms, a 5 or 6-membered heterocyclic ring having 1 to 4 heteroatoms selected from O, N or S, -NO2, -NRsRe, -N(RS)COR6, -CN, - CHFCN, -CF2CN, alkynyl of 2-7 carbon atoms, or alkenyl of 2-7 carbon atoms; wherein the alkyl or alkenyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl, trifluoroalkoxy, -CORs, -CO2Rg, -NO2, CONRgRe, NRsRe or N(R5)COR6; R2 and R2a are each, independently, hydrogen, hydroxyl, halogen, alkyl of 1-6 carbon atoms, alkoxy of 1-4 carbon atoms, alkenyl of 2-7 carbon atoms, alkynyl of 2-7 carbon atoms, trifluoroalkyl of 1-6 carbon atoms, or trifluoroatkoxy of 1-6 carbon atoms; wherein the alkyl, alkenyl, or alkynyl moieties are optionally substituted with hydroxyf, -CN, halogen, trifluoroalkyl, trifluoroalkoxy, -COR5, -CO2R5, -NO2, CONRSR6, NRSR6 or N(R5)COR<;; R3, and R3a are each, independently, hydrogen, alky] of 1-6 carbon atoms, alkenyl of 2-7 carbon atoms, alkynyl of 2-7 carbon atoms, halogen, alkoxy of 1r4 carbon atoms, trifluoroalkyl of 1-6 carbon atoms, or trifluoroalkoxy of 1-6 carbon atoms; wherein the alkyl, alkenyl, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl, trifluoroalkoxy, -CORS, - C02R5, -N02) CQNRsRe. NR5R6 or N{R5)COR6; R5, R6 are each, independently hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -CORs, -CO2R5 or a pharmaceutically acceptable salt thereof, which are useful as estrogenic agents. Pharmaceuticaliy acceptable salts can be formed from organic and inorganic acids, for example, acetic, propionic, lactic, citric, tartaric, succinfc, fumaric, mateic, maionic, mandelic, mafic, phthalic, hydrochloric, hydrobromic, phosphoric, nitric, sulfuric, methanesulfonic, naphthatenesulfonic, benzenesulfonic, toluenesulfonic, camphorsulfonic, and similarly known acceptable acids when a compound of this invention contains a basic moiety. Salts may also be formed from organic and inorganic bases, such as alkali metal salts (for example, sodium, lithium, or potassium), alkaline earth metal salts, ammonium salts, alkytemmonium salts containing 1-6 carbon atoms or dialkylammonium salts containing 1-6 carbon atoms in each alkyl group, and trialkylammonium salts containing 1-6 carbon atoms in each alkyl group, when a compound of this invention contains an acidic moiety. The terms alkyr, alkenyl, and alkynyf include both branched and straight chain moieties. Examples include methyl, ethyl, propyl, butyl, isopropyl, sec-butyl, terf-butyl, vinyl, ally!, acetylene, 1-methyl vinyl, and the like. When alkyl or alkenyl moieties are substituted, they may typically be mono-, di-, tri- or persubstituted. Examples for a halogen substituent include 1-bromo vinyl, 1-fluoro vinyl, 1,2-difluoro vinyl, 2,2-difluorovinyl, 1,2,2-trifluorovinyl, 1,2-dibromo ethane, 1,2 difluoro ethane, 1- fluoro-2-bromo ethane, CF2CF3, CF2CF2CF3, and the like. The term halogen includes bromine, chlorine, fluorine, and iodine. The term aryl includes an aromatic of 6-10 carbon atoms e.g., phenyl, 1-naphthyl, or 2-naphthyl. Preferred 5-6 membered heterocycfic rings include furan, thiophene, pyrrole, isopyrrole, pyrazole, imidazole, triazole, dithiole, oxathiole, isoxazole, oxazole, thiazole, isothiazolem oxadiazole, furazan, oxatriazole, dioxazole, oxathiazole, tetrazole, pyran, pyridine, pyridazine, pyrimidine, pyrazine, triazine, oxazine, oxathiazine, or oxadiazine. More preferred heterocyclic rings are furan, thiophene, or thiazole. In some embodiments of the compounds of formula I, R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl, trifluoroalkoxy, -CORs, -CO2Rs, -NO2, CONRgRe, NRgRe or Of the compounds of this invention, it is preferred that the compound of . formula I has the structure: wherein: and Q2 are independently H, a modified or unmodified hexose residue, or S(O)r OH, provided that QI and Q2 are not both H; RI is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl, trifluoroalkoxy, -COR5, -CO2Rs, - NO2, CONRsRe, NRsRe or N(R5)COR6; R2 and R2a are each, independently, hydrogen, hydroxyl, halogen, alkyl of 1-6 carbon atoms, alkoxy of 1-4 carbon atoms, alkenyl of 2-7 carbon atoms, alkynyl of 2-7 carbon atoms, trifluoroalkyl of 1-6 carbon atoms, or trifluoroalkoxy of 1-6 carbon atoms; wherein the alkyl, alkenyl, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl, trifluoroalkoxy, -COR5, -CO2R5l -NO2, CONR5R6, NR5RS or N(R6)COR6; R3 and R3a are each, independently, hydrogen, alkyl of 1-6 carbon atoms, alkenyl of 2-7 carbon atoms, alkynyl of 2-7 carbon atoms, halogen, alkoxy of 1-4 carbon atoms, trifluoroalkyl of 1-6 carbon atoms, or trifluoroalkoxy of 1-6 carbon atoms; wherein the alkyl, alkenyl, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl, trifluoroalkoxy, -COR5, - CO2RS,-NO2, CONRsRs, NR5R6 or N(R5)COR6; R5, R6are each, independently, hydrogen, alkyl of 1-6 carbon atoms, arylof 6-10 R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or a pharmaceutically acceptable salt thereof. It is more preferred that X is O, and still more preferred that X is O, and R1 is alkenyl of 2-3 carbon atoms, which is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl, trifluoroalkoxy, -COR5, -CO2Rs, -NO2, CONR5R6l NR5R6 or It is more preferred that Qi and Q2 are selected from -SO3H and glucuronide residues. In some particularly preferred embodiments, the compound is a mono- or disulfate derivative, a mono- or di-glucuronide derivative, or a glucuronide-sulfate derivative of 2-(3-fluoro-4'-hydroxyphenyl)-7-vinyl-1,3-benzoxazol-5-ol, or a pharmaceutically acceptable salt thereof. In some embodiments, the compound is 2- (3'-fluoro-4'-glucuronide phenyl)-7-vinyl-1,3-benzoxazol-5-ol; 2-(3'-fluoro-4'-sulfate phenyl)-7-vinvl-1,3-benzoxazol-5-ol; 2-(3'-fluoro-4'-hydroxy phenyl)-7-vinyl-1,3- benzoxazol-5-glucuronide; 2-(3I-fluoro-4'-hydroxy phenyf)-7-vinyM ,3-benzoxazol-5- sulfate; 2-(3I-fluoro-4'-glucuroride phenyl)-7-vinyl-1,3-benzoxazol-5-glucuronide; 2- (3'-fluoro-4'-glucuromde phenyl)-7-vinyl-1,3-benzoxazol-5-sulfate; 2-(3'-fluoro-4'- sulfate phenyl)-7-vinyM,3-benzoxazol-5-glucuronide; 2-(3'-fluoro-4'-sulfate phenyl)- 7-vinyM ,3-benzoxazol-5-sulfate; 2-(2'-fluoro-4'-glucuronide phenyJ)-7-vjnyl-1,3- benzoxazol-5-ol; 2-{2'-fluoro-4'-sulfate phenyl)-7-vinyl-1,3-benzoxazot-5-oI; 2-(2'- fluoro-4'-hydroxy phenyl)-7-vinyl-1,3-benzoxazol-5-glucuronide; 2-(2'-fluoro-4'- hydroxy phenyl)-7-vinyl-1,3-benzoxazol-5-sulfate; 2-(2'-fluoro-4'-gIucuronide phenyl)- 7-vinyH ,3-benzoxazol-5-glucuronide; 2-(2'-fluoro-4'-glucuronide phenyl)-7-vinyH,3- benzoxazol-S-sulfate; 2-{2'-fluoro-4'-sulfate phenyl)-7-vinyl-1,3-benzoxazol-5- glucuronide; 2-(2'-fluoro-4'-sulfate phenyl)-7-vinyl-1,3-benzoxazol-5-sulfate; 2-(2',3'- difluoro-4-glucuronide phenyl)-7-vinyH ,3-benzoxazol-5-ol,- 2-(2',3I-dif!uoro-4'-sulfate phenyl)-7-vinyM ,3-benzoxazol-5-ol; 2-(2I,3'-difluoro-4'-hydroxyphenyl)-7-vinyI-1,3- benzoxazol-5-glucuronide;2-(2',3'-difluoro-4'-hydroxyphenyl)-7-vinyl-1,3-ben2oxazol- 5-su!fate; 2-(2',3'-difluoro-4'-glucuronide pheny])-7-vinyH ,3-benzoxazol-5- glucuronide; 2-(2',3'-difluoro-4'-gIucuronide phenyl)-7-vinyl-1,3-benzoxazol-5-sulfate 2-(2',3'-difluoro-4'-sutfate phenyl)-7-vinyl-1,3-benzoxazol-5-gIucuronide; 2-(2',3'- difluoro-4'-sulfate phenyl)-7-vinyl-1,3-benzoxazol-5-sulfate; 4-bromo-2-(3'-fluoro-4'- glucuronide phenyl)-7-vinyl-1 )3-benzoxazo5-ol,• 4-bromo-2-(31-fluoro-4-sulfate phenyl)-7-vinyl-1,3-benzoxazoJ-5I;4-bromo-2-(3-fluoro-4'-hydroxyphenyl)-7-vinyl- 1,3-benzoxazol-5-glucoronide; 4-bromo-2-(3'-fluoro-4'-hydroxyphenyl)-7-vinyl-1,3- benzoxazol-5-sulfete; 4-bromo-2-{3I-fluoro-4I-glucuronide phenyl)-7-vinyl-1,3- benzoxazol-5-gIucuronide; 4-bromo-2-(3 -fluorcM'-glucuronide phenyl)-7-vinyH ,3- benzoxazol-5-sulfate; 4-bromo-2-(31-fluoro-4'-sulfate phenyl)-7-vinyH,3-benzoxazol- 5-glucuronide; 4-bromo-2-{3I-fluoro-4-sulfate phenyl)-7-vinyl-1,3-benzoxazol-5- sulfate; 4,6-dibromo-2-(3'-fluoro-4'- glucuronide phenyl)-7-vinyM,3-benzoxazol-5-oi; 4,6-dibromo-2-(3'-fluoro-4'-sulfate phenyl)-7-vinyl-1,3-benzoxazol-5-ol; 4,6-dibromo 2-{3'-fluoro-4'- hydroxyphenyl)-7-vinyl-1,3-benzoxazot-5-glucuronide; 4,6-dibromo-2- (3'-fIuoro-4'- hydroxyphenyl)-7-vinyl-1,3-benzoxazol-5-sulfate; 4,6-dibromo-2-(3'- fluoro-4'- glucuronide phenyl)-7-wnyl-1,3-benzoxazol-5-glucuronide; 4,6-dibromo-2- (3'-f1uoro-4'- glucuronide phenyl)-7-vinyl-1,3-benzoxazo|-5-sulfate; 4,6-dibromo-2-(3- fluoro-4'- sulfate phenyl)-7-vinyl-1,3-benzoxazol-5-glucuronide; 4,6-dibromo-2-(3'- fluoro-4- sulfate phenyl)-7-vinyl-1,3-benzoxazol-5-sulfate; 7-(1-bromovinyl)-2-(2Ifluoro- 4'-glucuronide phenyl)-1,3-benzoxazoJ-S-ol; 7-(1-bromovinyJ)-2-{2'-fluoro-4- sulfate phenyl)-1,3-benzoxazol-5-ol; 7-(1-bromovinyl)-2-(2'-fluoro-4'-hydroxyphenyl)- 1,3-benzoxazol-5-gIucuronide; 7-{1-bromovJnyI)-2-{2I-fluoro-4-hydroxyphenyl)-1,3- benzoxazol-5-sulfate; 7-(1-bromovinyl)-2-(2I-fluoro-4I-g!ucuronide phenyl)-1,3-. benzoxazol-&-glucuronide; 7-(1 -bromovinyl)-2-(2-fluoro-4'-g!ucurcnide phenyl)-1,3- benzoxazol-5-suIfate; 7-(1-bromovinyl)-2-(2 -fluoro-4'-sulfate phenyl)-1,3-benzoxazof5- glucuronide; 7-(1-bromovinyl)-2-(2'-f]uoro-4'-suIfate phenyl)-1,3-benzoxazol-5- sulfate; 7-(1-bromovinyl)-2-(2',3'-difluoro-4'-glucuronide phenyl)-1,3-benzoxazol-5-ol; 7-(1-bromovinyl)-2-(2',3'-difluorcH4'-sulfatephenyl)-1,3-benzoxazot-5-oJ;7-(1- bromovinyl)-2-(2',3'-difluoro-4'-hydroxyphenyl)-1,3-benzoxazo!-5-gIucuronide; 7-(1 - bromovinyl)-2-(2',3'-dJfluoro-4'-hydroxyphenyl)-1,3-benzoxazol-5-sulfate; 7-(1 - bromovinyl)-2-(21,3'-difluoro-4'-glucuronide phenyl)-1,3-benzoxazol-5-glucuronide; 7- (1-bromovinyl)-2-(2l,3'-difluoro-4I-glucuronide phenyl)-1,3-benzoxazol-5-suIfate; 7-(1- bromovinyl)-2-(2',31-difluoro-4'-sulfate pheny!)-1,3-benzoxazoi-5-glucuronide; 7-(1 - bromovinyl)-2-(2',3'-difluoro~4'-sulfate phenyl)-1,3-benzoxazol-5-sulfate; 7-allyl-2-(3'- fluoro-4'-glucuronide phenyl)-1,3-benzoxazol-5-ol; 7-aIlyl-2-(3'-fluoro-4'-sulfate phenyt)-1,3-benzoxazol-5-ol; 7-aIlyl-2-(3'-fluoro-4'-hydroxyphenyl)-1,3-benzoxazoJ-5- glucuronide; 7-allyl-2-(3 -fluoro-4'-hydroxyphenyl)-1,3-benzoxazol-5-suifate; 7-allyl-2- (3'-fIuoro-4'-glucuronide phenyl)-1,3-benzoxazof-5-glucuronide; 7-allyl-2-(3'-fluoro-4'- glucuronide phenyl)-1,3-benzoxa7ol-5-sulfate; 7-alfyl-2-(3'-fluoro-4'-suffate phenyl)- 1,3-benzoxazol-5-glucuronide; 7-ally2-(3'-fluoro-4I-sulfate phenyl)-1,3-benzoxazol- 5-sulfate; 2-(3',5'-difJuoro-4'-glucuronide phenyl)-7-vinyH,3-benzoxazo!-5-ol; 2-(3',5'- dif!uoro-4'-sulfate phenyl)-7-vinyl-1,3-benzoxazol-5-oI; 2-(31,5'-difluoro-4I-hydroxy phenylH-vinyl-I.S-benzoxazol-S-glucuronideS'.S'-dffluorcMt-hydroxyphenyl- vinyl-1,3-benzoxazol-5-sulfete; 2-{31,5-difluoro-4'-glucuronlde phenyl)-7-vinyH ,3- benzoxazol-5-gluguronide; 2-(3',5'-difluoro-4'-glucuronide phenyl)-7-vinyl-1,3- benzoxazol-5-suIfate; 2-(3',5'-difluoro-4'-sulfiate phenyl)-7-vinyl-1,3-benzoxazol-5- glucuronide; 2-(3'I5I-difluoro-4'-sulfate phenyl)-7-vinyH,3-benzoxazo5-sulfete,• 2-(3- fluoro-4'-glucuronide phenyl)-7-(1-fluorovinyl)-1,3-benzoxazol-5-ol; 2-(3'-fluoro-4'- sulfate phenyOI-fluonovinyQ-I.S-benzoxazol-S-ol; 2-(3'-fluoro-4'-hydroxyphenyl)-7- (1 -fluorovinyl)-1,3-benzoxazol-5-glucuronide; 2-(3'-fIuoro-4-hydroxyphenyl)-7-(1 - fluorovinyl)-1,3-benzoxazol-5-sulfate; 2-(3'-fluoro-4'-glucuronide phenyl)-7-(1- fluorovinyl)-1,3-benzoxazoI-5-glucuronide; 2-{3'-fluoro-4'-glucuronide phenyl)-7-(1- fluorovinyl)-1,3-benzoxazol-5-sulfate; 2-(3'-fIuoro-4'-suIfate phenyl)-7-{1-fluorovinyl)- 1,3-benzoxazol-5-glucuronide; or 2-{3'-fluoro-4'-sulfate phenyl)-7-(1-fluorovJnyl)-1,3- benzoxazol-5-sutfate. In further embodiments, the compound is glucuronide derivative, a sulfate derivative, or a glucuronide-sulfate derivative of 2-(5-hydroxy- 1,3-benzoxazol-2-yl) benzene-1,4-diol; 3-(5-hydroxy-1,3-benzoxazo2-yl)benzene- 1,2-diol; 2-(3-fluoro-4-hydroxyphenyl)-1,3-benzoxazol-5-ol; 2-(3-chloro-4- hydroxyphenyl)-1,3-benzoxazol-5-ol; 2-(2-chloro4-hydroxyphenyl)-1,3-benzoxazol-5- ol; 2-(3-fluoro-4-hydroxyphenyI)-1,3-benzoxazoi-6-ol; 2-(3-terf-butyl-4- hydroxyphenyl)-1,3-benzoxazol-6-ol; 2-(6-hydroxy-1,3-benzoxazc2-yl)benzene-1,4- dioJ; 3-(6-hydroxy-1,3-benzoxazol-2-yl)benzene-1,2-dioI; 4-(6-hydroxy-1,3- benzoxazol-2-yl)benzene-1,2-diol; 2-(3-chloro-4-hydroxyphenyl)-1,3-benzoxazol-6-ol; 4-(5-hydroxy-1,3-benzoxazol-2-yl)benzene-1,3-dioI; 4-(6-hydroxy-1,3-benzoxazol-2- yl)benzene-1,3-diol; 6-chIoro-2-(3-fluoro-4-hydraxyphenyl)-1,3-benzoxazo!-5-of; 6- bromo-2-{3-fluoro-4-hydroxyphenyl)-1,3-benzoxazol-5-ol; 6-chloro-2-(4- hydroxyphenyl)-1,3-benzoxazol-5-ol; 5-chloro-2-(4-hydroxyphenyl)-1,3-benzoxazol-6- ol; 7-bromo-2-(3-fluoro-4-hydroxyphenyI)-1,3-benzoxazol-5-ol; 7-bromo-2-(2-fluoro-4- hydroxyphenyl}-1,3-benzoxazol-5-ol; 7-bromo-2-(2I3-dlfluoro-4-hydroxyphenyl)-1,3- bezoxazo5-ol; 2-(4-hydroxyphenyl)-7-vinyH,3-benzoxazol-5-ol.; 7-(1,2- dibromoethyl)-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol;7-{1-bromovinyl)-2-(4- hydroxyphenyl)-1,3-benzoxazol-5-ol; 7-ethynyl-2-(4-hydroxyphenyl)-1,3-benzoxazo!- 5-oi; 2-(4-hydroxyphenyl)-7-propyl-1,3-benzoxazol-5-ol; 7-butyl-2-(4-hydroxyphenyl)- 1,3-benzoxazol-5-ol; 7-cycfopentyl-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol; ethyl 5- hydroxy-2-(4-hydroxyphenyl)-1,3-benzoxazote-7-carboxylate; 2-{4-hydroxyphenyl)-7- phenyl-1,3-benzoxazol-5-oI; 2-(4-hydroxyphenyl)-7-methoxy-1,3-benzoxazol-5-ol; 7- ethyl-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol; 7-ethyl-2-(2-ethyl-4-hydroxypheny1)- 1,3-benzoxazol-5-ol; 5-hydroxy-2-(4-hydroxyphenyI)-1,3-benzoxazole-7- carbaldehyde; 7-(hydroxymethyl)-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-oJ; 7- (bromomethyl)-2-<4-hydroxyphenyl)-1,3-benzoxazol-5-ol; [5-hydroxy-2-(4- hydroxyphenyl)-1,3-benzoxazol-7-yl] acetonitrile; 7-(1-hydroxy-1-methylethyl)-2-(4- hydroxyphenyl)-1,3-benzoxazol-5-ol],- 2-(4-hydroxyphenyl)-7-isopropenyl-1,3- benzoxazol-5-ol; 2-{4-hydroxyphenyl)-7-isopropyf-1,3-benzoxazoI-5-ol]; 7-bromo-2- (4-hydroxy-3-(trifIuoromethy1)phenyl)-1,3-benzoxazo!-&-ol; 7-(2-furyl)-2-(4- hydroxyphenyl) -1,3-benzoxazol-5-ol; 2-(3-fluoro-4-hydroxyphenyl)- 7-(2-furyl)-1,3- benzoxazol-5-ol; 2-(4-hydroxyphenyl)- 7-thien-2-yH,3-benzoxazol-5-ol; 2-(4- hydroxyphenyl)-7-(1,3-thiazol-2-yl)-1,3-benzoxazol-5-ol; 2-(3-fluoro-4- hyd roxyphenyl)-5-hydroxy-1,3-benzoxazote-7-carbonitrile; 4-bromo-2-(4- hydroxyphenyl}-7-methoxy-1,3-benzoxazo5-ol;4,6-djbromo-2-(4-hydroxyphenyl)-7- methoxy-1,3-benzoxazol-5-ol; or 7-brom&-2-(3,5-difluoro-4-hydroxyphenyl)-1,3- benzoxazol-5-ol. The present invention provides prodrug derivatives of substituted benzoxazoles, which are useful as estrogenic agents. In some embodiments, the compounds of the invention are derivatives that possess one or more appended suJfate (i.e., -O-S(=O)2-O-H), unmodified or modified hexose (for example, glucuronide) or both. Suitable compounds that can be derivatized to form compounds of the present invention can be found in U.S. Patent Application Ser. No. 10/309,699 filed December 4,2002, which is incorporated herein by reference in its entirety. As used herein, sugar refers to at least monosaccharides having 5 to 6 carbon atoms such as pentoses, e.g., ribose, and hexoses, e.g., glucose, galactose or fructose. Sugar also includes dissacharides, i.e., sugars comprising two monosaccharides, such as sucrose, lactose and maltose. The sugar residue can be of a naturally or synthetically-modified form, including, for example, phosphates, acids and lactones. As used herein, the term hexose means a sugar containing six carbon atoms. Suitable hexoses include but are not limited to glucose, mannose, galactose and fructose, in both their straight chain and pyranose forms. Modified hexoses include naturally occurring derivatives of hexoses, for example, phosphates, and corresponding acid and lactone forms. For example, the term modified hexose includes gluconic acid, gluconolactone, glucuronic acid, amino derivates including Nacetyl derivatives, phosphoate derivatives, and the like. As used herein, the term glucuronide derivative, as applied to a specific compound, refers to a derivative of such compound where one or more hydroxyl groups of the compound have been replaced with a moiety of formula XX: As used herein, the term sulfate derivative, as applied to a specific compound, refers to a derivative of such compound where one or more hydroxyl groups of,the compound have been replaced with a moiety of formula -O-S(=O)2-OH. The term glucuronide-sulfate derivative, as applied to a specific compound, refers to a derivative of such compound where at least one hydroxyl group of the compound has been replaced with a moiety of formula XX, and at least one hydroxyl group of the compound has been replaced with a moiety of formula O-S(=O)2-O-H. The compounds of the present invention are substituted benzoxazole estrogenic agents, which have been derivatized to possess one or more appended moieties. After administration of the derivatized compound, the appended moieties are removed by endogenous enzymes to provide the underivatized compound. Such compounds are referred to here as metabolites of the compounds of the invention. As used in accordance with this invention, the term providing, with respect to providing a compound or substance covered by this invention, means either directly administering such a compound or substance, or administering a prodrug, derivative, or analog that will form the effective amount of the compound or substance within the body. As used in accordance with this invention, the term ERp selective ligand means that the binding affinity (as measured by ICso, where the ICso of 17p-estradiol is not more than 3 fold different between ERa and ERP) of the ligand to ERp is at least about 10 times greater than its binding affinity to ERa in a standard pharmacological test procedure that measures the binding affinities to ERa and ERp. It is preferred that the ERp selective ligand will have a binding affinity to ERp that is at least about 20 times greater than its binding affinity to ERa. It is more preferred that the ERp selective ligand will have a binding affinity to ERp that is at least about 50 times greater than its binding affinity to ERa. It is further preferred that the ERp selective ligand is non-uterotrophic and non-mammotrophic. As used in accordance with this invention, the term non-uterotrophic means producing an increase in wet uterine weight in a standard pharmacological test procedure of less than about 50% of the uterine weight increase observed for a maximally efficacious dose of 17p-estradiol or 17a-ethinyl-17p-estradiol in the same procedure. It is preferred that the increase in wet uterine weight will be less than about 25% of that observed for estradiol, and more preferred that the increase in wet uterine weight will be less than about 10% of that observed for estradiol. It is most preferred that the non-uterotrophic ERp selective ligand will not increase wet uterine weight significantly (p 0.05) compared with a control that is devoid of uterotrophic activity (e.g., vehicle). As used in accordance with this invention, the term non-mammotrophic means having activity that is <10% as efficacious as 17beta-estradiol at facilitating the development of Iqbular-alveolar end buds as assessed by histological examination. Examples of such determination by histological examination are well known in the art. See, for example, Harris, HA, et al., Endocrinology 144(10} 4241- 4249 (2003); Mulac-Jericevic, B., etal., Proc. Nati. Acad. S.ci. 100 (17) 9744-9749 (2003); Bocchinfuso, W.P., et al., Endocrinology 141(8) 2982-2994 (2002); and Lewis, B.C., et al., Toxicological Sciences 62,46-53 (2001), each of which is incorporated by reference herein in its entirety. This invention also provides the use of the disclosed derivatized ERp selective ligands in the treatment or inhibition of arthritis, inflammatory bowel disease, and endometriosis. More particularly, the derivatized ERp selective ligands are useful in the treatment or inhibition of rheumatoid arthritis, osteoarthritis or spondyloarthropathies; and Crohn's disease, ulcerative colitis, indeterminate colitis, infectious colitis, or ulcerafive proctitis. This invention further provides for the use of a derivatized ERp selective ligand in treating or inhibiting joint swelling or erosion; or treating or inhibiting joint damage secondary to arthroscopfc or surgical procedures. It is preferred that the ERp selective ligand is non-uterotrophic and non-mammotrophic. The present invention also provides the disclosed derivatized ERp selective ligands for use in lowering cholesterol, triglycerides, Lp(a), or LDL levels; inhibiting or treating hypercholesteremia, hyperlipidemia, cardiovascular disease, atherosclerosis, hypertension, peripheral vascular disease, restenosis, or vasospasm; or inhibiting .vascular wall damage from cellular events leading toward immune mediated vascular damage in a mammal in need thereof. Further, the disclosed derivatized ERp selective ligands are useful in providing cognition enhancement or neuroprotection; or treating or inhibiting senile dementias, Alzheimer's disease, cognitive decline, stroke, anxiety, or neurodegenerative disorders in a mammal in need thereof. The invention further provides the use of the disclosed ERp ligands for the treatment and inhibition of free radical induced disease states, vaginal or vulvar atrophy, atrophic vaginitis, vaginal dryness, pruritus, dyspareunia, dysuria, frequent urination, urinary incontinence, urinary tract infections, vasomotor symptoms, psoriasis or dermatitis, ischemia, reperfusion injury, asthma, pleurisy, multiple sclerosis, systemic lupus erythematosis, uveitis, sepsis, hemmorhagic shock, or type II diabetes, in a mammal in need thereof. The ERp selective ligands of the present invention of formula I are also useful in inhibiting conception in a mammal in need thereof. In some embodiments, the mammal is a human, e.g., a woman. The present invention further provides a pharmaceutical composition comprising a compound of formula I, as described hereinbefore, and a pharmaceutical carrier. The reagents used in the preparation of the compounds of this invention can be either commercially obtained or can be prepared by standard procedures described in the literature. The general preparation of compounds of formula I that can be derivatized by the addition of one or more moieties selected from sulfate and modified and unmodified hexoses, can be prepared according to the following synthetic Schemes In Scheme I, commercially available dimethoxy aniline (1) was treated with commercially available benzoyl chloride (2) in the presence of triethylamine to produce an amide (3). The required benzoyl chloride (2) was also prepared from commercially available benzoic acid (4) upon refluxing with thionyl chloride. The amide (3) was converted to the phenolic benzoxazole (5) upon treatment with pyridine hydrochloride at high temperature (200 °C). In Scheme II, commercially available nitre-phenol (6) was brominated with Br2/NaOAc in acetic acid to produce bromo-phenol (7). Catalytic hydrogenation of (7) with Ra-Ni in EtOAc afforded aniline (8). Coupling of (8) with benzoyl chloride (9) (commercially available, or prepared from the corresponding benzoic acid and thionyl chloride) in the presence of pyridine produced amide-ester (10). Conversion of (10) to benzoxazole (11) was accomplished under acidic conditions (p-toluenesulfonic acid) at high temperature (150 °C). Demethylation of (11) with boron tribromide in dichloromethane afforded the phenolic benzoxazole (12). In Scheme III, the aniline (8) was converted to benzoxazole (14) upon treatment with benzoic acid (13) and boric acid in p-xylene at high temperature (150 °C). Demethylation of (14) with boron tribromide in dichloromethane produced the phenolic benzoxazole (15). In Scheme IV, nitration of (16) with nitric acid in acetic acid produced (17), which was reduced with hydrogen in the presence of Ra-Ni to afford aniline (18). Aniline (18) was converted to benzoxazole (19) in a similar manner as described in Scheme II, with the exemption that the demethylation step was accomplished with pyridine hydrochloride at high temperature (200 °C). In Scheme V, the hydroxyl groups of benzoxazole (20) were protected either as the siiyl ethers (21) (R3 = Me3C(CH3)2Si) with terf-butyldimethylsilyl chloride/imidazole/4-dimethylaminopyridine in N.N-dimethylformamide, or as the esters (21) (R3 = CH3CO) with acetic anhydride/4-dimethylaminopyridine in dichloromethane. Benzoxazoles (20) and (21) were coupled with a variety of tin reagents (i.e., tributyl(vinyl)tin, tributyl(allyl)tin, tributyl(2-furyl)tin, boronic acids or zinc chlorides in the presence of a palladium catalyst [i.e., dichlorobis(tri-otolylphosphine) palladium(H) or tetrakis(triphenylphosphine) palladium(O)] in p-xylene, toluene, tetrahydrofuran, dimethoxymethane or 1,2-dimethoxyethane, with the presence of a base (i.e., Na2CO3) for the boronic acid coupling reaction, at temperatures in the range of 20 °C to 150 °C, to produce benzoxazoles (22) and (23). Deprotection of the silyl ethers of (22) (R3 = Me3C(CH3)2Si) with hydrofluoric acid (48 wt.% in water) or tetrabutylammonium fluoride produced benzoxazole (24). Saponification of (22) (R3= CH3CO) with potassium carbonate in dioxane produced. benzoxazole (24). Benzoxazole 23 (R = CH3) was demethylated with boron tribromide in dichloromethane or pyridine hydrochloride at high temperature (200 °C) to afford benzoxazole (24). In Scheme VI, benzoxazole (24) was treated with n-butyllithium at low temperatures (-78 °C) followed by the addition of an electrophile (i.e. CNCO2Et, Ph(CH3)NCHO, Etl, etc.) to produce compound (25). Deprotection of (25) with boron tribromide (R = CH3) or tetrabutyiammonium fluoride (R = Me3C(CH3)2Si) afforded benzoxazole (26) [R = CHO, CO2Et, CH2CH3f C(CH3)2OH]. The tertiary alcohol (25) (R = C(CH3)OH) was treated with pyridine nydrochloride at high temperature (200 °C) to produce 1-methyl-vinyl benzoxazole (27). Reduction of (27) with H2 / Pd-C afforded the isopropyl analog (28). In Scheme VII, reduction of the benzoxazole (29) with sodium borohydride in methanol produced alcohol (30). Treatment of (30) with boron tribromide in CHt for 1 hour furnished benzoxazole (31), while prolonged (18 hours) treatment afforded bromide (32). Bromide (32) was converted to acetonitrile (33) upon treatment with potassium cyanide and 18-crown-6 ether in N,N-dimethylforrnamide. In Scheme VIII, bromo-benzoxazole (35) (R = CH3) was first treated with copper(l) cyanide in DMF to produce the corresponding aryl-nitrile, which upon treatment with boron tribromide afforded benzoxazole (36). Benzoxazole (36) was also prepared from a second synthetic Route, where the bromo-benzoxazole (35) was treated with zinc cyanide in the presence of a palladium catalyst [i.e. tetrakis(triphenylphosphine)palladiurn(0)] to afford the corresponding aryl-nitrile, which upon demethylation with boron tribromide produced benzoxazole (36). Benzoxazole (35) (R = H) was treated with copper (I) bromide, and freshly prepared sodium methoxide in DMF to produce methoxy-benzoxazote (37). Bromination of (37) with N-bromosuccinimide in acetonitrile afforded the monobromo benzoxazole (38) (major product) and the dibromobenzoxazole (39) (minor product). Glucuronide, sulfate, and glucuronide-sulfate derivatives of the compounds prepared by the procedures of Schemes I-VI1I can be prepared according to Schemes IX and X: PAPS = 3'-phosphoadenosine-5'-phosphosulfate In addition, the glucuronide, sulfate and glucuronide-sulfate derivatives of the invention can be prepared according to standard organic chemical synthetic techniques. For example, functional groups (e.g., ons or more hydroxyl groups) of compounds prepared in accordance with Schemes (-V11I can be protected by standard techniques, and then a free hydroxyl can be coupled to a unmodified or modified hexose (e.g., a glucuronide) or a sulfonic acid group, to yield a compound of the invention. Suitable protecting groups for use in such syntheses can be found in, for example, Greene, T.W., and Wuts, P.G.M., Protective Groups in Organic Synthesis, 2nd ed., New York: John Wiley & Sons, N.Y. 1991. PHARMACOLOGICAL TEST PROCEDURES Standard pharmacological test procedures are readily available to determine the activity profile of a given test compound. The following briefly summarizes several representative test procedures and may include data for representative compounds of the invention. All assays, except the radioligand binding assay, can be used to detect estrogen receptor agonist or antagonist activity of compounds. In general, estrogen receptor agonist activity is measured by comparing the activity of the compound to a reference estrogen (e.g., 17p-estradiol, 17a-ethinyl, 17p-estradiol, estrone, diethylstilbesterol, etc). Estrogen receptor antagonist activity is generally measured by co-treating the test compound with the reference estrogen and comparing the result to that obtained with the reference estrogen alone. Standard pharmacological test procedures for SERMs are also provided in US Patents 4,418,068 and 5,998,402, which are hereby incorporated by reference. Evaluation of binding affinities to ERg and ERB Representative examples of metabolites of compounds of the invention were evaluated for their ability to compete with 17p-estradiol for both ERa and ERp in a conventional radioligand binding assay. This test procedure provides the methodology for one to determine the relative binding affinities for the ERa or ERp receptors. The procedure used is briefly described below. Preparation of receptor extracts for characterization of binding selectivity. The ligand binding domains, conveniently defined here as all sequence downstream of the DNA binding domain, were obtained by PCR using full length cDNA as templates and primers that contained appropriate restriction sites for subcloning while maintaining the appropriate reading frame for expression. These templates contained amino acids Maso-Vsss of human ERa [Green, et al., Nature 320:134-9 (1986)] and M2u-Qs3o of human ERp [Ogawa, et al., Biochemical & Biophysical Research Communications 243:122-6 (1998)]. Human ERp was cloned into pET15b (Novagen, Madison, Wl) as a Nco1-BamH1 fragment bearing a C-terminal Flag tag. Human ERa was cloned as for human ERp except that an N-terminal His tag was added. The sequences of all constructs used were verified by complete sequencing of both strands. BL21(DE3) cells were used to express the human proteins. Typically, a 10 ml overnight culture was used to inoculate a 1 L culture of Luria-Bertani (LB) medium containing 100 ng/mL of ampicillin. After incubation overnight at 37 °c, isopropyl-p-D-thiogulactoside (IPTG) was added to a final concentration of 1 mM and incubation proceeded at 25 °C for 2 hours. Cells were harvested by centrifugation (1500 x g), and the pellets washed with and resuspended in 100 mL of 50 mM Tris- Cl (pH 7.4) and 150 mM NaCl. Cells were lysed by passing twice through a French press at 12000 psi. The lysate was clarified by centrifugation at 12,000 x g for 30 minutes at 4 °C and stored at -70 °C. Evaluation of extracts for specific fHJ-estradiol binding. Dulbecco's phosphate buffered saline (1x final concentration Gibco; nitrogen, Carlsbad, CA) supplemented with 1 mM ethylenediamine-tetraacetic acid (EDTA) was used as the assay buffer. To optimize the amount of receptor to use in the assay, [3HJ-17pestradiol (final concentration = 2 nM; New England Nuctear (NEN); Perkin Elmer, Shelton, CT) ± 0.6 uM diethlystilbestrol and 100 jtL of various dilutions of the E. coll lysate were added to each well of a high binding masked microtiter plate (EG&G Wallac). The final assay volume was 120 fiL and the concentration of DMSO was <, 1 %. After incubation at room temperature for 5-18 hours, unbound material was aspirated and the plate washed three times with approximately 300 uL of assay buffer. After washing, 135 ML of scintillation cocktail (Optiphase Supermix, EG&G Wallac) was added to the wells, and the plate was sealed and agitated for at least 5 minutes to mix scintillant with residual wash buffer. Bound radioactivity was evaluated by liquid scintillation counting (Plus EG&G Wallac, Microbeta). After determining the dilution of each receptor preparation that provided maximum specific binding, the assay was further optimized by estimating the ICgo of unlabelled 17p-estradiol using various dilutions of the receptor preparation. A final working dilution for each receptor preparation was chosen for which the ICso of unlabelled 17p-estradiol was 2-4 nM. Ligand binding competition test procedure. Test compounds were initially solubilized in dimethylsulfoxide (DMSO) and the final concentration of DMSO in the binding assay was 1 %. Eight dilutions of each test compound were used as an unlabelled competitor for [3HJ-17(5-estradiol. Typically, a set of compound dilutions were tested simultaneously on human ERa and ER0. The results were plotted as measured disintegrated per minute (DPM) vs. concentration of test compound. For dose-response curve fitting, a four parameter logistic model on the transformed, weighted data was fitted and the ICso was defined as the concentration of compound that decreased maximum [3HJ-estradiol binding by 50%. Binding affinities for ERa and ERp (as measured by ICSO) for representative metabolites of compounds of the invention are shown in Table 1. Table 1: ER Binding Affinities of Representative Metabolites of Compounds The results obtained in the standard pharmacologic test procedure described above demonstrate that the tested compounds bind both subtypes of the estrogen receptor. The ICsoS are generally lower for ER0, indicating that these compounds are preferentially ERp selective ligands, but are still considered active at ERa. The compounds will exhibit a range of activity based, at least partially, on their receptor affinity selectivity profiles. Since the metabolites of the compounds of the invention bind ERp with higher affinity than ERa, the compounds of the invention will be useful in treating or inhibiting diseases than can be modulated via ERp. Additionally, since each receptor ligand complex is unique and thus, its interaction with various coregulatory proteins is unique, the compounds of this invention will display different and unpredictable activities depending on cellular context For example, in some cell types, it is possible for a compound to behave as an estrogen receptor agonist while in other tissues, as an estrogen receptor antagonist Compounds with such activity have sometimes been referred to as SERMs (Selective Estrogen Receptor Modulators). Unlike many estrogens, however, many of the SERMs do not cause increases in uterine wet weight These compounds are antiestrogenic in the uterus and can completely antagonize the trophic effects of estrogen receptor agonists in uterine tissue. These compounds, however, act as estrogen receptor agonists in the bone, cardiovascular, and central nervous systems. Due to this tissue selective nature of these compounds, they are useful in treating or inhibiting in a mammal disease states or syndromes that are caused or associated with an estrogen deficiency (in certain tissues such as bone or cardiovascular) or an excess of estrogen (in the uterus or mammary glands). In addition, metabolites of compounds of this invention have the potential to behave as estrogen receptor agonists on one receptor type while behaving as estrogen receptor antagonists on the other. For example, it has been demonstrated that compounds can antagonize the action of 17{3-estradiol via ER|3 while exhibiting estrogen receptor agonist activity with ERcc [Sun, et al., Endocrinology 140:800-804 (1999)]. Such ERSAA (Estrogen Receptor Selective Agonist Antagonist) activity provides for pharmacologically distinct estrogenic activity within this series of compounds Regulation of metallothionein II mRNA Estrogens acting through ERp, but not ERa, can upregulate metallothionein II mRNA levels in Saos-2 cells, as described by Harris et al. [Endocrinology 142(2): 645-652 (2001)]. Results from this test procedure can be combined with results from the test procedure described below (ERE reporter test procedure) to generate a selectivity profile for metabolites of compounds of this invention (see also, WO 00/37681). Data for representative metabolites of compounds of the invention are shown in Table 2. Table 2: Regulation of Metallothionein-ll mRNA in Saos-2 Cells EvaJuation of test compound using an ERE-reoorter test procedure in MCF-7 breast cancer cells Stock solutions of test compounds (usually 0.1 M) are prepared in DMSO and then diluted 10 to 100-fold with DMSO to make working solutions of 1 or 10 mM. The DMSO stocks are stored at either 4 °C (0.1 M) or-20 °C (< 0.1M). MCF-7 cells are passaged twice a week with growth medium [D-MEM/F-12 medium containing 10% (v/v) heat-inactivated fetal bovine serum, 1% (v/v) Penicillin-Streptomycin, and 2 mM gfutaMax-1]. The cells are maintained in vented flasks at 37 °C inside a 5% CO2/S5% humidified air incubator. One day prior to treatment, the cells are plated with growth medium at 25,000 cells/well into 96 well plates and incubated at 37 °C overnight The cells are infected for 2 hours at 37 °C with 50 nl/well of a 1:10 dilution of adenovirus 5-ERE-tk-luciferase in experimental medium [phenol red-free D-MEM/F- 12 medium containing 10% (v/v) heat-inactived charcoal-stripped fetal bovine serum, 1% (v/v) Penicillin-Streptomycin, 2 mM glutaMax-1, and 1 mM sodium pyruvate]. The wells are then washed once with 150 n\ of experimental medium. Finally, the cells are treated for 24 hours at 37 °C in replicates of 8 wells/treatment with 150 I/well of vehicle (< 0.1 % v/v DMSO) or test compound that is diluted 1000-fold into experimental medium. Initial screening of test compounds is done at a single dose of 1 \M that is tested alone (estrogen receptor agonist mode) or in combination with 0.1 nM 17pestradiol (ECso; estrogen receptor antagonist mode). Each 96 well plate also includes a vehicle control group (0.1% v/v DMSO) and an estrogen receptor agonist control group (either 0.1 or 1 nM 17p-estradiol). Dose-response experiments are performed in either the estrogen receptor agonist and/or estrogen receptor antagonist modes on active compounds in log increases from 10~14 to 105 M. From these dose-response curves, ECsQ and ICso values, respectively, are generated. The final well in each treatment group contains 5 1 of 3 x 105 M ICI-182,780 (106 M final concentration) as an estrogen receptor antagonist control. After treatment, the cells are lysed on a shaker for 15 minutes with 25 uJ/well of 1X cell culture lysis reagent (Promega Corporation, Madison, Wl). The cell lysates (20 uJ) are transferred to a 96 well luminometer plate, and luciferase activity is measured in a MicroLumat LB 96 P luminometer (EG & G Berthold; Perkin Elmer, Shelton, CT) using 100 nt/well of luciferase substrate (Promega Corporation). Prior to the injection of substrate, a 1 second background measurement is made for each well. Following the injection of substrate, luciferase activity is measured for 10 seconds after a 1 second delay. The data are transferred from the luminometer to a Macintosh personal computer and analyzed using the JMP software (SAS Institute, Gary, NC); this program subtracts the background reading from the luciferase measurement for each well and then determines the mean and standard deviation of each treatment. The luciferase data are transformed by logarithms, and the Huber Mestimator is used to down-weight the outlying transformed observations. The JMP software is used to analyze the transformed and weighted data for one-way ANOVA (Dunnetfs test). The compound treatments are compared to the vehicle control results in the estrogen receptor agonist mode, or the positive estrogen receptor agonist control results (0.1 nM 17p-estradiol) in the estrogen receptor antagonist mode. For the initial single dose experiment, if the compound treatment results are significantly different from the appropriate control (p<0.05), then the results are reported as the percent relative to the 17p-estradiol control [i.e., ((compound - vehicle controf)/(17p-estradiol control- vehicle control)) x 100]. The JMP software is also used to determine the ECso and/or ICso values from the non-linear dose-response curves. Evaluation of uterotrophicacfiyitv Uterotrophfc activity of a test compound can be measured according to the following standard pharmacological test procedures. Procedure 1: Sexually immature (1d days of age) Sprague-Dawley rats are obtained from Taconfc (Germantown, NY) and provided unrestricted access to a casein-based diet (Purina Mills 5K96C, Purina Mills, LLC, St Louis, MO) and water. On day 19, 20 and 21, the rats are dosed subcutaneously with 17a-ethinyl-17pestradiol (0.06 ng/rat/day), test compound or vehicle (50% DMSO/50% Dulbecco's PBS). To assess estrogen receptor antagonist activity, compounds are coadministered with 17a-ethinyH7p-esiradio! (0.06 u.g/rat/day). There are six rats/group and they are euthanized app'oximately 24 hours after the last injection by CO2 asphyxiation and pneumothorax. Uteri are rernoved and weighed after trimming associated fat and expressing any internal fluid. A tissue sample can also be snap frozen for analysis of gene expression (e.g., complement factor 3 mRNA). Results obtained from representative metabolites of compounds of the invention are shown in Procedure 2: Sexually immature (18 days of age) 129 SvE mice are obtained from Taconic and provided unrestricted access to a casein-based diet (Purina Mills® 5K96C) and water. On day 22, 23,24 and 25, the mice are dosed subcutaneously with compound or vehicle (com oil). There are six mice/group and they are euthanized approximately 6 hours after the last injection by CO2 asphyxiation and pneumothorax. Uteri are removed and weighed after trimming associated fat and expressing any internal fluid. The following results (Table 4) were obtained for representative metabolites of compounds from the invention. Evaluation of osteoporosis and lipid modulation (cardioprotection) Female Sprague-Dawley rats, ovariectomized or sham operated, are obtained 1 day after surgery from Taconic (weight range 240 - 275 g). They are housed 3 or 4 rats/cage in a room on a 12/12 (light/dark) schedule and provided with food (Purina Mills® 5K96C) and water ad libitum. Treatment for all studies begin 1 day after arrival and rats are dosed 7 days per week as indicated for 6 weeks. A group of age matched sham operated rats not receiving any treatment serve as an intact, estrogen replete control group for each study. All test compounds are prepared in a vehicle of 50% DMSO (JT Baker, Phillipsburg, NJ) / 1x Dulbecco's phosphate saline (Gibco BRL, Grand Island, NY) at defined concentrations so that the treatment volume is 0.1 mL/100 g body weight. 17p-estradiol is dissolved in corn oil (20 yg/mL) and delivered subcutaneously, 0.1 mL/rat. All dosages are adjusted at three week intervals according to group mean body weight measurements, and given subcutaneously. Five weeks after the initiation of treatment and one week prior to the termination of the study, each rat is evaluated for bone mineral density (BMD). The total and trabecular density of the proximal tibia are evaluated in anesthetized rats using an XCT-960M peripheral quantitative computerized tomography (pQCT); Stratec Medizintechnik, Pforzheim, Germany). The measurements are performed as follows: Fifteen minutes prior to scanning, each rat is anesthetized with an intraperitoneal injection of 45 mg/kg ketamine, 8.5 mg/kg xylazine, and 1.5 mg/kg acepromazine. The right hind limb is passed through a polycarbonate tube with a diameter of 25 mm and taped, to an acrylic frame with the ankle joint at a 90° angle and the knee joint at 180°. The polycarbonate tube is affixed to a sliding platform that maintains it perpendicular to the aperture of the pQCT. The platform is adjusted so that the distal end of the femur and the proximal end of the tibia is in the scanning field. A two dimensional scout view is run for a length of 10 mm and a line resolution of 0.2 mm. After the scout view is displayed on the monitor, the proximal end of the tibia is located. The pQCT scan is initiated 3.4 mm distal from this point The pQCT scan is 1 mm thick, has a voxel (three dimensional pixel) size of 0.140 mm, and consists of 145 projections through the slice. After the pQCT scan is completed, the image is displayed on the monitor. A region of interest including the tibia but excluding the fibula is outlined. The soft tissue is mathematically removed using an iterative algorithm. The density of the remaining bone (total density) is reported in mg/cm3. The outer 55% of the bone is mathematically peeled away in a concentric spiral. The density of the remaining bone (Trabecular density) is reported in mg/cm3. One week after BMD evaluation the rats are euthanized by CO2 asphyxiation and pneumothorax, and blood is collected for cholesterol determination. The uteri also are removed and weighed after trimming associated fat and expressing any luminal fluid. Total cholesterol is determined using a Boehringer-Mannheim Hitachi 911 clinical analyzer (Roche, Alameda, CA) using the Cholesterol/HP kit. Statistics were compared using one-way analysis of variance with Dunnef s test. The following results were obtained with representative metabolites of compounds of the invention (Table 5). Table 5: Evaluation of Bone Mineral Density in the Ovariectomized Rat After Administration of Select Metabolites of Compounds of the 1/nventJon Porcine aortas are obtained from an abattoir, washed, transported in chilled PBS, and aortic endothelial cells are harvested. To harvest the cells, the intercostal vessels of the aorta are tied off and one end of the aorta clamped. Fresh, sterile filtered, 0.2% collagenase (Sigma Type I) is placed in the vessel and the other end of the vessel then clamped to form a closed system. The aorta is incubated at 37 °C for 15-20 minutes, after which the collagenase solution is collected and centrifuged for 5 minutes at 2000 x g. Each pellet is suspended in 7 ml of endothelial cell culture medium consisting of phenol red free DMEM/Ham's F12 media supplemented with charcoal stripped FBS (5%), NuSerum (5%), L-glutamine (4mM), penicillinstreptomycin (1000U/ml, 100ng/ml) and gentamycin (75ng/ml), seeded in 100mm petri dish and incubated at 37 °C in 5% CO2. After 20 minutes, the cells are rinsed with PBS and fresh medium added, this was repeated again at 24 hours. The cells are confluent after approximately 1 week. The endothelial cells are routinely fed twice a week and, when confluent, trypsinized and seeded at a 1:7 ratio. Cell mediated oxidation of 12.5 g/mL LDL is allowed to proceed in the presence of the compound to be evaluated (5 piM) for 4 hours at 37 °C. Results are expressed as the percent inhibition of the oxidative process as measured by the TEARS (thiobarbituric acid reactive substances) method for analysis of free aldehydes {Yagi K., Biochemical Medicine 15: 212-6 (1976)]. Progesterone receptor mRNA regulation standard pharmacological test procedure This test procedure can be used to evaluate the estrogenic or antiestrogenic activity of compounds from this invention [Shughrue, et al., Endocrinology 138:5476- 5484 (1997)]. Data for representative metabolites of compounds of the invention are shown in Table 6. The effect of test compounds on hot flushes can be evaluated in a standard pharmacological test procedure that measures the ability of a test compound to blunt the increase in tail skin temperature, which occurs as morphine-addicted rats are acutely withdrawn from the drug using naloxone [Merchenthaler, et al., Maturitas 30: 307-1 6 (1 998)]. It can also be used to detect estrogen receptor antagonist activity by co-dosing test compound with the reference estrogen. The following data were obtained from representative metabolites of compounds of the invention (Table 7). Table 7: Effect of Select Metabolites of Compounds of the Invention in a Rat Model of Hot Flush Evaluation of vasomotor: function in isolated rat aortic rings Sprague-Dawley rats (240-260 grams) are divided into 4 groups: 1. Normal non-ovariectomized (intact) 2. Ovariectomized (ovex) vehicle treated 3. Ovariectomized 17B-estradioI treated (1 mg/kg/day) 4. Ovariectomized animals treated with test compound (various doses) Animals are Ovariectomized approximately 3 weeks prior to treatment. Each animal receives either 17-p estradiol sulfate (1 mg/kg/day) or test compound suspended in distilled, deionized water with 1% tween-80 by gastric gavage. Vehicle treated animals received an appropriate volume of the vehicle used in the drug treated groups. Animals are euthanized by CO2 inhalation and e sanguination. Thoracic aortae are rapidly removed and placed in 37 °C physiological solution with the following composition (mM): NaCI (54.7), KG! (5.0), NaHCO3 (25.0). MgCI2 2H2O (2.5), D-glucose (11.8) and CaCI2 (0.2) gassed with COO2, 95%/5% for a final pH of 7.4. The advantitia is removed from the outer surface and the vessel is cut into 2- 3 mm wide rings. The rings are suspended in a 10 mL tissue bath with one end attached to the bottom of the bath and the other to a force transducer. A resting tension of 1 gram is placed on the rings. The rings are equilibrated for 1 hour, signals are acquired and analyzed. After equilibration, the rings are exposed to increasing concentrations of phenylephrine (1fJ-8to 1(HM) and the tension recorded. The baths are then rinsed 3 times with fresh buffer. After washout, 200 mM nitro-L-arginine-methyl ester (LNAME) is added to the tissue bath and equilibrated for 30 minutes. The phenylephrine concentration response curve is then repeated. Evaluation of cardioprotective activity Apolipoprotein E-deficient C57/B1J (apo E KO) mice were obtained from Tacontc. All animal procedures were performed under strict compliance to Institutional Animal Care and Use Committee (IACUC) guidelines. Ovariectomized female apo E KO mice, 4-7 weeks of age, were housed in shoe-box cages and allowed free access to food and water. The animals were randomized by weight into groups (n=12-15 mice per group). The animals were dosed with test compounds or estrogen (17p-estradiol sulfate at 1 mgykg/day) in the diet using a Precise-dosing Protocol, where the amount of diet consumed is measured weekly, and the dose adjusted accordingly, based on animal weight The diet used was a Western-style diet (57U5) that is prepared by Purina and contains 0.50% cholesterol, 20% lard and 25IU/KG Vitamin E. The animals were dosed/fed using this paradigm for a period of 12 weeks. Control animals are fed the Western-style diet and receive no compound. At the end of the study period, the animals were euthanized and plasma samples obtained. The hearts were perfused in situ, first with saline and then with neutral buffered 10% formalin solution. For the determination of plasma lipids and lipoproteins, total cholesterol and triglycerides are determined using enzymatic methods with commercially available kits from Boehringer Mannheim (Roche, Alameda, CA) and Wako Biochemicals (Osaka, Japan), respectively, and analyzed using the Boehringer Mannheim Hitachi! -a 911 Analyzer. Separation and quantification of plasma lipoproteins were performed using FPLC size fractionation. Briefly, 50-100 mL of serum was filtered and injected into Superose® 12 and Superose® 6 columns connected in series and eluted at a constant flow rate with 1 mM sodium EDTA and 0.15 M NaCl. Areas of each curve representing Very Low Density Lipoprotein (VLDL), (LDL) and High Density Lipoprotein (HDL) were integrated using Waters Millennium™ software, and each lipoprotein fraction quantified by multiplying the Total Cholesterol value by the relative percent area of each respective chromatogram peak. For the quantification of aortic atherosclerosis, the aortas were carefully isolated and placed in formalin fixative for 48-72 hours before handling. Atherosclerotic lesions were identified using Oil Red O staining. The vessels were briefly destained, and then imaged using a Nikon SMU800 microscope fitted with a Sony 3CCD video camera system in concert with IMAQ Configuration Utility (National Instrument, Austin, TX) as the image capturing software. The lesions were quantified en face along the aortic arch using a custom threshold utility software package (Coleman Technologies, Surrey, BC, Canada). Automated lesion assessment was performed on the vessels using the threshold function of the program, specifically on the region contained within the aortic arch from the proximal edge of the brachiocephalic trunk to the distal edge of the left subclavian artery. Aortic atherosclerosis f data were expressed as percent lesion involvement strictly within this defined luminal Evaluation of cognition enhancement Ovariectomized rats (n=50) are habituated to an Sarm radial arm maze for 10-minute periods on each of 5 consecutive days. Animals are water-deprived prior to habituation and testing. A100 uL aliquot of water placed at the ends of each arm serves as reinforcement Acquisition of a win-shift task in the radial arm maze is accomplished by allowing the animal to have access to one baited arm. After drinking, the animal exits the arm and re-enters the central compartment, where it now has access to the previously visited arm or to a novel arm. A correct response is recorded when the animal chooses to enter a novel arm. Each animal is given 5 trials per day for 3 days. After the last acquisition trial, the animals are assigned to one of the following 4 groups: 1. Negath/e controls: injected with 10% DMSO/ sesame oil vehicle once daily for 6 days (1 mL/kg, SC) 2. Positive controls: injected with 17p-estradiol benzoate for 2 days and tested 4 days after the second injection (17p-estradiol benzoate at 10 pg/0.1 mL per rat) 3. Estradiol: injected with 17p-estradiol will be injected daily for 6 days (20 jjg/kg, SC) 4. Test compound: injected daily for 6 days (doses vary). All injections will begin after testing on the last day of acquisition. The last injection for groups 1, 3, and 4 will take place 2 hours before testing for working memory. The test for working memory is a delayed non-matching-to-sample task (DNMS) utilizing delays of 15, 30, or 60 seconds. This task is a variation of the acquisition task in which the rat is placed in the central arena and allowed to enter one arm as before. A second arm is opened once the rat traverses halfway down the first arm, and again the rat is required to choose this arm. When it has traveled halfway down this second ami, both doors are closed and the delay is instituted. Once the delay has expired, both of the original two doors, and a third novel door, are opened simultaneously. A correct response is recorded when the animal travels halfway down the third, novel arm. An incorrect response is recorded when the animal travels halfway down either the first or second arms. Each animal will receive 5 trials at each of the three delay intervals for a total of 15 trials per subject. Evaluation of effect on pleurisy The ability to reduce the symptoms of experimentally-induced pleurisy in rats can be evaluated according to the procedure of Cuzzocrea S., et al. [Endocrinology 141 (4): 1455-63 (2000)]. Evaluation of protection against glutamate-lnduced cytotoxicity (neuroprotection) The neuroprotective activity of compounds of this invention, or metabolites V. thereof, can be evaluated in an in vitro standard pharmacological test procedure using glutamate challenge (Zaulyanov, et al., Cellular & Molecular Neurobiology 19: 705-18 (1999); Prokai, etal., Journal of Medicinal Chemistry 44:110-4 (2001)]. Evaluation in the Mammary End Bud Test Procedure by Histological Examination Estrogens are required for full ductal elongation and branching of the mammary ducts, and the subsequent development of lobulo-alveolar end buds under the influence of progesterone. The non-mammotrophic activity of compounds can be determined by histological assessment of their ability to facilitate the development of lobular-alveolar end buds. Examples of such determination by histological examination are well known in the art. See, for example, Harris, H.A., et al., Endocrinology 144(10): 4241-4249 (2003); Mulac-Jericevic, B., et al., Proc. Natl. Acad. Sci. 100(17): 9744-9749 (2003); Bocchinfuso, W.P., et al., Endocrinology 141(3): 2982-2994 (2002); and Lewis, B.C., et al., Toxicological Sciences 62:46-53 (2001), each of which is incorporated by reference herein in its entirety. In the context of the present invention, a compound is considered non-mammotrophic if it has activity that is <10% as efficacious as 17beta-estradiol at facilitating the development of lobular-alveolar end buds as assessed by histological examination. Evaluation in the HLA Rat Standard Pharmacological Test Procedure for inflammatory bowel disease Representative metabolites of compounds of the invention were evaluated in the HLA rat standard pharmacological test procedure, which emulates inflammatory bowel disease in humans. The following briefly describes the procedure used and results obtained. Male HLA-B27 rats were obtained from Taconic and provided unrestricted access to food (PMI Lab Diet 5001, Purina Mills, Inc., St Louis) and water. Stool qualify was observed daily and graded according to the following scale: Diarrhea = 3; soft stool - 2; normal stool = 1. At the end of the study, serum was collected and stored at -70 °C. A section of colon was prepared for histological analysis and an additional segment was analyzed for myeloperoxidase activity. In Study A, rats (22-26 weeks old) were dosed subcutaneously once per day for seven days with one of the regimens listed below. There were five rats in each group and the last dose was administered two hours before euthanasia. Vehicle (50% DMSO/50% Dulbecco's PBS) Example 24 (50 mg/kg) The results from Study A are shown in Table 8. Rats dosed with vehicle continued to have diarrhea throughout the course of the study. Stool quality was improved in rats treated with Example 24. Table 8: Evaluation 'of Stool Character of HLA Rats Treated Subcutaneously for 5 Days With Representative Compounds of the Invention In Study B, rafe (8-10 weeks old) were dcsed orally for twenty-six days as follows: • Vehicle (2% Tween-8070.5% methylcellulose) • Example 25 (10 mg/kg from days 1-14; then increased to 20 mg/kg at day 15) • Example 34 (10 mg/kg) The following results were obtained (Table 9) and show that stool character improved in all rats treated with representative metabolites of compounds of the invention. Hi'stoloqical analysis. Colonic tissue was immersed in 10% neutral buffered formalin. Each specimen of colon was separated into four samples for evaluation. The formalin-fixed tissues were processed in a Tissue-Tek vacuum infiltration processor (Miles, Inc; West Haven, Connecticut) for paraffin embedding. The samples were sectioned at 5 urn and then stained with hematoxyiin and eosin (H&E) for blinded histologic evaluations using a scale modified after Boughton-Smith. After the scores were completed, the samples were unblinded, and data were tabulated and analyzed by ANOVA linear modeling with multiple mean comparisons. Sections of colonic tissue were evaluated for several disease indicators and given relative scores. As shown in Table (11) (a composite of two subcutaneous dosing studies, including Study A), Example 24 is effective in reducing several measurements of tissue injury. Intestinal tissue from Study B (see above) was also examined histotogically. As shown below (Table 12), both compounds significantly reduced total disease score. Table 12: Histological Scoring of Disease Severity in the Colon from Animals Treated Orally for 4 weeks with Representative Metabolites of Compounds from the Invention Intestinal tissue from Study C (see above) was also examined histologically. As shown below (Table 13), Example 24 significantly reduced total disease score. The scores of Example 21 on all disease parameters, although not statistically significant, were lower than corresponding scores from vehicle-treated rats. Table 13: Histological Scoring of Disease Severity in the Colon from Animals Treated Orally for 7 Weeks with Representative Metabolites of Compounds from the Lewis rat assay of adjuvant-induced arthritis. Sixty, female, 12 weeks old, Lewis rats are housed according to standard facility operating procedures. They receive a standard regimen of food and water ad libitum. Each animal is identified by a cage card indicating the project group and animal number. Each rat number is marked by indelible ink marker on the tail. At least 10-21 days before study, they are anesthetized and ovariectomized by standard aseptic surgical techniques. Freund's Adjuvant-Complete (Sigma Immuno Chemicals, SL Louis, MO) is used to induce arthritis, each mL containing 1 mg Mycobacterium tuberculosis heat killed and dried, 0.85 mL mineral oil and 0.15 mL mannide monooleate (Lot No. 084H8800). The following are examples of two test procedures. Inhibition test procedure: Thirty rats are injected intradermally with 0.1 mL of Freund's Adjuvant-Complete at the base of the tail. The animals are randomized to four groups, each group containing six rats. Each day, the groups receive vehicle (50% DMSO (JT Baker, Phillipsburg, NJ) / 1x Dulbecco's phosphate saline (GibcoBRL, Grand Island, NY)) or test compound (administered subcutaneously). All rats began treatment on Day 1. Data for representative metbolites of compounds of the invention are shown in Table 14. Treatment test procedure: Thirty rats are injected intradermally with 0.1 mL of Freund's Adjuvant-Complete at the base of the tail. The animals are randomized to four groups, each group containing six rats. Each day, the groups receive vehicle (50% DMSO (JT Baker, Phillipsburg, NJ) / 1x Dulbecco's phosphate saline (GibcoBRL, Grand Island, NY)) or test compound (administered subcutaneously). All rats began treatment on Day 8 after adjuvant injection. Data for representative metabolites of compounds of the invention are shown in Tables 15,16 and 17, hereinbelow. Statistical analysis was performed using Abacus Concepts Super ANOVA. (Abacus Concepts, Inc., Berkeley, CA). All of the parameters of interest were subjected to Analysis of Variance with Duncan's new multiple range post hoc testing between groups. Data are expressed throughout as mean ± standard deviation (SD), and differences were deemed significant if p<0.05. The degree of arthritis severity is monitored daily in terms of the following disease indices: Hindpaw erythema, hindpaw swelling, tenderness of the joints, and movements and posture. An integer scale of 0 to 3 is used to quantify the level of erythema (0= normal paw, 1= mild erythema, 2= moderate erythema, 3= severe erythema) and swelling (0=normal paw, 1=mild swelling, 2= moderate swelling, 3= severe swelling of the hind paw). The maximal score per day is 12. At the end of the study, the rats are euthanized with CO2, hindlimbs removed at necropsy and fixed in 10% buffered formalin, and the tarsal joints decalcified and embedded in paraffin. Histologic sections are stained with Hematoxylin and Eosin or Saffranin O - Fast Green stain. Slides are coded so that the examiner is blinded to the treatment groups. Synovial tissue from tarsal joints is evaluated based on synovial hyperplasia, inflammatory cell infiltration, and pannus formation [Poole and Coombs, International Archives of Allergy & Applied Immunology 54: 97-113 (1977)], as outlined below. Category 1 . Synovial liningLcells a. No change b. Cells enlarged, slightly thickened c. Cells enlarged, increase in numbers, moderately thickened. No villus present d. Cells enlarged, thickened. Villlus present 2. Fibroplasia a. No change b. Fibroplasia present under lining cells c. Small areas of areolar tissue replaced by fibrous tissue d. Replacement of areolar tissue by fibrous tissue 3. Inflammatory cells a. Occasionally seen, scattered throughout selection b. Cells present in small numbers in or just under Oning cell layer and/or around blood vessels. c. Small focal collection of cells may be present d. Large numbers of cells present in capsule and in or under lining cell layers. Large foci often seen. In addition, articular cartilage and bone are evaluated using Mankin's histotogical grading system [Mankin, et a/., Journal of Bone & Joint Surgery - American 53:523-37 (1971)] as shown below. Evaluation in the HLA-B27 Rat model of arthritis. Representative metabolites of compounds of the invention were evaluated in the HLA-B27 rat standard pharmacological test procedure, which emulates arthritis in humans. The following briefly describes the procedure used and results obtained. Male HLA-B27 rats were obtained from Taconic and provided unrestricted access to a food (PMl LabDiet 5001) and water. Joint scores and histology were evaluated as described above for the Lewis rat model of adjuvant-induced arthritis. Study 1: Rats (8-10 weeks old) were dosed orally once per day for forty-six days with one of the formulations listed below. There were 4 rats in each group and the last dose was administered two hours before euthanasia. • Vehicle (2% Tween-80/0.5% methylcellulose) • Example 21 (10 mg/kg from days 1-18; then increased to 20 mg/kg at day 19) • Example 24 (10 mg/kg from days 1 -24; then increased to 20 mg/kg at day 25) The following results were obtained for representative metabolites of compounds of the invention (Tables 18 and 19). Study 2: Rats (8-10 weeks old) were dosed orally for twenty-six days with one of the formulations listed below. There were 4 rats in each group and the last dose was administered two hours before euthanasia. • Vehicle (2% Tween-80/0.5% methylcellulose) • Example 25 (10 mg/kg from days 1-14; then increased to 20 mg/kg at day 15) • Example 34 (10 mg/kg) The following results were obtained for representative metabolites of :ompounds of the invention (Table 20). aluation in in vivo models of carcinoqeneisis The ability of compounds of this invention, and metabolites thereof, to treat id inhibit various malignancies or hyperprolific disorders can be evaluated in standard pharmacological test procedures that are readily available in the literature, and include the following two procedures. Breast cancer. Athymic nu/nu (nude) mice are obtained ovariectomized from Charles River Laboratories (Wilmington, MA). One day prior to tumor cell injection, animals are implanted with time-release pellets containing 0.36-1.7 mg 17p-estradiol (60 or 90 day release, Innovative Research of America, Sarasota, FL) or a placebo. The pellet is introduced subcutaneously into the intrascapular region using a 10- gauge precision trochar. Subsequently, mice are injected subcutaneously into the breast tissue with either 1x107 MCF-7 cells or 1x107 BG-1 cells. The cells are mixed with an equal volume of matrigel, a basement membrane matrix preparation to enhance tumor establishment. Test compounds can be evaluated either by dosing one day after tumor cell implantation (inhibition regimen) or after tumors have reached a certain size (treatment regimen). Compounds are administered either intraperitoneally or orally in a vehicle of 1% Tween-80 in saline each day. Tumor size is evaluated every three or seven days. Colon cancer. The ability to treat or inhibit colon cancer can be evaluated in the test procedure of Smirnoff P., et al. [Oncology Research 11:255-64 (1999)]. Evaluation of neuroprotection in two in vivo test procedures Transient global ischemia in the Mongolian gerbil. The effect of test compounds on preventing or treating brain injury in response to oxygen deprivation/reperfusion were measured using the following test procedure. Female Mongolian gerbils (60-80 g; Charles River Laboratories, Kingston, NY) were housed in the Wyeth-Ayerst animal care facffity Association for Assessment and Acred'rtation of Laboratory Annual Care (AAALAC) certified with a 12-hour light, 12-hour dark photoperiod and free access to tap water and a lowestrogen casein diet (Purina; Richmond, IN). After acclimation (3-5 days), gerbils were anesthetized with isoflurane (2-3% mixture with OJ, ovariectomized (Day 0). Beginning the following morning (Day 1), gerbils were treated subcutaneously each day with either vehicle (10% ETOH/corn oil), 17p-estradiol (1 mg/kg, sc) or an experimental compound. On Day 6, gcrbils (n=4-5/group) were anesthetized with isoflurane, the common carotid arteries visualized via a mid-line neck incision and both arteries simultaneously occluded for 5 minutes with non-traumatic micro aneurysm clips. After occlusion, the clips were removed to allow cerebral reperfusion and the neck incision closed with wound clips. All animals were fasted overnight prior to the global ischemia surgery, a step that facilitates consistent ischemic injury. On Day 12, gerbils were exposed to a lethal dose of CO2, and the brains frozen on dry ice and stored at -80 °C. The animal protocols used for these studies were reviewed and approved by the Radnor/Collegeville Animal Care and Use Committee (RACUC/CACUC) at Wyeth-Ayerst Research. The degree of neuronal protection was evaluated by in situ hybridization analysis of neurogranin mRNA. Briefly, 20 jim coronal cryostat sections were collected on gelatin-coated slides, dried and stored at -80 °C. At the time of processing, the desiccated slide boxes were warmed to room temperature, the slides postfixed in 4% paraformakJehyde, treated with acetic anhydride and then delipidated and dehydrated with chloroform and ethanoi. Processed section-mounted slides were then hybridized with 200 \d (6x106 DPM/ slide) of an antisense or sense (control) riboprobe for Neurogranin (3SS-UTP-labeled NG-241; bases 99-340) in a 50% formamide hybridization mix and incubated overnight at 55 C in a humidified slide chamber without coverslipping. The following morning, the slides were collected in racks, immersed in 2xSSC (0.3 M NaCI, 0.03 M sodium citrate; pH 7.0) /10 mM DTT, treated with RNase A (20 jig/ml) and washed (2 x 30 min) at 67 °C in 0.1x SSC to remove nonspecific label. After dehydration, the slides were opposed to BioMax® (BMR-1; Kodak, Rochester, NY) X-ray film overnight The level of neurogranin hybridization signal was used to quantitatively assess the degree of neuronal loss in the CA1 region after injury and to evaluate the efficacy of 17p-estradiol and experimental compounds. Neurogranin mRNA was selected for these studies because it is highly expressed in the hippocampal neurons including CA1, but absent in glia and other cell types present in this brain region. Therefore, measurement of the amount of neurogranin mRNA present represents surviving neurons. Relative optical density measurements of neurogranin hybridization signal were obtained from film autoradiograms with a computer based image analysis system (C-lmaging Inc., Pittsburgh, PA). The results from 6 sections (40 nm apart) per animal were averaged and statistically evaluated. Numerical values are reported as the mean ± SEM. One-way analysis of variance was used to test for differences in the level of neurogranin mRNA and all statements of non-difference in the results section imply that p0.05.. The following results were obtained with representative metabolites of compounds of the invention (Table 21). Middle cerebral artery occlusion in mice. Neuroprotection can be evaluated according to the test procedures described by Dubai [see, Dubai, et al., Proceedings of the National Academy of Sciences of the United States of America 98:1952-1957 (2001) and Dubai, etal., Journal of Neuroscience 19:6385-6393 (1999)]. Ovulation inhibition standard pharmacological test procedure The test procedure is used to determine whether test compounds can inhibit or change the timing of ovulation. It can also be used to determine the number of oocytes ovulated [Lundeen, et al., J Steroid Biochem Mol Bid 78: 137-143 (2001)]. The following data were obtained from representative metabolites of compounds from the invention (Table 22). evaluation in an endometriosis standard pharmacologic test procedure This procedure is slightly modified from a published method {Bruner-Tran. et al.. Journal of Clinical Investigation 99: 2851-2857 (1997)]. In brief, normal human endometrial tissue (cycle day ~12) is treated in vitro overnight with 10nM 17pestradiol and then implanted into ovariectomized athymic nude mice. For the purposes of these studies, the mice do not receive estrogen/placebo implants, as described in the paper. Lesions are allowed to establish for at least 10 days, then oral daily dosing begins and continues for at least 15 days. It should be noted that all mice have visible lesions at the start of dosing. At necropsy, the number of mice with lesions is determined, as well as the lesions per mouse. The compound of Example 24 was evaluated three times in this procedure at a dose of 10 mg/kg. In each test procedure, mice dosed with the compound of Example 24 had fewer lesions at necropsy than those mice dosed with vehicle. For example, in Study 1, each of the four mice in the vehicle group had at least one lesion and there were 10 total lesions in this group. In contrast, only two of six mice treated with Example 24 had any lesions and only one lesion was found per animal. Therefore, because all mice had lesions at the start of treatment, the compound of Example 24 caused lesion regression in four of six mice Based on the results obtained in the standard pharmacological test procedures, the prodrug compounds of this invention are expected to yield compounds that are estrogen receptor modulators useful in the treatment or inhibition of conditions, disorders, or disease states that are at least partially mediated by an estrogen deficiency or excess, or which may be treated or inhibited through the use of an estrogenic agent. Such compounds are particularly useful in treating a perjmenopausal, menopausal, or postmenopausal patient in which the levels of endogenous estrogens produced are greatly diminished. Menopause is generally defined as the last natural menstrual period and is characterized by the cessation of ovarian function, leading to the substantial diminution of circulating estrogen in the bloodstream. As used herein, menopause also includes conditions of decreased estrogen production that may be caused surgically, chemically, or by a disease state that leads to premature diminution or cessation of ovarian function. The prodrug compounds of the invention are also useful in inhibiting or treating other effects of estrogen deprivation including, hot flushes, vaginal or vulvar atrophy, atrophic vaginitis, vaginal dryness, pruritus, dyspareunia, dysuria, frequent urination, urinary incontinence, urinary tract infections. Other reproductive tract uses include the treatment or inhibition of dysfunctional uterine bleeding. The compounds are also useful in treating or inhibiting endometriosis. The prodrug compounds of this invention are also active in the brain and therefore, are useful for inhibiting or treating Alzheimer's disease, cognitive decline, decreased libido, senile dementia, neurodegenerative disorders, depression, anxiety, insomnia, schizophrenia, and infertility. The compounds of this invention are also useful in treating or inhibiting benign or malignant abnormal tissue growth including, glomerulosclerosis, prostatic hypertrophy, uterine leiomyomas, breast cancer, scleroderma, fibromatosis, endometrial cancer, polycystic ovary syndrome, endometrial polyps, benign breast disease, adenomyosis, ovarian cancer, melanoma, prostate cancer, cancers of the colon, CNS cancers, such as glioma or astioblastomia. The prodrug compounds of this invention are cardioprotective and are antioxidants, and are useful in lowering cholesterol, triglycerides, Lp(a), and LDL levels; inhibiting or treating hypercholesteremia, hyperiipidemia, cardiovascular disease, atherosclerosis, peripheral vascular disease, restenosis, and vasospasm, and inhibiting vascular wall damage from cellular events leading toward immune mediated vascular damage. The prodrug compounds of this invention are also useful in treating disorders associated with inflammation or autoimmune diseases, including inflammatory bowel disease (Crohn's disease, ulcerative colitis, indeterminate colitis), arthritis (rheumatoid arthritis, spondyloarthropathies, osteoarthritis), pleurisy, ischemia/reperfusion injury (e.g., stroke, transplant rejection, myocardial infarction, etc.), asthma, giant cell arteritis, prostatitjs, uveitis, psoriasis, multiple sclerosis, systemic lupus erythematosus and sepsis. The prodrug compounds of this invention are also useful in treating or inhibiting ocular disorders including cataracts, uveitis, and macular degeneration and in treating skin conditions such as aging, alopecia, and acne. The prodrug compounds of Ms invention are also useful in treating or inhibiting metabolic disorders such as type-ll diabetes, of lipid metabolism, appetite (e.g., anorexia nervosa and bulimia). Prodrug compounds in this invention are also useful in treating or inhibiting bleeding disorders such as hereditary hemorrhagJc telangiectasia, dysfunctional uterine bleeding, and combating hemorrhagic shock. Prodrug compounds of this invention are useful in disease states where amenorrhea is advantageous, such as leukemia, endometrial ablations, chronic renal or hepatic disease or coagulation diseases or disorders. The prodrug compounds of this invention can be used as a contraceptive agent, particularly when combined with a progestin. When administered for the treatment or inhibition of a particular disease state or disorder, ft is understood that the effective dosage may vary depending upon the particular compound utilized, the mode of administration, the condition, and severity thereof, of the condition being treated, as well as the various physical factors related to the individual being treated. Effective administration of the compounds of this invention may be given at an oral dose of from about 0.1 mg/day to about 1,000 mg/day. Preferably, administration will be from about 10 mg/day to about 600 mg/day, more preferably from about 50 mg/day to about 600 mg/day, in a single dose or in two or more divided doses. The projected daily dosages are expected to vary with route of administration. Such doses may be administered in any manner useful in directing the active compounds herein to the recipient's bloodstream, including orally, via implants, parentally (including intravenous, intraperitoneal, intraarticulariy and subcutaneous injections), rectally, intranasally, topically, ocularly (via eye drops), vaginally, and transdermally. Oral formulations containing the compounds of this invention may comprise any conventionally used oral forms, including tablets, capsules, buccal forms, troches, lozenges and oral liquids, suspensions or solutions. Capsules may contain mixtures of the active compound(s) with inert fillers and/or diluents such as the pharmaceuticalfy acceptable starches (e.g., com, potato or tapioca starch), sugars, artificial sweetening agents, powdered celluloses, such as crystalline and microcrystalline celluloses, flours, gelatins, gums, etc. Useful tablet formulations may be made by conventional compression and wet granulation or dry granulation methods, and utilize pharmaceutically acceptable diluents, binding agents, lubricants, disintegrants, surface modifying agents (including surfactants), suspending or stabilizing agents, including, but not limited to, magnesium stearate, stearic acid, talc, sodium lauryl suifaie, microcrystalllne cellulose, carboxymethylcellulose calcium, polyvinylpyrrolidone, gelatin, alginic acid, acacia gum, xanthan gum, sodium citrate, complex silicates, calcium carbonate, glycine, dextrin, sucrose, sorbitol, dicalcium phosphate, calcium sulfate, lactose, kaolin, mannitol, sodium chloride, talc, dry starches and powdered sugar. Preferred surface modifying agents include nonionic and anionic surface modifying agents. Representative examples of surface modifying agents include, but are not limited to, poloxamer 188, benzalkonium chloride, calcium stearate, cetosteari alcohol, cetomacrogol emulsifying wax, sorbitan esters, colloidol silicon dioxide, phosphates, sodium dodecylsulfate, magnesium aluminum silicate, and triethanolamine. Oral formulations herein may utilize standard delay or time release formulations to alter the absorption of the active compound(s). The oral formulation may also consist of administering the active ingredient in water or a fruit juice, containing appropriate solubilizers or emulsifiers as needed. In some cases it may be desirable to administer the- compounds directly to the airways in the form of an aerosol. The prodrug compounds of this invention may also be administered parenterally or intraperitoneally. Solutions or suspensions of these active compounds as a free base or pharmacologically acceptable salt can be prepared in water suitably mixed with a surfactant such as hydroxy-propylcellulose. Dispersions can also be prepared in glycerol, liquid polyethylene glycols and mixtures thereof in oils. Under ordinary conditions of storage and use, these preparations contain a preservative to inhibit the growth of microorganisms. The pharmaceutical forms suitable for injectabie use include sterile aqueous solutions or dispersions and sterile powders for the extemporaneous preparation of sterile injectabie solutions or dispersions. In all cases, the form must be sterile and must be fluid to the extent that easy syringability exists. It must be stable under the conditions of manufacture and storage and must be preserved against the contaminating action of microorganisms such as bacteria and fungi. The carrier can be a solvent or dispersion medium containing, for example, water, ethanol, polyol (e.g., gJycerol, propylene glyr/l and liquid polyethylene glycol), suitable mixtures thereof, and vegetable oils. For the purposes of this disclosure, transdermaf administrations are understood to include all administrations across the surface of the body and the inner linings of bodily passages including epithelial and mucosal tissues. Such administrations may be carried out using the present compounds, or pharmaceutically acceptable salts thereof, in lotions, creams, foams, patches, suspensions, solutions, and suppositories (rectal and vaginal). Transderm/il administration may be accomplished through the use of a transdermal patch containing the active compound and a carrier that is inert to the active compound, Is non toxic to the skin, and allows delivery of the agent for systemic absorption into the bl'xxl stream via the skin. The carrier may take any number of forms such as creams and ointments, pastes, gels, and occlusive devices. The creams and ointments may be viscous liquid or semisolid emulsions of either the Oit-in-water or water-in-oil type. Pastes comprised of absorptive powders dispersed in petroleum or hydrophilic petroleum containing the active ingredient may also be suitable. A variety of occlusive devices may be used to release the active ingredient into the blood stream such as a semi-permeable membrane covering a reservoir containing the active ingredient v/ith or without a carrier, or a matrix containing the active ingredient. Oilier occlusive devices are known in the literature. Suppository formulations may be made from traditional materials, including cocoa butter, with or without the addition of waxes to alter the suppository's melting point, and glycerin. Water soluble suppository bases, such as polyethylene glycols of various molecular weights, may also be used. EXAMPLES The preparation of representative examples of compounds that can be derivatized to form compounds of the invention is described below. EXAMPLE 1 2-(5-HYDROXY-1,3-BENZOXAZOL-2-YL) BENZENE-1,4-DIOL Step a) /?-(2,5-dimethoxyphenyI)-2I5-dimethoxybenzamide A mixture of 2,5-dimethoxybenzoic acid (5.0 g, 27.5 mmol) and thionyl chloride (15 mL) was refluxed for 1 hour. The volatiles then were removed under vacuum. The reskJue was dissolved in THF (20 mL) and added into a cold (0 °C) solution of 2,5- dimethoxyaniline (4.6 g, 30.2 mmol), triethylamine (5 mL, 35.9 mmol) and THF (40 mL). The reaction mixture was stirred for 30 mins., poured into water, acidified with HC! (2N) and extracted with EtOAc. The organic extracts were dried over MgSO4. Evaporation and purification by flash chromatography (hexanes / EtOAc 2/1) gave a white solid (8.1 g, 93% yield, m.p. 121-123 °C); MS m/e 318 (M+H)+. Analysis for Ci7Hi9NO5 Cate'd: C, 64.34; H, 6.03; N.4.41 Found: C, 64.29; H, 5.95; N, 4.44 Step b) 2-(5-Hydroxy-1,3-benzoxazol-2-yl) benzene-1,4-diol. A mixture of A/-(2,5-dimethoxyphenyl)-2,5-dimethoxybenzamide (1.0 g, 3.1 mmol) and pyridine hydrochloride (2.0 g, 17.3 mmol) was stirred at 200 °C for 1 hour. The reaction mixture was cooled to room temperature and HCI (10 mL, 2 N) was added. The reaction mixture was then extracted with EtOAc and the organic extracts were dried over MgSO4. Evaporation and purification by flash chromatography (hexanes / EtOAc 2/1) gave a white solid (0.8 g, 76% yield, m.p. 309-311 °C); MS m/e 242 (MH)+. 3-(5-HYDROXY-1,3-BEN20XA20L-2-YL)BENZENE-1,2-DIOL The title compound was prepared in substantially the same manner as described in Example 1, from 2,5-dimethoxyaniline and 2,3-dimethoxybenzoic acid. The product was obtained as a tan solid, m.p. 239-241 °C; MS m/e 244 {M+H)+. Analysis for: C13HgNO4 Calc'd: C, 64.20; H, 3.73; N, 5.76 Found: C, 63.86; H, 3.90; N, 5.74 EXAMPLES ' 2-<3-FLUORO-4-HYDROXYPHENYL)-1.3-BENZOXAZOL-5-OL The title compound was prepared in substantially the same manner as described in Example 1, from 2,5-dimethoxyaniline and 3-fluoro-4-methoxybenzoic acid, and was obtained as a white solid, m.p. 262-268 C; MS m/e 244 (M-H)+. Analysis for Ci3HBFNO3 Calc'd: C, 63.68; H, 3.29; N, 5.71 Found: C, 64.01; H, 3.25; N, 5.63 EXAMPLE 4 2-(3-CHLORO-4-HYDROXYPHENYL)-1l3-BENZOXAZOL-5-OL The title compound was prepared in substantially the same manner as described in Example 1, from 2,5-dimethoxyaniline and 3-chloro-4-methoxybenzoic acid and was obtained as a white solid, m.p. 254-256 °C; MS m/e 260 (M-H)+. Analysis for: Ci3H8CINO3 Calc'd: C, 59.67; H, 3.08; N, 5.35 Found: C, 59.59; H, 3.02; N, 5.25 EXAMPLES 2-{2-CHLORO-4-HYDROXYPHENYL)-1,3-BENZOXAZOL-5-OL The title compound was prepared in substantially the same manner as described in Example 1, from 2,5-dimethoxyaniline and 2-chloro-4-methoxybenzoic acid, and was obtained as a white solid, m.p. 253-255 CC; MS m/e 262 (M+H)+. Analysis for: C13H8CINO3 Calc'd: C, 59.67; H, 3.08; N, 5.35 Found: C, 59.79; H, 2.87; N, 5.36 EXAMPLE 6 2-(3-FLUORO-4-HYDROXYPHENYL)-1,3-BENZOXAZOL-6-OL The title compound was prepared in substantially the same manner as described in Example 1, from 2,4-dimethoxyaniline and 3-fluoro-4-methoxybenzoic acid, and was obtained as a white solid, m.p. 269-271 C; MS m/e 244 (M-H)+. Analysis for: dyHuNOa Calc'd: C, 63.68; H, 3.29; N, 5.71 Found: C, 63.53; H, 3.71; N, 5.38 EXAMPLE 7 2-(3-TERT-BUTYL-4-HYDROXYPHENYL)-1,3-BENZOXAZOL-6-OL The title compound was prepared in substantially the same manner as described in Example 1, from 2,4-dimethoxyaniline and 3-terf-butyW-methoxybenzoic acid, and was obtained as a white solid, m.p. 220-222 °C; MS m/e 284 (M+H)+. Analysis for C17H17NO3 Calc'd: C, 72.07; H, 6.05; N, 4.94 Found: C, 72.03; H, 6.43; N, 4.72 EXAMPLE 8 2-(6-HYDROXY-1,3-BENZOXAZOL-2-YL)BENZENE-1,4-DIOL The titte compound was prepared in substantially the same manner as described in Example 1, from 2,4-dimethoxyaniline and 2,5-dimethoxybenzoic acid, and was obtained as a tan solid, m.p. 278-280 °C; MS m/e 244 (M+H). Analysis for Ci3H9NO4 Caic'd: C, 64.20; H, 3.73; N, 5.76 Found: C, 64.09; H, 3.14; N, 5.65 EXAMPLES 3-(6-HYDROXY-1,3-BENZOXAZOL-2-YL)BENZENE-1,2-DIOL The title compound was prepared in substantially the same manner as described in Example 1, from 2,4-dimethoxyaniline and 2,3-dimethoxybenzoic acid, and was obtained as a tan solid, m.p. 256-258 °C; MS m/e 244 (M+Hf. Analysis fon Ct3H9NO4 Cafc'd: C, 64.20; H, 3.73; N, 5.76 Found: C, 63.91; H, 3.98; N, 5.72 EXAMPLE 10 4-(6-HYDROXY-1,3-BENZOXAZOL-2-YL)BENZENE-1,2-DIOL Thie title compound was prepared in substantially the same manner as described in Example 1, from 2,4-dimethoxyaniline and 3,4-dimethoxybenzoic acid, and was obtained as a white solid, m.p. 282-284 °C; MS m/e 242 (M-H)+. Analysis for C<3H9NO4 Calc'd: C, 64.20; H, 3.73; N, 5.76 Found: C, 63.57; H, 3.68; N, 5.63 II 2-(3-CHLORCM-HYDROXYPHENYL)-1,3-BENZOXAZOL-6-OL The titte compound was prepared in substantially the same manner as described in Example 1, from 2,4-dimethoxyaniline and 3-chloro-4-methoxybenzoic acid, and was obtained as an off-white solid, m.p. 254-256 °C; MS m/e 262 (M+Hf. Analysis for. C13HgNO4 Calc'd: C, 64.20; H, 3.73; N, 5.76 Found: C, 63.57; H, 3.68; N, 5.63 EXAMPLE 12 2-(4-HYDROXYPHENYL)-1.3-BENZOXAZOL-5-OL The title compound was prepared in substantially the same manner as described in Example 1, from 2,5-dimethoxyaniline and 4-methoxybenzoyl chloride, and was obtained as a light yellow solid, m.p. 264-267 °C; MS m/e 228 (M+H). Analysis for Ci3H9NO3 Calc'd: C, 68.72; H, 3.99; N, 6.16 Found: C, 67.87; H, 4.05; N, 6.23 EXAMPLE 13 4-(5-H YDROXY-1,3-BENZOXAZOL-2-YL)BENZENE-1,3-DIOL The title compound was prepared in substantially the same manner as described in Example 1, from 2,5-dimethoxyaniline and 2,4-dimethoxybenzoic acid, and was obtained as a white solid, m.p. greater than 300 °C; MS m/e 242 (M-H). Analysis for Ci3H9NO4 Calc'd: C, 64.20; H, 3.73; N, 5.76 Found: C, 63.92; H, 3.74; N, 5.56 EXAMPLE 14 2-(4-HYDROXYPHENYL)-1,3-BENZOXA2OL-6-OL The title compound was prepared rn substantially the same manner as described in Example 1, from 2,4-dimethoxyaniline and 4-methoxybenzoyl chloride, and was obtained as a white solid, m.p. greater than 300 °C; MS m/e 226 (M-H)+. Analysis for Ci3HgNO3 Caic'd: C, 68.72; H, 3.99; N, 6.16 Found: C, 68.09; H, 4.01; N, 6.05 EXAMPLE 15 4-(6-HYDROXY-1,3-BENZOXAZOL-2-YL)BENZENE-1,3-DIOL The title compound was prepared in substantially the same manner as described in Example 1, from 2,4-dimethoxyaniline and 2,4-dimethoxybenzoic acid, and was obtained as a white solid, m.p. 293-296 °G; MS m/e 242 (M-H)+. Analysis for C13H9NO4 Caic'd: C, 64.20; H, 3.73; N, 5.76 Found: C, 64.43; H, 3.77; N, 5.74 EXAMPLE 16 6-CHLORO-2-(3-FLUORO-4-HYDROXYPHENYL)-1,3-BENZOXAZOL-5-OL STEP A) N-(4-CHLORO-2,5-DIMETHOXYPHENYL3-FLUORO-4- METHOXYBENZAMIDE. The title compound was prepared in substantially the same manner as described in Example 1, Step a, from 4-ch!oro-2,5-dimethoxyaniline and 3-fluoro-4- methoxybenzoic acid, and was obtained as a white solid, m.p. 197-199 C; MS m/e 340 {M+H)+. Analysis for Ci6Hi5CIFNO4 Caic'd: C, 56.56; H, 4.45; N, 4.12 Found: C, 56.33; H, 4.35: N, 4.05 Step b) A/-(4-Chloro-2,5-dihydroxyphenyl}-3-fluoro-4-hydroxybenzamide. Boron trifluoride dimethyl sulfide complex (70 mL) was added into a mixture of /V-(4- chloro-2,5-dimethoxyphenyl)-3-fluoro-4H7iethoxybenzamide (1.75 g, 5.15 mmol) and CH2CI2 (35 mL). After stirring for 20 hours, the solvent and the excess reagent were evaporated under a nitrogen stream in the hood. The residue was taken into a mixture of ice and HCI (1 N) and extracted with EtOAc. The organic layer was washed with HCI (1N) and dried over MgSO4. Evaporation and purification by flash chromatography (CH2CI2/hexanes/EtOAc 5/3/2, and AcOH 10 mL per 1 liter of the eluting solvent) gave a white solid (1.4 g, 91% yield, m.p. 254-256 °C); MS m/e 296 Analysis for: C13H9CIFNO4 Calc'd: C, 52.46; H, 3.05; N, 4.71 Found: C, 51.98; H, 2.98; N, 4.56 Step c) 6-Chloro-2-(3-fluoro-4-hydroxyphenyl)-1,3-benzoxazol-5-o! The title compound was prepared in substantially the same manner as described in Example 1 , step b, from /V-(4-chloro-2,5-dihydroxyphenyl)-3-fluoro-4- hydroxybenzamide and pyridine hydrochloride, and was obtained as a white solid, m.p. 258-260 °C; MS m/e 278 (M-H)+. Analysis for Ci3H17CIFNO3 CaJc'd: C, 55.83; H, 2.52; N, 5.01 Found: C, 55.35; H, 2.59; N, 4.91 EXAMPLE 17 6-BROMO-2-(3-FLUORO-4-HYDROXYPHENYL)-1,3-BENZOXA2OL-5-OL The title compound was prepared In substantially the same manner as described in Example 16, from 4-bromo-2,5-dimethoxyaniline and 3-fluoro-4-methoxybenzoic acid, and was obtained as a white solid, m.p. 224-226 °C; MS m/e 322 (M-H). Analysis for: C13Hi7BrFNO3 Calc'd: C, 48.18; H, 2.18; N, 4.32 Found: C, 48.'69; H, 2.36; N, 4.59 EXAMPLE 18 6-CHLORO-2-(4-HYDROXYPHENYL)-1,3-BENZOXAZOL-5-OL The title compound Was prepared in substantially the same manner as described in Example 16, from 4-chloro-2,5-dimethoxyaniline and 4-methoxybenzoyl chloride, and was obtained as an off-whffe solid, m.p. 260-262 °C; MS m/e 260 (M-H). Analysis for C13HBCINO3 Calc'd: C, 59.67; H, 3.08; N, 5.35 Found: C, 59.09; H, 3.06; N, 5.11 EXAMPLE 19 5-CHLORO-2-(4-HYDROXYPHENYL)-1,3-BENZOXAZOL-6-OL The title compound was prepared in substantially the same manner as described in Example 16, from 5-chloro-2,4-dimethoxyaniline and 4-methoxybenzoyl chloride, and was obtained as an off-white solid, m.p. 254-256 °C; MS m/e 262 (M+H)+. Analysis for Ci3H8CIN03 Calc'd: C, 59.67; H, 3.08; N, 5.35 Found: C, 59.40; H, 2.97; N, 5.22 EXAMPLE 20 7-BROMO-2-(4-HYDROXYPHENYLh1,3-BENZOXAZOL-5-OL Step a) 2-Bromo-4-methoxy-6-nitrophenol. Bromine (16.0 g, 100 mmol) in acetic acid (20 mL) was added into a mixture of 4- methoxy-2-nitrophenol (16.9 g, 100 mmol), sodium acetate (16.4 g, 200 mmol) and acetic acid (100 mL). The reaction mixture was stirred for 30 mins. at room temperature, and then at 70 °C for 2 hours and poured into water (1.51) containing concentrated sulfuric acid (10 mL). The precipitated solid was filtered and crystallized from chloroform /hexane to give a brownish solid, m.p. 116-118 °C; MS m/e 246 (M-H). Analysis for C7H6BrNO4 Calc'd: C, 33.90; H, 2.44; N, 5.65 Found: C, 34.64; H. 2.16; N, 5.43 Step b) 2-Amino-6-bromo-4-methoxyphenol. Raney/Ni (2.5 g) was added into a solution of 2-bromo-4-methoxy-6-nitrophenol (8.8 g, 35.5 mmol) in EtOAc (100 ml). The mixture was shaken in a Parr apparatus under hydrogen at 25psi for 2.5 hours. The reaction mixture was filtered through Celrte® and concentrated under vacuum to give a gray solid (7.4 g, 96% yield; 95-97 °C); MS m/e 218 (M+H)+. Analysis for C7H8BrNO2 Calc'd: C, 38.56; H, 3.70; N, 6.42 Found: C, 38.32; H, 3.77; N, 6.24 Step c) 2-Bromo-4-methoxy-6-[(4-methoxybenzoyl)amino]phenyl-4- methoxybenzoate Anhydrous pyridine (37.0 mL, 468.5 mmol) was added dropwise into a cold (0 °C) mixture (mechanically stirred) of 2-amino-6-bfomo-4-methoxyphenol (20.0 g, 91.7 mmol), 4-methoxybenzoyl chloride (38.9 g, 229.0 mmol), and CH2CI2 (250 mL). During the pyridine addition, a precipitate was formed. The reaction mixture was stirred for 30 mins. and then ethyl ether (250 mL) was added. The precipitated solids were filtered off and washed with ethyl ether. The solids were taken into water and stirred for 20 min. The solids were then filtered off and dried to give an off-white solid (42.5 g, 95% yield, m.p. 73-75 °C); MS m/e 484 (M-H)+. Analysis for. CasHsoBrNOs Calc'd: C, 56.80; H, 4.15; N, 2.88 Found: C, 56.50; H, 3.78; N, 2.83 Step d) 7-Bromo-5-methoxy-2-(4-methoxyphenyl)-1-benzoxazole. Route a) A suspension of 2-bromo-4-methoxy-6-[(4-methoxybenzoyl)amino]phenyl 4- methoxybenzoate (42.0 g, 86.4 mmol), p-toluenesulfonic acid monohydrate (32.8 g, 172.8 mmol) and anhydrous p-xylene (800 mL) was refluxed for 1 hour with continuous water removal (Dean-Stark Trap). The initial suspension turned into a brown solution at refluxing temperature. The reaction mixture was cooled to room temperature and washed with NaOH (2N). The organic layer was dried over MgSO4. Evaporation and crystallization from acetone/ethyl ether gave an off-white solid (23.5 g, 82% yield, m.p. 139-141 °C); MS m/e 334 (M+H)+. Analysis for: CisHBnMOa Cafc'd.-C, 53.91; H, 3.62; N, 4.19 Found: C, 53.83; H, 3.37; N, 4.01 Route b) A mixture of 2-amino-6-bromo-methoxyphenoI (100 mg, 0.46 mmol), 4-methoxybenzoic acid (77 mg, 0.5 mmol), and boric acid (31 mg, 0.5 mmol) in p-xylene (9 ml) was refluxed for 24 hours using a Dean-Stark water separator. The reaction mixture was cooled to room temperature, and concentrated under vacuum. The residual product was purified by flash chromatography (30% EtOAc/petroIeum ether) to give a light pink solid (99 mg, 65% yield, m.p. 136-138 °C); MS m/e 334 (M+H)+. Analysis for: Ci5Hi2BrNO3 Calc'd: C, 53.91; H, 3.62; N, 4.19 Found; C, 53.78; H, 3.55; N, 4.01. Step e) 7-Bromo-2-{4-hydroxyphenyl)-1,3-benzoxazol-5-ol. Route a) Boron tribromide (1M, 89.9 ml, 89.8 mmol) was added dropwise into a cold (-70 °C) suspension of 7-bromo-5-methoxy-2-(4-methoxyphenyl)-1,3-benzoxazole (10.0 g, 29.94 mmol) and CH2CI2 (50 mL). The reaction mixture was allowed to warm up to room temperature. During the warming up period, the suspension turned into a dark solution. The reaction mixture was stirred at room temperature for 2 days and then poured slowly into cold (0 ° C) ethyl ether (1000 mL). Methyl alcohol (200 ml) was added slowly into the new reaction mixture over a 20 mins. period. The reaction mixture was then poured into water (1.51). The organic layer was washed three times with water, and dried over MgSO4. Evaporation and crystallization from acetone/ethyl ether/hexanes gave an off-white so/id (8.4 g, 92% yield, m.p. 298-299 °C);MSmfe306(M+H)+. Anafysis for Ci3HaBrNQ3 Calc'd: C, 51.01; H, 2.63; N, 4.58 Found: C, 50.96; H, 2.30; N, 4.42 Route b) Boron tribromide (0.25 ml, 2.7 mmol) was added dropwise into a cold (-78 °C) mixture of 7-bromo-5-methoxy-2-(4-methoxyphenyl)-1,3-benzoxazole (130 mg, 0.39 mmol), and dichloromethane (1.5 mL). The reaction mixture was allowed to come gradually to room temperature and stirred for 1 hour. The reaction mixture was poured into ice and extracted with EtOAc. The organic extracts were washed with brine and dried over MgSCty. Evaporation and flash chromatography (30%-40% EtOAc/petroleum ether) gave (102 mg, 86% yield) of the product as a light pink solid, m.p. 295-298 °C; MS m/e 304 (M-H)+. Analysis fon C13H8BrNO3 Calc'd: C, 51.01; H, 2.63; N, 4.58 Found: C, 51.06; H, 2.77; N, 4.36. EXAMPLE 21 7-BROMO-2-(3-FLUORO-4-HYDROXYPHENYL)-1,3-BEN20XA20L-5-OL Step a) 2-Bromo-6-[(3-fluoro-4-methoxybenzoyl)amino]-4-methoxyphenyl 3- fluoro-4-methoxybenzoate. A mixture of 3-fluoro-4-methoxybenzoic acid (39.0 g, 229 mmol), thionyl chloride (100 mL), and N,N-dimethylformamide (0.5 mL) was refluxed for 1 hour. The volatiles were removed under vacuum. The solids were taken in benzene (twice) and the volatiles were removed under vacuum. The residue was dissolved in CH2CI2 (100 mL) and added into a cold (0 °C) mixture (mechanically stirred) of 2-amino-6-bromo- 4-methoxyphenol (20.0 g, 91.7 rnmol) and CH2CI2 (150 mL). Anhydrous pyridine (37.0 m'-, 468.5 mmoi) was added dropwise into the new reaction mixture. During the pyridine addition, a precipitate was formed. The reaction mixture was stirred for 30 mins. and then ethyl ether (250 mL) was added. The precipitated solids were filtered off and washed with ethyl ether. The solids were taken into water and stirred for 20 mins. The solids were then filtered off and dried to give an off-white solid (46.5 g, 97% yield, m.p. 184-186 °C); MS m/e 520 (M-H)+. Analysis for. CaHuBrfNOe Calc'd: C, 52.89; H, 3.47; N, 2.68 Found: C, 52.79; H, 3.23; N, 2.63 Step b) 7-Bromo-2-(3-fluoro-4-methoxyphenyl)-5-methoxy-1,3-benzoxazole. A suspension of 2-bromo-6-[(3-fluoro-4-methoxybenzoyl)amino]-4-methoxyphenyl 3- fluoro-4-methoxybenzoate (46.0 g, 88.1 mmol), p-toluenesulfonic acid monohydrate (33.5 g, 177.2 mmol) and anhydrous p-xylene (11) was refluxed for 3 hours with continuous water-removal (Dean Stark Trap). The initial suspension turned into a brown solution at refluxing temperature. The solids were filtered off and washed with ethyl ether. The solids were suspended in ethyl ether (200 ml), stirred for 10 mins., filtered off and dried to give a tan solid (25.1 g, m.p. 175-177 °C). The ethyl ether layer was concentrated to 20 mL and 2.5 g of additional product was obtained (90% overall yield). MS m/e 352 (M+H). Analysis for C15HuBrFNO3 Calc'd: C, 51.16; H, 3.15; N, 3.98 Found: C, 51.10; H, 2.92; N, 3.89 step c) 7-bromo-2-(3-fluoro-4-hydroxyphenyl)-1,3-benzoxazoI-5-ol The title compound was prepared in substantially the same manner as described in Example 20, Step e, and was obtained as a white solid, m.p. 265-267 °C; MS m/e 332 (M-H)+. Analysis for Ci3H7BrFNO3 Calc'd: C, 48.18; H, 2.18; N, 4.32 Found: C, 48.19; H, 2.29; N, 4.19 EXAMPLE 22 7-BROMO-2-(2-FLUORO-4-HYDROXYPHENYL)-1,3-BENZOXAZOL-S-OL ' Step a) 2-Fluoro-4-methoxybenzoic acid. Into a warm (55 °C) mixture of Ag20 (13.5 g, 58.4 mmol), NaOH (19.5 g, 487 mmol) and water (200 mL), was added 2-fluoro-4-methoxybenzaldehyde (15 g, 97.4 mmol). The reaction mixture was stirred for 1 hour, filtered off and the precipitated solids were washed with hot water (10 mL). The filtrate was added slowly into cold (0 °C) HCI (5N) with vigorous stirring. The precipitated solid was filtered, washed with water and dried to give a white solid (13.6 g, 82%yield, m.p. 194-196 °C); MS m/e 169 (MH). Analysis for: C8H7FO3 Calc'd:C, 56.48; H, 4.1 5 Found: C, 56.12; H, 4.12 Step b) 7-Bromo-2-(2-tluoro-4-hydroxyphenyi)-1,3-benzoxazol-5-ol The title compound was prepared in substantially the same manner as described in Example 21, from 2-fluoro-4-methoxybenzoic acid, and was obtained as a white solid, m.p. 248-250 °C; MS m/e 324 (M+H)+. Analysis for C13H7BrFNO3 CaJc'd: C, 48.18; H, 2.18; N, 4.32 Found: C, 47.89; H, 1.95; N, 4.18 EXAMPLE 23 7-BROMO-2-(2,3-DIFLUORO-4-HYDROXYPHENYL)-1 .3-BENZOXAZOL-5-OL Step a) Methyl 2,3-difluoro-4-methoxybenzoate lodomethane (10.7 ml, 172.5 mmol) was added into a mixture of 2,3-difluoro-4- hydroxybenzoic acid (10.0 g, 57.5 mrnol), lithium carbonate (12.7 g, 172.5 mmol) and N.N-dimethylformamide (100 mL). The reaction mixture was stirred at 40 °C for 12 h, and then poured into water and extracted with EtOAc. The organic extracts were dried over MgSO4. Evaporation and purification by flash chromatography (hexanes / EtOAc 5/1) gave a white solid (10.2 g, 88% yield, m.p. 66-68 °C); MS m/e 203 Analysis for Calc'd: C, 53.47; H, 3.99 Found: C, 53.1 5; H. 3.83 Step b) 2,3-Difluoro-4-methoxybenzoic acid. Sodium hydroxide (2N, 50 ml) was added into a mixture of methyl 2,3-difluoro-4- methoxybenzoate (10.0 g, 49.5 mmol), THF (100 ml) and MeOH (100 mL). The reaction mixture was stirred at room temperature for 6 hours, and acidified with HCI (2N). The precipitated solid was filtered off, washed with water and dried to give a white solid (8.9 g, 96% yieid, m.p. 194-196 °C); MS m/e 187 (M-H)+. Analysis for CaH6F2O3 Calc'drC, 51.08; H. 3.21 Found: C, 50.83; H, 2.92 Step c) 7-Bromo-2-(2,3-difluoro-4-hydroxyphenyl)-1,3-benzoxa2ol-5-of The title compound was prepared in substantially the same manner as described in Exampte 21, from 2,3-difluorc~4-methoxybenzdic acid, and was obtained as a white solid, m.p. 258-260 °C; MS m/e 342 (M+H)+. Analysis for. C13H6BrF2NO3 Calc'd: C, 45.64; H, 1.77; N, 4.09 Found: C, 45.33; H, 1.62; N, 4.02 EXAMPLE 24 2-(3-FLUORO-4-HYDROXYPHENYL)-7-VINYL-1,3-BEN2OXA2OL-5-OL Route a) Step a) 7-Bromo-5-aferf-butyl(dimethyl)silyl]oxy}-2-(4-{[tertb uty/(dimethyl)silyl]oxy}-3-fluorophenyl)-1 ,3-benzoxazole. terf-Butyl(chloro)dimethyfsilane (23.2 g, 154 mmof) was added portionwise into a mixture of 7-bromo-2-(3-fluoro-4-hydroxyphenyl)-1,3-ben2oxazol-5-oI (16.6 g, 51.4 mmol), imidazote (17.5g, 257mmol), /v/V-dimethylpyridin-4-amine (1.0g, 8.1 mmol) and DMF (300 mL). The reaction mixture was stirred for 3 hours, poured into water and extracted with ethyl ether. The organic extracts were dn'ed over MgSO4. Evaporation and purification by flash chromatography (hexanes / EtOAc 50/1) gave a white solid (27.5 g, 97% yield, m.p. 98-99 °C); MS m/e 552 (M+H)+. Calc'd: C, 54.34; H, 6.38; N, 2.53 Found: C, 54.06; H, 6.52; N, 2.24 Step b) 5-{[terf-Buty|(dimethyl)silyl]oxy}-2-(4-{[ferf-butyl(dimethyI)silyl]oxy}-3- fluorophenyl)-7-vinyI-1 ,3-benzoxazole. Dichlorobis(tri-o-tolylphosphine)pa!ladium (II) (0.63 g. 0.79 mmol) was added into a mixture of 7-bromo-5-{Iferf-butyl(dimethyl)silyl]oxy}-2-(4-{[terfbutyl( dimethyl)silyl]oxy}-3-fluorophenyl)-1 ,3-benzoxazole (14.7 g, 26.6 mmol), tributyl(vinyl)tin (10.5 g, 33.25 mmof) andp-xylene (85 mL). The reaction mixture was stirred at 90 °C for 24 hours, cooled to room temperature, diluted with ethyl ether (1 00 mL) and treated with activated carbon. The reaction mixture was filtered through MgSO4 and concentrated. Purification by flash cbromatography (hexanes / EiOAc 50/1) gave a white solid (11.8 g, 89% yield, m.p. 93-95 °C); MS m/e 500 Calc'd: C, 64.89; H, 7.66; N, 2.80 Found: C, 64.59; H, 7.70; N, 2.73 Step c) 2-(3-Fluoro-4-hydroxyphenyl)-7-vinyM,3-benzoxazol-5-oI. Hydrofluoric acid (48 wt.% in water, 1 mL) was added into a solution of 5-ffte/tbutyl( dimethyl)silynoxy}-2K4-flferbutyl(dimethyl)silyOoxy}-3-fluorophenyl)-7-vinyN 1,3-benzoxazoIe (1.5 g, 3.0 mmol), THF (6 mL) and acetonitrite (3 mL). The reaction mixture was stirred at 65 °C for 8 hours, and then poured into water. The precipitated solid was filtered off and dried. Crystallization of the product from acetone/ethyl ether gave a white solid (0.72 g, 81% yield, m.p. 249-251 C); MS m/e 272 (M+H). Analysis for CisHtoFNOa Calc'd: C, 66.42; H, 3.72; N, 5.16 Found: C, 66.31 ; H, 3.85; N, 4.96 Route b) 2-{3-Fluoro-4-hydroxyphenyl)-7-vinyl-1,3-benzoxazol-5-ol. Dichlorobis(tri-o-tolylphosphine)palladium (II) (0.87 g, 1.1 mmol) was added into a mixture of 7-bromo-2-(3-fluoro-4-hydroxyphenyl)-1,3-benzoxazol-5-ol (7.16 g, 22.1 mmol), tributyl(vinyl)tin (10.5 g, 33.25 mmol) and ethylene giycol diethyl ether (65 mL). The reaction mixture was stirred at 1 1 5 °C for 48 hours, cooled to room temperature and treated with activated carbon. The reaction mixture was filtered 75 through MgSO4 and concentrated. Purification by flash chromatography, on acidic silica gel (hexanes / EtOAc / CH2CI2 1/1/1), gave a white solid (4.35 g, 72% yield, m.p. 250-252 °C); MS m/e 272 (M+Hf. Analysis for. C15H10FNO3 Calc'd: C, 66.42; H. 3.72; N, 5.16 Found: C, 66.03; H, 3.68; N, 5.09 Route c) N Step a) 4-[5-(Acetyloxy)-7-bromo-1,3-benzoxazol-2-yI]-2-fluorophenyI acetate. Acetic anhydride (1.0 ml_, 9.95 mmol) was added into a cold (0 °C) solution of 7- bromc-2-(3-fluoro-4-hydroxyphenyl)-1.3-benzoxazol-5-ol(1.24g, 3.8 mmot), N,Ndtmethylpyridin- 4-amine (1.1 g, 9.18 mmol) and 1,4-dioxane (13 mL). The reaction mixture was allowed to warm up to room temperature and stirred for 20 hours. Water (50 ml) was added to the reaction mixture extracted with EtOAc and dried over MgSO Evaporation and crystallization from EtOAc/hexane gave an off-white solid (0.87 g, 56% yield); MS m/e 408 (M+H)+. Analysis fon CoHnBrFNOs Calc'd: C, 50.02; H, 2.72; N, 3.43 Found: C, 49.58; H, 2.59; N, 3.37 Step b) 2-[4Acetyloxy)-3-fluorophenyI]-7-vfnyl-1,3-benzoxazol-5-yl acetate. D»ch!orobis(trHtory1phosphine)paUadium (I!) (46 mg, 0.06 mmol) was added into a mixture of 4-[5-(acety1oxy)-7-bromo-1I3-benzpxazol-2-yll-2-fluorophenvl acetate (0.8 g, 1 .98 mmo!}, tributyl(vinvj)tin (0.9 g, 2.8 mmol) and p-xylene (9 ml). The reaction mixture was stirred at 130 C for 5 hours, cooled to room temperature, diluted with ethyl ether (10 ml) and treated with activated carbon. The reaction mixture was filtered through MgSO4 and concentrated. Purification by flash chromatography (hexanes / EtOAc 5/1) gave a white sofid (0.4 g, 56% yield, m.p. 154-156 C); MS Analysis for. C19H14FNO5 Calc'd: C, 64.23; H, 3.97; N, 3.94 Found: C, 63.94; H, 3.78; N, 3.76 Step c) 2-(3-Fluoro-4-hydroxyphenyI)-7-vinyl-1,3-benzoxazol-5-ol. Potassium carbonate (55 mg) was added into a solution of 2-[4-(acetyloxy)-3- fluorophenylJ-7-vinyl-1,3-benzoxazol-5-yl acetate (0.14 g, 0.39 mmol) and 1,4- dioxane (3 ml). The reaction mixture was stirred at 90 °C for 1 hour, poured into water, acidified with HCI (2N) and extracted with EtOAc. The organic extracts were dried over MgSCv Evaporation and crystallization from EtOAc/hexanes, gave a white solid (0.06 g, 46% yield, m.p. 250-252 °C); MS m/e 272 (M+H)+. Analysis for C1SH10FNO3 Calc'd: C, 66.42; H, 3.72; N, 5.16 Found: C, 66.32; H, 3.47; N, 5.18 EXAMPLE 25 2-(2-FLUORO-4-HYDROXYPHENYL)-7-VINYL-1,3-BENZOXAZOL-5-OL The title compound was prepared in substantially the same manner as described in Example 24, Route a), from 7-bromo-2-(2-fluoro-4-hydroxyphenyl)-1,3-benzoxazol-5- ol, and was obtained as a white solid, m.p. 274-275 °C; MS m/e 272 (M+H)+. Analysis for Ci5H10FNO3 Calc'd: C, 66.42; H, 3.72; N, 5.16 Found: C, 66.18; H, 3.47; N, 4.97 EXAMPLE 26 2-(2,3-DIFLUORO-4-HYDROXYPHENYLH-VINYL-1,3-BENZOXAZOL-5-OL The title compound was prepared in substantially the same manner as described in Example 24, Route b), from 7-bromo-2-(2,3-difluoro-4-hydroxyphenyl)-1,3- benzoxazoi-5-ol, and was obtained as an off-white solid, m.p. 276-278 °C; MS m/e 290 (M+Hf. Analysis for: CisHgFaNOa Calc'd: C. 62.29; H, 3.14; N, 4.84 Found: C, 61.90; H, 3.05; N, 4.52 EXAMPLE 27 2-(4-HYDROXYPHENYL)-7-VIN YL-1,3-B ENZOXAZOL-5-OL The title compound was prepared in substantially the same manner as described in Example 24, Route b), from 7-bromo-2-(4-hydroxyphenyl)-1,3-benzoxazoJ-5-ol, and was obtained as a white solid, m.p. 249-250 °C; MS m/e 254 (M+H)+. Analysis for: CtsHNOa Caic'd: C, 70.99; H, 4.39; N, 5.52 Found: C, 70.75; H, 4.34; N, 5.46 EXAMPLES 28 AND 29 4-BROMO-2-(3-FLUORO-4-HYDROXYPHENYL)-7-VINYL-1,3-BENZOXAZOL-5-OL (EX. 28) AND 4I6-DIBROMO-2-(3-FLUORO-4-HYDROXYPHENYL)-7-VINYL-1.3- BENZOXAZOL-5-OL (EX. 29). /V-Bromosuccinimide (0.49 g, 2.77 mmol) was added into a mixture of 2-(3-fluoro-4- hydroxyphenyl)-7-vinyH,3-benzoxazol-5-ol (0.75 g, 2.77 mmol) and acetonitrile (30 mL). The reaction mixture was stirred at room temperature for 16 hours, poured into water and extracted with EtOAc. The organic extracts were dried over MgSO4. Evaporation and purification by flash chromatography (hexanes / EtOAc /CH2CI2 2/1/1) gave Ex. 28 as a white solid (0.45 g, m.p. 226-228 °C); MS m/e 349 (M+H). Analysis for CisHgBrNOa Caic'd: C, 51.45; H, 2.59; N, 4.00 Found: C, 51.08; H, 2.40; N, 3.90; and Ex. 29 as a white solid (0.18 g, m.p. 272-274 °C); MS m/e 428 (M+H). Analysis for dsHaBNOa Caic'd: C, 41.99; H, 1.88; N, 3.26 Found: C, 42.25; H, 1.90; N, 3.14 EXAMPLE 30 7-(1,2-DIBROMOETHYL)-2-(4-HYDROXYPHENYL)-1.3-BENZOXAZOL-5-OL Step a) 5-Methoxy-2-(4-methoxyphenyl)-7-vinyl-1,3-benzoxa2ole. The title compound was prepared in substantially the same manner as described in Example 24, Route c), Step b) from 7-bromo-5-methoxy-2-(4-methoxyphenyl)-1,3- benzoxazole, and was obtained as a white solid, MS m/e 282 (M+H)+. Analysis for Ci7H15NO3 Calc'd: C, 72.58; H, 5.37; N, 4.98 Found: C, 72.33; H, 5.26; N, 4.72 Step b) 7-(1,2-Dibromoethyl)-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol. Boron tribromide (0.85 mL, 8.95 mmol) was added dropwise into a cold (-78 °C) mixture of 5-memoxy-2-(4-methoxyphenyl)-7-vinyl-1,3-benzoxazole (0.31 g, 1.12 mmol) and CH2CI2 (4 mL). The reaction mixture was allowed to warm up to room temperature. After stirring for 18 hours at room temperature the reaction mixture was slowly poured into cold (0 °C) ethyl ether (20 mL). Methyl alcohol (10 mL) was then slowly added into the reaction mixture. The new reaction mixture was washed with water (three times) and dried over MgSO4. Evaporation and purification by flash chromatography (hexanes / EtOAc 3/1) gave a light yellow solid (0.27 g, 59% yield, m.p. 175-177 °C); MS m/e 412 (M+H)+. Analysis for CHnBraNOa Calc'd: C, 43.62; H, 2.68; N, 3.39 Found: C, 43.85; H, 2.44; N, 3.33 EXAMPLE 31 7-(1-BROMOVINYL)-2-{4-HYDROXYPHENYL)-1t3-BENZOXAZOL-5-OL 1,8-Diazabicyclo[5.4.0]undec-7-ene (0.25g, 1.65mmol) was added into a solution of 7-(1,2-dibromoethyl)-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol (0.4 g, 0.96 mmol) and acetonitrile (4 mL). The reaction mixture was stirred for 24 hours, poured into cold (0 °C) HCI (1N, 10 mL) and extracted with EtOAc. The organic extracts were dried over MgSO4. Evaporation and purification by flash chromatography (CH2Cfe / hexanes / tsopropyl alcohol 15/5/1) gave a white solid (185 mg, 58% yield, m.p. 228-230 °C)- MS m/e 332 (M+H)+. Analysis for: C15H10BrNO3 Calc'd: C, 54.24; H, 3.03; N, 4.22 Found: C, 54.27; H. 2.94; N, 4.20 EXAMPLE 32 7-(1-BROMOVINYL)-2-(2-FLUORO-4-HYDROXYPHENYL)-1)3-BENZOXAZOL-5-OL The title compound was prepared in substantially the same manner as described in Examples 29-30, from 7-bromo-2-(2-fluoro-4-methoxyphenyl)-5-methoxy-1,3- benzoxazole, and was obtained as an off-white solid, m.p. 235-237 °C; MS m/e 350 (M+H)+. Analysis for C15H9BrFNO3 Calc'd: C, 51.45; H, 2.59; N, 4.00 Found: C, 51.63; H, 2.38; N, 3.98 EXAMPLE 33 7-(1-BROMOVINYL)-2-(2,3-DIFLUORO-4-HYDROXYPHENYL)-1,3-BENZOXA2OL- 5-OL The title compound was prepared in substantially the same manner as described in Examples 29-30, from 7-bromo-2-(2I3-difluoro-4-metnoxyphenyl)-5-methoxy-1,3- benzoxazole, and was obtained as an off-white solid, m.p. 240-242 °C; MS m/e 366 (M-H)+. Analysis for C1sHaBrF2NO3 Calc'd: C, 48.94; H, 2.19; N, 3.80 Found: C, 49.63; H, 2.33; N, 3.61 EXAMPLE 34 7-ALLYL-2-(3-FLUORO-4-HYDROXYPHENYL)-1,3-BENZOXX\ZOL-5-OL The title compound was prepared in substantially the same manner as described in Example 24, Route c, Step b, from 7-bromo-2-(3-fluoro-4-methoxyphenyl)-5- methoxy-1,3-benzoxazoIe, allyftributyltln and dichforobis(tri-otolylphosphine) palladium, followed by demethylation according to Example 20, Step e. The desired product was obtained as a light pink solid, m.p. 169-171 °C; MS m/e 284 (M-H)4. Analysis for: Ci6H12FNO3 Calc'd: C, 67.37; H, 4.24; N, 4.91 Found: C, 67.37; H, 4.16; N, 4.66 EXAMPLE 35 7-ETHYNYL-2-(4-HYDROXYPHENYL)-1I3-BENZOXAZOL-5-OL Tetrakis(triphenylphosphine)palladium(0) (52 mg, 0.045 mmol) was added into a mixture of 7-bromo-5-methoxy-2-(4-methoxyphenyl)-1,3-benzoxazole (0.3 g, 0.9 mmol), copperfl) iodide (17.1 mg, 0.09 mmol), ethynyl(trimethyOsilane (0.2 g mg, 2 mmol) and triethylamine (12 mL). The reaction mixture was stirred at 110 °C for 4 hours, poured into aqueous ammonium chloride and extracted with EtOAc/THF (1/1). The organic extracts were dried over MgSO4. Evaporation and purification by flash chromatography (hexanes/EtOAc 6/1) gave an off-white solid (0.27 g, 85% yield). The product was dissolved tn CH2Cl2(2 mL), cooled to -78 °C and boron tribromide (0.6 mL) was added dropwise. The reaction mixture was allowed to warm up to room temperature. After stirring for 18 hours at room temperature, the mixture was slowly poured into cold (0 °C) ethyl ether (10 mL). Methyl alcohol (3 mL) was then slowly added into the reaction mixture. The new reaction mixture was washed with water (three times) and dried over MgSO4. Evaporation and purification by flash chromatography (hexanes / EtOAc 3/1) gave a yellow solid (86 mg, 38% yield, m.p. 2-(4-HYDROXYPHENtL)-7-PROPYL-1,3-BENZOXAZOL-5-OL Tetrakis(triphenylphosphine)pallac ium(O) (70 mg, 0.06 mmol) was added into a mixture of 7-bromo-5-methoxy-2-(4-methoxyphenyl)-1,3-benzoxazole (0.4 g, 1.2 mmol), bromo(propyl)zinc (0.5 M ir reaction mixture was stirred at roci i temperature for 48 hours, poured into HCI (1N) and extracted with EtOAc. The ore off-white solid (0.14 g). The produ< and boron tribromide (0.35 ml) wa allowed to warm up to room tempe THF, 3.6 m(_, 1.8 mmol), and THF (4 mL). The anic extracts were dried over MgSO4. Evaporation and purification by flaj h chromatography (hexanes/EtOAc 6/1) gave an t was dissolved in CH2Cl2 (2 ml), cooled to -78 °C ; added dropwise. The reaction mixture was ature. After stirring for 18 hours at room temperature, the reaction mixture vi as slowly poured into cold (0 °C) ethyl ether (10 ml). Methyl alcohol (3 ml) was the new reaction mixture was washed v n slowly added into the reaction mixture. The rtth water (three times) and dried over MgSO4. Evaporation and purification by flash chromatography (hexanes / EtOAc 4/1) gave a white solid (90 mg, 27% yield, m.p. [110-112 °C); MS m/e 270 (M+H)+. Analysis for CHNOs Calc'd: C, 71.36; H, 5.61; N, 5.20 Found: C, 71.02; H, 5.58; N, 4.94 I EXAMPLE 37 7-BUTYL-2-(4-HYDROXYPHENYL)-1,3-BENZOXAZOL-5-OL rtPLE 38 7-CYCLOPENm-2K4-HYDfeOXYPHENYL)-1,3-BENZOXAZOL-5-OL The title compound was prepared in: Example 35, from 7-bromo-5-methox bromo(cyclopentyl)zinc. The desired 222 °C; MS m/e 296 (M+H). ubstantialfy the same manner as described in f-2-(4-methoxyphenyl)-1,3-benzoxazole and roduct was obtained as a white solid, m.p. 220- Analysis for C18H17NO3 ! Calc'd: C, 73.20; H, 5.80; N, 4.7 Found: C, 73.05; H, 5.74; N, 4.5f | EXAMPLE 39 ETHYL 5-HYDROXY-2-(4f HYDROXYPHENYLM.3-BENZOXAZOLE-7- | CARBQXYLATE Step a) 7-Bromo-5-([ferf-butyl(4imethyl)silyl]oxy}-2-(4-{fte/. butyl(dimethyl)si!yl]oxy}pheny|)-1I3-benzoxazo(e. The title compound was preparec in substantially the same manner as described in Example 24, Route a, Step a, froih 7rbromo-5-methoxy-2-(4-methoxyphenyl)-1,3- benzoxazole and te/f-butyl(chtoro|dimethylsilane. The desired product was obtained as a white solid, m.p. 90-91 °C; MS m/e 534 (M+H). Analysis for: CjsHaeBrNOaSfe, ] Calc'd: C, 56.16; H, 6.79; N, 2.621 Found: C, 55.66; H, 6.86; N, 2.681 Step b) Ethyl 5-hydroxy-2-(4-hy{iroxyphenyl)-1,3-benzoxazole-7-carboxylate. n-Butyl!ithium (2.5 M, 0.3 mL, 0.7{ solution of 7-bromo-5-{[ten'-butyl{d methyl)sifyl]oxy}r2-(4-{[tertbutyl( dimethyl)silyfjoxy}phenyl)-1,$-benzoxazole (0.4 g, 0.75 mmol) and THF (4 mL). The reaction mixture was allowed [(Cyanocarbonyl)oxy]ethane (84 tr mmol) was added dropwise into a cold (0 °C) to warm up to 40 °C, and then stirred for 2 hours, g) in THF (1 ML) was added into the reaction mixture and the reaction mixture was allowed to warm up to 0 °C and stirred for 1 hour. The reaction was quenchedlwith aqueous ammonium chloride, extracted with EtOAc, and dried over MgSO. Evaporation and purification by flash chromatography (hexanes / CH2CI2 /isopropyl alcohpl 18/2/1) gave a colorless oil (340 mg). The product was dissolved in THF (3.5[mL)3nd treated with tetrabutylammonium fluoride (1M in THF, 1.4 mL). The reaction] mixture was stirred for 30 mins., poured into HCI (1 N) and extracted with EtOAc. Thfe organic extracts were dried over MgSO4. Evaporation and purification by flasjh chromatography (hexanes / CHaCfe /isopropyl alcohol 5/2/1) gave a white solid (119 mg, 53% yield, m.p. 305-307 °C); MS m/e 300 2-(4-HYDROXYPHENYL)-7-PHENYL-1,3-BENZOXAZOL-5-OL Step a) 5-Methoxy-2-(4-methoxyphenyl)-7-phenyl-1,3-benzoxazole 7-Bromo-5-methoxy-2-(4-methoxyphenyl)-1,3-benzoxazole (200 mg, 0.60 mmol) and tetrakis(triphenylphosphine)pa!ladium(0) (63 mg, 0.03 mmol) were dissolved in toluene (5 mL) and stirred for 10 mins. at room temperature under a nitrogen atmosphere. Benzene boronic acid (110 mg, 0.90 mmol) was added, followed by aqueous sodium carbonate (2 M, 1.5 mL) and ethanol (2 mL). The reaction mixture was refluxed for 12 hours, diluted with water and extracted with EtOAc. The organic extracts were dried over MgSO. Evaporation and purification by flash chromatography (20% - 40% EtOAc/petroleum ether) gave the title compound as a light pink solid, mp 92 °C; MS m/e 332 (M+H)+. Analysis for C2iHi7NO3 Calcd: C, 76.12; H, 5.17; N, 4.23 Found: C, 75.86; H, 5.08; N, 4.07 Step b) 2-(4-Hydroxyphenyl)-7-pnenyl-1,3-benzoxazol-5-ol The title compound was prepared according to the procedure of Example 20, Step e (Route b), and was obtained as a purple solid, m.p. 255-258 °C; MS m/e 302 (M-H)+. Analysis for C19Hi3NO3 x 0.25 H2O Calcd: C, 74.14; H, 4.42; N, 4.55 Found: C, 73.81; H, 4.40; N, 4.35 EXAMPLE 41 5-HYDROXY-2-(4-HYDROXYPHENYL)-1,3-BENZOXAZOL-7-CARBONITRILE Step a) 5-Methoxy-2-(4-methoxyphenyl)-1,3-benzoxazole-7-carbonitrile. A solution of 7-bromo-5-methoxy-2-(4-methoxyphenyl)-1,3-benzoxazole (200 mg, 0.60 mmol) in anhydrous N,N dimethylformamide (1.5 mL) was stirred and heated to reflux under dry nitrogen with copper(l) cyanide (80 mg, 0.90 mmol) for 4 hours. The reaction mixture was cooled and poured into an excess of aqueous ethylenediaminetetraacetic acid. Isolation of the crude product gave the n'rtrile (164 mg, 98% yield) as tan needles from 30% EtOAc/petroleum ether; m.p. 180-183 °C; MS /n/e281(M+H)+. Analysis for Ci6H12N2O3 x 0.2 H2O Calcd: C, 66.84; H, 4.48; N, 9.74 Found: C, 66.63; H, 4.33; N, 9.60 Step b) 5-Hydroxy-2-{4-Hydroxyphenyl)-1I3-benzoxazol-7-carbonitriIe The title compound was prepared according to the procedure of Example 20, Step e (Route b), and was obtained as a light pink solid, mp 297-303 °C; MS m/e 253 (M+H)+. Analysis for C14H8N2O3 x 0.5 H2O Calcd: C, 64.37; H, 3.47; N, 10.72 Found: C, 64.44; H, 3.49; N, 9.92 EXAMPLE 42 5-HYDROXY-2-(4-HYDROXYPHENYL)-1,3-BENZOXAZOL-7-CARBOXAMlDE The title compound was isolated as a minor product from the reaction of Example 40, Step b, as a light tan solid, m.p. 325 °C; MS m/e 271 (M+H)+. Analysis for: C14H10N2O4 x 0.5 H2O Calcd: C, 60.22; H, 3.97; N, 10.03 Found: C, 59.71; H, 3.91; N, 9.84 EXAMPLE 43 2-(4-HYDROXYPHENYL)-7-METHOXY-1.3-BENZOXAZOL-5-OL A mixture of 7-bromo-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol (100 mg, 0.33 mmol) and copper(l) bromide (56 mg, 0.39 mmol) in anhydrous N,N dimethylformamide (1.5 ml) was stirred with freshly prepared sodium methoxide (15 wt % in methanol, 1 mJ) and heated to 120 °C for 4 hours. The reaction mixture was cooled and diluted with HCI (1N, 5 ml). Isolation of the crude product with ethyl acetate followed by flash chromatography (40% - 50% EtOAc/petroleum ether) gave the title compound as an off-white solid (50 mg, 60% yield, mp 225 - 228 °C); MS m/e 258 (M+H)+. Analysis for C14HnNO4x 0.75 H2O Calcd: C, 62.11; H, 4.65; N, 5.17 Found: C, 62.53; H, 4.73; N, 5.02. EXAMPLE 44 7-ETHYL-2-(4-HYDROXYPHENYD-1,3-BENZOXA20L-5-OL Step a) 7-Ethyl-5-methoxy-2-(4-methoxyphenyl)-1,3-benzoxazole. n-ButyJIithium (2.5 N, 0.43 mL, 1.08 mmol) was added dropvyise into a cold (-78 °C) mixture of 7-bromo-5-methoxy-2-(4-methoxyphenyl)-1,3-benzoxazole (300 mg, 0.90 mmol) and THF (2 mL). The reaction mixture was allowed to stir for 0.5 hours, lodoethane (0.14 mL, 1.8 mmol) was added dropwise into the reaction mixture. The reaction mixture was allowed to warm to room temperature and stirred for 2 hours. The reaction was quenched with aqueous ammonium chloride, poured into water, and extracted with EtOAc. The organic extracts were washed with brine and dried over MgSO4. Evaporation and flash chromatography (20% EtOAc/petroleum ether) gave the product (231 mg, 91% yield) as a light brown solid: m.p. 85 C; MS m/e 284 (M+H)+. Analysis for: C17H17NO3 x 0.2 H2O Calc'd: C, 70.28; H, 6.17; N, 4.94. Found: C, 70.12; H, 5.74; N, 4.82. Step b) 7-EthyI-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-oI The title compound was prepared according to the procedure of Example 20, Step e (Route b), and was obtained as a light brown solid (98% yield), m.p. 110 -115 °C; MS m/e256(M+H)+. EXAMPLE 45 7-ETHYL-2-(2-ETHYL-4-HYDROXYPHENYL)-1,3-BENZOXAZOL-5-OL Step a) 7-Ethyl-5-methoxy-2-(2-ethyI-4-methoxyphenyl)-1f3-benzoxa20le The title compound was prepared according to the procedure of Example 43, Step a, employing two equivalents of n-butyllithium, and the crude product was used directly in the next step. Step b) 7-Ethyl-2-(2-ethyl-4-hydroxyphenyl)-1,3-benzoxazol-5-ol The title compound was prepared from 7-ethyl-5-methoxy-2-(2-ethyl-4- methoxyphenyl)-1,3-benzoxazole according to the procedure of Example 20, Step e (Route b), and was obtained as a gray solid (87% yield); MS m/e 284 (M+H). EXAMPLE 46 5-HYDROXY-2-(4-HYDROXYPHENYL)-1,3-BENZOXAZOLE-7-CARBALDEHYDE Step a) 5-Methoxy-2-(4-methoxyphenyl)-1,3-berizoxazole-7-carbaldehyde. The title compound was prepared according to the procedure of Example 43, Step a, employing N-methylformanilide as the electrophile to give a light orange solid (94%, m.p. 153 - 155 °C); MS m/e 284 (M+H)+. Analysis for C16H13NO4 Calc'd: C, 67.84; H, 4.63; N, 4.94 Found: C, 67.58; H, 4.53; N, 4.75 Step b) 5-Hydroxy-2-(4-hydroxyphenyl)-1,3-benzoxazole-7-carbaldehyde The title compound was prepared from 5-methoxy-2-(4-methoxyphenyl)-1,3- benzoxazole-7-carbaldehyde according to the procedure of Example 20, Step e (Route b) and was obtained as a dark yellow solid (99% yield, m.p. 273 - 275 °C); MS m/e 256 (M+H)+. Analysis for: C14H9NO4x 0.25 H2O Calcd.: C, 64.74; H, 3.69; N, 5.39 Found: C, 64.32; H, 3.59; N, 5.18. EXAMPLE 47 7-(HYDROXYMETHYL)-2-(4-HYDROXYPHENYL)-1,3-BENZOXAZOL-5-OL Step a) 5-Methoxy-7-(hydroxymethyl)-2-(4-methoxyphenyl)-1,3-benzoxazole Sodium borohydride (66.8 mg, 1.76 mmol) was added into a solution of 5-methoxy-2- (4-methoxyphenyl)-1,3-benzoxazoIe-7-carbaldehyde (250 .mg, 0.88 mmol) in anhydrous MeOH (8 mL) at 0 °C. The reaction mixture was stirred for 30 mins. and then evaporated in vacuum. The residue was dissolved in diethyf ether and washed with water and brine, dried over MgSO4 and filtered. Evaporation and flash chromatography (50% EtOAc/petroteum ether) gave (210 mg, 83%) of the product, which was used directly in the next reaction. Step b) 7Hydroxymethyl)-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol. The title compound was prepared from 5-metnoxy-7-(hydroxymethy/)-2-(4- methoxyphenyl)-1,3-benzoxazole according to the procedure of Example 20, Step e (Route b), and was obtained as a light brown solid, m.p. 282 C (dec); MS m/e 258 (M+H)+. Analysis for: C14Hi]NO4x 0.5 H2O Calcd.: C, 63.16; H, 4.54; N, 5.26 Found: C, 63.33; H, 4.36; N, 5.04 EXAMPLE 48 7-(BROMOMETHYL)-2-(4-HYDROXYPHENYL)-1,3-BENZOXA2OL-5-OL The title compound was prepared according to the procedure of Example 20, step e (Route b), from 5-methoxy-7-(hydroxymethyl)-2-(4-methoxyphenyl)-1,3-benzoxazole wrri prolonged stirring in the presence of boron tribromide, and was obtained as a iicnt brown solid, m.p. 250 - 260 °C (dec); MS m/e 321 (M+H)+. Analysis for. C14H10BrNO3 Caicd: C, 52.52; H, 3.15; N, 4.38 Fojnd: C, 52.26; H, 3.17; N, 4.07 EXAMPLE 49 [5-HYDROXY-2-(4-HYDROXYPHENYL)-1,3-BENZOXAZOU7-YL] ACETONITRILE Tc a solution of 7-(bromomethyl)-2-(4-hydroxyphenyl)-1)3-benzoxazol-5-ol (122 mg, 0.40 mmol) in N,N-dimethylformamide (1.5 ml) was added 18-crown-6-ether (202 me, 0.80 mmol) and potassium cyanide (131 mg, 2 mmol). The reaction mixture was alfowed to stir for 2 hours and then poured into water and extracted with EtOAc. The organic extracts were washed with brine and dried over MgSO4. Evaporation and flash chromatography (50%-60% EtOAc/petroleum ether) gave the product (80 mg, 75 yield) as a gray solid, m.p. 170-180 C; MS m/e 265 (M-Hf. Analysis for C15H10N2O3X 1.5 H2O Caicd: C, 61.43; H, 4.47; N, 9.55 Found: C, 61.41; H, 4.21; N, 9.19 EXAMPLE 50 7-{ 1 -HYDROXY-1-METHYLETHYL)-2-(4-HYDROXYPHENYL)-1,3-BENZOXAZOL-SOLJ Step a) 2-[5-Wlethoxy-2-(4-methoxyphenyl)-1,3-benzoxazole-7-yI] propan-2-ol Trre title compound was prepared according to the procedure of Example 43, Step a, from 7-bromo-5-methoxy-2-(4-methoxyphenyl)-1,3-ben2oxazole, employing acetone as the electrophile, to give a white solid (78% yield, m.p. 149 °C); MS m/e 314 (M+H) Analysis for: Ci8HigNO4 Cate'd: C, 68.99; H, 6.11; N, 4.47. Found: C, 68.78; H, 6.13; N, 4.35. Step b) 7-(1-Hydroxy-1-methylethyl)-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol] The title compound was prepared from 2-[5-methoxy-2-(4-methoxyphenyl)-1,3- benzoxazole-7-yl] propan-2-ol according to the procedure of Example 20, Step e (Route b), and was obtained as a dark brown solid (90% yield, m.p. 180-185 °C); MS Analysis for C16H1SNO4 x 0.5 H2O Gated.: C, 65.30; H, 5.48; N, 4.76 Found: C, 65.03; H, 5.20; N, 4.72 EXAMPLE 51 2-(4-HYDROXYPHENYL)7-ISOPROPENYL-1,3-BENZOXAZOL-5-OL Pyridine hydrochloride (400 mg) was heated to 190 °C. To the melt was added 2-[5- methoxy-2-(4-methoxyphenyl)-1,3-benzoxazole-7-yl] propan-2-ol (114mg, 0.36 mmol) and the reaction was stirred for 2 hours. The reaction mixture was cooled to room temperature, dissolved in water and extracted with EtOAc. The organic layers were combined and washed with HCI (1N), water then brine and dried over MgSO4. Evaporation and purification by flash chromatography (50%-60% EtOAc/petroleum ether) gave (40 mg, 41% yield) of the product as a light red-brown solid, m.p. 225- 228 °C; MS m/e 268 (M+H)+. Analysis for C16H13NO3x 0.5 H20 Calcd.: C, 69.56; H, 5.11; N, 5.06 Found: C, 69.46; H, 5.22; N, 4.56 EXAMPLE 52 2-(4-HYDROXYPHENYL)-7-ISOPROPYL-1,3-BENZOXAZOL-5-OL] 2-(4-Hydroxyphenyl)-7-isopropenyI-1,3-benzoxazol-5-ol (64 mg, 0.24 mmol) was dissolved in a mixture of EtOAc (5 mL) and absolute ethanol (5 mL), and placed under an inert atmosphere with argon. To the solution was added 10% Pd-C. (25 mg). The solution was hydrogenated on a Parr apparatus at 25 psi for 3 hours. The solution was filtered through Celite and rinsed with ethanol. The filtrate was concentrated and the residue purified by flash chromatography (50% EtOAc/petroleum ether) to give the product (58 mg, 90% yield) as a tan solid, m.p. 200 °C; MSm/e270(M+H)+. EXAMPLE 53 7-BROMO-2-(4-HYDROXY-3-(TRIFLUOROMETHYL)PHENYL)-1,3-BENZOXAZOL- 5-OL Stepa)2-Bromo-4-methoxy-6-{[4-methoxy-3-(trifluoromethyl)benzoyl]amino} phenyl4-methoxy-3-(trifluoromethyl)benzoate. The title compound was prepared in substantially the same manner as described in Example 20, Step c, from 2-amino-6-bromo-4-methoxyphenol and 4-methoxy-3- trifluoromethyl benzoyi chloride. The product was obtained as an off-white solid, m.p. 205-208 °C; MS m/e 622 (M+H)+. Analysis for CzsHBrFeNOe Calc'd: C, 48.25; H, 2.92; N, 2.25 Found: C, 48.47; H, 2.76; N, 2.16 Step b) 7-Bromo-5-methoxy-2-{4-methoxy-3-{trifluoromethyl)phenyl]-1J3- benzoxazole The title compound was prepared in substantially the same manner as described in Example 20, Step d (Route a), from 2-bromo-4-methoxy-6-{[4-methoxy-3- - hydroxyphenyl)-7-vinyl-1,3-benzoxazol-5-glucoronide or a pharmaceutically acceptable salt thereof. 36. The compound according to claim 1, which is 4-bromo-2-(3'-fluoro-4'- hydroxyphenyl^T-vinyl-I.S-benzoxazol-S-suIfate or a pharmaceutically acceptable salt thereof. 37. The compound according to claim 1, which is 4-bromo-2-(3 -fluoro-4'- glucuronide phenyl)-7-vinyl-1,3-benzoxazol-5-glucuronide or a pharmaceutically acceptable salt thereof. 38. The compound according to claim 1, which is 4-bromo-2-(3'-fluoro-4'- glucuronide phenyl)-7-vinyl-1,3-benzoxazol-5-sulfate or a pharmaceutically acceptable salt thereof. 39. The compound according to claim 1, which is 4-bromo-2-(3'-fluoro-4'-sulfate phenyl)-7-vinyl-1,3-benzoxazol-5-glucuronide or a pharmaceutically acceptable salt thereof. 40. The compound according to claim 1, which is 4-bromo-2-(3'-fluoro-4'-sulfate phenyl)-7-vinyl-1,3-benzoxazol-5-sulfate or a pharmaceutically acceptable salt thereof. 41. The compound according to claim 1, which is 4,6-dibromo-2-{3'-fluoro-41- glucuronide phenyl)-7-vinyH ,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 42. The compound according to claim 1, which is 4,6-dibromo-2-(3'-fluoro-4'- sulfate phenyl)-7-vinyl-1,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 43. The compound according to claim 1, which is 4,6-dibromo-2-(3'-fluoro-4'- hydroxyphenyl)-7-vinyl-1,3-benzoxazol-5-glucuronide or a pharmaceutically acceptable salt thereof. 44. The compound according to claim 1, which is 4,6-dibromo-2-(3'-fluoro-4'- hydroxyphenyl)-7-vinyl-1,3-benzoxazol-5-sulfate or a pharmaceutically acceptable salt thereof. 45. The compound according to claim 1, which is 4,6-dibromo-2-(3'-fluoro-4Iglucuronide phenyI)-7-vinyl-1,3-benzoxazol-5-glucuronide or a pharmaceutically acceptable salt thereof. 46. The compound according to claim 1, which is 4,6-dibromo-2-(3'-fluoro-4'- glucuronide phenyl)-7-vinyl-1,3-benzoxazol-5-sulfate or a pharmaceutically acceptable salt thereof. 47. The compound according to claim 1, which is 4,6-dibromo-2-(3'-fluoro-4'- sulfate phenyl)-7-vinyH,3-benzoxazol-5-glucuronide or a pharmaceutically acceptable salt thereof. 48. The compound according to claim 1, which is 4,6-dibromo-2-(31-fluoro-4'- sulfate phenyl)-7-vinyH,3-benzoxazol-5-sulfate or a pharmaceutically acceptable salt thereof. 49. The compound according to claim 1, which is 7-(1-bromovinyl)-2-(2'-fluoro-4'- glucuronide phenyl)-1,3-benzoxazol-5-ol or a pharmaceutically acceptable 50. The compound according to claim 1, which is 7-(1 -bromovinyl)-2-(2'-fluoro-4'- sulfate phenyl)-1,3-benzoxazol-5-ol or a pharrnaceutically acceptable salt thereof. 51. The compound according to claim 1, which is 7-(l-bromovinyl)-2-(2f-fluoro-4'- hydroxyphenyI)-1,3-benzoxazol-5-glucuronide or a pharmaceuticaHy acceptable salt thereof. 52. The compound according to claim 1, which is 7-(1-bromovinyl)-2-(2'-fluoro-4'- hydroxyphenyl)-1,3-benzoxazol-5-sulfate or a pharmaceuticaHy acceptable salt thereof. * 53. The compound according to claim 1, which is 7-(1-bromovinyl)-2-{2I-fluoro-4Iglucuronide phenyl)-1,3-benzoxazol-5-glucuronide or a pharmaceuticaHy acceptable salt thereof. 54. The compound according to claim 1, which is 7-(1-bromovinyl)-2-(2'-fluoro-4'- glucuronide phenyl)-1,3-benzoxazol-5-sulfate or a pharmaceuticaHy acceptable salt thereof. 55. The compound according to claim 1, which is 7-(1-bromovinyl)-2-(2'-fIuoro-4'- sulfate phenyl)-1,3-benzoxazol-5-glucuronide or a pharmaceuticaHy acceptable salt thereof. 56. The compound according to claim 1, which is 7-(1-bromovinyl)-2-(2'-fluoro-4'- sulfate phenyl)-1,3-benzoxazol-5-sulfate or a pharmaceuticaHy acceptable salt thereof. 57. The compound according to claim 1, which is 7-(1-bromovinyl)-2-(2',3'- difluoro-4'-glucuronide phenyl)~1,3-benzoxazol-5-ol or a pharmaceuticaHy acceptable salt thereof. 58. The compound according to claim 1, which is 7-(1-bromovinyl)-2-(2',3'- difluoro-4'-sulfate phenyl)-1,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 59. The compound according to claim 1, which is 7-(1-bromovinyl)-2-(2',3'- difIuoro-4'-hydroxyphenyl)-1,3-benzoxazol-5-glucuronide or a phdrmaceutically acceptable salt thereof. 60. The compound according to claim 1, which is 7-(1-bromovinyl)-2-(2',3'- difluoro-4'-hydroxyphenyl)-1,3-benzoxazol-5-sutfate or a pharmaceutically acceptable salt thereof. 61. The compound according to claim 1, which is 7-(1-bromovinyl)-2-(2',3'- difluoro-4'-glucuronide phenyl)-1,3-benzoxazol-5-glucuronide or a pharmaceutically acceptable salt thereof. 62. The compound according to claim 1, which is 7-(1-bromovinyl)-2-(2')3'- d ifluoro-4'-glucuronide phenyl)-1,3-benzoxazol-5-sulfate or a pharmaceutically acceptable salt thereof. 63. The compound according to claim 1, which is 7-(1-bromovinyl)-2-(2',3'- difluoro-4'-sulfate pheny!)-1,3-benzoxazo!-5-glucuronide or a pharmaceutically acceptable salt thereof. 64. The compound according to claim 1, which is 7-(1-bromovinyl)-2-(2',3'- difluoro-4'-sulfate phenyl)-1,3-benzoxazol-5-suIfate or a pharmaceutically acceptable salt thereof. 65. The compound according to claim 1, which is 7-allyl-2-(3'-fluoro-4'- glucuronide phenyl)-1,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 66. The compound according to claim 1, which is 7-al|yl-2-(3'-fluoro-4'-suIfate pheny!)-1,3-benzoxazo^-ol or a pharmaceutically acceptable salt thereof. 67. The compound according to claim 1, which is 7-allyl-2-(3'-fluoro-4'- hydroxyphenyi)-1,3-bertzoxazo!-5-glucuronide or a pharmaceutically acceptable salt thereof. 68. The compound according to claim 1, which is 7-allyl-2-(3'-fluoro-4'- hydroxyphenyl)-1,3-benzoxazol-5-sulfate or a pharmaceutically acceptable salt thereof. 69. The compound according to claim 1, which js 7-aIlyl-2-(3'-fluoro-4Iglucuronide phenyI)-1,3-benzoxazol-5-glucuronide or a pharmaceutically acceptable salt thereof. 70. The compound according to claim 1, which is 7-ally!-2-(3'-fluoro-4'- glucuronide phenyl)-1,3-benzoxazol-5-sulfate or a pharmaceutically acceptable salt thereof. 71. The compound according to claim 1, which is 7-alIyl-2-(3'-fluoro-4'-sulfate pheny])-1,3-benzoxazo!-5-g!ucuronide or a pharmaceutically acceptable salt 72. The compound according to claim 1, which is 7-allyl-2-(3'-fluoro-4'-sulfate phenyI)-1,3-benzoxazol-5-sulfate or a pharmaceuticalfy acceptable salt thereof. 73. The compound according to claim 1, which is 2-(3',5'-difluoro-4'-glucuronide phenyl)-7-vinyl-1,3-benzoxazo!-5-ol or a pharmaceutically acceptable salt thereof. 74. The compound according to claim 1, which is 2-(3',5'-difluoro-4'-sulfate phenyl)-7-vinyl-1,3-benzoxazol-5-ol or a pharmaceutically acceptable salt 75. The compound according to claim 1, which is 2-(3> 15'-difluoro-4'-hydroxy phenyl)-7-vinyl-1 s3-benzoxazol-5-g!ucuronide or a pharmaceutically acceptable salt thereof. 76. The compound according to claim 1, which is 2-(3',5'-difluoro-4'- hydroxyphenyl)-7-vinyl-1,3-benzoxazol-5-sulfate or a pharmaceutically acceptable salt thereof. 77. The compound according to claim 1, which is 2-(3',5'-difluoro-4 -glucuronide phenyl)-7-vinyl-1,3-benzoxazol-5-gluguronide or a pharmaceutically acceptable salt thereof. 78. The compound according to claim 1, which is 2-(3',5'-difIuoro-4'-glucuronide phenyl)-7-vinyl-1,3-benzoxazol-5-sulfate or a pharmaceutically acceptable salt thereof. 79. The compound according to claim 1, which is 2-(3',5'-difluoro-4'-sulfate phenyl)-7-vinyl-1.,3-benzoxazol-5-glucuronide or a pharmaceutically acceptable salt thereof. 80. The compound according to claim 1, which is 2-(3',5'-difluoro-4'-sulfate phenyl)-7-vinyl-1,3-benzoxazol-5-sulfate or a pharmaceutically acceptable salt thereof. 81. The compound according to claim 1, which is 2-(3'-fluoro-4'-glucuronide phenyl)-7-(1-fluorovinyl)-1,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 82. The compound according to claim 1, which is 2-(3'-fluoro-4'-sulfate phenyl)-7- (1-fluorovinyl)-1,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 83. The compound according to claim 1, which is 2-(3 -fluorcM'-hydroxyphenyl}- 7-(1 -fluorovinyl)-1,3-benzoxazol-5-glucuronide or a pharmaceutically acceptable salt thereof. 84. The compound according to claim 1, which is 2-(3'-fluoro-4'-hydroxyphenyl)- 7-(1-fluorovinyl)-1,3-benzoxazol-5-sulfate or a pharmaceutically acceptable 85. The compound according to claim 1, which is 2-(3-fluoro-4'-glucuronide phenyl}-7-(1-fluorovinyl)-1,3-benzoxazol-5-glucuronide or a pharmaceutically acceptable salt thereof. 86. The compound according to claim 1, which is 2-(3'-fluoro-4'-glucuronide phenyl)-7-(1-fluorovinyi)-1,3-benzoxazol-5-suifate or a pharmaceutically acceptable salt thereof. 87. The compound according to claim 1, which is 2-(3'-fluoro-4'-sulfate phenyl)-7- (1-fluorovlnyl)-1,3-benzoxazol-5-glucuronide or a pharmaceutically acceptable 88. The compound according to claim 1, which is 2-(3'-fluoro-4'-sulfate phenyl)-7- (1-f!uorovinyl)-1,3-benzoxazol-5-sulfate or a pharmaceutically acceptable salt thereof. 89. The compound according to claim 1, which is 2-(3'-fluoro-4'-glucuronide phenyl)-7-vinyl-1,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. SO. The compound according to claim 1, which is 2-(3'-fluoro-4'-sulfate phenyl)-7- vinyH ,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 91. The compound according to claim 1, which is 2-(3'-fluoro-4'-hydroxy phenyl)- 7-vinyH ,3-benzoxazol-5-glucuronide or a pharmaceutically acceptable salt thereof. 92. The compound according to claim 1, which is 2-(3'-fluoro-4'-hydroxy phenyl)- 7-vinyM ,3-benzoxazol-5-suffate or a pharmaceutically acceptable salt * 93. A compound which is a gluocuronide derivative, a sulfate derivative, or a glucuronide-sulfate derivative of: .a) 2-(5-hydroxy-1,3-benzoxazol-2-y!)benzene-1,4-diol; b) 3-(5-hydroxy-1,3-benzoxazol-2-yl)benzene-1,2-diol; c) 2-(3-fluoro-4-hydroxyphenyl)-1,3-benzoxazol-5-ol; d) 2-(3-chloro~4-hydroxyphenyl)-1,3-benzoxazol-5-ol; e) 2-{2-chloro-4-hydroxyphenyl)-1,3-benzoxazol-5-ol; 0 2-(3-fluoro-4-hydroxyphenyl)-1,3-benzoxazol-6-ol; g) 2-(3-ferf-butyl-4-hydroxyphenyl)-1,3-benzoxazol-6-ol; h) 2-(6-hydroxy-1,3-benzoxazoI-2-yl)benzene-1,4-diol; i) 3-(6-hydroxy-1,3-benzoxazol-2-yl)benzene-1,2-diol; j) 4-(6-hydroxy-1,3-benzoxazol-2-yl)benzene-1,2-diol; k) 2-(3-chloro-4-hydroxyphenyl)-1,3-benzoxazol-6-of; I) 4-(5-hydroxy-1,3-benzoxazol-2-yl)benzene-1,3-diol; m) 4-(6-hydroxy-1,3-benzoxazol-2-yl)benzene-1,3-diol; n) 6-chloro-2-(3-fIuoro-4-hydroxyphenyl)-1,3-benzoxazol-5-ol; o) 6-bromo-2-(3-fluoro-4-hydroxyphenyl)-1,3-benzoxazoI-5-ol; p) 6-ch!oro-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol; q) 5-ch!oro-2-{4-hydroxypnenyl)-1,3-benzoxazol-6-6l; r) 7-bromo-2-(3-fIuoro-4-hydroxyphenyl)-1,3-benzoxazof-5-ol; s) 7-bromo-2-(2-fluoro-4-hydroxyphenyl)-1,3-benzoxazo!-5-ol; t) 7-bromo-2-(2,3-difluoro-4-hydroxyphenyl)-1,3-benzoxazol-5-ol; u) 2-(4-hydroxyphenyl)-7-vinyM ,3-benzoxazoH5-ol.; v) 7-(1,2-dibrornoethyl)-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol; w) 7-(1-bromovinyl)-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol; x) 7-ethynyl-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-oI; y) 2-(4-hydroxyphenyl)-7-propyl-1,3-benzoxazol-5-ol; z) 7-butyl-2-(4-hydroxyphenyl)-1>3-benzoxazoJ-5-ol; aa) 7-cyclopentyl-2-(4-hydroxyphenyl)-1,3-benzoxazoi-5-ol; bb) ethyl 5-hydroxy-2-(4-hydroxyphenyl)-1,3-benzoxazole-7-carboxylate; cc) 2-(4-hydroxyphenyl}-7-phenyM,3-benzoxazol-5-ol; dd) 2-(4-hydroxyphenyl)-7-methoxy-1,3-benzoxazol-5-ol; ee) 7-ethyl-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol; ff) 7-ethyJ-2-(2-ethyl-4-hydroxyphenyl)-1,3-benzoxazol-5-ol; gg) 5-hydroxy-2-(4-hydroxyphenyl)-1,3-benzoxazole-7-carbaldehyde; hh) 7-(hydroxymethyl)-2-{4-hydroxyphenyl)-1,3-benzoxazol-5-ol; ii) 7-(bromomethyl)-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol; jj) [5-hydroxy-2-(4-hydroxyphenyl)-1,3-benzoxazo)-7-yl] acetonitrile; kk) 7-(1 -hydroxy-1 -methyIethyl)-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol]; II) 2-(4-hydroxyphenyl)-7-isopropenyl-1,3-benzoxazol-5-ol; mm) 2-(4-hydroxyphenyl)-7-isopropyl-1,3-benzoxazol-5-ol]; nn) 7-bromo-2-(4-hydroxy-3-{trifluoromethyl)phenyl)-1,3-benzoxazol-5-ol; oo) 7-(2-fijryl)-2-(4-hydroxyphenyl) -1,3-be^zoxazo^5-ol ; pp) 2-(3-fluoro-4-hydroxyphenyl)- 7-(2-furyl)-1l3-benzoxazol-5-ol; qq) 2-(4-hydroxyphenyl)-7-thien-2-yH,3-benzoxazol-5-ol; rr) 2-(4-hydroxyphenyl)-7-(1,3-thiazol-2-yl)-1,3-benzoxazol-5-ol; ss) 2-(3-fluoro-4-hydroxyphenyl)-5-hydroxy-1,3-benzoxazoIe-7- carbonitrile; tt) 4-bromo-2-(4-hydroxyphenyl)-7-methoxy-1,3-benzoxazol-5-ol; uu) 4,6-dibromo-2-(4-hydroxyphenyl)-7-mefhoxy-1l3-benzoxazol-5-ol; or w) 7-bromo-2-(3,5-difIuoro-4-hydroxyphenyl)-1,3-benzoxazol-5-ol; or a pharmaceutically acceptable salt thereof. 94. A method of treating or inhibiting prostatitis or interstitial cystitis in a mammal in need thereof, which comprises providing to said mammal an effective amount of a compound of any one of claims 1 to 93. 95. A method of treating or inhibiting inflammatory bowel disease, Crohn's disease, ulcerative proctitis, or colitis in a mammal in need thereof, which comprises providing to said mammal an effective amount of a compound of any one of claims 1 to 93. 96. A method of treating or inhibiting prostatic hypertrophy, uterine leiomyomas, breast cancer, endometrial cancer, polycystic ovary syndrome, endometrial polyps, benign breast disease, adenomyosis, ovarian cancer, melanoma, prostrate cancer, colon cancer, glioma or astioblastomia in a mammal in need thereof, which comprises providing to said mammal an effective amount of a compound of any one of claims 1 to 93. 97. A method of lowering cholesterol, triglycerides, Lp(a), or LDL levefs; inhibiting or treating hypercholesteremia, hyperlipidemia, cardiovascular disease, atherosclerosis, hypertension, peripheral vascular disease, restenosis, or vasospasm; or inhibiting vascular wall damage from cellular events leading toward immune mediated vascular damage in a mammal in need thereof, which comprises providing to said mammal an effective amount of a compound of any one of claims 1 to 93. 98. A method of providing cognition enhancement or neuroprotection; or treating or inhibiting senile dementias, Alzheimer's disease, cognitive decline, stroke, anxiety, or neurodegenerative disorders in a mammal in need thereof, which comprises providing to said mammal an effective amount of a compound of any one of claims 1 to 93. 99. A method of treating or inhibiting free radical induced disease states in a mammal in need thereof, which comprises providing to said mammal an effective amount of a compound of ^ny one of claims 1 to 93. 100. A method of treating or inhibiting vaginal or vulvar atrophy, atrophic vaginitis, vaginal dryness, pruritus, dyspareunia, dysuria, frequent urination, urinary incontinence, urinary tract infections in a mammal in need thereof, which comprises providing to said mammal an effective amount of a compound of any one of claims 1 to 93. 101. A method of treating or inhibiting vasomotor symptoms in a mammal in need thereof, which comprises providing to said mammal an effective amount of a compound of any one of claims 1 to 93. 102. A method of inhibiting conception in a mammal in need thereof, which comprises providing to said mammal an effective amount of a compound of any one of claims 1 to 93. 103. A method of treating or inhibiting arthritis in a mammal in need thereof, which comprises providing to said mammal an effective amount of a compound of any one of claims 1 to 93. 104. The method according to claim 103, wherein the arthritis is rheumatoid arthritis, osteoarthritis, or spondyloarthropathies. 105. A method of treating or inhibiting joint swelling or erosion; or treating or inhibiting joint damage secondary to arthroscopic or surgical procedures in a mammal in need thereof, which comprises providing to said mammal an effective amount of a compound of any one of claims 1 to 93. 106. A method of treating or inhibiting psoriasis or dermatitis in a mammal in need thereof, which comprises providing to said mammal an effective amount of a compound of any one of claims 1 to 93. 107. A method of treating or inhibiting ischemia, reperfusion injury, asthma, pleurisy, multiple sclerosis, systemic lupus erythematosis, uveitis, sepsis, hemmorhagic shock, or type II diabetes in a mammal in need thereof, which comprises providing to said mammal an effective amount of a compound of any one of claims 1 to 93. 108. A method of treating or inhibiting endometrtosis in a mammal in need thereof, which comprises providing to said mammal an effective amount of a compound of any one of claims 1 to 93. 109. A pharmaceutical composition which comprises a compound of any one of claims 1 to 93, and a pharmaceutical carrier. 110. The Invention substantially such as herein before described.