TOs invention retoes ,o eH-mbenzopyranoW-bJquinolines and their use as es.rogenic agents FIELD OF THE INVENTION This invention relates to 6H-[1lbenzopyrano[4,3-b]qulno!ine compounds, their use as estrogenic agents, and methods of their preparation. BACKGROUND OF THE INVENTION The pleiotropic effects of estrogens In mammalian tissues have been weil documented, and it is now appreciated that estrogens affect many organ systems (see Mendelsohn and Karas, New England Jpumal of Medicine 340: 1801-1811 (1999), Epperson, et al., Psychosomatic Medicine 61: 676-697 (1999), Crandall, Journal ofWomens Health & Gender Based Medicine 8: 1155-1166 (1999), Monk and Brodaty, Dementia & Geriatric Cognitive Disorders 11: 1-10 (2000), Hurn and Macrae, Journal of Cerebral Blood Flow & Metabolism 20: 631-652 (2000), Calvin, Maturitas 34: 195-210 (2000), Finking, etal., Zeitschrift fur Kardiologie 89: 442-453 (2000), Brincat, Maturitas 35: 107-117 (2000), AI-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 interaction with estrogen receptors leading to alterations in gene transcription. Estrogen receptors are ligand-activated transcription factors and belong to the nuclear hormone receptor superfamily. Other members of this family include the progesterone, androgen, glucocorticoid and mlneralocorticoid receptors. Upon binding ligand, these receptors dimerize and can activate gene transcription either by directly binding to specific sequences on DNA (known as response elements) or by interacting with other transcription factors (such as AP1), which in turn bind directly to specific DNA sequences (see Moggs and Orphanides, EMBO Reports 2:775-781 (2001), Hall, et al., Journal of Biological Chemistry 27 Q: 36869-36872 (2001), McDonnell, Principles of Molecular Regulation 351-361 (2000)), A class of "coregulatory" proteins can also interact with the ligand-bound receptor and further modulate its transcriptional activity (see McKenna, et al., Endocrine Reviews 20: 321-344 (1999)). It has also been shown that estrogen receptors can suppress NFicB-mediated transcription in both a ligand-dependent and independent manner (see Quaedackers, et al., Endocrinology 142: 1156-1166 (2001), Bhat, et al., Journal of Steroid Biochemistry & Molecular Biology 67: 233-240 (1998), Pelzer, et al., Biochemical & Biophysical Research Communications 286:1153-7 (2001)). Estrogen receptors can also be activated by phosphorylation. This phosphorylation is mediated by growth factors such as EOF and causes changes in gene transcription in the absence of ligand (see Moggs and Orphanides, EMBO Reports 2: 775-781 (2001), Half, et a!,, Journal of Biological Chemistry 276: 36869- 36872 (2001)). A less well-characterized means by which estrogens can affect ceils 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 (see Levin, Journal of Applied Physiology 91: 1860-1867 (2001), Levin, Trends in Endocrinology & Metabolism 10: 374-377 (1999)). Two estrogen receptors have been discovered to date. The first estrogen receptor was cloned about 15 years ago and is now referred to as ERa (see Green, et al., Nature 320: 134-9 (1986)). The second form of the estrogen receptor was found comparatively recently and is called ERp (see Kuiper, et al., Proceedings of the National Academy of Sciences of the United Slates of America 93: 5925-5930 (1996)). Early work on ERp focused on defining its affinity for a variety of ligands and indeed, some differences with ERa were seen. The tissue distribution of ERp has been well mapped in the rodent and it is not coincident with ERa. Tissues such as the mouse and rat uterus express predominantly ERa, whereas other tissues such as the mouse and rat lung express predominantly ERp (see 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 ERp can be compartmentalized. For example, in the mouse ovary, ERp is highly expressed in the granulosa cells and ERa is restricted to the thecal and stromal cells (see Sar and Welsch, Endocrinology 140: 963-971 (1999), Fitzpatrick, et al., Endocrinology 140: 2581-2591 (1999)). However, there are examples where the receptors are coexpressed and there Is evidence from in vitro studies that ERa and ERp can form heterodimers (see Cowley, et al., Journal of Biological Chemistry 272:19858-19862 (1997)). A large number of compounds have been described that either mimic or block the activity of 17{J-estradiol. Compounds having roughly the same biological effects as 17p-estradiol, the most potent endogenous estrogen, are referred to as "estrogen receptor agonists". Those which, when given in combination with 17p-estradiol, block its effects are called "estrogen receptor antagonists". In reality there is a continuum between estrogen receptor agonist and estrogen receptor antagonist activity, and indeed, some compounds behave as estrogen receptor agonists in some tissues and estrogen receptor antagonists in others. These compounds with mixed activity are called selective estrogen receptor modulators (SERMS) and are therapeutically useful agents (e.g., EVtSTA®) (see McDonnell, Journal of the Society for Gynecologic Investigation 7: S10-S15 (2000), Goldstein, et al., Human Reproduction Update 6: 212-224 (2000)). The precise reason why the same compound can have cell-specific effects has not been elucidated, but the differences in receptor conformation and/or in the milieu of coregulatory proteins have been suggested. It has been known for some time that estrogen receptors adopt different conformations when binding ligands. However, the consequence and subtlety of these changes have been only recently revealed. The three dimensional structures of ERa and ERp have been solved by co-crystallization with various ligands and clearly show the repositioning of helix 12 in the presence of an estrogen receptor antagonist, which sterically hinders the protein sequences required for receptorcoregulatory protein interaction (see 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 (see Paige, etal., Proceedings of the National Academy of Sciences of the United Stales of America 96: 3999-4004 (1999)). For example, a peptide was identified that distinguished between ERa bound to the full estrogen receptor agonists 17B-estradiol and diethylstilbesterol. A different peptide was shown to distinguish between clomiphene bound to ERa and ERp. These data indicate that each ligand potentially places the receptor in a unique and unpredictable conformation that is likely to have distinct biological activities. As mentioned above, estrogens affect a panoply of biological processes. In addition, where gender differences have been described (e.g. disease frequencies, responses to challenge, etc.), it is possible that the explanation involves the difference in estrogen levels between males and females. Given the importance of these compounds, it can be seen that there is a need for new estrogenic agents. This invention is directed to these, as well as other, important ends. SUMMARY OF THE INVENTION The present invention provides 6H-[1]benzopyrano[4,3-b]quinoline compounds that find use as estrogenic agents. In certain embodiments, the compounds have the formula I: A and A' are each independently OH, H or OR; each R is independently selected from the group consisting of Ct-C6 alkyl, alkenyl, benzyl, acyl, aroyf, -C(=O)-OR', sulfonyl and phosphoryl, wherein each R' is independently selected from Cj-Cs alkyl, Ca-C7 alkenyl, C2-C7 alkynyl, or ,C3-C10 cycloalkyl, each of which are optionally substituted by 1 to 3 substituents selected from Ci-C6 alkyl or halogen; R1 and R2 are independently selected from the group consisting of H, halogen, CrC6 alkyl, d-Cs perhaloalkyl, CF3, Cz-C7 alkenyl and CrC6 alkoxy; R3, R4, R5 and Re are each independently selected from the group consisting of H, halogen, CF3) C,-C6 perhaloalkyl, Ci-C6 alkyl, C2-C7 alkenyl, Cz-C7 alkynyl, C3- C7 cycloalkyl, CM-CS alkoxy, CN, -CHO, acyl, phenyl, aryl and heteroaryl; wherein the alky! or alkenyl moieties of R3, R4, Rs and Re can each be optionally substituted with up to three substituents independently selected from halogen, OH, CN, trifluoroalkyl, trifluoroalkoxy, NO2 or phenyl, wherein said phertyl is optionally substituted with up to three independently selected R10 groups; wherein the alkyhyl moiety of R3, R4, R5 and R6 can each be optionally substituted with up to three substituents selected from halogen, -CN, -CHO, acyl, trifluoroalkyl, trialkylsilyl or phenyl, wherein said phenyi is optionally substituted with up to three independently selected R10 groups; wherein the phenyl, aryl or heteroaryl moiety of R3, R4, R5 and R6 can each be optionally substituted with up to three substituents selected from halogen, -CN, alky!, alkoxy, perfluoroalkyl or perfluoroalkoxy; each R10 is independently selected from the group consisting of halogen, Cr C6 alkyl, C2-C7 alkenyl, -OH, CrC6 alkoxy, -CN, -CHO, -NO2, amino, CrC6 alkylamino, di-(Ci-Ce)alkylamino, thiol, and CrC6 alkylthio; and n is 0,1,2, or 3; provided that: at least era of A and A' is not H; if n is 0, then Rz is not halogen; and at least one of R3, R4 and R5 is halogen, CrCB alkyl, C2-C7 alkenyl, Cy-C7 aikynyl, C3-C7 cycloalkyl, Ci-C6 alkoxy, -CN, -CHO, acy!, phenyl, aryl or heteroaryl; or an N-oxide thereof or a pharmaceutically acceptable salt thereof or a prodrug thereof. The compounds of the 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. Thus, in some aspects, the invention is directed to the use of the compounds of the invention in the treatment or prevention of diseases such as osteoporosis, inflammatory bowel diseases, Crohn's disease, ulcerative proct'rtis, colitis, estrogen dependent cancers, hypercholesteremia, hyperlipidemia, cardiovascular disease, atherosclerosis, senile dementias, Alzheimer's disease, anxiety disorders, neurodegenerative disorders, infertility, or arthritis. DETAILED DESCRIPTION OF THE INVENTION The present invention provides 6H-[1]benzopyrano[4,3-b]quinoline compounds, compositions containing the compounds, and methods for use of the compounds as estrogenic agents. The compounds of the invention are useful in the treatment and prevention of diseases associated with the estrogen receptor, particularly ERp. In some embodiments, the estrogenic compounds of the invention A and A' are each independently OH, H or OR; each R is independently selected from the group consisting of CrC6 alkyl, alkenyl, benzyl, acyl, aroyl, -C(=0)-OR', sulfonyi and phosphoryl, wherein each R' is independently selected from Calkyl, CrCy alkenyl, Ca-C? alkynyl, or C3-Ci0 cycloalkyl, each of which are optionally substituted by 1 to 3 substituents selected from d-CB alkyl or halogen; R1 and R2 are independently selected from the group consisting of H, halogen, Ci-CB alkyl, Ci-Ce perhaloalkyl, CF3, C2-C7 alkenyl and d-Ce alkoxy; • R3, R4, Rs and R6 are each independently selected from the group consisting of H, halogen, CF3l CrC6 perhaloalkyl, CrC6 alkyl, C2-C7 alkenyl, C^C-, alkynyl, C3- C7 cycloalkyl, CrC6 alkoxy, CN, -CHO, acyl, phenyl, aryl and heteroaryl; wherein the alkyl or alkenyl moieties of R3, R4, R5 and R8 can each be optionally substituted with up to three substituents independently selected from halogen, OH, CN, trifluoroalkyl, trifluoroalkoxy, NO2 or phenyl, wherein said phenyl is optionally substituted with up to three independently selected R10 groups; wherein the alkynyl moiety of R3, R4, R5 and R8 can each be optionally substituted with up to three substituents selected from halogen, -CN, -CHO, acyl, trifluoroalkyl, trialkylsilyl or phenyl, wherein said pheny! is optionally substituted with up to three independently selected R10 groups; wherein the phenyl, aryl or heteroaryl moiety of R3, R4, Rs and Rs ean each be optionally substituted with up to three substituents selected from halogen, -CN, alkyl, alkoxy, perfluoroalkyl or perfiuoroalkoxy; each R10 is independently selected from the group consisting of halogen, Cr C6 alkyl, C2-C7 alkenyl, -OH, 0,-Cs alkoxy, -CN. -CHO, -NO2, amino, CrC6 alkylamino, di-(C1-C6)aIkylamino, thiol, and CrC6 alkylthio; and n is 0,1,2, or 3; provided that: at least one of A and A' is not H; if n is 0, then R3 is not halogen; and at least one of R3, R4 and R5 is halogen, CrC6 alkyl, C2-C7 alkenyl, C2-C7 alkynyl, C3-C7 cycloalkyl, Ct-C6 alkoxy, -CN, -CHO, acyl, phenyl, aryl or heteroaryl; or an H-oxide thereof or a pharmaceutically acceptable salt thereof or a prodrug thereof. In some embodiments, A and A' are each OH. In some further embodiments, one of A and A' is OH, and the other of A and A' is OR. In some further embodiments, one of A and A' is OH, and the other of A and A' is O-CrCe alkyl- In some further embodiments, A and A' are each OR. In still further embodiments, A and A' are each -O-C,-C6 alkyl. In still further embodiments, one of A and A' is H, and tie other of A and A' is OH or OR. In further embodiments, one of A and A' is H, and he other of A and A1 is OH or O-CrC6 alkyl. In some embodiments, Rs and R5 are each, independently, H, halogen, C^e ilkyl, C2-C7 alkenyl, C2-C7 alkynyl, -CN, -CHO, acyl or optionally substituted phenyl, as previously described. In some such embodiments, R3 is other than H. In some embodiments, R3 Is halogen, C^CB alkyl, CrC? alkenyl, C2-C7 alkynyl, -CN, -CHO, or phenyl optionally substituted with up to three groups selected rom halogen, -O-CrCa alkyl {i.e., Ci-C6 alkoxy), perfluoroalkyl and CN; and R5 is H, lalogen, d-C6 alkyl, Cz-C7 alkenyi, C2-C7 alkynyl, -CN, -GHO, or phenyl optionally substituted with up to three groups selected from halogen, Ci-C6 alkoxy, perfluoroalkyl and CN. In some such embodiments, the phenyl of R3 is optionally substituted with up to three substituents selected from F, CI, Br, CN, OCH3 and CF3. In some embodiments, R3 is halogen, C2-C7 aikynyl or -CN. In some further embodiments, R3 and R5 are each independently halogen, C2-C7 aikynyl or -CN. In some embodiments, one of R1 and R2 is halogen. In some preferred embodiments, one of R1 and R2 is fluorine. In some further embodiments, one of R1 and R2 is halogen, and the other of R1 and R2 is H. In some further embodiments, one of R1 and R2 is fluorine, and the other of R1 and R2 is H. In some further embodiments, R1 and R2 are each independently halogen. In some further embodiments, R1 and R2 are each fluorine. In some further embodiments, R1 and R2 are each H. In some embodiments, R4 is H, halogen or-CN, preferably H. In some embodiments, R3 is halogen, CrC6 alkyl, C2-C7 alkenyl, C2-C7 aikynyl, -CN, -CHO, or phenyl optionally substituted with up to three groups selected from halogen, CrC6 alkoxy, perfluoroalkyl and CN; R5 is H, halogen, CrCa alkyl, C2- C7 alkenyl, C2-C7 aikynyl, -CN, -CHO, or phenyl optionally substituted with up to.three groups selected from halogen, d-Cs alkoxy, perfluoroalkyl and CN; and one of R1 and R2 is halogen; and R4 is H, halogen or-CN. In some embodiments, preferably those wherein A and A' are each OH, R1, R1-, R4, R5 and R6 are hydrogen, and R3 is halogen, or R3 is OH, or R3 is C2-C7 alkenyl, or R3 is CN, or R3 is C2-C7 aikynyl, or R3 is CrC6 alkyl, or R3 is optionally substituted phenyl, preferably wherein the substituents of the phenyl are halogen, Cr C6 alkoxy, perfluoroalkyl or CN. In some embodiments of each of the foregoing, n is 1. In some embodiments, the invention provides compositions containing one or more compounds of the invention, or pharmaceutically acceptable salts, chelates, complexes or prodrugs thereof. It is to be understood that, when the compounds according to the present invention may be present either in their free base forms, as depicted in the formulae set forth herein, or as salts and/or hydrates thereof, and in particular as pharmaceutically acceptable salts thereof. Pharmaceutically acceptable salts are known in the art, as are hydrates, and the person having skill in the art will find it conventional to prepare such salts using art-recognized techniques. Pharmaceutically acceptable salts can be formed from organic and inorganic acids, for example, acetic, propionic, lactic, citric, tartaric, succinic, fumaric, maleic, malonic, nandelic, malic, phthalic, hydrochloric, hydrobromic, phosphoric, nitric, suifuric, nethanesulfonic, naphthaienesulfonic, benzenesulfonic, toiuenesuifonic, ;amphorsulfonic, and similariy known acceptable acids when a compound of this nvention contains a basic moiety. Salts may also be formed from organic and norganic 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 trialkylarnmonium salts containing 1-6 carbon atoms in-each alkyl group, when a compound of this invention contains an acidic moiety. Exemplary salts further include acid-addition salts, e.g., HCI, H2SO4, HBr, HI, HNO3, H3P04, NaH2P04, Na2HP04l H3PO3, NaH2PO3, Na2HPO4, H2SO4, NaHSO4, carboxylic acids, such as acetic acid, malonic acid, capric acid, lauric.acid, dichloroacetic acid, trichloroacetic acid, etc., and other pharmacologically tolerated salts. Hydrates include hemihydrates, monohydrates, dihydrates, etc. Unless otherwise modified herein, the use of a free base formula is intended to include the salt and/or hydrate thereof. The instant invention also encompasses N-oxide derivatives of the compounds disclosed herein. These N-oxides can be prepared by methods known for preparing analogous compounds. For example, the compounds maybe oxidized with a peracid, hydrogen peroxide, an alkali metal peroxide or an alkyl peroxide. One useful N-oxide derivative is a composition where the nitrogen atom of the quinoline ring forms the N-oxide group. The instant invention also encompasses prodrug derivatives. "Prodrug derivative" or "prodrug" means derivatives of the instant compounds that are converted in vivo to the corresponding non-derivattzed form of the instant compounds. The term "alkyl", as used'herein, whether used alone or as part of another group, refers to an aliphatic hydrocarbon chain and includes, but is not limited to, straight and branched chains containing from 1 to 12 carbon atoms, preferably 1 to 6 carbon atoms, unless explicitly specified otherwise. For example, methyl, ethyl, propyl, isopropyl, butyl, Isobutyl, tert-butyl, etc. are encompassed by the term "alkyl." The number of carbon atoms as used in the definitions herein refers to the carbon backbone and carbon branching of the moiety, but does not include carbon atoms of the substituents, such as alkoxy substitutions and the like, of the moiety. The term "alkenyl", as used herein, whether used alone or as part of another group, refers to an aliphatic hydrocarbon chain and includes, but is not limited to, straight and branched chains having 2 to 8 carbon atoms, e.g., 2-7 carbon atoms and containing at least one double bond. Preferably, the alkenyl moiety has 1 or 2 double bonds. For example, vinyl, allyl, 1-methyl vinyl, etc. are encompassed by the term "alkenyl". Such alkenyl moieties may exist in the E or Z conformations and the compounds of this invention include both conformations. The term "alkynyl", as used herein, whether used alone or as part of another group, refers to an aliphatic hydrocarbon chain and includes, but is not limited to, straight and branched chains having 2 to 8 carbon atoms, e.g., 2-7 carbon atoms and containing at least one triple bond. Preferably, the alkynyl moiety has 1 or 2 tn'ple bonds. For example, ethynyl, propynyi, etc. are encompassed by the term "alkynyl". The term "acyl" refers to alkylcarbonyi groups, e.g., where alkyl is as defined herein. The term "benzyl" has its accustomed meaning as a phenyimethyl group. The term "aroyl" refers to an aryl moiety connected through a carbonyl group, such as a benzoyl group. The alkyl, alkenyl, alkynyl, aryl, cycloalkyl, heteroaryl, aroyl, acyl and phenyl groups that are described herein for variables R1, R2 R3, R4, R5, R8, A and A1 can be optionally substituted with one or more substituents, preferably, with up to three substituents. The substituents are independently selected, and include nitro, cyano, halo, hydroxy, carboxy, alky!, alkenyl, alkynyl, cycloalkyl, aryl, heteroaryl, alkoxy, aryloxy, heteroaryloxy, alkylalkoxy, alkoxyalkoxy, perfluoroalkyl, perfluoraalkoxy, arylalkyl, alkylaryl, hydroxyalkyl, alkoxyalkyl, alkylthio, S(O)t-aryI (where s=0-2) S(O}rheteroaryl (where s=0-2),'or -C(=O)-OR', where R' is as previously described. In certain embodiments of the invention, preferred substituents include halogen, OH, CM, trifluoroalkyl, trifluoroalkoxy, perfluoroalkyl, perfluoraalkoxy, arylalkyl, alkylaryl, NO2 and phenyl, wherein said phenyl is optionally substituted with up to three independently selected R10 groups as described herein. For example, when alkyl or alkenyl moieties are substituted, they can typically be mono-, di-, tri- or persubstituted. Examples for a halogen substituent include 1- bromo vinyl, 1-fluoro vinyl, 1,2-difluoro vinyl, 2,2-difluorovinyl, 1,2,2-trifluorovinyl, 1,2- dibromo ethane, 1,2-fluoro ethane, 1-fluoro-2-bromo ethane, CF2CF3, CFzCF2CF3l and the like. The term "halogen" includes fluorine, chlorine, bromine, and iodine. Exemplary cycloalkyl groups include cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl, adamantyl, etc. In some embodiments, the cycloaikyl groups have 3-10 carbon atoms. Preferably cycloalkyl groups have 3-7 carbon atoms. As used herein, cycloalkyl further includes unsaturated cycloalkyl groups, i.e., cycloalkeny! groups. Exemplary unsaturated cycloalkyl groups include cyclopentenyl, cyclohexenyl, cycloheptenyl, etc. Aryl'groups are moieties that possess at least one aromatic ring containing no hetero (i.e., non-carbon) ring atoms. The term "aryl" includes mono- and polycyclic aromatic ring systems, e.g., of 6-15 carbon atoms, for example, phenyl, naphthyl, etc. Aryl groups can have fully or partially saturated rings fused to the aromatic ring. Thus, exemplary aryl groups include phenyl, naphthyl, pyrenyl, 5,6,7,8- tetrartydronaphth-1-yl, and the like. The term heteroary! is intended to mean an aromatic ring system that contains at least one non-carbon ring atom (e.g., one to three heteroatoms) selected from O, N and S and having for example five to 14 ring atoms. Exemplary heteroaryl groups include pyrrolyl, imidazolyl, pyridyl, pyrimidinyl, pyridazinyl, pyrazinyl, quinolyl, quoxalinyl, quinazolinyl, thiophenyl, furanyl, oxazolyl, thiazolyl, thienyl, pyranyl, thiopyranyl, benzofuranyl, indolyl, indazolyl, benzimidazolyl, benzothiazolyl, benzopyranyl, benzothiopyranyl, indazolyl, pyridopyrrolyl, and the like. In some embodiments, the R1 group of the -C(=O)-OR' moiety of A or A', is Ci-C6 alkyl. In some embodiments, R' is d* alkyl. In some embodiments, the- C(=O)-OR'moiety is t-butoxycarbonyl (BOC), As used in accordance With this invention, the term "providing," with respect to providing a compound or substance covered by this invention, means either directly administering such a compound or substance, or administering a prodrug, derivative, or analog that will form the effective amount of the compound or substance within the body. Based on the results obtained in the standard pharmacological test procedure, as described below, the compounds of the 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 corhpounds 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 caused surgically, chemically, or by a disease state that leads to premature diminution or cessation of ovarian function. Accordingly, the compounds of this invention are useful in treating or inhibiting osteoporosis and in the inhibition of bone demineralization, which may result from an imbalance in formation of new bone tissues and the resorption of older tissues in an individual, leading to a net loss of bone. Such bone depletion results in a range of individuals, particularly in post-menopausal women, women who have undergone bilateral oophorectomy, those receiving or who have received extended corticosteroid therapies, those experiencing gonadal dysgenesls, and those suffering from Cushing's syndrome. Special needs for bone replacement, including teeth and oral bone, can also be addressed using these compounds in individuals with bone fractures, defective bone structures, and those receiving bone-related surgeries and/or the implantation of prosthesis. In addition to those problems described above, these compounds can be used in treatment or inhibition for osteoarthritis, spondyloarthropathies, hypocalcemia, hypercalcemia, Paget's disease, osteomalacia, osteohalisteresis, multiple myeloma and other forms of cancer having deleterious effects on bone tissues. The compounds of this invention are further useful in treating or inhibiting joint damage secondary to arthroscopic or surgical procedures. The compounds of this invention are also useful in treating or inhibiting benign or malignant abnormal tissue growth, including prostatic hypertrophy, uterine leiomyomas, breast cancer, endometriosis, endometriaJ 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 they are useful in lowering cholesterol, triglycerides, Lp(a) lipoprotein, and low density lipoprotein (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. These cardiovascular protective properties are of great importance when treating postmenopausal patients with estrogens to inhibit osteoporosis and in the male when estrogen therapy is indicated. The compounds of this invention are also antioxidants, and therefore, are useful in treating or inhibiting free radical induced disease states. Specific situations in which antioxidant therapy is indicated to be warranted are with cancers, central nervous system disorders, Alzheimer's disease, bone disease, aging, inflammatory disorders, peripheral vascular disease, rheumatoid arthritis, autoimmune diseases, respiratory distress, emphysema, asthma, pleurisy, uveitis, sepsis, hemorrhagic shock, prevention of reperfusion injury, viral hepatitis, chronic active hepatitis, tuberculosis, psoriasis, systemic lupus erythematosus, adult respiratory distress syndrome, central nervous system trauma and stroke. The compounds of this invention are also useful in providing cognition enhancement, and in treating or inhibiting senile dementias, Alzheimer's disease, cognitive decline, neurodegenerative disorders, providing neuroprotection or cognition enhancement. The compounds of this invention are also useful in treating or inhibiting inflammatory bowel disease, ulcerative proctitis, Crohn's disease, and colitis; •nenopausal related conditions, such as vasomotor symptoms, including hot flushes, /aginal or vulvar atrophy, atrophic vaginitis, vaginal dryness, pruritus, dyspareunia, tysuria, frequent urination, urinary incontinence, urinary tract infections, myalgia, arthralgia, insomnia, irritability, and the like; male pattern baldness; skin atrophy; acne; type II diabetes; dysfunctional uterine bleeding; and infertility. 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 being treated, and severity thereof, as well as, the various physical factors related to the individual being treated. Effective administration of the compounds of this invention may be given at an oral dose of from about 0.1 mg/day to about 1,000 mg/day. Preferably, administration will be from about 10 mg/day to about 600 mg/day, more preferably from about 50 mg/day to about 600 mg/day, in a single dose or in two or more divided doses. The projected daily dosages are expected to vary with route of administration. Such doses may be administered in any manner useful in directing the active compounds herein to the recipient's bloodstream, including orally, via implants, parenterally (including intravenous, intraperitoneal and subcutaneous injections), rectally, intranasally, vaginally, and transdermally. 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 pharmaceutically 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 pharmaceutically acceptable diluents, binding agents, lubricants, disintegrants, surface modifying agents (including surfactants), suspending or stabilizing agents, including, but not limited to, magnesium stearate, stearic acid, talc, sodium lauryl sulfate, microcrystalline cellulose, carboxymethylcellulose calcium, polyvinylpyrrolidone, gelatin, alginic acid, acacia gum, xanthan gum, sodium citrate, complex silicates, calcium carbonate, glycine, dextrin, sucrose, sorbitol, dicalctum 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 parenterally or intraperitoneally. Solutions or suspensions of these active compounds as a free base or pharmacologically acceptable salt can be prepared in water suitably mixed with a surfactant such as hydroxy-propylcellulose. Dispersions can also be prepared in glycerol, liquid polyethylene glycols and mixtures thereof in oils. Under ordinary conditions of storage and use, these preparations contain a preservative to prevent 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, N-oxides thereof, prodrugs thereof, or pharmaceutically 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 liquids or semisolid emulsions of either the oil-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. Synthesis Of Compounds Of The Invention The compounds of this invention can be prepared by methods known in the art of organic chemistry. The reagents used in the preparation of the compounds of this invention can be either commercially obtained or can be prepared by standard procedures described in the literature. The syntheses of representative examples of this invention are described in the following Schemes 1-4. The Synthetic Methods A-M referred to in 'Schemes 1-4 Synthesis Of Representative Compounds Of The Invention: General Method Aldrich Sure Seal™ solvents, anhydrous without further purification, may be used for the reactions described herein and may be obtained from Aldrich Chemical Company (St. Louis, MO). All reactions were carried out under a nitrogen atmosphere. Chromatography was performed using 230-400 mesh silica gel (Merck Grade 60, Aldrich Chemical Company). Thin layer chromatography was performed with Silica Gel 60 F2S4 plates from EM Science ( ). nH and 19F NMR spectra were obtained on a Bruker AM-400 or Bruker DPX-300 instrument (Bruker, Bilterica, MA) in deuterated solvents such as CDCI3, DMSO-d6 or acetone-d6. Chemical shifts (6) are given in parts per million (ppm) down field from tetramethylsilane (TMS). Melting points were determined on a Thomas-Hoover apparatus and are uncorrected. Infrared (IR) spectra were recorded on a Perkin-Elmer diffraction grating or Perkin- Elmer 784 spectrophotometers (Perkin-Elmer, Shelton, CT). Mass spectra were recorded on a Kratos MS 50 or Finnigan 8230 mass spectrometers. Compound nomenclature was generally arrived at by use of the Beilstein Autonom™ program. EXAMPLE 1 3-(3-METHOXY-PHENOXY)-PROPIONIC ACID (1) Method A: To a mixture of 3-bromopropionic acid (14.70 g, 118 mmol) in water (100 mL) was added slowly NaHCO3 (8.40 g, 100 mmoi) and the resulting mixture was stirred for 5 mins. To this solution was aaaed a 70-mL solution of 3-methoxyphenol (14.70 g, 96 mmol) in aqueous NaOH (4.67 g, 119 mmol), and the resulting mixture was heated at 100 °C for 3 hours. After cooling to room temperature, the reaction mixture was acidified with 1N HCI, and extracted with Et2O. The EtzO layer was washed with aqueous NaHCO3 (3x). The aqueous layer was again acidified with 1N HCI and extracted with Et2O. The Et2O layer was washed with water, brine, dried (NaaSO^), filtered and concentrated to give a crude brown solid, which was recrystallized (Et2O/-20 °C) to give a pure product as a yellow solid. Yield: 17.0 g (23%), 1H-NMR (300 MHz, CDCI3): 5 2.85 (t, J = 6.3 Hz, 2H), 3.79 (s, 3H), 4.24 (t, J = 6.3 Hz, 2H), 6.50 (m, 3H), 7.18 (t, J = 8.2 Hz, 1H), 11.45 (br, 1H); MS (ESI) m/z 195 ([M-HV); Anal. Calcd forC10H12O4: C:61.22, H:6.16. Found: 0:61.24, H:6.12. EXAMPLE 2 7-METHOXY-CHROMAN-4-ONE (2) Method B: To a reaction vessel containing 3-(3-methoxy-phenoxy)-propionic acid (1) (7.00 g, 35.6 mmol) at 0 "C was added slowly trifluoromethanesulfonic acid (15 mL). f The reaction mixture was stirred for 3 hours while allowing to warm up to room temperature. After cooling to 0 "C, the reaction mixture was quenched with crushed ice, then extracted with EfcO (2 x 300 ml). The organic layer was washed with water (2x), aqueous NaHCO3l water, brine, then dried (Na2SO4), filtered and concentrated to give a crude oil, which was purified by silica gel chromatography to give a pure product as a yellow solid. Yield: 4.26 g (67%). 1H-NMR (300 MHz, CDCI3): 6 2.76 ({, J = 6.3 Hz, 2H), 3.84 (s, 3H), 4.52 (t, J = 6.3 Hz, 2H), 6.41 (d, J= 2.3 Hz, 1H), 6.58 (dd, J = 8.8, 2.3 Hz, 1H), 7.84 (d, J= 8.8 Hz, 1H); MS (ESI) m/z 179 ([M+Hft. . - EXAMPLE 3 3,9-DIMETHOXY-6H-CHROMENO[4,3-b]QUINOLIN-7-OL(3) Method C: A mixture of 2-amino-5-methoxybenzoic acid (1.839 g, 11.00 mmol) and 7-methoxy-chroman-4-one (2) (1.960 g, 11.00 mmol) in Ph2O (10 mL) was heated at 170 °C for 1 hour and at 200 °C for 7 hours. After cooling to room temperature, hexane was added. The yellow precipitate formed was collected by filtration and washed successfully with hexane and Et2O and dried in vacua. Yield: 2.171 g (64%). mp 298 °C (dec.); 1H-NMR (300 MHz, DMSO-d6) 6 3.82 (s, 3H), 3.84 (s, 3H), 5.17 (s, 2H), 6.64 (d, J = 2,4 Hz, 1H), 6.79 (dd, J = 8.7, 2.4 Hz, 1H), 7.31 (dd, J = 9.0, 2.9 Hz, 1H), 7.50 (d, J = 2.8 Hz, 1H), 7.74 (d, J = 9.0 Hz, 1H), 7.99 (d, J = 8.7 Hz, 1H), 11.56 (s, 1H); MS (ESI) m/z 308 ([M-HD, 310 «M+H]*); HRMS (ESI*) calcd for Ci6HisN04 310.1074 ([M+Hf), found 310.1068. EXAMPLE 4 7-CHLORO-3,9-DIMETHOXY-6H-CHROMENO[4,3-b]QUINOLJNE(4) Method C: A mixture of 3,9-dimethoxy-6H-chromeno[4,3-b]quino!in-7-ol (3) (124 mg, 0.400 mmol) and POCI3 (1 mL) was heated at reflux for 1 hour. After cooling, excess POCIj was removed under reduced pressure. Water and then aqueous K2CO3 were slowly added to the solid residue and the reaction mixture was extracted with EtOAc. The organic layer was washed with brine, then dried (Na2SO4), filtered and concentrated to give a crude solid, which was passed through a short pad of silica gel and recrystailized (hot heptane/-20 °C) to give a pure product as a yellow powder. Yield: 124 mg (95%); mp 190-191 °C; nH-NMR (300 MHz, CDCI3) 5 3.85 (s, 3H), 3.97 (s, 3H), 5.50 (s, 2H), 6.53 (d, J = 2.4 Hz, 1H), 6.71 (dd, J = 8.7, 2.4 Hz, 1H), 7.35 (dd, J = 8.9, 2.8 Hz, 1H), 7.38 (d, J = 3.2 Hz, 1H), 7.98 (d, J = 8.8 Hz, 1H), 8.29 (d, J = 8.7.Hz, 1H); MS (ESI) m/z 328/330 (fJvU-Hf); HRMS (ESI*) calcd for C1BH14CINO3 328.0735 ([M+Hf), found 328.0728; Anal, calcd for CiBHi4CIN03: C:65.96, H:4.31, N:4.27. Found: C:65.71, H:4.17, N:3.92. EXAMPLE 5 7-BROMO-3,9-DlMETHOXY-6H-CHROMENO[4,3-b]QUINOL!NE (5) Method E. A mixture of 3,9-dimethoxy-6H-chromeno[4,3-b3quinolin-7-o! (3) (1.025 g, 3.31 mmol) and POBr3 (1.430 g, 5.00 mmol, 1.5 equiv.) in DMF (15 mL) was heated at 70 "C for 30 mins. After cooling to room temperature, water and then aqueous K2CO3 were slowly added, and the reaction mixture was extracted with warm CHCIj (2x). The organic layer was washed with water (2x) and brine, then dried (Na2SO4), filtered through a short pad of silica gel and concentrated to give a crude yellow solid, which was recrystallized (hot EtOAc/-20 °C) to give a pure product as yellow needles. Yield: 1.127 g (91%); mp 196-197 °C; 1H-NMR (300 MHz, CDCI3) 5 3.85 (s, 3H), 3.98 (s, 3H), 5.48 (s, 2H), 6.53 (d, J = 2.4 Hz, 1H), 6.71 (dd, J = 8.7, 2.5 Hz, 1H), 7.35 (dd, J = 9.0, 2.7 Hz, 1H), 7.39 (d, J = 2.7 Hz, 1H), 7.97 (d, J = 9.0 Hz, 1H), 8.30 (d, J = 8.7 Hz, 1H); MS (ESI) m/z 372/374 ([M+Hf); HRMS (ESI*) calcd for C18H14BrN03 372.0230 ([M+H]*), found 372.0228; Anal, calcd for C1BHi4BrNO3: C:53.08, H:3.79, N:3J6. Found: 0:57.94, H:3.68, N:3.73. EXAMPLE 6 7-CHLORO-3,9-DIHYDROXY-6H-CHROMENOt4,3-b]QUINOLINE(6) Method F: To a solution of 7-chloro-3,9-dimethoxy-6H-chromeno[4,3-b]quinoIine (4) (68 mg, 0.21 mmol) in 1,2-dichloroethane (3 mL) was added slowly a solution of BBr3 (1.0 M, 1 ml, 1 mmol) in CH2CI2. The reaction mixture was stirred at room temperature for 30 mins. and then at 40 "C for 2 hours. After cooling in an ice bath, aqueous NaHCO3 was added very slowly with vigorous stirring to quench the reaction, and the resulting reaction mixture was extracted with EtOAc. The organic layer was washed with brine, then dried (Na2SO4), filtered through a short pad of silica gel, and concentrated to give a yellow solid, which was recrystallized (THF/hexane). Yield: 56 mg (90%); mp 235 *C (dec.); 1H-NMR (300 MHz, DMSOd6) 6 5.47 (s, 2H), 6.40 (s, 1H), 6.60 (d, J = 8.0 Hz, 1H), 7.34 (d, J = 2.1 Hz, 2H), 7.89 (d, J = 9.6 Hz, 1H), 8.09 (d, J = 8.6 Hz, 1H), 10,10 (s, 1H), 10.35 (s, 1H); HRMS (ESl+) calcd for Ci6H,0ClNO3 300.0422 ([M-t-H]*), found 300.0411. EXAMPLE 7 7-BROMO-3,9-DlHYDROXY-6H-CHROMENO[4,3-b]QUINOLINE(7) Method G: To a solution of 7-bromo-3I9-dimethoxy-6H-chromeno[4,3-b]quinoline (5) (881 mg, 2.37 mmol) in 1,2-dichloroethane (20 mL) was added slowly AJCI3 (3.16 g, 23.7 mmol) and EtSH (2.7 mL, 36 mmol) and the reaction mixture was stirred at room temperature for 3 hours. After cooling in an ice bath, aqueous NaHCOg was added very slowly with vigorous stirring to quench the reaction, and the resulting reaction mixture was extracted with EtOAc. The precipitate formed was filtered through Celite*. The organic layer was washed with brine, then dried (NajSO^), filtered and concentrated to give a crude yellow solid, which was purified by silica gel chromatography to give a pure product as an orange solid. Yield: 478 mg (59%); mp 240 °C (dec.); 'H-NMR (300 MHz, DMSO-d6) 6 5.44 (s, 2H). 6.41 (d, J = 2.3 Hz, 1H), 6.59 (dd, J = 8.6, 2.3 Hz, 1H), 7.33 (dd, J = 8.7, 2.6 Hz, 1H), 7.35 (s, 1H), 7.88 (d, J = 8.7 Hz, 1H), 8.09 (d, J = 8.6 Hz, 1H), 10.09 (s, 1H), 10.35 (s, 1H); MS (ESI) m/z 342/344 ([M-HJO, 344/346 ([M+Hf); HRMS (ESI+) calcd for C1sH,0BrNG3 343.9917 ([M+H]+), found 343.9911. EXAMPLE 8 3,9-DIHYDROXY-7-VINYL-6H-CHROMENO[4,3-b]QUINOLINE(8) Method H: A mixture of 7-bromo-3,9-dihydroxy-6H-chromeno[4,3-b]quinoline (7) (34.5 mg, 0.100 mmol), tributyi(vinyl)tin (38 mg, 0.120 mmol, 1.2 equiv.), and Pd(PPh3)4 (11.6 mg, 0.0100 mmol, 10 mo!%) in toluene (1.5 mL) was refluxed under nitrogen until all starting material was consumed (1-2 hour(s)). Filtration through Celite® and purification by passing through a short pad of silica gel gave a pure product as an orange powder. Yield: 24 mg (83%); mp 160 °C (dec.); 1H-NMR (400 MHz, DMSO-d6) 6 5.36 (s, 2H), 5.47 (dd, J = 17.9, 1.4 Hz, 1H), 5.91 (dd, J = 11.6, 1.4 Hz, 1H), 6.38 (d, J = 2.3 Hz, 1H), 6.58 (dd, J = 8.5, 2.3 Hz, 1H), 7.10 (dd, J = 17.7,11.6 Hz, 1H), 7.22 (d, J = 2.5 Hz, 1H), 7.26 (dd, J= 9.1, 2.6 Hz, 1H), 7.84 (d, J = 8.9 Hz, 1H), 8.10 (d, J= 8.5 Hz, 1H), 9.94 (s, 1H), 9.95 (s, 1H); MS (ESI) m/z 290 ([M-H]-), 292 ([M+HD; HRMS (ESI+) calcd for C18H13N03 292.0968 ([M+H]*), found 292.0962. EXAMPLE 9 3,9-DIHYDROXY-7-[(TRIMETHYLS!LYL)ETHYNYL]-6H-CHROMENO[4,3- b]QUINOL!NE (9) Method I: A mixture of 7-bromo-3,9-dihydroxy-6H-chromeno[4,3-b]quinoline (7) (51.6 mg, 0.150 mmol), (trimethylsilylethynyl)tributyltin (70 mg, 0.180 mmol, 1.2 equiv.), and Pd(PPh3)4 (17 mg, 0.015 mmol, 10 mol%) in toluene (2 mL) was refluxed under nitrogen until all starting material was consumed (1-2 hour(s)). Filtration through Celite* and purification by passing through a short pad of silica gel gave a pure product as a red solid. Yield: 54 mg (99.6%); mp 160 °C (dec.); 1H-NMR (300 MHz, acetone-d6) 5 0.43 (s, 9H), 5.53 (s, 2H), 6.52 (d, J = 2.3 Hz, 1H), 6.71 (dd, J = 8.6, 2.3 Hz, 1H), 7.42 (dd, J = 9.1, 2.7 Hz, 1H), 7.61 (d, J = 2.7 Hz, 1H), 7.97 (d, J = 9.0 Hz, 1H), 8.26 (d, J - 8.6 Hz, 1H), 8.94 (s, 1H), 9.16 (s, 1H); MS (ESI) m/z 360 ([MHr), 362 ([M+H]+); HRMS (ES!+) calcd for C2,H19NO3Si 362.1207 ([M+H]), found 362.1207. EXAMPLE 10 3,9-DIHYDROXY-7-ETHYNYL-6H-CHROMENO[4,3-b]QUINOLINE{10) Method J: To a solution of 3,9-dihydroxy-7-[(trimethy!si!yl)ethynylJ-6H-chromeno[4,3- b]quinoline (9) (54 mg, 0.15 mmol) in MeOH (2 ml_) was added K2CO3 (104 mg, 0.75 mmol, 5 equiv.) and the reaction mixture was stirred for 30 mins. at room temperature. The reaction mixture was quenched with aqueous NH4CI (5 mL). Mathanol {MeOH} was removed under reduced pressure and the reaction mixture was extracted with EtOAc. The organic layer was washed with water and brine, then dried (Na2SO4), filtered and concentrated to give a crude yellow solid, which was purified by passing through a short pad of silica gel to give a pure product as a burgundy powder. Yield: 27 mg (63%); mp 220 °C (dec.); 1H-NMR (300 MHz, DMSO-d6) 5 5.27 (s, 1H), 5.46 (s, 2H), 6.41 (d, J = 2.1 Hz, 1H), 6.59 (dd, J = 8.5, 2.1 Hz, 1H), 7.31 (dd, J = 9.1, 2.6 Hz, 1H), 7.41 (d, J= 2.5 Hz, 1H), 7.87 (d, J= 9.0 Hz, 1H), 8.09 (d, J= 8.5 Hz, 1H), 10.04 (s, 1H), 10.23 (s, 1H); MS (ESI) m/z 288 ([M-Hf ), 290 ([M+H]); HRMS (ESI calcd for C18HuNO3 290.0812 ([M+H]*), found 290.0808. EXAMPLE 11 3,9-DIHYDROXY-7-ETHYL-6H-CHROMENO[4,3-b]QUlNOLINE (11) METHOD K: A mixture of 3,9-dihydroxy-7-ethynyl-6H-chromeno[4,3-b]quinoline (10) (13 mg, 0,045 mmol) and Pd/C (10 wt. %) in EtOAc/THF (1.5 mL) was stirred under hydrogen atmosphere (1 atm, balloon) for 30 mlns. The reaction mixture was filtered through Celite and concentrated to give a yellow solid, which was recrystallized (EtOAc/hexane/-20 °C). Yield: 13 mg (98%). mp 145 °C (dec.); 1H-NMR (300 MHz, DMSO-d6) 5 1.18 (t, J = 7.4 Hz, 3H), 2.95 (q, J = 7.6 Hz, 2H), 5.41 (s, 2H), 6.38 (d, J = 2.2 Hz, 1H), 6.56 (dd, J = 8.5, 2.3 Hz, 1H), 7.24 (dd, J = 8.3, 2.4 Hz, 1H), 7.26 (s, 1H), 7.82 {d, J = 9.0 Hz, 1H), 8.09 (d, J = 8.5 Hz, 1H), 9.90 (s, 1H), 9.93 (s, 1H); MS (ESI) m/z 292 ([M-HD, 294 ([M+H]+); HRMS (ESI+) calcd for CiaH15NO3 294.1125 \[M+H]*), found 294.1123. EXAMPLE 12 7-CYANO-3,9-DlHYDROXY-6H-CHROMENO[4,3-b]QU!NOUNE{12} Method L: A mixture of 7-bromo-3,9-dihydroxy-6H-chromeno[4,3-b]quinoline (7) (47 mg, 0.14 rrtmol), CuCN (370 mg, 4.13 mmol) in anhydrous DMF (2 mL) was heated at 200 "C in a sealed tube until all starting material was consumed (5 hours). After cooling to room temperature, the reaction mixture was filtered through Celite* and rinsed with EtOAc. Water was added to the filtrate and the reaction mixture was extracted with EtOAc. The organic layer was washed with water (2x) and brine, then dried (Na2SO4), filtered and concentrated to give a crude solid, which was purified by silica gel chromatography to give a pure product as a brown powder. Yield: 9 mg (23%); 1H-NMR (300 MHz, DMSO-d6) 5 5.52 (s, 2H), 6.44 (d, J = 2.1 Hz, 1H), 6.63 (dd, J = 8.6, 2.1 Hz, 1H), 7.27 (d, J = 2.4 Hz, 1H), 7.41 (dd, J = 9.1, 2.5 Hz, 1H), 7.98 (d, J = 9.1 Hz, 1H), 8.09 (d, J = 8.6 Hz, 1H), 10.19 (s, 1H), 10.63 (s, 1H); MS (ESI) m/z 289 ([M-H]-), 291 ([M+H]+); HRMS (ES!+) calcd for C17H,oN2O3 291.0764 ([M+H]*), found 291.0758. EXAMPLE 13 7-(4-CHLOROPHENYL)-3,9-DIHYDROXY-6H-CHROMENO[4,3-b]QUINOLiNE(13) Method M. A mixture of 7-bromo-3,9-dihydroxy-6H-chromeno[4,3-b]quinoline (7) (40 mg, 0.12 mmol) and Pd(PPh3)4 (7 mg, 0.006 mmol, 5 mol%) in DME (3 ml) was stirred for 10 mins. at room temperature. To this mixture were added sequentially 4- chlorophenylboronic acid (22 mg, 0.14 mmol, 1.2 equiv.) and aqueous Na2CO3 (2 M soln, 5 equiv.), and the reaction mixture was refluxed until all starting material was consumed (2-3 hours). After cooling, aqueous NH