WO 2005/092854 PCT/US2005/005240 -2- BICYCLIC SUBSTITUTED INDOLE-DERIVATIVE STEROID HORMONE NUCLEAR RECEPTOR MODULATORS BACKGROUND OF THE INVENTION Nuclear hormone receptors are an evolutionarily conserved class.of intracellular receptor proteins which have been termed "ligand dependent transcription factors". Evans et al., SCIENCE, 240: 889 (1988). The nuclear hormone receptor gene superfamily encodes structurally-related receptor proteins for glucocorticoids (e.g. cortisol, . corticosterone, cortisone), androgens, mineralocorticoids (e.g. aldosterone), progestins, estrogen, and thyroid hormone. Also included within diis superfamily of nuclear receptors are receptor proteins for vitamin D, retinoic acid, 9-cis retinoic acid, as well as those receptors for which no cognate ligands have been identified ("orphan receptors") Ribeiro et al.,Annual Rev. Med., 46:443-453 (1995). Steroid hormone receptors represent a subset of the nuclear hormone, receptor superfamily. So named according to the cognate ligand which complexes with the receptor in its native state, the steroid hormone nuclear receptors include the glucocorticoid receptor (GR), the androgen receptor (AR), the mineralocorticoid receptor (MR), the estrogen receptor (ER), and the progesterone receptor (PR). Tenbaum et al, Lit. J. Biochem. Cell. Bio., 29(12):1325-1341(1997). In contrast to membrane bound receptors, nuclear hormone receptors encounter . their respective ligands following entry of the ligand into the cell. Once ligand binding occurs, the ligand-receptor complex modulates transcription of target genes within the cell nucleus. For example, most ligand-free nuclear receptors are bound in a complex with heat shock proteins (HSPs) in the cytoplasm. Following entry of circulating hormone into the cell, binding elicits a conformational change in the receptor, dissociating the receptor from the hsp. The ligand bound receptors translocate to the nucleus, where they as monomers as well as hetero-and homodimers in binding to particular hormone response elements (HREs) in the promoter regions of target genes. The HRE-receptor complex then, in turn, regulates transcription of proximally-located genes, (see Ribeiro et al., supra.). On the other hand, thyroid hormone receptors (TRs) and other non-steroid receptors such as vitamin D receptor (VDR) and retinoic acid receptors (RAR) are bound WO 2005/092854 PCT/US2OO5/005240 3 to their respective HRE in the absenceof HSPs and/or cognate ligand. Hormones released from the circulation enter the cell, binding in the nucleus to these receptors which, in turn, hetero-dimerize to other nuclear receptors such as 9-cis retinoic acid (RXR). As with the steroid hormone nuclear receptors, following ligand binding, the ligand-bound receptor complex again regulates transcription of neighboring genes. Mineralocorticoids and glucocorticoids exert profound influences on a multitude of physiological functions,by virtue of their diverse roles in growth, development, and maintenance of homeostasis. The actions are mediated by the MR and GR which share approximately 94% homolpgy in their respective DNA binding regions, and approximately 57% homology in their respective ligand-binding domains. Kino et al, J. of Endocrinology, 169,437-445 (2001). In visceral tissues, such as the kidney and the gut, MR regulates sodium retention, potassium excretion, and water balance in response to aldosterone. Li addition, MR expression in the brain appears to play a role in the control of neuronal excitability, in the negative feedback regulation.of the hypothalamic-pituitary-adrenal axis, and hi the cognitive aspects of behavioral performance. Castren et al., J. of Neuroendocrinology, 3,461-466 (1993). GR, which is ubiquitously expressed in almost all tissues and organ systems, is crucial for the integrity of central nervous system function and the maintenance of cardiovascular, metabolic, and immune homeostasis. Kino et al, J. of Endocrinology, 169,437-445 (2001). Elevations in aldosterone levels, or excess stimulation of mineralocorticoid receptors, are linked to several physiological disorders or pathologic disease states including, Conn's Syndrome, primary and secondary hyperaldosteronism, increased sodium retention, increased magnesium and potassium excretion (diuresis), increased water retention, hypertension (isolated systolic and combined systolic/diastolic), arrhythmias, myocardial fibrosis, myocardial infarction, Bartter's Syndrome, and disorders associated with excess catecholamine levels. Hadley, M.E., ENDOCRINOLOGY, 2nd Ed.;1 pp. 366-381, (1988); and Brilla et al, Journal of Molecular and Cellular Cardiology, 25 (5), pp. 563-575 (1993). Additionally, elevated aldosterone levels have been increasingly implicated with congestive heart failure (CHF). In CHF, the failing heart triggers hormonal mechanisms in other organs in response to the attending reductions in blood flow and blood pressure seen with CHF. In particular, the kidney activates the renin-angiotensin-aldosterone system (RAAS) causing an increase in WO 2005/092854 PCT/US2005/005240 1 aldosterone production by,the adrenals which, in turn, promotes water and sodium retention, potassium loss, and further edema. Although historically it was believed that aldosterone participated in the etiology of CHF only as a result of its salt retaining effects, several recent studies have implicated elevated aldosterone levels with events in extra-adrenal tissues and organs! such as myocardial and vascular fibrosis, direct vascular damage, and baroreceptor dysfunction. Pitt etal, New Eng. J. Med., 341:709-717 (1999). These findings are particularly significant since angiotensin converting enzyme (ACE) inhibitors, which were once thought to completely abolish aldosterone production, are • now believed to only transiently suppress aldosterone production which has been shown to occur in extra-adrenal tissues including the heart and vasculature. Weber, New Eng. J. Med., 341:753-755 (1999); Fardella and Miller, Annu. Rev. Nutr., 16:443-470 (1996). The involvement of aldosterone acting via MR in CHF was confirmed in the recently completed RALES (Randomized Aldactone Evaluation Study) study. Pitt ei al., New Eng. J. Med., 341:709-717 (1999). The RALES study demonstrated that the use of Aldactone(tm) (spironolactone), a well-known competitive MR antagonist, in combination with standard CHF therapy, reduced cardiac related mortality by 30% and frequency of hospitalization by 35% in patients suffering from advanced CHF. However, spironolactone therapy has also been associated with attending side effects such as gastric bleeding, diarrhea, azotemia, hyperchloremic metabolic acidosis an type-4 renal tubule acidosis, nausea, gynecomastia, erectile dysfunction, hyperkalemia, and irregular menses. Thus, the mineralocorticoid receptor represents a viable target for CHF therapy either alone or in combination with conventional CHF therapies such as vasodilators (ACE inhibitors), inotropics (digoxin), diuretics, or beta blockers. Molecules, preferably non-steroids, which bind to the mineralocorticoid receptor and modulate receptor activity without the attending side effects of current therapies would be particularly desirable. Recently, selective aldosterone blockers have also been implicated in the treatment of atherosclerosis. S. Keider, et al., Cardiovascular Pharmacology 41 (6), 955-963 (2003). Finally, published international PCT application WO 02/17895 discloses that aldosterone antagonists are useful in the treatment of subjects suffereing from one or more cognitive dysfunctions including, but not limited to psychoses, cognitive disorders (such as memory disturbances), mood disorders (such as depression and bipolar disorder), anxiety disorders, and personality disorders. WO 2005/092854 PCT/US2005W05240 Glucocorticoids (e.g. cortisol, corticosterone, and cortisone), and the glucocorticoid receptor, have also been implicated in the etiology of a variety of physiological disorders or pathologic disease states. For example, cortisol hyposecretion is implicated in the pathogenesis of Addison's Disease and may result in muscle weakness, increased melanin pigmentation of the skin, weight loss, hypotension, and hypogiycemia. On the other hand, excessive or prolonged secretion of glucocorticoids has been correlated to Cushing's Syndrome and may also result in obesity, hypertension, i glucose intolerance, hyperglycemia, diabetes mellitus, osteoporosis, polyuria, and polydipsia. Hadley, M.E., ENDOCRINOLOGY, 2nd Ed., pp. 366-381, (1988). Further, United States Patent No. 6,(166,013, issued December 26,2000, discloses that GR selective agents could modulate GR activity and, thus, be useful in the treatment of inflammation, tissue rejection, auto-immunity, malignancies such as leukemias and lymphomas, Cushing's syndrome, acute adrenal insufficiency, congenital adrenal hyperplasia, rheumatic fever, polyarteritis nodosa, granulomatous polyarteritis, inhibition of myeloid cell lines, immune proliferation/apoptosis, HP A axis suppression and regulation, hypercortisolemia, modulation of the (Th 1/Th2 cytokine balance, chronic kidney disease, stroke and Ispinal cord injury, hypercalcemia, hyperglycemia, acute' adrenal insufficiency, chronic primary adrenal insufficiency, secondary adrenal insufficiency, congenital adrenal hyperplasia, cerebral edema, thrombocytopenia, and Little's syndrome. United States Patent No. 6,166,013 also discloses that GR modulators are especially useful in disease states involving systemic inflammation such as ! inflammatory bowel disease, systemic lupus erythematosus, polyartitis nodosa, Wegener's granulomatosis, giant cell'arthritis, rheumatoid arthritis, osteoarthritis, hay fever, allergic rhinitis, urticaria, angioneurotic edema, chronic obstructive pulmonary disease, asthma, tendonitis, bursitis, Crohn's disease, ulcerative colitis, autoimmune chronic active hepatitis, organ transplantation, hepatitis, and cirrhosis; and that GR modulating compounds have been used as immunostimulants, repressors, and as wound healing and tissue repair agents. In addition, United States Patent No. 6,166,013 also discloses that GR modulators have also found use in a variety of topical diseases such as inflammatory scalp alopecia, panniculitis, psoriasis, discoid lupus erythematosus, inflamed cysts, atopic dermatitis, pyoderma gangrenosum, pemphigus vulgaris, bullous pemphigoid, systemic lupus WO 2005/092854 PCT/US2005/005240 A erythematosus, dermatomyositis, eosinophilic fasciitis, relapsing polychondritis, inflammatory vasculitis, sarcoidosis, Sweet's disease, type 1 reactive leprosy, capillary hemangiomas, contact dermatitis, atopic dermatitis, lichen planus, exfoliative dermatitis, erythema nodosum, acne, hirsutism, toxic epidermal necrolysis, erythema multiform, and cutaneous T-cell lymphoma. Thus, it is clear that a ligand which has affinity for steroid hormone nuclear receptors, and particularly for MR and/or GR, could be used to modulate (i.e. repress, antagonize, agonize, partially antagonize, partially agonize) receptor activity and target gene expression, thereby influencing a multitude of physiological functions related to alterations in steroid hormone levels and/or steroid hormone receptor activity. In this regard, such ligands could be useful to treat a wide range of physiological disorders susceptible to steroid hormone nuclear receptor modulation. - Published literature references disclose indole derivative molecules useful in a broad range of indications from electroluminescent agents to marine anti-fouling agents.' Further, indole-derivative compounds have also been disclosed as having pharmacological utility as, inter alia, serotonin 5HT-6 receptor (modulators, anticoagulant agents, antiangiogenics, antiparasitics, integrin inhibitors, phospholipase inhibitors, i' endothelian receptor antagonists, antiarrhythmics, and dopamine antagonists. Surprisingly, however, and in accordance with the present invention, applicants have | discovered a series of non-steroidal indole derivative compounds, particularly bicyclic substituted indole derivatives, with affinity for steroid hormone nuclear receptors, and particularly for MR and GR. Such compounds could modulate nuclear receptor activity and, therefore, have utility in treating physiological disorders related to alterations in steroid hormone level and/or to alterations in steroid hormone nuclear receptor activity. Furthermore, such compounds could address a long felt and continuing need for safe and effective pharmaceutical interventions without the attending side effects of steroidal-type agents. The treatment of steroid hormone related disorders is hereby furthered. The following references describe examples of the state of the art as it relates to the present invention. Published International PCT Application WO 96/19458 and U.S. Patent Nos. 5,696,130; 5,994,544; 6,017,924, and 6,121,450 disclose quinoline derivative analogs as steroid hormone receptor modulators. WO 2005/092854 PCMJS2005/005240 Published International PCT Application WO 00/06137 and U.S. Patent No. 6,166,013 disclose triphenylmethane compounds as glucocorticoid receptor modulators. U.S. Patent No. 6,147,066 discloses anti-mineralocorticoid receptor compounds for use in treating drug withdrawal syndrome. U.S. Patents Nos. 6,008,210 and 6,093,708 disclose spirolactone compounds, such as spironolactone and epoxymexrenone, with affinity for the mineralocorticoid receptor for use in the treatment of myocardial fibrosis. Published International PCT Application WO 02/17895 discloses that aldosterone antagonists are useful in the treatment of subjects suffereing from one or more cognitive dysfunctions. ' • Published International PCT Application WO 02/09683 discloses aldosterone blockers useful to treat inflammation disoders. ii Published International PCT Application WO 02/051832 discloses i heterocyclalkylindoles as 5HT-6 ligands. ii Published International PCT Application WO 02/0163.48 discloses indole derivatives molecules as antiangiogenic agents. II Published International PCT Application WO 02/012227 discloses nine- and ten - II membered bicyc'lic heteroaryl molecules as angiogenesis inhibitors. Published International PCT Application WO 01/058893 discloses indpl-3-yl II propionates as integrin inhibitors. Published International PCT Application WO 99/43672 discloses indole derivatives as phospholipase enzyme inhibitors. Published International PCT Application WO 98/42696 and related family members disclose inhibitors of nitric oxide synthase. Published International PCT Application WO 97/43260 and related family members disclose indole derivatives useful as endothelin receptor antagonists. Published International PCT Application WO 96/03377 and related family members disclose heterocyclic compounds useful as allosteric effectors of muscarinic receptors. European Patent EP683166 dislcoses l-(3-indolylalkyl)-4-(3-indolyl) piperidines as dopamine agonists or antagonists. WO 2005/092854 PCT/US2005/005240 Japanese Patents JP 05339565 and JP 3229654 disclose indole derivatives for electroluminescent devices. United States Patent No. 5,342,547 dislcoses indole derivatives for controlling underwater fouling. Whitehead and Whitesitt. Journal of Medicinal Chemistry (1974), 17(12), 1298-304 discloses the effects of lipohilic substituents on biological properties of indoles. Co-pending International Patent Application PCT/US04/00017 discloses indole derivative agents as mineralocorticoid and glucocorticoid receptor modulators. - . SUMMARY OF THE INVENTION The present invention is directed to the discovery that certain indole-deriva'tive compounds, as defined below, are modulators of steroid hormone nuclear receptors and, i therefore, may have utility as pharmaceutical agents. Accordingly, the present invention provides a compound of the formula: ° wherein, X represents -CH2-, -CH2CH2-, -CH2CH2CH2-, -CH2O-, -CH2S-, or -CH2NRl0-; R* represents hydrogen, (Cj-C^alkyl, (C3-C7)cycloalkyl, hydroxy(Ci-C4)alkyl, halo(Ci-C4)alkyl, (Ci-C4)alkyl-heterocycle, (Ci-C4)alkyl-NH(Ci-C4)alkylamine, or (Ci-C4)alkyl-N,N-(C1-C4)dialkylamine; ii R^ represents hydrogen, halo, (Cj-C4)alkyl, heterocycle, or substituted heterocycle; R3 represents hydrogen, halo, (Ci-C4)alkyl, heterocycle, or substituted heterocycle; ' R4 represents hydrogen, halo, amino, nitro, (Ci-C4)alkyl, (Ci-C4)alkoxy, NH SO2R7, NHCORS," or COR9; WO 2"05/092854 PCT/US2005/005240 R5 represents hydrogen or halo; R6 represents hydrogen or (Cj-C^alkyl; R7 represents (Ci-C4)alkyl, aryl, NH(Ci-C4)alkylamine, or N,N-(Ci-C4)dialkylaniine; R8 represents (Ci-C4)alkyl, (Ci-C4>alkoxy, or aryl(Ci-C4)alkoxy; and R9 represents (Ci-C4)alkyl or (Ci-C4)alkoxy; R10 represents hydrogen, (Ci-C4)alkyl, (C3-C7)cycloalkyl, (Ci-C4)alkyl-(C3-C7)cycloalkyl; or a pharmaceutically acceptable salt thereof. As another aspect, the present invention provides a method of treating a physiological disorder susceptible to steroid hormone nuclear receptor modulation comprising administering to a patient in need thereof an effective amount of a compound of Formula I as described herein and above. Examples of such disorders include Conn's Syndrome, primary and secondary hyperaldosteronism, increased sodium retention, increased magnesium and potassium excretion (diuresis), increased water retention, hypertension (isolated systolic and combined systolic/diastolic), arrhythmias, myocardial fibrosis, myocardial infarction, atherosclerosis, Banter's Syndrome, disorders associated with excess catecholamine levels, diastolic and systolic congestive heart failure (CHF), peripheral vascular disease, diabetic nephropathy, cirrhosis with edema and ascites, esophageal varicies, Addison's Disease, muscle weakness, increased melanin pigmentation of the skin, weight loss, hypotension, hypoglycemia, Cushing's Syndrome, obesity, hypertension, glucose intolerance, hyperglycemia, diabetes mellitus, osteoporosis, 'I polyuria, polydipsia, inflammation, autoimmune disorders, tissue rejection associated with organ transplant, malignancies such as leukemias and lymphomas, acute adrenal insufficiency, congenital adrenal .hyperplasia, rheumatic fever, polyarteritis nodosa, granulomatous polyarteritis, inhibition of myeloid cell lines, immune proliferation/apoptosis, HPA axis suppression and regulation, hypercortisolemia, modulation of the Thl/Th2 cytokine balance, chronic kidney disease, stroke and spinal cord injury, hypercalcemia, hyperglycemia, acute adrenal insufficiency, chronic primary adrenal insufficiency, secondary adrenal insufficiency, congenital adrenal hyperplasia, cerebral edema, thrombocytopenia, and Little's syndrome, systemic inflammation, inflammatory bowel disease, systemic lupus erythematosus, discoid lupus erythematosus, WO 2005/092854 PCT/US2005/005240 polyartitis nodosa, Wegener's granulomatosis, giant cell arthritis, rheumatoid arthritis, osteoarthritis, hay fever, allergic rhinitis, contact dermatitis, atopic dermatitis; exfoliative dermatitis, urticaria, angioneurotic edema, chronic obstructive pulmonary disease, asthma, tendonitis, bursitis, Crohn's disease, ulcerative colitis, autoimmune chronic active hepatitis, hepatitis, cirrhosis, inflammatory scalp alopecia, panniculitis, psoriasis, inflamed cysts, pyoderma gangrenosum, pemphigus vulgaris, bullous pemphigoid, dermatomyositis, eosinophilic fasciitis, relapsing polychondritis, inflammatory vasculitis, sarcoidosis, Sweet's disease, type 1 reactive leprosy, capillary hemangiomas, lichen planus, erythema nodosum, acne, hirsutism, toxic epidermal necrolysis, erythema multiform, cutaneous T-cell lymphoma, psychoses, cognitive disorders'(such as memory disturbances), mood disorders (such as depression and bipolar disorder), anxiety disorders, and personality disorders. As a further aspect, the present invention provides a method of treating a physiological disorder susceptible to mineralocorticoid or glucocorticoid receptor modulation comprising administering to a patient in need thereof an effective amount of a compound of Formula I as described herein and above. As a/more particular aspect, the present invention provides a method of treating a physiological disorder susceptible to mineralocorticoid or glucocorticoid receptor antagonism comprising administering to a patient in need thereof an effective amount of a compound of Formula I. As an even more particular aspect the present invention provides a method of treating hypertension (isolated systolic and combined systolic/diastolic), systolic and/or diastolic congestive heart failure, atherosclerosis, rheumatoid arthritis or inflammation comprising administering to a patient in need thereof an effective amount of a compound of Formula I as described herein and above - II As a separate aspect, the present invention also provides a method of modulating a steroid hormone nuclear recpetor comprising contacting said receptor with an effective amount of a compound of Formula I More particularly, the present invention provides a method of modulating the mineralocorticoid or glucocorticoid receptor comprising contacting said receptor with an effective amount of a compound of Formula I. More particularly still, the present invention provides a method of antagonizing the mineralocorticoid or glucocorticoid receptor comprising contacting said receptor with an effective amount of a compound of Formula I, as described herein and above. WO 2005/092854 PCT/US2005/005240 u In addition, the present invention provides pharmaceutical compositions of compounds of Formula ^including any pharmaceutically acceptable salts and hydrates thereof, comprising a compound of Formula I in combination with a pharmaceutically acceptable carrier, diluent or excipient. This invention also encompasses novel intermediates, and processes for the synthesis of the compounds of Formula L The present invention also provides the use of a compound of Formula I, or a il pharmaceutically acceptable salt thereof, for the treatment of a physiological disorder susceptible to steroid hormone nuclear receptor modulation. More particularly, the present ii invention provides the use of a compound of Formula I, or a pharmaceutically acceptable salt thereof, for treating' hypertension, congestive heart failure, atherosclerosis, rheumatoid arthritis or inflammation. Further still, the present invention also provides the use of a compound of Formula I, or a pharmaceutically acceptable' salt thereof, for the manufacture of a medicament for treating a physiological disorder susceptible to steroid hormone nuclear receptor modulation. More particularly, the present invention provides the use of a compound of Formula I, or a pharmaceutically acceptable salt thereof, for the manufacture of a medicament for treating hypertension, congestive heart failure, atherosclerosis, rheumatoid arthritis or inflammation. } * 'i DETAILED DESCRIPTION OF THE INVENTION II The present invention provides compounds of Formula I with affinity for steroid hormone nuclear receptors, particularly MR and/or GR, which could be used to modulate 11 (i.e. repress, antagonize, agonize, partially antagonize, partially agonize) nuclear receptor activity and target gerie expression, thereby influencing physiological functions related to steroid hormone levels and/or steroid hormone receptor activity: In this regard, compounds of Formula I are believed to be useful in treating or preventing a multitude of physiological disorders susceptible to steroid hormone nuclear receptor modulation. Thus, methods for the treatment or prevention of physiological disorders susceptible to " steroid hormone nuclear receptor modulation constitute another important embodiment of the present invention. As a particular aspect, the present invention provides compounds useful as mineralocoirticoid or glucocorticoid receptor modulators. As a more particular II aspect, the present invention provides compounds useful as mineralocorticoid or glucocorticoid receptor antagonists. WO 2005/092854 PCT/US2005/005240 As will be understood by the skilled artisan, some of the compounds useful for the methods of the present invention may be available for prodrug formulation. As used I herein, the term "prodrug" refers to a compound of Formula I which has been structurally modified such that in vivo the prodrug is converted, for example, by hydrolytic, oxidative, reductive, or enzymatic cleavage, into the parent molecule ("drug") as given by Formula I. Such prodrugs may be, for example, metabolically labile ester derivatives of the parent compound where said parent molecule bears a carboxylic acid group. Conventional procedures for the selection and preparation of suitable prodrugs are well known to one of ordinary skill in the art. • It is also understood that many of the steroid hormone nuclear receptor modulators of the present invention may exist as pharmaceutically acceptable salts and, as such, pharmaceutically acceptable salts are therefore included within the scope of the present invention. The term "pharmaceutically acceptable salt" as used herein, refers to salts of the compounds of Formula I, which are substantially non-toxic to living organisms. - -Typical pharmaceutically 'acceptable salts include those salts prepared by reaction of the compounds of the present invention with a pharmaceutically acceptable mineral or organic acid or an organic or inorganic base. Such salts are known as acid addition and base addition salts. It is further understood by the skilled reader that salt forms of pharmaceutical compounds are commonly used because they are often more readily crystallized, or more readily purified, than are the free bases. In all cases, the use of the •" • pharmaceutical compounds of the present invention as salts is contemplated in the description herein. Hence, it is understood that where compounds of Formula I are capable of forming salts, the pharmaceutically acceptable salts and isoforms thereof are encompassed in the names provided herein. Acids commonly employed to form acid addition salts are inorganic acids such as . hydrochloric acid, hydrobromic acid, hydroiodic acid, sulfuric acid, phosphoric acid, and the like, and organic acids such as p-toluenesulfonic, methanesulfonic acid, oxalic acid, p-bromophenylsulfonic acid, carbonic acid, succinic acid, citric acid, benzoic acid, acetic acid, and the like. Examples of such pharmaceutically acceptable salts are the sulfate, pyrosulfate, bisulfate, sulfite, bisulfite, phosphate, monohydrogenphosphate, dihydrogenphosphate, metaphosphate, pyrophosphate, bromide, iodide, hydroiodide, dihydroiodide, acetate, propionate, decanoate, caprylate, acrylate, formate, hydrochloride, H WO 2005/092854 PCT/US200S/005240 dihydrochloride, isobutyrate, caproate, heptanoate, propiolate, oxalate, malonate, succinate, suberate, sebacate, fumarate, maleate, butyne-l,4-dioate, hexyne-l,6-dioate, benzoate, chlorobenzoate, methylbenzoate, hydroxybenzoate, methoxybenzoate, phthalate, xylenesulfonate, phenyl acetate, phenyl propionate,- phenyl butyrate, citrate, lactate, oc-hydroxybutyrate, glycolate, tartrate, methahesulfonate, propanesulfonate, naphthalene-1-sulfonate, napththalene-2-sulfonate, mandelate and the like. Base addition salts include those derived from inorganic bases, such as ammonium or alkali or alkaline earth metal hydroxides, carbonates, bicarbonates, and the like. Such bases useful in preparing the salts of this invention thus include sodium hydroxide, potassium hydroxide, ammonium hydroxide, potassium carbonate, sodium carbonate, sodium bicarbonate, potassium bicarbonate, calcium hydroxide, calcium carbonate, and the like. As used herein, the term "stereoisomer" refers to a compound made up of the same atoms bonded by the same bonds but having different three-dimensional structures which are not interchangeable. The three-dimensional structures are called configurations. As used herein, the term "enantiomer" refers to two stereoisomers whose molecules are nonsuperimposable mirror images of one another. The term "chiral center" refers to a carbon atom to which four different groups are attached. As used herein, the term "diastereomers" refers to stereoisomers which are not enantiomers. In addition, two diastereomers which have a different configuration at only one chiral center are referred to herein as "epimers". The terms "racemate", "racemic mixture" or "racemic modification" refer to a mixture of equal parts of enantiomers. The term "enantiomeric enrichment" as used herein refers to the increase in the amount of one enantiomer as compared to the other. A convenient method of expressing the enantiomeric enrichment achieved is the concept of enantiomeric excess, or "ee", which is found using the following equation: wherein E1 is the amount of the first enantiomer and E2 is the amount of the second enantiomer. Thus; if the initial ratio of the two enantiomers is 50:50, such as is present in a racemic mixture, and an enantiomeric enrichment sufficient to produce a final ratio of 50:30 is achieved, the ee with respect to the first enantiomer is 25%. However, if the .final WO 2005/092854 PCT/US2005/005240 i ratio is 90:10, the ee with respect to the first enantiomer is 80%. An ee of greater than 90% is preferred, an ee of greater than 95% is most preferred and an ee of greater than 99% is most especially preferred. Enantiomeric enrichment is readily determined by one of ordinary skill in the art using standard techniques and procedures, such as gas or high performance liquid chromatography with a chiral column. Choice of the appropriate chiral column, eluent and conditions necessary to effect separation of the enantiomeric pair is well within the knowledge of one of ordinary skill in the art. In addition, the enantiomers of compounds of Formula I can be resolved by one of ordinary skill in the art using standard techniques well known in the art, such as those described by J. Jacques, et al., "Enantiomers, Racemates, and Resolutions", John Wiley and Sons, Inc., 1981. The compounds of the present invention may have one or more chiral centers and may, therefore, exist in a variety of stereoisomeric configurations. As a consequence of these chiral centers the compounds of the present invention may occur as racemates, mixtures of enantiomers, and as individual enantiomers as well as diastereomers and mixtures of diastereomers. All such racemates, enantiomers, and diastereomers are within the scope of the present invention. Enantiomers of the compounds provided by the present invention can be resolved, for example, by one of ordinary skill in the art using standard techniques such as those described by J. Jacques, et al., "Enantiomers, Racemates, and Resolutions", John Wiley and Sons, Inc., 1981. The terms "R" and "S" are used herein as commonly used in organic chemistry to denote specific configuration of a chiral center. The term "R" (rectus) refers to that configuration of a chiral center with a clockwise relationship of group priorities (highest to second lowest) when viewed along the bond from the chiral carbon toward the lowest priority group. The term "S" (sinister) refers to that configuration of a chiral center with a counterclockwise relationship of group priorities (highest to second lowest) when viewed along the bond from the chiral carbon toward the lowest priority group. The priority of groups is based upon their atomic number (in order of decreasing atomic number). A partial list of priorities and a discussion of stereochemistry is contained in "Nomenclature of Organic Compounds: Principles and Practice", (J.H. Fletcher, et al., eds., 1974) at pages 103-120. The specific stereoisomers and enantiomers of compounds of Formula I can be prepared by one of ordinary skill in the art utilizing well known techniques and processes, WO 2005/092854 PCT/US2005/005240 1ST such as those disclosed by Eliel and Wilen, "Stereochemistry of Organic Compounds", John Wiley & Sons, Inc., 1994, Chapter 7; Separation of Stereoisomers, Resolution, Racemization; and by Collet and Wilen, "Enantiomers, Racemates, and Resolutions", ¦ John Wiley & Sons, Inc., 1981. For example, specific stereoisomers and enantiomers can be prepared by stereospecific syntheses using enantiomerically and geometrically pure, or enantiomerically or geometrically enriched starting materials. In addition, the specific stereoisomers and enantiomers can be resolved and recovered by techniques such as chromatography on chiral stationary phases, enzymatic resolution or fractional recrystallization of addition salts formed by reagents used for that purpose. In addition, as will be appreciated by one of ordinary skill in the art compounds of the present invention containing a carbon-carbon double bond may exist as geometric -isomers. Two methods are commonly used to designate the specific isdmers, the "cis-trans" method and the "E and Z" method, which methods designate a particular isomer based on whether the groups attached to each of the ethylene carbons are the same or different. A discussion of geometric isomerism and the naming of specific isomers is found in March, "Advanced Organic Chemistry", John Wiley & Sons, 1992, Chapter 4. All such geometric isomers, as well as mixtures of individual isomers, are contemplated and provided by the present invention. As appreciated by one of ordinary skill in the ait, suitable oxygen or nitrogen protecting groups are used as needed. Suitable oxygen or nitrogen protecting groups, as used herein, refers to those groups intended to protect or block the oxygen or nitrogen group against undesirable reactions during synthetic procedures. The suitability of the oxygen or nitrogen protecting group used will depend upon the conditions that will be employed in subsequent reaction steps wherein protection is required, and is well within the knowledge of one of ordinary skill in the art. Commonly used protecting groups suitable for practicing the present invention are disclosed in "Protective Groups in Organic Synthesis, 3rd Edition" by Theodara Greene, Peter G. M. Wuts, John Wiley & Sons, New York (1999). As used herein the term "(Ci-GOalkyl" refers to a straight or branched, monovalent, saturated aliphatic chain of 1 to 4 carbon atoms and includes, but is not limited to methyl, ethyl, n-propyl, isopropyl, n-butyl, isobutyl and the like. WO 2005/092854 PCT/US2005/005240 i As used herein the term "(Ci-C6)alkyl" refers to a straight or branched, monovalent, saturated aliphatic chain of 1 to 6 carbon atoms and includes, but is not limited to methyl, ethyl, n-propyl, isopropyl, n-butyl, isobutyl, t-butyl, n-pentyl, n-hexyl, and the like. It is understood that the term "(Ci-C4)alkyl" is included within the definition of I1(Ci-C6)alkyl". As used herein the term "(Ci-C]0)alkyl" refers to a straight or branched, monovalent, saturated aliphatic chain of 1 to 10 carbon atoms and includes, but is not limited to methyl, ethyl, propyl, isopropyl, n-butyl, isobutyl, tertiary butyl, pentyl, isopentyl, hexyl, 2,3-dimethyl-2-butyl, heptyl, 2,2-dimethyl-3-pentyl, 2-methyl-2-hexyl; octyl, 4-methyl-3-heptyl and the like. It is understood that the terms "(Ci-C4)alkyl" and "(Ci-C6)alkyl" are included within the definition of "(C1-Cio)alkyl". As used herein, the terms "Me", "Et", "Pr", "I-Pr", "Bu" and "t-Bu" refer to methyl, ethyl, propyl, isopropyl, butyl and tert-butyl respectively. As used herein, the term "(Cj-C^alkoxy" refers to an oxygen atom bearing a straight or branched, monovalent, saturated aliphatic chain of 1 to 4 carbon atoms and includes, but is not limited to methoxy, ethoxy, n-propoxy, isopropoxy, n-butoxy, and the like. As used herein the term "(Ci-C6)alkoxy" refers to an oxygen atom bearing a straight or branched, monovalent, saturated aliphatic chain of 1 to 6 carbon atoms and includes, but is not limited to methoxy, ethoxy, n-propoxy, isopropoxy, n-butoxy; n-pentpxy, n- hexoxy, and the like. It is understood that the term "(Ci-C4)alkoxy" is included within the definition of "(Q-C^alkoxy". • * • • As used herein, the term "hydroxy(Ci-C4)alkyl" refers to a straight or branched, monovalent, saturated aliphatic chain of 1 to 4 carbon atoms bearing a hydroxyl group-attached to one of the carbon atoms. As used herein, the term "hydroxy(Ci-C6)alkyl" refers to a straight or branched, monovalent, saturated aliphatic chain of 1 to 6 carbon atoms bearing a hydroxyl group attached to one of the carbon atoms. It is understood that the term "hydroxy(Ci-C4)alkyl" is included within the definition of "hydroxy(Ci-C6)alkyF\ As used herein, the term "hydroxy(Ci-C4)alkoxy" refers to an oxygen atom bearing a straight or branched, monovalent, saturated aliphatic chain of 1 to 4 carbon atoms, further bearing a hydroxyl group attached to one of the carbon atoms. As used herein, the term "hydroxy(Ci-C6)alkoxy" refers to an.oxygen atom bearing a straight or branched, monovalent, saturated aliphatic chain of 1 to 6 carbon atoms, further bearing a WO 2005/092854 PCT/US2005/005240 Mr -&r- hydroxyl group attached to one of the carbon atoms. It is understood that the term "hydroxy(C]-C4)alkoxy" is included within the definition of "hydroxy(Ci-C6)alkoxy". As used herein, the terms "halo", "halide" or "hal" of "Hal" refer to a chlorine, bromine, iodine or fluorine atom, unless otherwise specified herein. As used herein, the term "halo(Ci-C4)alkyi" refers to a straight or branched, monovalent, saturated aliphatic chain of 1 to 4 carbon atoms bearing one or more halo groups attached to one or more of the carbon atoms. As used herein, the term "halo(Ci-C6)alkyl" refers to a straight or branched, monovalent, saturated aliphatic chain of 1 to 6 carbon atoms bearing one or more halo groups attached to one or more of the carbon atoms. It is understood that the term "haloCCi-GOalkyl" is included within the definition of "halo(Ci-C6)alkyl". As used herein, the term "halo(Q-C4)alkoxy" refers to an oxygen atom bearing a straight or branched, monovalent, saturated aliphatic chain of 1 to 4 carbon atoms, further bearing one or more halo groups attached to one or more of the carbon atoms. As used herein, the term "halo(Ci-C6)alkoxy" refers to an oxygen atom bearing a straight or branched, monovalent, saturated aliphatic chain of 1 to 6 carbon * > atoms, further bearing one or more halo groups attached to one or more of the carbon atoms. It is understood that the term "halo(Ct-Gi)alkoxy" is included within the definition of "halo(Ci-Q;)alkoxy". As used herein the term "(C2-C6)alkenyl" refers to a straight or branched, monovalent, unsaturated aliphatic chain having from two to six carbon atoms and having a double bond. Typical (C2-Ce)alkenyl groups include ethenyl (also known as vinyl), 1-methylethenyl, 1-methyl-1-propenyl, 1-butenyl, 1-hexenyl, 2-methyl-2-propenyl, 1-propenyl, 2-propenyl, 2-butenyl, 2-pentenyl, and the like. As used herein the term "(C2-C6)alkynyl"refers to a straight or branched, monovalent, unsaturated aliphatic chain having from two to six carbon atoms and having ¦ a triple bond. Typical (C2-C6)alkynyl groups include p'ropynyl, ethynyl, and the like As used herein, the term "acyl" refers to a hydrogen or a (Ci-Q>)alkyl group attached to a carbonyl group. Typical acyl groups include formyl, acetyl, propionyl, butyryl, valeryl, and caproyl. , As used herein, the term "aryl" refers to a monovalent carbocyclic group containing one or more fused or non-fused phenyl rings and includes, for example, phenyl, 1- or 2-naphthyl, 1,2-dihydronaphthyl, 1,2,3,4-tetrahydronaphthyl, and the like. WO 2005/092854 PCT/US2005/005240 I? The term "substituted aryl" refers to an aryl group optionally substituted with one to three moieties, preferably one or two, chosen from the group consisting of halo, amino, cyano, (C,-C4)alkyl, (Ci-C4)alkoxy, -S-(CrC4)alkyl. As used herein, the term "aryl(Ci-C6)alkoxy" (or "(Ci-C^alkoxy-aryl") refers to an oxygen atom bearing a straight or branched, monovalent, saturated aliphatic chain of 1 to 6 carbon atoms wherein said aliphatic chain, in turn, bears an aryl group. Examples of "aryl(Ci-C6)alkoxy" include benzyloxy, phenyl ethoxy, and the like. As used herein the term "(C3-Cio)cycloalkyl"-refers to a saturated hydrocarbon ring structure composed of one or more fused or unfused rings containing from three to ten carbon atoms. Typical (C3-Cjo)cycloalkyl groups include cyclopropyl, cyclobutyl, cyclopentyl, cyclohexyl, cycloheptyl, cyclooctyl, adamantanyl, and the like. "(C3-C7)cycloalkyl" refers to a saturated hydrocarbon ring structure composed of one or more fused or unfused rings containing from three to seven carbon atoms. It is understood that the definition of "(C3-C7)cycloalkyl" is included within the definition of "(C3-Cio)cycloalkyr. The term "substituted (C3-C7)cycloalkyl" refers to a "(C3-C7)cycloalkyl group optionally substituted with one or tw<> moieties chosen from the group consisting of halogen, hydroxy, pyano, nitro, amino, (Ci-C6)alkyl, (Ci-C6)alkoxy, (Ci-C4)alkyl-(C3-Cio)cycloalkyl, (Ci-C4)alkyl-aryl, (Ci-C6)alkoxycarbonyl, NJSf(Ci-C6)dialkylamine, NH(Ci-C6)alkylamine, (Ci-C4)alkyl-N,N-Ci-C6dialkylamine, difluoromethyl, difluoromethoxy, trifluoromethyl, and trifluoromethoxy. As used herein, the term "(Ci-C4)alkyl-(C3-C7)cycloalkyl" refers to a straight or . branched, monovalent, saturated aliphatic chain of 1 to 4 carbon atoms which has a (C3-C7)cycloalkyl attached to the aliphatic chain. Included within the term "(Cj-C4)alkyl-(C3-C7)cyclbalkyr are the following: WO 2005/092854 PCT/US2005/005240 and the like. As used herein, the term "(Ci-C4)alkyl-substituted (C3-C7)cycloalkyr' refers to a straight or branched, monovalent, saturated aliphatic chain of 1 to 4 carbon atoms bearing an optionally substituted (C3-C7)cycloalkyl group attached to the aliphatic chain. As used herein the term "heterocycle" refers to a saturated or unsaturated, five- or six-membered ring, which contains one to four heteroatoms selected from the group consisting of oxygen, sulfur, and nitrogen. It is understood that the remaining atoms are carbon and that the heterocycle may be attached at any point which provides for a stable structure. Examples of heterocycle groups include thiophenyl, furanyl, tetrahydrofuryl, pyrrolyl, imidazolyl, pynazolyl, thiazolyl, thiazolidinyl, isothiazolyl, oxazolyl, isoxazolyl, triazolyl, thiadiazolyl, oxadiazolyl, tetrazolyl, pyridyl, pyridinyl, pyrimidyl, pyrazinyl, pyridiazinyl, triazinyl, imidazolyl, dihydropyrimidyl, tetrahydropyrimdyl, pyrrolidinyl, piperidinyl, piperazinyl, pyrazolidinyl, pyrimidinyl, imidazolidimyl, morpholinyl, pyranyl, thiomorpholinyl, and the like. The term "substituted heterocycle" represents a heterocycle group optionally substituted with one or two moieties chosen from the group consisting of halo, ammo, cyano, (Ci-C4)alkyl, (Ci-C4)alkoxy, -S-(Ci-C4)alkyl. As used herein, the term "(Ci-C4)alkyl-heterocycle" refers to a straight or • branched, monovalent, saturated aliphatic chain of 1 to 4 carbon atoms which has a . heterocycle group attached to the aliphatic chain. Examples of "(Ci-C4)alkyl-heterocycle" include: WO 2005/092854 PCT7US2005/005240 and the like. The term "(Ci-Oalkyl-substituted heterocycle" refers to a straight or branched, monovalent, saturated aliphatic chain of 1 to 4 carbon atoms bearing an optionally substituted heterocycle group attached to the aliphatic chain. As used herein, the term "NHKCi-GO alkylamine" refers to a nitrogen atom substituted with a straight or branched, monovalent, saturated aliphatic chains of 1 to 4 carbon atoms. Included within the term "NH-(Ci-Gt) alkylamine" are -NH(CH3), -NH(CH2CH3), -NH(CH2CH2CH3), -NH(CH2CH2CH2CH3), and the like. As used herein the term "N,N-(Ci-C4)dialkylamine" refers to a nitrogen atom substituted with two straight or branched, monovalent, saturated aliphatic chains of 1 to 4 carbon atoms. Included within the term "N,N-(Ci-C4)dialkylamine" are -N(CH3)2, -N(CH2CH3)2, -N(CH2CH2CH3)2, -N(CH2CH2CH2CH3)2, -N,N(CH3)(CH2CH3), -N,N(CH2CH3)(CH2CH3) and the like. As used herein the term "(Ci-C4)alkyl-N,N-(Ci-C4)dialkyJamine" refers to straight, or branched, monovalent, saturated aliphatic chain of 1 to 4 carbon atoms which has an N,N-(Ci-C4)dialkylamine attached to the aliphatic chain. Included within the term "(Q-C4)alkyl-N,N-(Ci-C4)dialkylamine" are the following: WO 2005/092854 PCT/US2005/005240 -202- and the like. As used herein the term "(Ci-C4)alkyl-NH(Ci-C4)alkylamine" refers to straight or branched, monovalent, saturated aliphatic chain of 1 to 4 carbon atoms which has an NH(Ci-C4)alkylamine attached to the aliphatic chain. Included within the terhi "(Ci-C4)alkyl-NH(Ci-C4)alkylamine" are the following: The designation " ""^** " refers to a bond that protrudes forward out of the plane of the page. The designation' '""I " refers to a bond that protrudes backward out of the plane of the page. As used herein, the term "steroid hormone nuclear receptor modulator" refers to . those nuclear hormone receptor ligands which bind to any one of GR, MR, AR, ER, or WO 2005/092854 PCT/US2005/005240 &/- PR, of the larger class of nuclear hormone receptors, and either agonize, antagonize, partially agonize, or partially antagonize the receptor's activity. As used herein the term "mineralocorticoid receptor" or "MR" refers to the mineralocorticoid receptor subtype, of the larger class of nuclear hormone receptors, which binds the mineralocorticoid hormone aldosterone, as its cognate ligand. The term "mineralocorticoid receptor modulator" or "mineralocorticoid modulator" or "MR modulator" as used herein, refers to those nuclear hormone receptor ligands which bind to the mineralocorticoid receptor subtype and modulate (i.e. agonize, antagonize, partially agonize, or partially antagonize) the receptor activity. As a particular embodiment, the present invention provides antagonists of MR activity As used herein the term "glucocorticoid receptor" or "GR" refers to the glucocorticoid receptor subtype, of the larger class of nuclear hormone receptors, which binds the glucocorticoid hormones cortisol, corticosterone, or cortisone as its cognate ligand. The term "glucocorticoid receptor modulator" or "glucocorticoid modulator" or "GR modulator", as used herein, refers to those nuclear hormone receptor ligands which bind to the glucocorticoid receptor subtype and modulate (i.e. agonize, antagonize, partially agonize, or partially antagonize) the receptor activity. As used herein, the term "disorder susceptible to steroid hormone nuclear receptor modulation" refers to any physiological disorder, of any origin, known or believed to be responsive to administration of a modulator (i.e. agonist, antagonist, partial agonist, or partial antagonist) of a steroid hormone nuclear receptor. Such disorders include Conn's Syndrome, primary and secondary hyperaldosteronism, increased sodium retention, increased magnesium and potassium excretion (diuresis), increased water retention, hypertension (isolated systolic and combined systolic/diastolic), arrhythmias, myocardial fibrosis, myocardial infarction, atherosclerosis, Bartter's Syndrome, disorders associated with excess catecholamine levels, diastolic and systolic congestive heart failure (CHF), peripheral vascular disease, atherosclerosis, diabetic nephropathy, cirrhosis with edema and ascites, esophageal varicies, Addison's Disease, muscle weakness, increased melanin pigmentation of the skin, weight loss, hypotension, hypoglycemia, Cushing's Syndrome, obesity, hypertension, glucose intolerance, hyperglycemia, diabetes mellitus, osteoporosis, polyuria, polydipsia, inflammation, autoimmune disorders, tissue rejection associated with organ transplant, malignancies such as leukemias and lymphomas, acute adrenal WO 2005/092854 PCT/US2005/005240 -af- insufflciency, congenital adrenal hyperplasia, rheumatic fever, polyarteritis nodosa, granulomatous polyarteritis, inhibition of myeloid cell lines, immune proliferation/apoptosis, HPA axis suppression and regulation, hypercortisolemia, modulation of the Thl/Th2 cytokine balance, chronic kidney disease, stroke and spinal cord injury, hypercalcemia, hyperglycemia, acute adrenal insufficiency, chronic primary adrenal insufficiency, secondary adrenal insufficiency, congenital adrenal hyperplasia, cerebral edema, thrombocytopenia, and Little's syndrome, systemic inflammation, inflammatory bowel disease, systemic lupus erythematosus, discoid lupus erythematosus, polyartitis nodosa, Wegener's granulomatosis, giant cell arthritis, rheumatoid arthritis, osteoarthritis, hay fever, allergic rhinitis, contact dermatitis, atopic dermatitis, exfoliative dermatitis, urticaria, angioneurotic edema, chronic obstructive pulmonary disease, asthma, tendonitis, bursitis, Crohn's disease, ulcerative colitis, autoimmune chronic active hepatitis, hepatitis, cirrhosis, inflammatory scalp alopecia, panniculitis, psoriasis, inflamed cysts, pyoderma gangrenosum, pemphigus vulgaris, bullous pemphigoid, dermatomyositis, eosinophilic fasciitis, relapsing polychondritis, inflammatory vasculitis, sarcoidosis, Sweet's disease, type 1 reactive leprosy, capillary hemangiomas, lichen planus,, erythema nodosum, acne, hirsutism, toxic epidermal necrolysis, erythema multiform, cutaneous T-cell lymphoma, psychoses, cognitive disorders (such as memory disturbances), mood disorders (such as depression and bipolar disorder), anxiety disorders, and personality disorders. • •' ¦ As used herein the term "congestive heart failure" (CHF) or "congestive heart disease" refers to a disease state of the cardiovascular system whereby the heart is unable to efficiently pump an adequate volume of blood to meet the requirements of the body's tissues and organ systems. Typically, CHF is characterized by left ventricular failure (systolic dysfunction) and fluid accumulation in the lungs, with the underlying cause being attributed to one or more heart or cardiovascular disease states including coronary artery disease, myocardial infarction, hypertension, diabetes, valvular heart disease, and cardiomyopathy. The term "diastolic congestive heart failure" refers to a state of CHF characterized by impairment in the ability of the heart to properly relax and fill with blood. Conversely, the term "systolic congestive heart failure" refers to a state of CHF characterized by impairment in the ability of the heart to properly contract and eject blood. WO 2005/092854 PCT/US2005/005240 As appreciated by one of skill in the art, physiological disorders may present as a "chronic" condition, or an "acute" episode. The term "chronic", as used herein, means a ¦ condition of slow progress and long continuance. As such, a chronic condition is treated when it is diagnosed and treatment continued throughout the course of the disease. Conversely, the term "acute"means an exacerbated event or attack, of short course, followed by a period of remission. Thus, the treatment of physiological disorders contemplates both acute events and chronic conditions. In an acute event, compound is administered at the onset of symptoms and discontinued when the symptoms disappear. As described above, a chronic condition is treated throughout the course of the disease. As used herein the term "patient" refers to a mammal, such a mouse, gerbil, guinea pig, rat, dog or human. It is understood, however, that the preferred patient is a human. As used herein, the terms "treating", "treatment", or "to treat" each mean to alleviate symptoms, eliminate the causation of resultant symptoms either on a temporary or permanent basis, and to prevent, slow the appearance, or reverse the progression or severity of resultant symptoms of the named disorder. As such, the methods of this invention encompass both therapeutic and prophylactic administration. f As used herein the term "effective amount" refers to the amount or dose of the compound, upon single or multiple dose administration to the patient, which provides the desired effect in the patient under diagnosis or treatment. An effective amount can be readily determined by the attending diagnostician, as one skilled in the art, by the use of known techniques and by observing results obtained under analogous circumstances. In . determining the effective amount or dose of compound administered, a number of factors are considered by the attending diagnostician, including, but not limited to: the species of mammal; its size, age, and general health; the degree of involvement or the severity of the disease involved; the response of the individual patient; the particular compound administered; the mode of administration; the bioavailability characteristics of the preparation administered; the dose regimen selected; the use of concomitant medication; and other relevant circumstances. A typical daily dose will contain from about 0.01 mg/kg to about 100 mg/kg of each compound used in the present method of treatment. Preferably, daily doses will be about 0.05 mg/kg to about 50 mg/kg, more preferably from about 0.1 mg/kg to about 25 mg/kg. WO 2005/092854 ^_ PCT/US2005/005240 4. After filtering off the drying agent, concentrate the filtrate in vaciio to a volume of ~1.5 L resulting in thin dark mixture. Gradually exchange the solvent using heptane (~ 4 L) to form a thick sand-like slurry and increase the bath temperature to 50-60 °C. Concentrate to a volume of -1.5 L, filter while hot (50-60 °C), wash with warm (45 °C) heptane (1L) and RT heptane (1 L), and dry to yield 683.5 g (96.7 %) of the title compound as light purple solid. 1H-NMR(DMSO-d6, 300MHz) 8 10.79 (br s, 1H), 9.42 (br s, 1H), 7.20-7.56 (m, 8H), 6.92 (t, 1H), 6.41 (dd, 1H), 5.18(s, 1H). WO 2005/(192854 _£3 PCT/US2005/005240 Combine l-ethyl-5-fluoro-indan-l-ol (502 mg, 2.79 mmol, 1.30 equivalents), N-(1H-Indol-7-yl)-methanesulfonamide (450 mg, 2.14 mmol, 1.00 equivalents), and • trifluoroacetic acid (0.2S ml, 3.21 mmol, 1.50 equivalents) in dichloromethane (5 ml) and stir at room temperature under nitrogen overnight. Load the solution on silica and purify eluting with 0 to 100% ethyl acetate/hexanes over 25 minutes to obtain the title compound (672 mg, 84%). LC-MS m/z 373.0 (MM). The racemic mixture is separated on a Chiralcel dJ 8 x 33 cm column eluting with methanol with 0.2% dimethylethylamine (flow: 375 ml/min, UV detection at 230 nm) to provide me individual enantiomers, Examples 1A and IB, in 96.3% ee and 97.4% ee, respectively. Utilizing l-ethyl-5-fluoro-indan-l-ol and 7-nitroindole, the title compound is prepared as in example 1. 0.37 g (42%). NMR (400 MHz, CDC13): 5 0.85 (t, 3H), 2.18 (m, 2H), 2.35 (m, 1H), 2.53 (m, 1H), 3.00 (m, 2H), 6.83 (t, 1H), 6.92 (t, 1H), 7.01 (m, 2H), 7.08 (s, 1H), 7.44 (d, 1H), 8.09 (d, 1H), 9.76 (s, 1H, NH). WO 2005/092854 / PCT/US2005/005240 Combine 3-(l-ethyl-5-fluoro-indan-l-yl)-7-nitro-lH-indole (0.33 g, 1.02 mmol), sodium methoxide (110 mg, 2.04 mmol), and iodomethane (0.10 ml, 1.53 mmol) in dimethylformamide (5ml) and stir at room temperature under nitrogen overnight. Dilute with ether, wash with water (2x), dry over sodium sulfate, filter, and concentrate to obtain the title compound as a yellow amorphous solid (0.33 g, 94%). LC-MS m/z 339.1 (M++l). ... Hydrogenate a mixture of 3-(l-ethyl-5-fluoro-indan-l-yl)-l-methyl-7-nitro-lH-indole (0.26 g, 0.77 mmol) and 5% palladium on carbon (26 mg) in ethanol (50 ml) at 60 psi at room temperature overnight. Filter catalyst and concentrate under high vacuum to obtain the title compound as oil (0.17 g, 71%). NMR (400 MHz, CDC13): 8 0.83 (t, 3H), 2.05 (m, 1H), 2.25 (m, 2H), 2.60 (m, 1H), 2.96 (m, 2H), 3.72 (broad s, 2H, NH2), 4.02 (s, 3H), 6.43 (m, 2H), 6.76 (d, 2H), 6.83 (t, 1H), 6.97 (d, 1H), 7.02 (m, 1H). WO 2005/092854 PCT/US2005/005240 6/ m- Dissolve 3-(l-ethyl-5-fluoro-indan-l-yl)-l-methyHH-indol-7-ylamine (0.18 g, 0.58 mmol) in pyridine (3 ml). Add rriethanesulfonyl chloride (0.05 ml, 0.70 mmol, 1.20 equivalents) and stir at room temperature under nitrogen overnight. Dilute with ether, ¦ wash with IN aqueous hydrochloric acid (2x), dry over anhydrous sodium sulfate, filter, and concentrate solution in vacuo. Purify the residue on silica eluting with 0 to 100% ethyl acetate/hexanes over 25 minutes to provide the title compound as a white solid (0.19 g, 86%). LC-MSm/z 387.1 (M++l). I Utilizing l-ethy]-5-fluoro-indan-l-ol and indole, the title compound is prepared as in example 1. 89 mg (54%). LC-MS m/z 280.0 (M++l). WO 2005/092854 . PCT/US2005/005240 It- Utilizing l-ethyl-5-fluoro-indan-l-ol and 7-fluoroindole, the title compound is prepared as in example 1. 217 mg (92%). NMR (400 MHz, CDC]3): 6 0.85 (t, 3H), 2.12 (m, 1H), 2.21 (m, 1H), 2.31 (m, 1H), 2.58 (m, 1H), 2.97 (m, 2H), 6.83 (m, 4H), 6.98 (m, 3H), 8.06 (s, 1H,NH). Utilizing l-ethyl-5-fluoro-indan-l-ol and 7-bromoindole, the title compound is prepared as in example 1. 51 mg (16%). NMR (400 MHz, CDC13): 8 0.82 (t, 3H), 2.12 (m, 1H), 2.21 (m, 1H), 2.30 (m, 1H), 2.59 (m, 1H), 2.97 (m, 2H), 6.82 (m, 2H), 6.90 (s, 1H), 6:99 (m, 2H), 7.12 (d, 1H), 7.28 (d, 1H), 8.08 (s, 1H, NH). WO 2005/092854 PCT/US2005/005240 Utilizing l-ethyl-5-fluoro-indan-l-ol and 7-chloroindole, the title compound is prepared as in example 1. 90 mg (60%). NMR (400 MHz, CDC13): 5 0.85 (t, 3H), 2.15 (m, 1H), 2.22 (m, 1H), 2.34 (m, 1H), 2.59 (m, 1H), 2.98 (m, 2H), 6.82 (t, 1H), 6.87 (m, 2H), 7.00 (m, 2H), 7.11 (d, 1H), 7.16 (d, 1H), 8.12 (s, 1H, NH). Utilizing l-ethyl-5-fluoro-indan-l-ol and 7-ethylindole, the title compound is prepared as in example. 1. 104 mg (58%). LC-MS ro/z 308.1 (M++l).' Utilizing l-ethyl-5-fluoro-indan-l-ol and lH-indole-7-carboxylic acid methyl ester, the title compound is prepared as in example 1. 103 mg (75%). LC-MS m/z 338.1 (M++l). WO 2005/092854 PCT/US2005/005240 Utilizing l-ethyl-5-fluoro-indan-l-ol and 7-melhoxyiiidole, the title compound is prepared as in example 1. 123 nag (59%). LC-MS m/z 310.2 (MM). Utilizing lrethyl-5-fluoro-indan-l-ol and (lH-indol-7-yl)-carbamic acid benzyl ester, the title compound is prepared as in example 1. 7.78 g (100%). LC-MS m/z 249.1 (M*+l) WO 2005/092854 PCT/US2005/005240 A mixture of [3-(l-ethyl-5-fluoro-indan-l-yl)-lH-indol-7-yl]-carbamic acid benzyl ester (7.78 g, 18.2 mmol) and 20% palladium hydroxide on carbon (1.6 g) in ethanol is hydrogenated at 50°C at 60 psi for 18 hours. After filtration of the catalyst the solution is concentrated in vacuo to furnish the title compound as a black solid (5.04 g, 94%). LC- MSm/z295.1(M++l). . r Dissolve 3-(l-ethyl-5-fiuoro-indan-l-yl)-lH-indol-7-ylamine (0.35 g, 1.19 mmol) in pyridine (3 ml). Add methyl chloroformate (0.10 ml, 1.31 mmol, 1.1 equivalents) and stir at room temperature under nitrogen overnight. Dilute with ether, wash with IN aqueous hydrochloric acid (2x), dry over anhydrous sodium sulfate, filter, and concentrate solution in vacuo. Purify the residue on silica eluting with 0 to 75% ethyl acetate/hexanes over 30 minutes to provide the title compound as a white solid (0.15 g, 36%). LC-MS m/z 353.1 (M++l). WO 2005/092854 PCT/US2005/005240 Utilizing 3-(l-ethyl-5-fluoro-indan-l-yl)-lH-indol-7-ylamine and acetic anhydride, the title compound is prepared as in example 15. 0.16 g (46%). LC-MS m/z 337.1 (M*+l). Utilizing 3-(l-ethyl-5-fluoro-indan-l-yl)-lH-indol-7-ylamine and dimethyl sulfamoyl chloride, the title compound is prepared as in example 15. 0.16 g (29%). LC-MS m/z 4O2.HM++n. WO 2005/092854 PCT/US2OO5/O0S240 Utilizing 3-(l-ethyl-5-fluoro-indan-l-yl)-lH-indol-7-ylamine and benzenesulfonyl chloride, the title compound is prepared as in example 15. 0.21 g (33%). LC-MS m/z 295.1 (MM). Utilizing 3-(l-ethyl-5-fluoro-indan-l-yl)-lH-indol-7-ylamine and ethanesulfonyl chloride, the title compound is prepared as in example 15. 0.18 g (35%). LC-MS m/z 387.1 (MM). The carbinols used in Examples 20-39 are prepared from the appropriate ketone as in Preparation 1. WO 20(15/092854 PCMJS2005/005240 Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-raethanesulfonamide, the title compound is prepared as in Example 1. 634 mg (74%). LC-MS m/z 341.1 (M*+l). Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the title compound is prepared as in Example 1. 737 mg (83%). LC-MS m/z 359.1 (NT+1). The racemic mixture is separated on a Chiralcel OJ 8 x 33 cm column eluting with 15/85 -acetonitrile/methanol with 0.2% dimethylethylamine (flow: 400 ml/min, UV detection at 275 nm) to give the individual enantiomers, Examples 21A and 21B, in greater than 99.9% ee and 97.4% ee, respectively. WO 2005/092854 PCT/US2005/005240 Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the title compound is prepared as in Example 1. 1.25 g (71%). LC-MS m/z 377.1 (M*+l). The racemic mixture is separated on a Chiralcel OJ 8 x 33 cm column eluting with 20/20/60 3A alcohol/methanol/heptane with 0.2% dimethylethylamine (flow: 375 ml/min, UV detection at 300 run) to provide the individual enantiomers, Examples 22A and 228, in 99.3% ee and 99.6% ee, respectively. Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the title compound is prepared as in Example 1. 0.41 g (69%). LC-MS m/z 391.0 (M++l). The racemic mixture is separated on a Chiralcel OD 8 x 34 cm column eluting with 30/10/60 isopropanol/methanoiyheptane with 0.2% dimethylethylamine (flow: 375 ml/min, UV detection at 300 run) to give the individual enantiomers, Examples 23A and 23B, in 97.2% ee and 98.5% ee, respectively. WO 2005/092854 PCT/US2005/005240 Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the title compound is prepared as in Example 1. 0.43 g (32%). LC-MS m/z 407.1 (M*+l).. Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the title compound is prepared as in Example 1. 197 mg (40%). LC-MS m/z 341.1 (M*+l). WO 2005/092854 PC17US2005/005240 Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the title compound is prepared as in Example 1. 541 mg (78%). LC-MS m/z 355.0 (M*+l). Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the titl compound is prepared as in Example 1. 140 mg (54%). LC-MS m/z 369.1 (M++l). WO 2005/092854 PCT/US2005/U05240 Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the title compound is prepared as in Example 1. 0.81 g (76%). LC-MS m/z 373.2 (M*+l). The racemic mixture is separated on a Chiralcel OJ 8 x 33 cm column eluting with 20/30 acetonitrile/methanol with 0.2% dimethylethylamine (flow: 375 ml/min, UV detection at 316 nm) to provide the individual enantiomers, Examples 28A and 28B, in greater than 99.9% ee and greater than 99.9% ee, respectively. Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the title compound is prepared as in Example 1. 2.23 g (74%). NMR (400 MHz, CDC13): 8 0.89 (t, 3H), 1.62-1.86 (m, 2H), 2.05 (m, 1H), 2.16-2.42 (m, 4H), 2.84 (t, 2H), 3.01 (s, 3H), 6.42 (s, 1H), 6.70 (s, 1H), 6.75 (t, 1H), 6.82-6.93 (m, 3H), 7.05 (m, 1H), 7.21 (d, 1H), 8.91 (broad s, 1H, NH). The racemic mixture is separated on a Chiralpak AD 8 x 30 cm column eluting with 100% 3A alcohol with 0.2% dimethylethylamine (flow: 300 ml/min, UV detection at 270 nm) to provide the individual enantiomers, Examples 29A and 29B, in 99.5% ee and 99.6% ee, respectively. WO 2005/092854 ~ , PCT/US200S/U0S240 Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the title compound is prepared as in Example 1. 3.12 g (68%). LC-MSm/z 391.0 (M++l). The racemic mixture is separated on a Chiralcel OJ 8 x 33 cm column eluting with 5/95 acetonitrile/methanol (flow: 375 ml/min, UV detection at 225 nm) to give the individual . . enantiomers, Examples 31A and 3 IB, in greater than 99.9% ee and 99.3% ee, respectively. Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the title compound is prepared as in Example 1. 380 mg (40%). NMR (400 MHz, CDC13): 5 0.82 (t, 3H), 1.58-1.78 (m, 2H), 2.08 (m, 1H), 2.17 (m, 1H), 2.40 (m, 1H), 2.55 (m, 1H), 2.82 (m, 2H), 3.01 (s, 3H), 6.47 (s, 1H), 6.57 (t, 1H), 6.67 (s, 1H), 6.74 (d, 1H), 6.87 (d, 1H), 6.94 (t, 1H), 7.31 (d, 1H), 8.94 (broad s, 1H, NH). The racemic mixture is separated on a WO 2005/092854 PCT/US2005/005240 Chiralcel OJ 8 x 33 cm column eluting with 5/95 acetonitrile/methanol (flow: 375 ml/min, UV detection at 230 nm) to give the individual enantiomers.'Examples 31A and 3 IB, in greater than 99.9% ee and 99.5% ee, respectively. Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the title compound is prepared as in Example 1. 226 mg (99%). LC-MS m/z 357.0 (NT^+l). Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonaraide, the title compound is prepared as in Example 1. 270 mg (99%). LC-MS m/z 375.0 (M++l). WO 2005/092854 s- PCT/US2005/005240 Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the title compound is prepared as in Example 1. 3.6 g (100%). LC-MS m/z 375.0 (NT+1). The racemic mixture is separated on a Chiralpak AD 8 x 30 cm column eluting with 100% 3A alcohol (flow: 375 ml/min, UV detection at 230 nm) to give the individual enantiomers, Examples 34A and 34B, in 98.9% ee and 99.1% ee, respectively. Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the title compound is prepared as in Example 1. 3.85 g (99%). LC-MS m/z 389.1 (M*+l). The racemic mixture is separated on a Chiralcel OJ 8 x 33 cm column eluting with 10/90 acetonitrile/methanol (flow: 375 ml/min, UV detection at 230 nm) to give the individual "-"itiomers, Examples 35 A and 35B, in 96.5% ee and 98.2% ee, respectively. WO 2005/092854 PCT/US2005/005240 "¥> Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-raethanesulfonamide, the title compound is prepared as in Example 1. 4.13 g (94%). LC-MS m/z 407.0 (MM). The racemic mixture is separated on a Chiralcel OJ 8 x 33 cm column eluting with 20/80 ¦ acetonitrile/methanol with 0.2% dimethylethylamine (flow: 375 ml/min, UV detection at 280 nm) to give the individual enantiomers, Examples 36A and 36B, in greater than 99.9% ee and 99.9% ee, respectively. Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the title compound is prepared as in Example 1. 195 mg (74%). LC-MS m/z 390.1 (M*+H.2O). WO 2005/092854 PCT/US2005/005240 Utilizing the appropriate carbinol and N-(lH-Indol-7-yl)-methanesulfonamide, the title compound is prepared as in Example 1. 213 mg (66%). NMR (400 MHz, CDC13): 8 1.47 (m, 1H), 1.75 (m, 1H), 1.78 (s, 3H), 1.87 (m, 3H), 2.60 (m, 1H), 2.67 (m, 1H), 2.79 (m, 1H), 6.43 (s, 1H), 6.67 (s, 1H), 6.87 (d, 1H), 6.93 (t, 1H), 7.11 (m, 1H), 7.16-7.21 (m, 3H), 7.41 (m, 1H), 8.91 (broad s, 1H, NH). Combine N-(lH-Indol-7-yl)-methanesulfonamide (0.95 g, 4.51 mmol), l-cyclopropyl-5-fluoro-indan-1-ol (1.30 g, 6.76 mmol, 1.50 equivalents), and trifluoroacetic acid (0.70 ml, 9.02 mmol, 2.00 equivalents) in dichloromethane (20 ml) and stir at room temperature under nitrogen overnight. Preload the solution on silica and purify on 40 g of silica eluting with 0 to 50 ethyl acetate/hexanes over 30 minutes. Isolate the product as a white crystalline solid (1.42 g). NMR analysis indicates a one to one mixture of the title compound and propyl-trifluoroacetate ester. Dissolve the product in methanol (20 ml) and 2M aqueous lithium hydroxide (20 ml) and stir at room temperature overnight. • . WO 2005/092854 PCT/US2005/005240 Dilute with ether, wash with IN hydrochloric acid (2x), dry over sodium sulfate, filter, and concentrate. Purify on 40 g of silica eluting with 0 to 100 ethyl acetate/hexanes over 30 minutes to obtain the title compound as a white solid (0.39 g). The title compound is the less polar component. NMR (400 MHz, CDC13): 8 1.47 (m, 1H), -0.15 (m, 1H), 0.11 (m, 1H), 0.49 (m, 2H), 1.45 (m, 1H), 2.21 (m, 1H), 2.67 (m, 1H), 2.94 (m, 1H), 3.01 (s, 3H), 3^05 (m, 1H), 6.55 (s, 1H), 6.72 (m, 2H), 6.83 (m, 3H), 6.97 (d, 1H), 7.33 .(s, 1H), 9.02 (broad s, 1H, NH). The racemic mixture is separated on a Chiralcel OJ 8 x-33 cm column eluting with 60/40 acetonitrile/methanol with 0.2% dimethylethylamine (flow: 375 ml/min, UV detection at 275 nm) to give the individual enantiomers, Examples 39A and 39B, in greater than 99.9% ee and 99.6% ee, respectively. The title compound is the more polar component of the final chromatography described in example 39. NMR (400 MHz, CDC13): 8 1.47-1.60 (m, 2H), 2.08-2.29 (m, 3H), 2.58 (m, 1H), 2.97 (m, 2H), 2.99 (s, 3H), 2.61 (m, 2H), 6.77 (t, 1H), 6.85-6.98 (m, 6H), 7.05 (d, 1H), 9.01 (broad s, 1H, NH). The racemic mixture is separated on a Chiralpak AD 8.x 30 cm column eluting with 40/10/50 isopropanol/methanol/heptane with 0.2% dimethylethylamine (flow: 350 ml/min, UV detection at 232 nm) to give the individual enantiomers, Examples 40A and 40B, in 98.2% ee and 96.8% ee, espectively. WO 2005/092854 PCT/US2005/005240 To a solution of triphenylphosphine (422 mg, 1.61 mmol, 1.30 equivalents) and imidazole (219 mg, 3.22 mmol, 2:60 equivalents) in anhydrous tetrahydrofuran (10 ml) add iodine (410 mg, 1.61 mmol, 1.30 equivalents). After stirring for 20 minutes at room temperature under nitrogen, add N-{3-[5-Fluoro-l-(3-hydroxy-propyl)-indan-l-yl]-lH-indol-7-yl}-methanesulfonamide (500 mg, 1.24 mmol) and stir for 48 hours. Dilute with ether, wash with water (2x), wash with IN aqueous hydrochloric acid (2x), dry over anhydrous sodium sulfate, filter, and concentrate the solution. Purify the residue on silica eluting with 50 to 100% ethyl acetate/hexanes over 25 minutes to obtain the title compound as a white solid (254 mg, 40%). LC-MS m/z 385.0 (M+-I). . StirN- {3- [5- fluoro-1- (3-iodo -propyl)- indan-1-yl]- lH-indol-7-yl}- methane sulfonamide (88 mg, 0.17 mmol) and methylamine (40% in water, 2ml) in tetrahydrofuran (1 ml) at room temperature under nitrogen for 30 minutes. Dilute with dichloromethane and 10% aqueous potassium carbonate. Filter the white solids that crush out and dry WO 2005/092854 PCT/US2005/005240 under high vacuum to obtain the title compound (35 mg, 49%). LC-MS m/z 416.1 (M++1). • Stir N- {3- [5- fluoro-1- (3-iodo -propyl)- indan-1-yl]- lH-indol-7-yl}- methane sulfonamide (65 mg, 0.13 mmol) and dimethyl amine (5.0 ml, 2.0 M in tetrahydrofuran) at room temperature under nitrogen overnight. Remove the volatiles under high vacuum, dissolve the residue in dichloromethane, wash with saturated aqueous sodium bicarbonate, dry over anhydrous sodium sulfate, filter, and concentrate in vacuo. Purify the residue on silica eluting with 10% methanol in dichloromethane to obtain the title compound as a white solid (34 mg, 65%). LC-MS m/z 430.2 (MM). WO 2005/092854 PCT/US2005/005240 Combine N- {3- [5- fluoro-1- (3-iodo -propyl)- indan-1-yl]- lH-indol-7-yl}- methane sulfonamide (65 mg, 0.13 mmol) and morpholine (2 ml) in anhydrous tetranydrofuran (2.5 ml) and stir at room temperature under nitrogen overnight. Remove the volatiles under high vacuum, dissolve the residue in dichloromethane, add solid potassium carbonate, stir for ten minutes, filter, and concentrate in vacuo. Purify the residue on silica eluting with 5 to 10% methanol in dichloromethane over 15 minutes to obtain the title compound as a white solid (50 mg, 83%). LC-MS m/z 472.2 (M++l). What is claimed is: 1. A compound of the formula: wherein, X represents -CH2-, -CH2CH2-, -CH2CH2CH2-, -CH2O-, -CH2S-, or -CH2NR10-; Rl represents hydrogen, (Ci-C4)alkyl, (C3-C7)cycloalkyl, hydroxy(Cj-C4)alkyl, halo(Ci-C4)alkyl, (Ci-C4)alkyl-heterocycle, (Ci-C4)alkyl-NH(Ci-C4)alkylamine, or (C i -C4)alkyl-N,N-(C i -C4)dialkylamine; R2 represents hydrogen, halo, (Cj-C4)alkyl, heterocycle, or substituted heterocycle; R3 represents hydrogen, halo, (Ci-C4)alkyl, heterocycle, or substituted heterocycle; R4 represents hydrogen, halo, amino, nitro, (Cj-C4)alkyl, (Ci-C4)alkoxy, NHSO2R7, NHCOR8, or COR9; R5 represents hydrogen or halo; R^ represents hydrogen or (Cj-C4)alkyl; R7 represents (Ci-C4)alkyl, aryl, NH(Ci-C4)alkylamine, or N,N-(Cj- C4)dialkylamine; R8 represents (Cj-C4)alkyl, (Ci-C4)alkoxy, or aryl(Ci-C4)alkoxy; R9 represents (Ci-C4)alkyl or (Ci-C4)alkoxy, and RlO represents hydrogen, (Ci-C4)alkyl, (C3-C7)cycloalkyl, or (Ci-C4)alkyl-(C3-C7)cycloalkyl, or a pharmaceutically acceptable salt thereof. 2. The compound according to Claim 1 wherein X represents -CH2-, -CH2CH2-, or -CH2O-. 3. The compound according to any one of Claims 1-2 wherein R.1 represents hydrogen, (Ci-C4)alkyl, (C3-C7)cycloalkyl, hydroxy(Ci-C4)alkyl, halo(Ci-C4)alkyl, (Ci-C4)alkyl-heterocycle, (Ci-C4)alkyl-NH(Ci-C4)alkylamine, or (Ci-C4)alkyl-N,N- (C \ -C4)dialkylamine. 4. The compound according to Claim 3 wherein Rl represents methyl, ethyl, propyl, isopropyl, (C3-C7)cycloalkyl, hydroxy(Cj-C4)alkyl, halo(Ci-C4)alkyl, (C]- C4)alkyl-heterocycle, (Ci-C4)alkyl-NH(Ci-C4)alkylamine, or (Ci-C4)alkyl-N,N-(Ci- C4)dialkylamine. 5. The compound according to any one of Claims 1-4 wherein R2 represents hydrogen, fluoro, chloro, bromo, methyl, ethyl, propyl, or isopropyl. 6. The compound according to any one of Claims 1-5 wherein R.3 represents hydrogen, fluoro, chloro, or bromo. 7. The compound according to any one of Claims 1-6 wherein R.4 represents hydrogen, halo, amino, nitro, (Ci-C4)alkyl, (Ci-C4)alkoxy, NHSO2R7, NHCOR8 wherein R8 represents (Ci-C4)alkyl or (Cj-C4)alkoxy, or COR^ wherein R9 represents (C1 -C4)alkyl or (C1 -C4)alkoxy. 8. The compound according to Claim 7 wherein R4 represents hydrogen, halo, amino, nitro, (Cj-C4)alkyl, (Cj-C4)alkoxy, or NH SO2R7 wherein R7 represents (C1 -C4)alkyl, aryl, or N,N-(C 1 -C4)dialkylamine. 9. The compound according to any one of Claims 1- 8 wherein R5 represents hydrogen, chloro, or flouro. 9. 10. The compound according to any one of Claims 1- 9 wherein R6 represents hydrogen, methyl, or ethyl. 11. A pharmaceutical composition comprising the compound according to any one of Claims 1-10 in combination with a pharmaceutically acceptable carrier, diluent, or excipient. 12. The use of a compound according to any one of Claims 1-10 for the manufacture of a medicament for the treatment of diastolic or systolic congestive heart failure, inflammation, hypertension, or rheumatoid arthritis. 13. A compound selected from the group consisting of N-[3-(l-Ethyl-5- fluoro-indan-1 -yl)-1 H-indol-7-yl]-methanesulfonamide; N-[3-(6-Fluoro-1 -methyl- 1,2,3,4-tetrahydro-naphthalen-1 -yl)-1 H-indol-7-yl]-methanesulfonamide; N- [3 -(6,8-Difluoro-l-methyl-l,2,3,4-tetrahydro-naphthalen-l-yl)-lH-indol-7-yl]-methanesulfonamide; N-[3-(6,8-Difluoro-l-methyl-l,2,3,4-tetrahydro-naphthalen-l-yl)-lH-indol-7-yl]-methanesulfonamide; N-[3-(4-Ethyl-7-fluoro-chroman-4-yl)-lH-indol-7-yl]-methanesulfonamide; andN-[3-(l-Cyclopropyl-5-fluoro-indan-l-yl)-lH-indol-7-yl]-methanesulfonamide, or a pharmaceutically acceptable salt thereof. 14. A compound, a pharmaceutical composition and use of a compound substantially as herein described with reference to the foregoing examples. Dated this 2nd day of August 2006 "BICYCLIC SUBSTITUTED INDOLE-DERIVATIVE STEROID HORMONE NUCLEAR RECEPTOR MODULATORS" The present invention provides a compound of the formula: or a pharmaceutically acceptable salt thereof, pharmaceutical compositions comprising an effective amount of a compound of Formula I in combination with a suitable carrier, diluent, or excipient, and methods for treating physiological disorders, particularly congestive heart disease, hypertension, and atherosclerosis, comprising administering to a patient in thereof an effective amount of a compound of Formula I.