BACKGROUND OF THE INVENTION This invention relates to substituted benzoxazoles which are useful as estrogencc agents. The pleiotropic effects of estrogens in mammalian tissues have been well documented, and it is now appreciated that estrogens affect many organ systems [Mendelsonn and Karas. New England Journal of Medicine 340: 1801-1811 (1999), Epperson, et al., Psychosomatic Medicine 61: 676-697 (1999), Crandal,, Journal of Womens Health & Gender Based Medicine 8: 1155-1166 (1999), Monk and Brodaty, Demeniia & Geriatric Cognitive Disorders 11:1-10 (2000). Hum and Macrae, Journal of Cerebral Blood Flow & Metaboiism 20: 631-652 (2000), Calvin, Maturitas 34: 195- 210 (2000.. Finking, et al.. Zeitschrift fur Kardiologie 89: 442-453 (2000). Brineat. Maturttas 35: 107-117 (2000), A1-Azzawi, 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 interaciion with estrogen receptors leading to alteraiions in gene transcription. Estrogen receptors are Hgand-activated transcription factors and belong to the nudlear hormone receptor superfamily. Other members of this famlly include the progesterone, androgen, glucocoriicoid 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 interaciing with other transcription factors (such as AP1). which in turn bind directly to specific DNA sequences {Moggs and Orphanide,, EMBO Reports 2: 775-781 (2001). Hall. et al.. Journal of Biological Chemistry 276: 36869-36872 (2001), McDonnell, Principles Of Molecular Regulation. p351-361(2000)]. A class of "coregulatory" proteins can also interact with the ligand- bound receptor and further modulate its transcriptionll activity [McKenna, et at., Endocrine Reviews 20: 321-344 (1999)]. It has also been shown that estrogen receptors can suppress NFκB-mediated transcription in both a ligand-dependent and independent manner [Quaedackers. et ar., Endocrinology 142: 1156-1166 (2001., Bhat, et aI., 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 phosphorylation is mediated by growth factors such as EGF and causes changes in gene transcription in the absence o( ligand [Maggs and Orphanides, EMBO Reports 2: 775-781 (2001), Hall, et aI., Journal of Biological Chemistry 276: 36869-36872 (2001)]. 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)1. 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 aI., Nature 320: 134-9 (1986)]. The second form of the estrogen receptor was found comparatively recently and is called ERI3 [Kuiper, et al., Proceedings of the National Academy of Sciences of the United States of America 93: 5925-5930 (1996)]. Early work on ERI3 focused on defining its affinity for a variety of ligands and indeed, some differences with ERa were seen. The tissue distribution of ERB 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 ERB [Couse, et al., Endocrinology 138: 4613-4621 (1997), Kuiper, et al., Endocrinology 138: 863-870 (1997)]. Even within the same organ, the distribution of ERa and ERB can be compartmentaiized. For example, in the mouse ovary, ERB is highly expressed in the granulosa cells and ERa is restricted to the thecal and stromal cells tSar and Welsch, Endocrinology 140: 963-971 (1999), Fitzpatrick, et aI., 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 i ERB can form heterodimers [Cowley, et at,, 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-esttadiol. 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)1. 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 Iigands 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 at, 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 17p-esttadiol and diethylstilbestero.. 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. DESCRIPTION OF THE INVENTION This invention provides estrogenic compound of formula I having the structure, wherein ~1 is hydrogen, hydroxyl, halogen, alkyl of 1-6 carbon atoms, triflouroalkyl of 1-6 carbon atoms, cycloalkyl 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 0, N or S, -NO2, -NR5R6, -N(R5)CORe, -CN, -CHFCN, -CFzCN, alkynyl of 2-7 carbon atoms, or alkenyl of 2-7 carbon atoms; wherein the alkyl or alkenyl moieties are optionally substituted with hydroxyl, -eN, halogen, trifluoroalkyoff 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5. -NO2. CONRsRa. NR5R6 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, or alkynyl of 2-7 carbon atoms, trifluoroalkyl of 1-6 carbon atoms, or trifluoroalkoxy of 1-6 carbon atoms; wherein the alkyl or alkenyl moieties are optionally substituted with hydroxyl,. -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5. -CO2R5. -NO2, CONR5R6. NR5R6 or N(R5)COR6; R3, R3a, and R4 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 or alkenyl moieties are optionally substituted with hydroxyl, -CN. halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 or N(R5)COR6; R5, R6 are each, independently hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms; X is O,S,orNR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or-SO2R5; or a pharmaceutically acceptable salt thereof. Pharmaceuticaly acceptable salts can be formed from organic and inorganic acids, for example, acetic, propionic, lactic, citric, tartaric, succinic, fumaric, maleic, malonic, mandelic, malic, phthalic, hydrochloric, hydrobromic, phosphoric, nitric, sulfuric, methanesulfonic, napthalenesulfonic, benzenesulfonic, toluenesulfonic, camphorsulfonic, and similarly known acceptable aids 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, alkylammonium 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 alkyl, alkenyl, and alkynyl include both branched and straight chain moieties. Examples include methyl, ethyl, propyl, butyl, isopropyl, see-butyl, tert-buty,, vinyl, allyl, acetylene, 1-methyl vinyl, and the like. When alkyl or alkenyl moieties are substituted, they may typically be mono-, di-, tri- or per-substituted. Examples for a halogen substituent include 1-bromo vinyl, 1-f1uoro vinyl, 1,2-difluoro vinyl, 2,2- difluorovinyl, 1,2,2-trifluorovinyl. 1,2-dibromo ethane, 1,2 difluoro ethane, 1-f1uoro-2- bromo ethane, CF2CF3, CF2CF2CF3. and the like. The term halogen includes bromine. chlorine, fluorine, and iodine. The term aryl means phenyl, 1-naphthyl, or 2-naphthyl. Preferred 5-6 membered heterocyclic 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. It is more preferred that the heterocyclic ring is turan, thiophene, or thiazole. Of the compounds of this invention, it is preferred that the compound of formula I has the structure wherein R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms. trifluoroalkoxy of 1-6 carbon atoms, -COR5. -CO2R5. -NO2, CONR5R6. NR5R6 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 of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5. -CO2RS. -NO2, CONR5R6, NR5R6 orN(R5)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 of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5. -CO2Rs, -NO2. CONR5R6, NR5R6 or N(R5)COR6; R5, R6 are each, independently hydrogen, alkyl of 1-6 carbon atoms. aryl of 6-10 carbon atoms; XisO,S,orNR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or-SO2R5; or a pharmaceutically acceptable salt thereof. It is more preferred that X is 0, and still more preferred that X is 0, and R1 is alkenyl of 2-3 carbon atoms, which is optionally substituted with hydroxy!. -CN, halogen, trifJuoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5. -NO2, CONR5R6, NR5R6 or N(R5)COR«. 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 which 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 IC50 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-esttadiol 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 significanlly (p > 0.05) compared with a control that is devoid of uterotropic activity (e.g. vehicle). As used in accordance with this invention, the term "non-mammotrophic" means producing an increase in casein kinase II mRNA In a standard pharmacological test procedure of less than about 50% of the casein kinase /I mRNA increase observed for a maximally efficacious dose of 17p-esrradiot or 17ct-ethinyl- 17p-estradiol in the same procedure. It is preferred that the increase casein kinase /I mRNA will be less than about 25% of that observed for estradiol, and more preferred that the increase in casein kinase /I mRNA will be less than about 10% of that observed for estradiol. It is most preferred that the non-mammotrophic ERp selective ligand will not increase casein kinase II mRNA significantly (p > 0.05) compared with a control that is devoid of mammotrophic actiVity (e.g. vehicle). This invention also provides the use of a ERp selective ligand in the treatment or inhibition of arthritis, inflammatory bowel disease, and endometriosis. More particUlarly, the ERp selective Iigands are useful in the treatment or inhibition of rheumatoid arthritis, osteoarthritis or spondyloarthropathies; and Crohn's disease, ulcerative colitis, indeterminate colitis, infectious colitis. or ulcerative proctitis. This invention further provides for the use of an ERp selective ligand in treating or inhibiting joint swelling or erosion; or treating or inhibiting joint damage secondary to arthroscopic or surgical procedures. It is preferred that the ERp selective ligand is non-uterotrophic and non-mammotrophic. 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. In another aspect, this invention relates to a process for the preparation of a compound of the invention comprising one of the following: a) reacting a compound of formula wherein R1, R2, R* and X are as defined above with a compound of formula wherein R3 and R3a are as defined above and Y is halogen, -OH or alkoxy of 1 to 6 carbon atoms; or b) converting a compound of formula II as defined above to a pharmaceutically acceptable salt thereof; or c) resolVing an isomeric mixture of compounds of formula II to isolate an enanliomer of a compound of formula II or a pharmaceutically acceptable salt thereof. The compounds of the present invention may for example be prepared according to the following synthetic Schemes (I-VIII) In Scheme I, commercially available dimethoxy aniline 1 was treated with commercially available benzoyl chloride 2 in the presence of triethylamine to produce amide 3. The required benzoyl chloride 2 was also prepared from commercially available benzoic acid 4 upon refluxing with thionyl chloride. Amide 3 was converted to the phenolic benzoxazole 5 upon treatment with pyridine hydrochloride at high temperature (200 °e). In Scheme II. commercially available nitro-phenol 6 was brominated with Br2/NaOAc in acetic acid to produce bromo-phenol 7. Catalytic hydrogeroion 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, aniline 8 was converted to benzoxazole 14 upon treatment with benzoic acid 13 and boric acid in p-xylene at high temperature (150°C). Oemethylation 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 silyl ethers 21 (R3 = Me3C{CH3)2Si) with tert-butyldimethylsilyl chlorldelimidazole/4- dimethylaminopyridine in N.N-dimethylformamide, or as the esters 21 (~3 = CHaCO) with acetic anhydridel4-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-o-tolylphosphine)palladium(ll) or tetrakis(triPhenylphosphine)palladium(0)] 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 (~3 = Me3C(CHa)2Sii with hydrofluoric acid (48 wt.% in water) or tetrabutylammonium fluoride produced benzoxazole 24. saponificaiion 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. CNCO2E,. Ph(CH3)NCHO. EtI, etc) to produce compound 25. Deprotection of 25 with boron tribromide (R = CH3) or tetrabutylammonium fluoride (R = Me3C(CH3)2Si) afforded benzoxazole 26 [R = CHO. CO2Et, CH2CH3, C(CH3)2OH]. The tertiary alcohol 25 (R = C(CH3)OH) was treated with pyridine hydrochloride at high temperature (200°C) to produce 1-methyl-vinyl benzoxazole 27. Reduction of 27 with H2 I Pd-C afforded the isopropyl analog 28. 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)palladium(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-benzoxazole 37. Bromination of 37 with N-bromosuccinimide in acetonitrile afforded the monobromo benzoxazole 38 (major product) and the dibromobenzoxazole 39 (minor product). 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,17(3-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 ERa and ERB Representative examples of the invention were evaluated for their ability to compete with 17B-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 ERprecptors. 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 M250-V595 of human ERa [Green, et aI., Nature 320: 134-9 (1986)] and M^-Qsao of human ERp [Ogawa, et al., Biochemical & Biophysical Research Communications 243: 122-6 (1998)]. Human ERp was cloned into pET15b (Novagen. Madison WI) 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 LB medium containing 100 ~g/mL of ampicillin. After incubation overnight at 37 °C, 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-CI (pH 7.4), 150 mM NaC!. 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 ^-esrradiol binding. Dulbecco's phosphate buffered saline (Gibco, 1x final concentration) supplemented with 1 mM EDTA was used as the assay buffer. To optimize the amount of receptor to use in the assay, [3H]-17p-estradiol (New England Nuclear; final concentration = 2 nM) ± 0.6 ^M diethlystilbestrol and 100 nL of various dilutions of the E. coli lysate were added to each well of a high binding masked microtiter plate (EG&G Wallac). The final assay volume was 120 uL 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 ~L of assay buffer. After washing, 135 uL 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 (EG&G Wallac Microbeta Plus). After determining the dilution of each receptor preparation that provided maximum specific binding, the assay was further optimized by estimating the IC* of unlabelled 17p-estradiol using various dilutions of the receptor preparation. A final working dilution for each receptor preparation was chosen for which the IC» of unlabelled 17p-estradiol was 2-4 nM. Ligand binding competition test procedure. Test compounds were initially solubilized in 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 [3H]-17f3-estradiol. Typically, a set of compound dilutions would be tested simultaneously on human ERa and ER\3. The results were plotted as measured DPM vs. concentration of test compound. For dose-response curve fitting, a four parameter logistic model on the transformed, weighted data was fit and the IC* was defined as the concentration of compound decreasing maximum [3H]-estradiol binding by 50%. Binding affinities for ERa and ERp (as measured by ICa,) for representative examples of the invention are shown in Table (1). The results obtained in the standard pharmacologic test procedure described above demonstrate that the compounds of this invention bind both subtypes of the estrogen receptor. The ICsoS are generally lower for ERp\ indicating these compounds are preferentially ER(3 selective Iigands, but are still considered active at ERa. Compounds of this invention will exhibit a range of activity based, at least partially, on their receptor affinity selectivity profiles. Since the compounds of the invention bind ER-~ with higher affinity than ER-a, they will be useful in treating or inhibiting diseases than can be modulated via ER-~. Additionally. since each receptor ligand complex is unique and thus its interaction with various coregulatory proteins is unique, 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, 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 which 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, compounds of this invention also 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 be antagonize the action of 17p-esttadiol via ERp while exhibiting estrogen receptor agonist activity with ERa[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 [Endocrinology 142: 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 compounds of this invention (see also WO 00/37681). Data for representative compounds of the invention are shown in Table (2). Evaluation of test compound using an ERE-reporter 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-MEMlF-12 medium containing 10% (v/v) heat-inactivated fetal bovine serum, 1% (vlv) Penicillin-Streptomycin, and 2 mM glutaMax-1]. The cells are maintained in vented flasks at 37°C inside a 5% CO2/95% humidified air incubator. One day prior to treatment, the cells are plated with growth medium at 25,000 cellslwell into 96 well plates and incubated at 37°C overnight. The cells are infected for 2 hr at 37 °C with 50 ^l/well of a 1:10 dilution of adenovirus 5-ERE-tk-Iuciferase in experimental medium [phenol red-free D-MEMlF-12 medium containing 10% (v/v) heat-inactived charcoal-stripped fetal bovine serum, 1% (v/v) Penicillin-Streptomycin. 2 mM glutaMax-1, 1 mM sodium pyruvate]. The wells are then washed once with 150 »l of experimental medium. Finally, the cells are treated for 24 hr at 37°>C in replicates of 8 wells/treatment with 150 nl/well of vehicle (< 0.1% vlv DMSO) or 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 17(3- estradiol (EC80; 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'" to 10-5 M. From these dose- response curves, EC50 and IC50 values, respectively, are generated. The final well in each treatment group contains 5 jd of 3 x 10s M ICI-182,780 (10~ M final concentration) as an estrogen receptor antagonist control. After treatment, the cells are lysed on a shaker for 15 min with 25 ^l/well of 1X cell culture lysis reagent (Promega Corporation). The cell Iysates (20 nl) are transferred to a 96 well luminometer plate, and luciferase activity is measured in a MicroLumat LB 96 P luminometer (EG & G Berthold) using 100 ~I/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); 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 M-estimator 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 (Dunnett's 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 17(3-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 17(3-estradiol control [i.e., ((compound - vehicle control)/(17p-esrradiol control - vehicle control)) x 100]. The JMP software is also used to determine the EC50 and/or IC50 values from the non-linear dose-response curves. Evaluation of uterotropic activity Uterotrophic activity of a test compound can be measured according to the following standard pharmacological test procedures. Procedure 1: Sexually immature (18 days of age) Sprague-Dawley rats are obtained from Taconic and provided unrestricted access to a casein-based diet (Purina Mills 5K96C) and water. On day 19, 20 and 21 the rats are dosed subcutaneously with 17a-ethinyl-17B-estradiol (0.06 ^g/rat/day). test compound or vehicle (50% DMSO/50% Dulbecco's PSS). To assess estrogen receptor antagonist activity, compounds are coadministered with 17a-ethinyl-17B-estradiol (0.06 > iig/rat/day). There are six rats/group and they are euthanized approximately 24 hours after the last injection by CO2 asphyxiation and pneumothorax. Uteri are removed 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 compounds of the invention 5 are shown in Table (3). 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 (corn 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 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 Farms (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 5K96C rat chow) 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 Oulbecco's phosphate saline (GibcoBRL, Grand Island, NY) at defined concentrations so that the treatment volume is 0.1 mU100 g body weight. 17~-estradiol is dissolved in corn oil (20 ug/mL) and delivered subcutaneously, 0.1 mUral. 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 (paCT; 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 mglkg ketamine, 8.5 mg/kg xylazine, and 1.5 mglkg 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 900 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 pOCT. 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 paCT scan is initiated 3.4 mm distal from this point. The pOCT 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 paCT 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 are also removed and the weighed after trimming associated fat and expressing any luminal fluid. Total cholesterol is determined using a Boehringer-Mannheim Hitachi 911 clinical analyzer using the Cholesterol/HP kit. Statistics were compared using one-way analysis of variance with Dunnefs test. The following results were obtained with representative compounds of the invention (Table (5)). Evaluation of antioxidant activity 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), penicillin- streptomycin (1000U/ml, 100ng/ml) and gentamycin (75^/ml), seeded in 100mm petri dish and incubated at 37°C in 5%CO2. After 20 minutes, the cells are rinsed with PSS 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 ng/mL LDL is allowed to proceed in the presence of the compound to be evaluated (5 MM) for 4 hours at 37 °C. Results are expressed as the percent inhibition of the oxidative process as measured by the TSARS (thiobarbituric acid reactive substances) method for analysis of free aldehydes [Vagi, 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 aI., Endocrinology 138: 5476- 5484 (1997)]. Data for representative compounds of the invention are shown in Table (6). Rat Hot Flush Test Procedure The effect of test compounds on hot flushes can be evaluated in a standard pharmacological test procedure which 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 aI., Maturitas 30: 307-16 (1998)]. 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 compounds of the invention (Table (7)) 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 17J3-estradiol trea!ed (1 mglkg/day) 4. Ovariectomized animals treated with test compound (various doses) Animals are ovariectomized approximately 3 weeks prior to treatment. Each animal receives either 17-pestradiol sulfated mglkg/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 exsanguination. Thoracic aortae are rapidly removed and placed in 37 0C physiological solution with the following composition (mM): NaCI (54.7), KCI (5.0), NaHCO3 (25.0), MgCI2 2H20 (2.5), D-glucose (11.8) and CaCI2 (0.2) gassed with CO2-02, 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. 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. Rings are equilibrated for 1 hour, signals are acquired and analyzed. After equilibration, the rings are exposed to increasing concentrations of phenylephrine (10-8 to 10-4 M) and the tension recorded. Baths are then rinsed 3 times with fresh buffer. After washout, 200 mM L-NAME 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 are obtained from Taconic Farms. All animal procedures are performed under strict compliance to IACUC guidelines. Ovariectomized female apo E KO mice. 4-7 weeks of age, are housed in shoe-box cages and were allowed free access to food and water. The animals are randomized by weight into groups (n=12-15 mice per group). The animals are dosed with test compounds or estrogen (17p-estradic4 sulfate at 1 mg/kg/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 is a Western-style diet (57U5) that is prepared by Purina and contains 0.50% cholesterol, 20% lard and 25 IU/KG Vitamin E. The animals are dosedlfed 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 are euthanized and plasma samples obtained. The hearts are 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 and Wako Biochemicals, respectively and analyzed using the Boehringer Mannheim Hitachii 911 Analyzer. Separation and quantification of plasma lipoproteins were performed using FPLC size fractionation. Briefly, 50-100 ml_ of serum is 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 NaC!. Areas of each curve representing VLDL, LDL and HDL are integrated using Waters Millennium™ software, and each lipoprotein fraction is 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 are carefully isolated and placed in formalin fixative for 48-72 hours before handling. Atherosclerotic lesions are identified using Oil Red 0 staining. The vessels are briefly destained, and then imaged using a Nikon SMU800 microscope fitted with a Sony 3CCD video camera system in concert with IMAC Configuration Utility (National Instrument) as the image capturing software. The lesions are quantified en face along the aortic arch using a custom threshold utility software package (Coleman Technologies.. Automated lesion assessment is 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 data are expressed as percent lesion involvement strictly within this defined luminal area. Evaluation of cognition enhancement Ovariectomy rats (n=50) are habituated to an 8-arm radial arm maze for 10- min periods on each of 5 consecutive days. Animals are water-deprived prior to habituation and testing. A 100 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. Negative controls: injected with 10% DMSOI sesame oil vehicle once daily for 6 days(1mUkg,Se) 2. Positive controls: injected with 17j3-estradiol benzoate for 2 days and tested 4 days after the second injection (17p-estradiol benzoate at 10 ug/0.1 mL per rat) 3. Estradiol: 17(3-estradiol will be injected daily for 6 days (20 ug/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-tosample 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 arm, 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 [Endocrinology 141: 1455-63(2000)]. Evaluation of protection against glutamate-induced cytotoxicity (neuroproteciion! The neuroprotective activity of compounds of this invention can be evaluated in an in vitro standard pharmacological test procedure using glutamate challenge [Zaulyanov, et aI., Cellular & Molecular Neurobiology 19: 705-18 (1999); Prokai, et al.. Journal of Medicinal Chemistry 44:11Q-4 (2001)]. Evaluation in the Mammary End Bud Test Procedure 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. In this test procedure. the mammotroph.c activity of selected compounds of the invention was evaluated according to the following standard pharmacological test procedure. Twenty-eight day old Sprague-Dawley rats (Taconic Farms) were ovariectomized and rested for nine days. Animals were housed under a 12-hour light/dark cycle. fed a casein-based Purina Laboratory Rodent Diet 5K96 (Purina, Richmond, IN) and allowed free access to water. Rats were then dosed subcutaneously for six days with vehicle (50% DMSO (JT Baker, Phillipsburg. NJ) I 50% 1x Dulbecco's Phosphate buffered saline (GibcoBRL), 17B-estradiol (0.1 mg/kg) or test compound (20 mg/kg). For the final three days, rats were also dosed subcutaneously with progesterone (30 mg/kg). On the seventh day, rats were euthanised and a mammary fat pad excised. This fat pad was analyzed for casein kinase II mRNA as a marker of end bud proliferation. Casein kinase II mRNA was anlayzed by real-time RT-PCR. Briefly, RNA was isolated following Trizol (GibcoBRL) according to the manufacture's directions, Samples were treated with DNAse I using DNA-free kit (Ambion), and casein kinase II mRNA levels were measured by real-time I RT-PCR using the Taqman Gold procedure (PE Applied Biosystems). A total of 50 n9 of RNA was analyzed in triplicate using casein kinase II specific primer pair (5' primer, CACACGGATGGCGCATACT; 3' primer, CTCGGGATGCACCATGAAG) and customized probe (TAMRA-CGGCACTGGTTTCCCTCACATGCT-FAM). Casein kinase II mRNA levels were normalized to 18s ribosomal RNA contained within each sample reaction using primers and probe supplied by PE Applied Biosystems.The following results were obtained for representative compounds of the invention (Table (8». Evaluation in the HLA Rat Standard Pharmacolonical Test Procedure for inflammatory bowel disease Representative 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 unrestridted access to food (PMI lab diet 5001) and water. Stool quality 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 (9). Rats dosed with vehicle continued to have diarrhea throughout the course of the stUdy. Stool quality was improved in rats treated with Example 24. In Study B. rats (8-10 weeks old) were dosed orally for twenty-six days as follows: • Vehicle (2% Tween-80/0.5% methylceululose) • Example 25 (10 mglkg from days 1-14; then increased to 20 mg/kg at d15) • Example 34 (10 mglkg) The following results were obtained (Table (10») and show that stool character improved in all rats treated with representative compounds of the inveniion. Table 10: Evaluaiion of stool character of HLA rats treated orally with vehicle or representative compounss from the inveniion. Value reported is the group's average score. In Study C, 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 mglkg from days 1-18; then increased to 20 mg/kg at d19) • Example 24 (10 mglkg from days 1-24; then increased to 20 mglkg at d25) The following results were obtained (Table (11)) and show that stool character improved with administration of all the ERB selective compounds: Table 11: Stool scores from HLA rats treated orally with vehicle or representative compounds from the invention. Value reported ;s the group's average Histological 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 hematoxylin 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 (12) (a composite of two subcutaneous dosing studies, including Study A), Example 24 is effective in reducing several measurements of tissue injury. Evaluation in two models of arthritis 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, St. 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 intradermal* 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) I 1x Dulbecco's phosphate saline (GibcoBRL, Grand Island, NY)) or test compound (administered subcutaneously). All rats began treatment on Day 1. Data for representative compounds of the invention are shown in Table (15). Treatment test procedure: Thirty rats are injected intradermal* 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) I 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 compounds of the invention are shown in Tables (16), (17) and (18). 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 (SO), 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 Oto 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 SaffraniNO-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. In addition, articular cartilage and bone is evaluated using Mankin's histological grading system [Mankin, et aI., Journal of Bone & Joint Surgery - American Volume 53: 523-37 (1971)J as shown below. Evaluation in the HLA-B27 Rat model of arthritis. Representative 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 (PMI Lab diet 5001) and water. Joint scores and histology are 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 d19) • Example 24 (10 mg/kg from days 1-24; then increased to 20 mg/kg at d25) The following results were obtained for representative compounds of the invention (Tables (19) and (20)). Study 2: Rats (8-10 weeks old) were dosed orally for twenty-six days with one of the formulations listed below. There were 4 rat~ in each group and the last dose was administered two hours before euthanasia. • Vehicle (2% Tween-80/0.5% methylceJlulose) • Example 25 (10 mglkg from days 1-14; then increased to 20 mglkg at d15) • Example 34 (10 mg/kg) The following results were obtained for representative compounds of the invention (Table (21)). Evaluation in in vivo models of i^nn^^u, The ability of compounds of this invention to treat and 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 17B-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 [Oncology Research 11: 255-64 (1999)]. Evaluation of neuroprotection in two in vivo test prnr.pH„rp« Transient global ischemia in the Mongolian gerbil. The effect of test compounds on preventing or treating brain injury in response to oxygen deprivation/reperfusion can be 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 facility (AAALAC certified) with a 12- hour light, 12-hour dark photoperiod and free access to tap water and a low-estrogen casein diet (Purina; Richmond, IN). After acclimation (3-5 days), gerbils were anesthetized with isoflurane (2-3% mixture with O2), ovariectomized (Day O). Beginning the following morning (Day 1), gerbils were treated subcutaneously each day with either vehicle (10% ETOH/com oil), 17p-esttadiol (1 mg/kg, sc) or an experimental compound. On Day 6, gerbils (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 -SOX. 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 de~ree of neuronal protection was evaluated by in situ hybridization analysis of neurogranin mRNA. Briefly, 20 Mm coronal cryostat sections were collected on gelatin-coated slides, dried and stored at -SOX. At the time of processing, the desiccated slide boxes were warmed to room temperature, the slides postfixed in 4% paraformaldehyde, treated with acetic anhydride and then delipidated and dehydrated with chloroform and ethanol. Processed section-mounted slides were then hybridized with 200 pi (6x106 DPM/ slide) of an antisense or sense (control) riboprobe for Neurogranin (^S-UTP-labeled NG-241; bases 99-340) in a 50% formamide hybridization mix and incubated overnight at 55X in a humidified slide chamber without coverslipping. The following morning. the slides were collected in racks, immersed in 2xSSC (0.3 M NaCl, 0.03 M sodium citrate; pH 7.0) 110 mM DTT. treated with RNase A (20 ng/ml) and washed (2 x 30 min) at 67X in 0.1x SSC to remove nonspecific label. After dehydration, the slides were opposed to BioMax (BMR-1; Kodak) 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-Imaging Inc., Pittsburgh, PAl. The results from 6 sections (40 urn 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 p>O.05. The following results were obtained with representative compounds of the invention (Table (22)). Middle cerebral artery occlusion in mice. Neuroprotection can be evaluated according to the test procedures described by Dubal [see, Dubal, et aI., Proceedings of the National Academy of Sciences of the United States of America 98:1952-1957 (2001), Dubal, et aI., 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 Bioi 78: 137-143 (2001)]. The following data were obtained from representative compounds from the invention (Table (23)) Evaluation in an endometriosis standard pharmacoloaic test procedure This procedure is slightly modified from a published method [Bruner-Tran. et aI., Journal of Clinical Investigation 99: 2851-2857 (1997)]. In brief, normal human endometrial tissue (cycle day -12) is treated in vitro overnight with 10nM 17(3-estradiol 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 10mg/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 compounds of this invention 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. The compounds of this invention are particularly useful in treating a peri-menopausal, 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 surgically, chemically, or be caused by a disease state which leads to premature diminution or cessation of ovarian function. The compounds of this 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 compounds of this invention are also active in the brain and are therefore 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 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, hyperlipidemia, cardiovascular disease, atherosclerosis, peripheral vascular disease, restenosis, and vasospasm, and inhibiting vascular wall damage from cellular events leading toward immune mediated vascular damage. The 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, ischemialreperfusion injury (e.g. stroke, transplant rejection, myocardial infarction, etc.), asthma, giant cell arteritis, prostatitis, uveitis, psoriasis, multiple sclerosis, systemic lupus erythematosus and sepsis. The 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 compounds of this 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). Compounds in this invention are also useful in treating or inhibiting bleeding disorders such as hereditary hemorrhagic telangiectasia, dysfunctional uterine bleeding, and combating hemorrhagic shock. The 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 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, it 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 mgJday 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, intraarticular^ and subcutaneous injections), rectally, intranasal^, topically, ocularly (via eye drops), vaginally and transdermal^. Oral formulations containing the active 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 pharmaceuticaly acceptable starches (e.g. corn, 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, wet granulation or dry granUlation methods and utilize pharmaceuiicaly 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 sulfate, microcrystalline cellulose, carboxymethylcellulose calcium, polyvinylpyrroiidone, 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, cetostearl 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 compounds of this invention may also be administered parenteral^ 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 injectable use include sterile aqueous solutions or dispersions and sterile powders for the extemporaneous preparation of sterile injectable 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.• glycerol, propylene glycol and liqUid polyethylene glycol). suitable mixtures thereof. and vegetable oils. For the purposes of this disclosure, transdermal 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 pharmaceuticaly acceptable salts thereof, in lotions, creams, foams, patches, suspensions solutions and suppositories (rectal and vaginal). Transdermal 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 blood 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 o«- 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 with or without a carrier, or a matrix containing the active ingredient. Other 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. The preparation of representative examples of this invention is described below. Example 1 2-(5-Hydroxy-1,3-benzoxazol-2-yl)benzene-1f4-diol Step a) /^2,5-Dimethoxyphenyl)-2>dimethoxyben2arnide. A mixture of 2,5-dimethoxybenzoic acid (5.0 g, 27.5 mmol) and thionyl chloride (15 mL) was refluxed for 1 h. The volatiles were removed under vacuum. The residue was dissolved in THF (20 mL) and added into a cold (O°C) solution of 2,5- dimethoxyaniline (4.6 g, 30.2 mmol), triethylamine (5 mL. 35.9 mmol) and THF (40 mL). The mixture was stirred for 30 min, poured into water, acidified with HCI (2N) and extracted with EtOAc. The organic extracts were dried over MgSO4. Evaporation and purification by flash chromatography (hexanes I EtOAc 2/1) gave a white solid (8.1 g, 93% yield, m.p. 121-123 0C); MS mle 318 {M+H)+. Analysis for: C17H,9NOs Calc'd:C, 64.34; H, 6.03; N, 4.41 Found: C, 64.29; H, 5.95; N, 4.44 Step b) 2-(S-Hydroxy-1,3.benzoxazo|.2.yl) benzene-1,4-diol. A mixture of N-(2,5-dimethoxyphenyl)-2,5Kiimethoxybenzamide (1.0 g, 3.1 mmol) and pyridine hydrochloride (2.0 Q, 17.3 mmol) was stirred at 200°C for 1 h. The mixture was cooled to room temperature and HCI (10 mL, 2 N) was added. The mixture was then extracted with EtOAc and the organic extracts were dried over MgSO4 Evaporation and purification by flash chromatography (hexanes I EtOAc 2/1) gave a white solid (0.8 g, 76% yield, m.p. 309-31rc); MS m/e 242 (M-H)+ Analysis for: C,3HgNO4 Calc'd:C, 64.20; H, 3.73; N, 5.76 Found: C, 63.98; H, 3.71; N, 5.62 Example 2 3-(5-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 2,5-dimethoxyaniline. and 2,3-dimethoxybenzoic acid. The product was obtained as a tan solid, m.p. 239-241°C; MS mle 244 (M+H)+ Analysis for: C,3HgNO4 Calc'd:C, 64.20; H, 3.73; N, 5.76 Found: C, 63.86; H, 3.90; N, 5.74 Example 3 2-(3-Fluoro-4.hydroxyphenyl)-1,3-benzoxazo|.5-ol The title compound was prepared in substantially the same manner as described in Example 1, from 2,5-dimethoxyaniline, and 3-fJuoro-4-methoxybenzoic acid and was obtained as a white solid, m.p. 262-268°C; MS mle 244 (M-H)'. Analysis for: C,3HeFNO3 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)-1,3-benZoxa2ol-5-ol The title compound was prepared in substantially the same manner as described in Example 1, from 2,5-dimethoxyaniline, and 3-chloro4-methoxybenzoic acid and was obtained as a white solid, m.p. 254-256 °C; MS mle 260 (M-H)Analysis for: C13HaCINO3 Calc'd:C, 59.67; H, 3.08; N, 5.35 Found: C, 59.59; H, 3.02; N, 5.25 Example 5 2-(2-Chloro-4-hydroxyphenyl).1,3-benzoxazol-5-ol The title compound was prepared in sUbstantiaily the same manner as described in Example 1, from 2.5-dimethoxyaniline, and 2-ehlor0-4-methoxybenzoic acid and was obtained as a white solid, m.p. 253-255°C; MS mle 262 (M+H)Analysis for: C13HeCINO3 Calc'd:C, 59.67; H, 3.08; N, 5.35 Found: C, 59.79; H. 2.87; N. 5.36 Example6 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-f1uoro-4-methoxybenzoic acid and was obtained as a white solid, m.p. 269-271X; MS mle 244 (M-H)Analysis for: C17H11NO3 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-ButyM-hydroxyphenyl)-1,3-benZoxazo|.6-ol The title compound was prepared in substantially the same manner as described in Example 1, from 2,4-dimethoxyaniline. and 3-terf-butyl-4-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 Example8 2-{6-Hydroxy-1,3-benzoxazol-2-yl)benzene-1,4-diol The title 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 X; MS m/e 244 (M+H)Analysis for: C'3HgNO4 Calc'd:C, 64.20; H, 3.73; N, 5.76 Found: C, 64.09; H, 3.14; N, 5.65 Example9 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+H)Analysis for: C13HgNO4 Calc'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-benzoxa2ol-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 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 Example 11 2-{3-Chloro-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-chloro-4-methoxybenzoic acid and was obtained as an off-white solid, m.p. 254-256°C; MS m/e 262 (M+H) 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 mle 228 (M+H)*. Analysis for: C13HgNO3 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-Hydroxy-1,3-benzoxazol-2-yl)benzene-d,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 X; MS mle 242 (M-H)t Analysis for: C13HgNO4 CalcttC, 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-benzoxazol-6-ol The title compound was prepared in 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 X; MS mle 226 (M-H)Analysis for: C13HgNO3 Calc'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 °C; MS m/e 242 (M-H)+. Analysis for: C13HgNO4 Calc'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 Stepa)N-(4-Chloro-2,5-dimethoxyphenyl)-3-fluoro-4-methoxybenzamide. The title compound was prepared in substantially the same manner as described in Example 1, step a, from 4-chloro-2,5-dimethoxyaniline, and 3-f1uoro-4- methoxybenzoic acid and was obtained as a white solid, m.p. 197-199 °C; MS m/e 340(M+H)Analysis for: C16H15CIFNO4 Calc'd:C, 56.56; H, 4.45; N, 4.12 Found: C, 56.33; H, 4.35; N, 4.05 Stepb)A/-(4-Chloro-2,5-dihydroxyphenyl)-3>fluoro-4.hydroxybenzamide. Boron trifluoride dimethyl sulfide complex (70 mL) was added into a mixture of A/-(4- chloro-2,5-dimethoxyphenyl)-3-fluoro-4-methoxybenzamide (1.75 g, 5.15 mmol) and CH2CI2 (35 mL). After stirring for 20 h, the solvent and the excess reagent were evaporated under a nitrogen stream in the hood. The residue was taken in a mixture of ice and HCI (1N) and extracted with EtOAc. The organic layer was washed with HCI (1N) and dried over MgSO4. Evaporation and purification by flash chromatography (CH2Cl2/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 (M-H)+. 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-ben2oxazol-5-ol 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-fluor<>4-hydroxybenz- amide and pyridine hydrochloride and was obtained as a white solid, m.p. 258-260 •C; MSmfe278{M-Ht. Analysis for: C13H17CIFNO3 Calc'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^-hydroxyphenyl)-1,3-benzoxazol-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-f1uoro-4-methoxybenzoic acid and was obtained as a white solid, m.p. 224-226 X; MS m/e 322 {M-H)Analysis for C13H17BrFNO3 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)-b,3-benzoxazol-5-ol The title compound was prepared in substantially the same manner as described in Example 16, from 4-chlorc~2,5-dimethoxyaniline, and 4-methoxybenzoyl chloride and was obtained as an off-white solid. m.p. 260•262 •C; MS m/e 260 {M-H)+. Analysis for: C13HeCINO3 Calc'd:C, 59.67; H, 3.08; N, 5.35 Found: C, 59.09; H, 3.06; N, 5.11 Example 19 S-ehloro-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: C,3HeC/NO3 CalcttC, 59.67; H, 3.08; N, 5.35 Found: C, 59.40; H, 2.97; N, 5.22 Example 20 7-Bromo-2-(4-hydroxyphenyl)-1,3-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 mixture was stirred for 30 min at room temperature, and then at 70°C for 2 h and poured into water (1.5I) containing concentrated sulfuric acid (10 mL). The precipitated solid filtered and crystallized from (chloroform I hexane) to give a brownish solid, m.p. 116-118 °C; MS mle 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 h. The reaction mixture was filtered through celite and concentrated under vacuum to give a gray solid (7.4 g. 96% yield; 95-97°C); MS mle 218(M+Ht+. Analysis for: C7HeBrNO2 CalcUC. 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-methoxyben2oyl)amino]phenyl-4- methoxybenzoate Anhydrous pyridine (37.0 mL. 468.5 mmol) was added dropwise into a cold (O°C) mixture (mechanically stirred) of 2-amino-6-bromo-4-methoxyphenll (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 mixture was stirred for 30 min and then ethyl ether (250 ml) was added. The precipitated solids were filtered off and washed with ethyl ether. The solids were taken in 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 mle 484 (M-H) Analysis for CaHaBrNO., 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-2K4-methoxyphenyl)-1,3-benzoxazole. Route a) A suspension of 2-bromo-4-methoxy-6[((4-methoxybenzoy))amino]phenyl 4-methoxy- benzoate (42.0 g, 86.4 mmol), p-toluenesulfonic acid monohydrate (32.8 g, 172.8 mmol) and anhydrous p-xylene (800 mL) was refJuxed for 1 h with continuous water removal (Dean-Stark Trap). The initial suspension turned into a brown solution at refJuxing temperature. The mixture was cooled to room temperature and washed with NaOH (2N). The organic layer was dried over MgSCv Evaporation and crystallization from acetone/ethyl ether gave an off-white solid (23.5 g, 82% yield, m.p. 139-141°C); MS/n/e334(M+H)Analysis for: C15H12BrNO3 Calc'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-methoxyphenol (100 mg, 0.46 mmol), 4-methoxy- benzoic acid (77 mg. 0.5 mmol), and boric acid (31 mg, 0.5 mmol) in p-xylene (9 mL) was refluxed for 24 h using a Dean-Stark water separator. The mixture was cooled to room temperature, and concentrated under vacuum. The residual product was purified by flash chromatography (30% EtOAclpetroleum ether) to give a light pink solid (99 mg, 65% yield, m.p. 136-138 'Q; MS mle 334 (M+H)*. Analysis for: C15H12BrNO3 CalcttC, 53.91; H, 3.62; N. 4.19 Found: C, 53.78; H. 3.55; N, 4.01. I Step e) 7•Bromo-2-(4-hydroxyphenyl)-1,3-benzoxazol-S-ol. Route a) Boron tribromide (1M, 89.9 mL, 89.8 mmol) was added dropwise into a cold (-70 °C) suspension of 7-bromo-S-methoxy-2-(4-methoxyphenyl)-1.3-benzoxazole (10.0 g. 29.94 mmol) and CH2CI2 (50 mL). The mixture was allowed to warm up to room temperature. During the warming up period the suspension turned into a dark solution. The mixture was stirred at room temperature for 2 days and then poured slowly into cold (0 0 C) ethyl ether (1000 mL). Methyl alcohol (200 mL) was added slowly into the new mixture over a 20 min period. The mixture was then poured into water (1.5 I). 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 solid (8.4 g, 92% yield. m.p. 298-299 °C); MS m/e 306 (M+H)*. Analysis for: C,3HeBrNO3 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*0 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 h. The mixture was poured into ice and extracted with EtOAc. The organic extracts were washed with brine and dried over MgSO4. Evaporation and flash chromatography (30%-40% EtOAd/petroleum ether) gave (102 mg, 86% yield) of the product as a light pink solid. m.p. 295-298°C; MS mle 304 (M-H)•; Analysis for: C'3HaBrNO3 Calc'd-.C, 51.01; H, 2.63; N. 4.58 Found: C. 51.06; H, 2.77; N, 4.36. Example 21 7-8romo-2-(3-fluoro-4-hydroxyphenyl)-1,3-benzoxazol-5-ol Step a) 2.Bromo-6-[(3-fluoro-4-methoxybenzoyl}amino]-4-methoxylhenyl 3- fluoro-4-methoxybenzoate. A mixture of 3-f1uoro-4-methoxybenzoic acid (39.0 g, 299 mmol), thionyl chloride (100 mL), and N,N-dimethylformamide (0.5 mL) was refluxed for 1 h. 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-brom0-4- methoxyphenol (20.0 g, 91.7 mmol) and CH2Cl2 (150 mL). Anhydrous pyridine (37.0 mL, 468.5 mmol) was added dropwise into the new mixture. During the pyridine addition a precipitate was formed. The mixture was stirred for 30 min and then ethyl ether (250 mL) was added. The precipitated solids were filtered off and washed with ethyl ether. The solids were taken in water and stirred for 20 min. The solids were then filtered off and dried to give an off-white solid (46.5 g 97% yield mp 184 186°C):MSmle520(M-H)+. , ," " Analysis for C^H^BrF^Oe 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^-[(3-f1uor0-4-methoxybenzoyl)aminO]-4-methoxyphenyl 3- f1uoro^-methoxybenzoate (46.0 g, 88.1 mmol), p-toluenesuffonic acid monohydrate (33.5 g, 177.2 mmol) and anhydrous p-xylene (1 I) was refluxed for 3 h 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 min, filtered off and dried to give a tan solid (25.1 9, 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 mle 352 (M+H)+. Analysis for: CsH^BrFNOa Calc^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-benzoxa2ol-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 mle 332 (M-H)+. Analysis for: C,3H7BrFNO3 CalcttC, 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-benzoxazo|.5-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-fluor0-4-methoxybenzaldehyde (15 g, 97.4 mmol) The mixture was stirred for 1 h, filtered off and the precipitated solids were washed with hot water (10 mL). The filtrate was added slowly into cold (O°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 °CV MS m/e 169 (M H( Analysis for: CaH7F03 ' Calc'd:C, 56.48; H, 4.15 Found: C, 56.12; H, 4.12 Step b) 7.Bromo.2^2.fluoro-4.hydroxyphenyl).1,3.benzoxazol-5K)l The title compound was prepared in substantially the same manner as described in Example 21, from 2-fJuoro-4-methoxybenzoic acid, and was obtained as a white solid m.p. 248-250 "C; MS m/e 3~4 (M+H)Analysis for C13H7BrFNO3 Calc'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-(2,3K«fluoro-*-hydroxyphenylM,3-benzoxazo|.5-ol Step a) Methyl 2,3-dlfluoro-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 mmol), lithium carbonate (12.7 g, 172.5 mmol) and N,N-dimethylformamide (100 mL). The 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 I EtOAc 5/1) gave a white solid (10.2 g, 88% yield, m.p. 66-68 'Q) MS m/e 203 (M+H)+ Analysis for: CgHaF203 CalcttC, 53.47; H, 3.99 Found: C, 53.15; 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 mixture was stirred at room temperature for 6 h, 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% yield, m.p. 194-196 •C); MS m/e 187 (M-H)+. Analysis for: CeHeF203 Calc'd:C, 51.08; H, 3.21 Found: C, 50.83; H, 2.92 Step c) 7-Bromo-2-(2,3-difluoro-4-hydroxyphenyl)-1,3-benzoxazol-5-ol The title compound was prepared in substantially the same manner as described in Example 21, from 2,3-difluor0-4-methoxybenzoic acid. and was obtained as a white solid, m.p. 258-260 °C; MS mle 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-vinyM,3-benzoxazol-5-ol Route a) Stepa)7-Bromo-5-{[tert-butyl(dimethyl)silyl]oxy}-2-(4-{[fert-butyl(dimethyl)silyl]- oxy}-3-f1uorophenyl)-1,3-benzoxazole. tert-Butyl(chloro)dimethylsilaee (23.2 9, 154 mmol) was added portionwise into a mixture of 7-bromo-2-(3-fluoro-4-hydroxyphenyl)-1,3-benzoxazol-5-ol (16.6 g, 51.4 mmol), imidazole (17.5 g, 257 mmol), A/,A/-dimethylpyridin-4-amine (1.0 g, 8.1 mmol) and DMF (300 ml). The mixture was stirred for 3 h, poured into water and extracted with ethyl ether. The organic extracts were dried over MgSO4. Evaporation and purification by flash chromatography (hexanes I EtOAc 50/1) gave a white solid (27.5 9.97% yield, m.p. 98-99°e); MS m/e 552 {M+H)+. Analysis for: C2sH3SBrFNO3Sii CalcttC. 54.34; H. 6.38; N, 2.53 Found: C, 54.06; H, 6.52; N. 2.24 Step b) 5K[terf.Butyl(dimethyl)sHyl]oxy}-2-(4Klterf-butyl(dimethyl)silyl]oxy>.3. fluorophenyl)-7-vinyMt3.benzoxazole. Dichlorobis(tri-o-tolylphosphine)palladium (II) (0.63 g, 0.79 mmol) was added into a mixture of 7-bromo-5-{(tert-butyl(dimethyl)silyl]oxy^2-(4H[tert-butyl(dimethyl)silylloxy}- 3-f1uorophenyl)-1,3-benzoxazole (14.7 g, 26.6 mmol), tributyl(vinyl)tin (10.5 g, 33.25 mmol) and p-xylene (85 mL). The reaction mixture was stirred at 90°C for 24 h cooled to room temperature, diluted with ethyl ether (100 mL) and treated with activated carbon. The mixture was filtered through MgSO< and concentrated Purification by flash chromatography (hexanes / EtOAc 50/1) gave a white solid (11 8 g, 89% yield, m.p. 93-95 -Q; MS mle 500 (M+H)+. Analysis for: C^FNOaSi, CalcttC, 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-vinyl-1,3-benzoxazol-5-ol. Hydrofluoric acid (48 wt.% in water, 1 mL) was added into a solution of 5-{[tert- butyl(dimethyl)silyl]oxy}-2((4-{[tert-butyl(dimethyl)silyrioxy}-3-fluorophenyl)-7-viny|.13- benzoxazole (1.5 g, 3.0 mmol), THF (6 mL) and acetonitrile (3 mL). The reaction mixture was stirred at 65 °C for 8 h. 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. 249-251X); MS m/e 272 (M+H)+ Analysis for: C1sH10FNO3 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.benzoxazoI-5-ol. Dichlorobis(tri-o-tolylphosphine)palladium (II) (0.87 g, 1.1 mmol) was added into a mixture of 7-bromo-2-(3-f1uoro-4-hydroxyphenyl)-1,3-benzoxazol-5-ol (7.16 g, 22.1 mmol), tributyl(vinyl)tin (10.5 g, 33.25 mmol) and ethylene glycol diethyl ether (65 mL). The reaction mixture was stirred at 115°C for 48 h, cooled to room temperature and treated with activated carbon. The mixture was filtered through MgSO4 and concentrated. Purification by flash chromatography, on acidic silica gel (hexanes I EtOAc I CH2CI21/1/1), gave a white solid (4.35 g, 72% yield, m.p. 250-252 X); MS m/e272(M+H)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) Step a) 4-[S-(Acetyloxy)-7-bromo-1(3-benzoxa2ol-2-yl]-2-fluorophenvl acetate. Acetic anhydride (1.0 mL, 9.95 mmol) was added into a cold (0°C) solution of 7- bromo-2-(3-f1uor0-4-hydroxyphenyl)-1,3-benzoxazol-5-ol (1.24 g. 3.8 mmol). N.N- dimethylpyridin-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 h. Water (50 mL) was added to the reaction mixture extracted with EtOAc and dried over MgSO4. Evaporation and crystallization from EtOAclhexane gave an oft-white solid (0.87 g. 56%yield);MSm/e408(M+Hr. Analysis for: CuH^BrFNOs Calc'd: C. 50.02; H. 2.72; N, 3.43 Found: C, 49.58; H. 2.59; N, 3.37 Step b) 2-[4-(Acetyloxy)-3-f1uorophenyl]-7-vinyl-1,3-benzoxazol-5-yl acetate. Dichlorobis(tri-o-tolylphosphine)palladium (II) (46 mg, 0.06 mmol) was added into a mixture 4-[5-(acetyloxy)-7-bromo-1,3-benzoxazol-2-yl]-2-fluorophenyl acetate (0.8 g, 1.98 mmol). tributyl(vinyJ)tin (0.9 g, 2.8 mmol) and p-xylene (9 mL). The reaction mixture was stirred at 130°C for 5 h, cooled to room temperature, diluted with ethyl ether (10 mL) and treated with activated carbon. The mixture was filtered through MgSO4 and concentrated. Purification by flash chromatography (hexanes / EtOAc 5/1) gave a white solid (0.4 g, 56% yield, m.p. 154-156 DC); MS m/e 356 (M+H)Analysis for: C,9H,4FNO5 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-hydroxyphenyl)-7-vinyl-1.3-benzoxazol-5-ol. Potassium carbonate (55 mg) was added into a solution of 2-[4-(acetyloxy)-3- f1uorophenyl]-7-vinyl-1,3-benzoxazol-5-yl acetate (0.14 g, 0.39 mmol) and 1,4-dioxane (3 mL). The mixture was stirred at 90 °c for 1 h, poured into wate,, acidified with HCI (2N) and extracted with EtOAc. The organic extracts were dried over MgSO4 Evaporation and crystallization from EtOAc/hexanes, gave a white solid (0 06 g 46y yield, m.p. 250-252 •C); MS mle 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 Exampee 25 2^2-Fluoro^-hydroxyphenyl)-7-vinyl-1,3-benzoxazol-5-ol. The title compoudd 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 DC; MS mle 272 (M+H.* Analysis for: C15H10FNO3 Calc'd: C, 66.42; H, 3.72; N, 5.16 Found: C. 66.18; H. 3.47; N,4.97 Exampee 26 2^2,3-Difluoro^.hydroxyPhenyl).7-vinyl-1,3-ben20xazol-5.ol. The title compoudd was prepared in substantially the same manner as described in Example 24, Route b), from 7-bromO-2-(2,3-difluorc~4-hydroxyphenyl)-1.3- benzoxazo5-5-ol, and was obtained as an Off-white solid, m p 276-278X MS m/e 290 (M+H)+. Analysis for: C1sHgF2NO3 Calc'd: C, 62.29; H, 3.14; N, 4.84 Found: C, 61.90; H, 3.05; N. 4.52 Exampee 27 2-<4.Hydroxyphenyl)-7-v;nyl-1,3-ben2oxa2ol.5-ol. The title compoudd was prepared in substantially the same manner as described in Example 24, Route b), from 7-bromo-2-(4-hydroxyphenyl)-1,3-benzoxazol-5-ol and was obtained as a white solid, m.p. 249-250 °C; MS m/e 254 (M+H.Analysis for: dsH"NOa Calc'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-fJuoro-4-hydroxyphenyl)-7-vlnyl-1,3-benzoxa2ol-5-ol (Ex. 28) and 4,6-Dibromo-2-{3-fluoro-4-hydroxyphenyl)-7-vinyl-1,3-benZoxazol-5-ol(Ex.29). N-Bromosuccinimide (0.49 g, 2.77 mmol) was added into a mixture of 2-(3-f1uor0-4- hydroxyphenylK-vinyM.S-benzoxazol-S-ol (0.75 g, 2.77 mmol) and acetonitrile (30 mL). The reaction mixture was stirred at room temperature for 16 h, poured into water and extracted with EtOAc. The organic extracts were dried over MgSO,. Evaporation and purification by flash chromatography (hexanes I EtOAc /CHzCI2 2/1/1) gave (a) as a white solid (0.45 g, m.p. 226-228 °C); MS mle 349 (M+H)Analysis for C1sH9BrNO3 Calc'd:C,51.45;H,2.59;N,4.00 Found: C, 51.08; H, 2.40; N, 3.90 and (b) as a white solid (0.18 g, m.p. 272-274 °C); MS mle 428 (M+H)Analysis for: C16H8Br2NO3 Calc'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-hydroxyphe1yl)-1,3-benzoxazol-5-ol Step a) S-Methoxy-2-{4.methoxyphenyl)-7-vinyl-1,3-benzoxazole. 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 mle 282 (M+H)Analysis for: C17H15NO3 Calc'd:C, 72.58; H, 5.37; Nt 4.98 Found: C, 72.33; H, 5.26; N, 4.72 Stepb)7-(1,2-Dibromoethyl)-2-(4-hydroxyphenyl)-1,3-benzoxa2ol-5-ol. Boron tribromide (0.85 mL, 8.95 mmol) was added dropwise into a cold (-78°C) mixture of 5-methoxy-2-(4-methoxyphenyl)-7-vinyl-1,3-benzoxazole (0.31 g, 1.12 mmol) and CHzCI2 (4 mL). The mixture was allowed to warm up to room temperature. After stirring for 18 h at room temperature the mixture was slowly poured into cold (0°C) ethyl ether (20 mL). Methyl alcohol (10 mL) was then slowly added into the mixture. The new mixture was washed with water (three times) and dried over ~gSO«. Evaporation and purification by flash chromatography (hexanes 1 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: dsH^BrzNOa 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)-1,3-ben2oxazol-5-ol 1,8-Diazabicyclo[5.4.0]undec-7-ene (0.259, 1.65mmol) was added into a solution of 7- (1,2-dibromoethyl)-2-(4-hydroxyphenyl)-3,3-benzoxazol-5-ol (0.4 g, 0.96 mmol) and acetonitrile (4 mL). The reaction mixture was stirred for 24 h, poured into cold (0°C) HCI (1N. 10 mL) and extracted with EtOAc. The organic extracts were dried over MgSO,. Evaporation and purification by flash chromatography (CH2CI2 1 hexanes 1 isopropyl alcohol 15/5/1) gave a white solid (185 mg, 58% yield, m.p. 228-230°C); MS m/e332(M+Hr. Analysis for: C15H10BrNO3 Calc^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-f1uoro-4-hydroxyphenyl)-1,3-ben2oxa2ol-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. 235-237X; MS m/e 350 (M+H)+. Analysis for: C1sHgBrFNO3 Calc^C, 51.45; H, 2.59; N, 4.00 Found: C, 51.63; H. 2.38; N, 3.98 Example 33 7-d-Bromovinyl)-2-(2,3-difluoro-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-(2,3-difluoro-4-methoxyphenyl)-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: C15H.BrF2No, CakAfcC, 48•94; H,Z.1~;N~ 3.80 Found: C, 49.63; H, 2.33; N, 3.61 Example 34 7-Allyl-2^3.fluoro^-hydroxyphenylH,34^nzoxazo|.5^l The title compound was prepared in substantially the same manner as described in Example 24, Route c, step b, from I-brorrH>-2^3-fluoro^^ethoxyphenyl)-5HT«thoxy. 1.3-benzoxazote. aMyltriburyltin anddichlorobls(tn^o-torylprK5sphir»)pattadlum, followed by demethytetion according to Example 20, step e. The desired product was obtained as a light pink solid, m.p. 169-171 "C; MS mle 284 (M-Hf Analysis for: C16H,2FNen20xazo|.5^l Tetrakis(triphenylphosphine)pallacJium(O) (70 mg, 0.06 mmol) was added into a mixture of >bromo-5-m^ 12 mmol), bromo(propyl)zinc (0.5 M in THF, 3.6 mL, 1.8 mmol), and THF (4 mL).. The mixture was stirred at room temperature for 48 h, poured into HCl (1N) and extracted with EtOAc. The organic extracts were dried over MgSO* Evaporation and purification by flash chromatography (hexanes/EtOAc 6/1) gave an off-white solid (0.14g). The product was dissolved in CH2CI?(2 mL), cooredto -7$ °C and boron tribromide (0.35 mL) was added dropwise. Th' mixture was allowed to warm up to room temperature. After stirring for 18 h at room temperature the mixture was slowly poured into cold (0 °CJ ethyl ether (10 mL). Methyl alcohol (3 mL) was then slowly added into the mixture. The new mixture was washed with water (three times) and dried over MgSO4. Evaporation and purification by flash chromatography (hexanes I EtOAc 4/1) gave a white solid (90 mg, 27% yield, m.p. 11D-112X); MS mle 270 (M+H)+. Analysis for: C^NCV C~lc'd:C, 71.36; H, 5.61; N, 5.20 Found:C. 71.02; H, 5.58; N~ 4.94 Example 37 7-Butyl-2-(4-hydroxyphenyl).1,3.benZoxa2ol-5K)l The title compound was prepared in substantially the same manner as described in Example 35, from 7-bromo-5-methoxy-2-(4-methoxyphenyl).1,3-benzoxazole, and bromo(butyl)zinc. The desired product was obtained as a ~hite solid, m.p 125-127'C MS/n/e282(M-H)Analysis for: C17H17NO3 Calc'd: C,72.07^,6.05;^ 4.94 Found: C, 72.78; H, 5.87; N. 4.69 Example 38 7-Cyclopentyl-2-(4-hydroxyphenyl).1,3-benzoxa2ol-5-ol The title compound was prepared in substantially the same manner as described in Example 35, from 7-bromo-5-methoxy-2-(4-methoxyphenyl)-1,3-benzoxazole, and bromo(cyclopenty1)zinc. The desired product was obtained as a white solid, m.p. 220- 222•C;MSmle296(M+H)+. Analysis for: C18H17NO3 CalcUC, 73.20; H, 5.80; N, 4.74 Found: C, 73.05; H, 5.74; N, 4.59 Example 39 Ethyl 5-hydroxy-2-(4-hydroxyphenyl)-1,3-benzoxazole.7-carboxylate Step a} 7-Bromo-5-{[fert-butyl(dimethyl)si1yl]oxy}-2-{4-{[feft- butyl(dimethyl)silyl]oxy}phenyl)-1,3-benzoxazole. The title compound was prepared in substantially the same manner as described in Example 24, Route a, Step a, from 7-bromo-5-methoxy-2-(4-methoxyphenyl)-1-3- benzoxazole, and tert-butyl(chloro)dimethylsilane. The desired product was obtained as a white solid, m.p. 90-9rC; MS mle 534 (M+Hf. Analysis for: C25H38BrNO3Si2 Calc'd:C, 56.16; H, 6.79; N, 2.62 Found: C, 55.66; H, 6.86; N, 2.68 Step b) Ethyl 5-hydroxy-2-(4-hydroxyphenyl)-1,3•benzoxa2ole-7-carboxylate. n-Butyllithium (2.5 M, 0.3 mL, 0.75 mmol) was added dropwise into a cold (0 °C) solution of 7-bronx)-5-{[tert-butyl(dimethyl)silyl]oxy}-2-(4-{[tert-butyl(dimethyl)silyl]oxy}- phenyl)-1.3-benzoxa2ole (0.4 g, 0.75 mmol) and THF (4 mL). The mixture was allowed to warm up to 40°C, and then stirred for 2 h. [(Cyanocarbony))oxy]ethane (84 mg) in THF (1 ML) was added into the reaction mixture and the reaction mixture was allowed to warm up to O°C and stirred for 1 h. The reaction was quenched with aqueous ammonium chloride, extracted with EtOAc, and dried over MgSO4. Evaporation and purification by flash chromatography (hexanes 1 CH2CI2 lisopropyl alcohol 18/2/1) gave a colorless oil (340 mg). The product was dissolved in THF (3.5 mL) and treated with tetrabutylammonium fluoride (1M in THF, 1.4 mL). The mixture was stirred for 30 min poured into HCI (1N) and extracted with EtOAc. The organic extracts were dried over MgSO<. Evaporation and purification by flash chromatography (hexanes 1 CH2CI2 lisopropyl alcohol 5/211) gave a white solid (119 mg, 53% yield, m.p. 305-307 °C); MS mle 300 (M+H) Analysis for: C1sH13NO5 Calc'd:C, 64.21; H, 4.38; N, 4.68 Found: C, 64.04; H, 4.43; N, 4.40 Example 40 2-(4-Hydroxyphenyl)-7-phenyl-1,3-benzoxa2ol-5-ol Step a) 5-Methoxy-2-(4-methoxyphenyl)-7-phenyl-1,3-benZoxa2ole 7-Bromo-5-methoxy-2-(4-methoxyphenyl)-1,3-ben20xazole (200 mg, 0.60 mmol) and tetrakis(triphenylphosphine)palladium(0) (63 mg, 0.03 mmol) were dissolved in toluene (5 mL) and stirred for 10 min 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 mixture was refluxed for 12 h, diluted with water and extracted with EtOAc. The organic extracts were dried over MgSO4. Evaporation and purification by flash chromatography (20% _ 40% EtOAclpetroleum ether) gave the title compound as a light pink solid, mp 92°C; MS mle332(M+H(+. Analysis for C21H17NO3 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-phenyl-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 mle 302 (M-H)+. Analysis for C19H13NO3x 0.25 H20 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•benzoxazo--7-earbonitrile Stepa)S-Methoxy-2-(4-methoxyphenyl)-1,3-benzoxazole-7-earbonitrile. 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 h. The mixture was cooled and poured into an excess of aqueous ethylenediaminetetraacetic acid. Isolation of the crude product gave the nitrile (164 mg, 98% yield) as tan needles from (30% EtOAclpetroteum ether); m.p. 180-183 °C; MS mle 281 (M+H)+. Analysis for C16H12N203 x 0.2 H20 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).1,3-ber«oxa2ol.7^arbonltrlle 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 mle 253 (M+H)* Analysis for C14HeN203 x 0.5 H20 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-hydroxyphenylM>benzoxazol-7eWoxazol.5^| Step a) 2-Broi"o^-methoxy-6-{[4.methoxy.3^trifIuoromethyl)ben2ovnamiNOi phenyl 4-methoxy^^trJf|Uoromethyl)benzoate. The title compound was prepared in sUbstantially the same manner as described in Example 20. Step c. from 2-amiNO-6-bromyl).1,3-benzoxazole. The title compound was prepared according to the procedure of Example 53, Step a. from 7-bromo-5-methoxy-2-{4-methoxyphenyl)-1,3-benzoxazole and 2-{tributyl. stannyl)thiazole. The product was obtained as an off white solid (93% yield, m.p. 132- 136•C);MS/n/e339(M+H)Analysis for C„H14N203S Calcd:C, 63.89; H, 4.17; N, 8.28 Found: C, 63.53; H, 3.94; N, 8.15 Step b) 2-(4-Hydroxyphenyl).7-(1,3-thia2ol-2-yl)-1,3-benzoxa2ol-5-ol. The title compound was prepared according to the procedure of Example 50, from 5- methoxy-2-(4-methoxyphenyl)-7-(1,3-thiazol-2-yl)-1.3-benzoxazole,and was obtained as a yellow solid (55% yield, m.p. 245-255°C;; MS mle 311 (M+H)+. Analysis for C16H10N2O3S x 1.5 H20 Caled:C, 56.97; H, 3.88; N, 8.30 Found: C, 57.24; H, 3.95; N, 7.50 Example 58 2-(3-Fluoro-4-hydroxyphenyl)-5-hydroxy-1,3-benzoxa20le-7-carbonitrile The title compound was prepared according to the procedure of Example 35, from 7- bromo-2-(3-f1uoro-4-methoxypheny))-5-methoxy-1,3-benzoxazole, and zinc cyanide. The product was obtained as a white solid, m.p. 308-310°C, MS mle 269 (M-H)Analysis for C14H7FN2~3 x 1.5 H20 Calcd:C, 61.01; H. 2.77; N, 10.16 Found: C, 60.68; H, 2.46; N, 9.77 Examples 59 and 60 4-Bromo-2-(4-hydroxyphenyl)-7-methoxy-1,3-benzoxa2ol-5-ol(Ex.59) 4,6-Dibromo-2-(4-hydroxyphenyl)-7-methoxy-1,3-benzoxazol-S-ol (Ex. 60) The title compounds were prepared according to the procedure of Example 28, from 2-(4-hydroxyphenyl)-7-methoxy-1,3-benzoxazol-5-ol. and N-bromosuccinimide. Product (a) was obtained as a white solid, m.p. 246-248°C. MS mle 336 (M+H)+. Analysis for C14H10BrNO4x.1H20 Calcd:C, 49.49; H, 3.08; N, 4.12 Found: C, 49.28; H, 2.89; N, 3.87. Product (b) was obtained as a white solid, m.p. 260-262 °C, MS m/e 414 (M+H)Analysis for C^Br^O, Caled:C, 40.52; H, 2.19; N, 3.37 Found: C, 40.21; H, 2.00; N, 3.3 Example 61 7-Bromo-2-(3,5-difluoro4-hydroxyphenyl)-1,3-benzoxazol-5-ol The title compound was prepared in substantially the same manner as described in Example 21, from 3,5-difluor0-4-methoxybenzoic acid, and 2-amino-6-bromo-4- methoxyphenol, and was obtained as a white solid, m.p. 270-272 °C; MS m/e 340 (M- H)+. Analysis for: C13H6BrF2NO3 Calc'd:C, 45.64; H, 1.77; N, 4.09 Found: C, 45.81; H, 1.73; N, 3.89 Example 62 2-(3.5-Difluoro-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 b, from 7-bromo-2-(3,5-difluoro-4-hydroxyphenyl)-1.3-benzoxazol- 5-ol, and was obtained as a white solid, m.p. 160-262 X; MS m/e 288 (M-H)+. Analysis for: C'5H9F2NO3 x 0.1 HzO Calc'd:C,61.52;H,3.23;N,4.78 Found: C, 61.53; H, 3.10; N, 4.72 Example 63 7-Sromo-2-(4-hydroxy-2-methylphenyl)-1,3-benzoxaZol-5-ol The title compound was prepared in substantially the same manner as described in Example 21, from 4-methoxy-2-methylbenzoic acid, and 2-amino-6-bromo^- methoxyphenol, and was obtained as a light purple solid, m.p. 120-135 °C; MS mle 320(M+H)Analysis for: C14H10BrNO3 Calc^C, 52.52; H, 3.15; N, 4.38 Found: C, 52.24; H, 2.97; N, 4.15 Example 64 2-(3-FIUoro-4-hydroxyphenyl)-7-(1-f1uorovinyl)-1,3-benzoxazol-5-ol Hydrogen fluoride pyridine (1.14 mL) was added dropwise into a cold (0 DC) solution of 2-[4-(acetyloxy)-3-fluoropheny)]-7-vinyl-1,3-ben20xazol-5-yl acetate (0.25 9, 0.7 mmol), in sulfolane (3 mL). The reaction mixture was stirred for 5 min and then 1,3- dibromo-5.5-dirnethylimidazolidine-2,4-dione (120 mg) was added in one portion. The mixture was stirred at room temperature for 24 h, diluted with HCI (1N) and extracted with EtOAc. The organic layer was dried over MgSO4. Evaporation and purification by flash chromatography (CH2CI2 I isopropyl alcohol 0.3%) gave 7-(2-bromo-1- f1uoroethyl)-2-(3-f1uoro^-hydroxyphenyl)-1,3-ben20xa20l-5-ol as a white solid (0.25 g, m.p. 185-186X). The product was taken in acetonitrile (2 mL) and 1,8- diazabicyclo[5.4.0]undec-7-ene (150 mg) was added. The reaction mixture was stirred for 24 h, poured into cold (O°C) HCI (1N, 10 mL) and extracted with EtOAc. The organic extracts were dried over MgSO4. Evaporation and purification by flash chromatography (20% EtOAc I hexanes) gave a white solid (160 mg, m.p. 213- 214°C);MSmle290(M+Hr. Analysis for: C15HgBrF2NO3 x 0.3 H20 CalcttC, 61.15; H, 3.28; N, 4.75 Found: C, 60.84; H, 3.41; N, 4.57 We Claim: 1. A process for the preparation of a compound of formula I, having the structure wherein R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2Rs, -NO2, CONR5R6, NR5R6 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 trifluoroalkoyy of 1-6 carbon atoms; wherein the alkyl, alkenyl, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 orN(R5)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 trifluoroalkoyy of 1-6 carbon atoms; wherein the alkyl, alkeny,, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 or N(R5)COR6; R5, R6 are each, independenlly hydrogen, alkyl of 1-6 carbon atoms or aryl of 6-10 carbon atoms; XiSO,5,orNR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or-SO2R5; or a pharmaceuiically acceptable salt thereof; comprising one of the following a) reacting a compound of formula wherein R1, R2, R2a and X are as defined above with a compound of formula wherein R3 and R3a are as defined above and Y is halogen. -OH or hydroxyalkyl of 1 to 6 carbon atoms; or b) converting a compound of formula I as defined above to a pharmaceutically acceptable salt thereof; or c) resolving an isomeric mixture of compounds of formula I as defined above to isolate an enantiomer of a compound of formula I or a pharmaceutically acceptable salt thereof. 2. A process according to claim 1, wherein X is O. 3. A process according to claim 1 or 2. wherein R1 is alkenyl of 2-3 carbon atoms, which is optionally substituted with hydroxy!, -CN. halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2 CONR5R6, NR5R6orN(R5)COR6. 4. A process according to claim 1, which is carried out to prepare 2-(3-fluoro-4- hydroxyphenyl)-7-vinyl-1,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 5. A process according to claim 1, which is carried out to prepare 2-(2-fluor0-4~ hydroxyphenyl)~7-vinyll1,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 6. A process according to claim 1, which is carried out to prepare 2-(2,3-djfluoro~ 4-hydroxyphenyl)-7-vinyl-1,3-benzoxazol~5-ol or a pharmaceutically acceptable salt thereof. 7. A process according to claim 1, which is carried out to prepare 4-bromo-2-(3- f1uoro-4-hydroxyphenyl)-7-vinyl-1,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 8. A process according to claim 1, which is carried out to prepare 4,6-d,bromo~2~ (3-fluoro-4-hydroxyphenyl)-7-vinyl-1,3~benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 9. A process according to claim 1, which is carried out to prepare 7-(1- bromovinyl)~2-(2-f1uoro-4-hydroxyphenyl)-1,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 10. A process according to claim 1, which is carried out to prepare 7-(1- bromovinyl)-2-(2,3-difluoro-4-hydroxyphenyl)-1,3~benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 11. A process according to claim 1, which is carried out to prepare 7-allyl-2-(3- fluoro-4-hydroxyphenyl)-1,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 12. A process according to claim 1, which is carried out to prepare 2-(3,5-difluoro- 4-hydroxyphenyl)-7-vinyl-1,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 13. A process according to claim 1, which is carried out to prepare 2-(3-fluoro-4- hydroxyphenyl)-7-(1-fluorovinyl)-1,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 14. Use of a compound of formula I, having the structure wherein R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6,. NR5R6 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 of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2 CONR5R6 NR5R6 or N(R5)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 of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 or N(R5)COR6; R5, R6 are each, independently hydrogen, alkyl of 1-6 carbon atoms or aryl of 6-10 i carbon atoms; X is O, S, or NR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2Rs or-SO2R5; or a pharmaceuiically acceptable salt thereof in the preparation of a medicament for treating or inhibiting osteoporosis or inhibiting bone demoraiization in a mammal in need thereof. 15. Use of a compound of formula I, having the structure wherein R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5. -NO2, CONR5R6, NR5R6 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 of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 orN(R5)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 of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 or N(R5)COR6; R5, R6 are each, independenlly hydrogen, alkyl of 1-6 carbon atoms or aryl of 6-10 carbon atoms; X is O, S, or NR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or-SO2R5; or a pharmaceutically acceptable salt thereof in the preparation of a medicament for treating or inhibiting inflammatory bowel disease, Crohn's disease, ulcerative proctitis or colitis in a mammal in need thereof. 16. Use of a compound of formula I, having the structure wherein R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 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 trifluoroalkoyy of 1-6 carbon atoms; wherein the alkyl, alkeny,, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 orN(R5)COR6; R3, and R3a are each, independently, hydrogen, alkyl of 1-6 carbon atoms, alkenyoff 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 of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 or N(R5)COR6; R5, R6 are each, independenlly hydrogen, alkyl of 1-6 carbon atoms or aryl of 6-10 carbon atoms; X is O, S, or NR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or-SO2R5; or a pharmaceuiically acceptable salt thereof in the preparation or a medicament for treating or inhibiting prostatic hypertrophy, uterine leiomyomas, breast cancer, endometrial cancer, polycystic ovary syndrome, endometrial polyps, benign breast disease, adenomyosis, ovarian cancer, glioma or astioblastomia in a mammal in need thereof. 17. Use of a compound of formula I, having the structure wherein R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 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 of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 or N(R5)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, alkeny,, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 or N(R5)COR6; R5, R6 are each, independenlly hydrogen, alkyl of 1-6 carbon atoms or aryl of 6-10 carbon atoms; X is O, 5, or NR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or-SO2R5; or a pharmaceuiically acceptable salt thereof in the preparation of a medicament for lowering cholestero,, triglycerides, Lp(a) or LDL levels, inhibiting or treating hypercholesteremia; hyperlipemia; 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. 18. Use of a compound of formula I, having the structure wherein R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 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 of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 orN(R5)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 of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5• -CO2R5, -NO2, CONR5R6, NRsRa or N(R5)COR6; R5, R6 are each, independently hydrogen, alkyl of 1-6 carbon atoms or aryl of 6-10 carbon atoms; XiSO,S,orNR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or-SO2R5; or a pharmaceutical acceptable salt thereof in the preparation of a medicament for 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. 19. Use of a compound of formula I, having the structure wherein R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 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 of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2Rs, -NO2, CONR5R6, NR5R6 or N(R5)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 of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6 NR5R6 or N(R5)COR6; Rs, Rs are each, independently hydrogen, alkyl of 1-6 carbon atoms or aryl of 6-10 carbon atoms; X is O,S,orNR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2Rs or-SO2R5; or a pharmaceutically acceptable salt thereof in the preparaiion of a medicament for treating or inhibiting free radical induced disease states in a mammal in need thereof. 20. Use of a compound of formula I, having the structure wherein R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, triftuoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONRsRa, NR5R6 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 trifluoroalkoyy of 1-6 carbon atoms; wherein the alkyl, alkeny,, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO,, CONR5R6, NR5R6 orN(R5)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 trifJuoroalkoxy of 1-6 carbon atoms; wherein the alkyl, alkeny,, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 or N(R5)COR6; R5, R6 are each, independenlly hydrogen, alkyl of 1-6 carbon atoms or aryl of 6-10 carbon atoms; X is O, 5, or NR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or-SO2R5; or a pharmaceuiically acceptable salt thereof in the preparation of a medicament for treating or inhibiting vaginal or vulvar atrophy; atrophic vaginitis; interstitial cystitis; vaginal dryness; pruritus; dyspateunia; dysuria; frequent urination; urinary incontinence; urinary tract infections in a mammal in need thereof. 21. Use of a compound of formula I, having the structure wherein R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 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 of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 or N(R5)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 trifluoroalkoyy of 1-6 carbon atoms; wherein the alkyl, alkeny,, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2Rs, -NO2, CONR5R6, NR5R6 or N(R5)COR6; R5, R6 are each, independenlly hydrogen, alkyl of 1-6 carbon atoms or aryl of 6-10 carbon atoms; XiSO,S,orNR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or-SO2R5; or a pharmaceuiically acceptable salt thereof in the preparation of a medicament for treating or inhibiting vasomotor symptoms in a mammal in need thereof. 22. A method of inhibiting conception in a mammal in need thereof, which comprises providing to said mammal an effective amount of a compound of formula I, having the structure wherein R1 isalkenll of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 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 of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 orN(R5)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 trifluoroalkoyy of 1-6 carbon atoms; wherein the alkyl, alkenyl, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2Rs, -NO2, CONR5R6 NR5R6 or N(R5)COR6; Rs, R6 are each, independenlly hydrogen, alkyl of 1-6 carbon atoms or aryl of 6-10 carbon atoms; XisO,5,orNR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or-SO2R5; or a pharmaceuiically acceptable salt thereof. 23. Use of a compound of formula I, having the structure wherein R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R6, -NO2, CONR5R6, NR5R6 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, alkeny,, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2Rs, -NO2, CONR5R6, NR5R6 orN(R5)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 of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5. -NO2, CONR5R6, NR5R6 or N(R5)COR6; R5, R6 are each, independently hydrogen, alkyl of 1-6 carbon atoms or aryl of 6-10 carbon atoms; X is O, 5, or NR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or.SO2 R5; or a pharmaceuiically acceptable salt thereof in the preparation of a medicament for treating or inhibiting arthritis in a mammal in need thereof. 24. Use according to claim 23, wherein the arthritis is rheumatoid arthritis, osteoarthritis, or spondyloarthropathies. 25. Use of a compound of formula I, having the structure wherein R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 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 trifluoroalkoyy of 1-6 carbon atoms; wherein the alkyl, alkenyl, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO,, CONR5R6, NR5R6 or N(R5)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 trifluoroalkoyy of 1-6 carbon atoms; wherein the alkyl, alkeny,, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO,, CONR5R6, NR5R6 or N(R5)COR6; R5, R6 are each, independently hydrogen, alkyl of 1-6 carbon atoms or aryl of 6-10 carbon atoms; X is O, 5, or NR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or-SO2R5; or a pharmaceuiically acceptable salt thereof in the preparation of a medicament for treating or inhibiting joint swelling or erosion; or treating or inhibiting joint damage secondary to arthroscopic procedures in a mammal in need thereof. 26. Use of a compound of formula I, having the structure wherein R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6,. NR5R6 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 of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 or N(R5)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 trifluoroalkoyy of 1-6 carbon atoms; wherein the alkyl, alkeny,, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 or N(R5)COR6; R5, R6 are each, independently hydrogen, alkyl of 1-6 carbon atoms or aryl of 6-10 carbon atoms; X is O, 5, or NR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or-SO2R5; or a pharmaceuiically acceptable salt thereof in the preparation of a medicament for treating or inhibiting psoriasis or dermatitis in a mammal in need thereof. 27. Use of a compound of formula I, having the structure wherein R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 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 of 1-6 carbon atoms, trifluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 orN(R5)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, alkeny,, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5. -NO2, CONR5R6, NR5R6 or N(R5)COR6; R5, R6 are each, independenlly hydrogen, alkyl of 1-6 carbon atoms or aryl of 6-10 carbon atoms; X is O, S, or NR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or-SO2R5; or a pharmaceuiically acceptable salt thereof in the preparation of a medicament for 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. 28. Use of a compound of formula I, having the structure wherein R1 is alkenyl of 2-7 carbon atoms; wherein the alkenyl moiety is optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 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 trifluoroalkoyy of 1-6 carbon atoms; wherein the alkyl, alkenyl, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, trifluoroalkoyy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 or N(R5)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 tnfluoroalkoxy of 1-6 carbon atoms; wherein the alkyl, alkenyl, or alkynyl moieties are optionally substituted with hydroxyl, -CN, halogen, trifluoroalkyl of 1-6 carbon atoms, tnfluoroalkoxy of 1-6 carbon atoms, -COR5, -CO2R5, -NO2, CONR5R6, NR5R6 or N(R5)COR6; R5, R6 are each, independently hydrogen, alkyl of 1-6 carbon atoms or aryl of 6-10 carbon atoms; X is O, S, or NR7; R7 is hydrogen, alkyl of 1-6 carbon atoms, aryl of 6-10 carbon atoms, -COR5, -CO2R5 or-SO2R5; or a pharmaceutically acceptable salt thereof in the preparation of a medicament for treating or inhibiting endometriosis in a mammal in need thereof. 29. Use or method according to anyone of claims 14 to 28, wherein X is O. 30. Use or method as claimed in anyone of claims 14 to 29 wherein R1 is as defined in claim 3. 31. Use or method according to any one of claims 14 to 28, wherein the compound used is 2-(3-f1uoro-4-hydroxyphenyl)-7-vinyl-1,3-benzoxazol-5-ol or a pharmaceutically acceptable salt thereof. 32. A process of manufacture of a pharmaceutical composition which comprises bringing a compound having formula I as defined and illustrated in claim 14 or a pharmaceutically acceptable salt into combination with a pharmaceutical carrier. 33. Use of an ER-1 selective ligand, wherein the binding affinity of the ER-1 selective ligand to ER-1 is at least about 20 times greater than its binding affinity to ER-a, in the preparation of a medicament for treating or inhibiting inflammatory bowel disease in a mammal in need thereof. 34. Use according to claim 33, wherein the inflammatory bowel disease is Crohn's disease, ulcerative colitis, indeterminate colitis, infectious colitis, or ulcerative proctitis. 35. Use according to claim 34, wherein the binding affinity of the ER-P selective ligand to ER-P is at least about 50 times greater than its binding affinity to ER-a. 36. Use according to claim 35, wherein the ERp selective ligand causes an increase in wet uterine weight which is less than about 10% of that observed for a maximally efficacious dose of 17p-estradiol in a standard pharmacological test procedure measuring uterotrophic activity, and the ERp selective ligand causes an increase in casein kinase II mRNA which is less than about 10% of that observed for a maximally efficacious dose of 17p-estradiol in a standard pharmacological test procedure measuring mammotrophic activity. 37. Use according to claim 36, wherein the ER-P selective ligand does not significantly (p > 0.05) increase wet uterine weight compared with a control that is devoid of uterotrophic activity, and does not significantly (p > 0.05) increase casein kinase II mRNA compared with a control that is devoid of mammotrophic activity. 38. Use of a non-uterotropic, non-mammotrophic ERp selective ligand, wherein the binding affinity of the ER-P selective ligand to ER-P is at least about 20 times greater than its binding affinity to ER-a, in the preparation of a medicament for treating or inhibiting arthritis in a mammal in need thereof. 39. Use according to claim 38, wherein the arthritis is rheumatoid arthritis, osteoarthritis, or spondyloarthropathies. 40. Use according to claim 39, wherein the binding affinity of the ER~ selective ligand to ER~ is at least about 50 times greater than its binding affinity to ERa. 41. Use according to claim 40, wherein the ER~ selective ligand causes an increase in wet uterine weight which is less than about 10% of that observed for a maximally efficacious dose of 17~-estradiol in a standard pharmacological test procedure measuring uterotrophic activity, and the ER~ selective ligand causes an increase in casein kinase II mRNA which is less than about 10% of that observed for a maximally efficacious dose of 17p-estradiol in a standard pharmacological test procedure measuring mammotrophic activity. 42. Use according to claim 41, wherein the ERp selective ligand does not significantly (p > 0.05) increase wet uterine weight compared with a control that is devoid of uterotrophic activity, and does not significantly (p > 0.05) increase casein kinase II mRNA compared with a control that is devoid of mammotrophic activity. 43. Use of a non-uterotrophic, non-mammotrophic ERp selective ligand. wherein the binding affinity of the ER-P selective ligand to ER-P is at least about 20 times greater than its binding affinity to ER-a, in the preparation of a medicament for 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. 44. Use according to claim 43, wherein the binding affinity of the ERp selective ligand to ERp is at least about 50 times greater than its binding affinity to ERa. 45. Use of an ER-P selective ligand, wherein the binding affinity of the ER-P selective ligand to ER-P is at least about 20 times greater than its binding affinity to ER-a, in the preparation of a medicament for treating or inhibiting endometriosis in a mammal in need thereof. 46. Use according to claim 45, wherein the binding affinity of the ER-P selective ligand to ER-P is at least about 50 times greater than its binding affinity to ER-a. 47. Use according to claim 46. wherein the ERp selective ligand causes an increase in wet uterine weight which is less than about 10% of that observed for a maximally efficacious dose of 17p-estradiol in a standard pharmacological test procedure measuring uterotrophic activity, and the ERp selective ligand causes an increase in casein kinase lI mRNA which is less than about 10% of that observed for a maximally efficacious dose of 17β-estradiol in a standard pharmacological test procedure measuring mammotrophic activity. 48. Use according to claim 47, wherein the ER-β selective ligand does not significantly (p > 0.05) increase wet uterine weight compared with a control that is devoid of uterotrophic activity and does not significantly (p > 0.05) increase casein kinase II mRNA compared with a control that is devoid of mammotrophic activity.