Glucopyranosides conjugates of...

Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Carbohydrate doai

Reexamination Certificate

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C536S017400, C536S018100

Reexamination Certificate

active

06537971

ABSTRACT:

BACKGROUND OF THE INVENTION
This invention provides glucopyranosides conjugates of 2-(4-hydroxy-phenyl)-3-methyl-1-[4-(2-amin-1-yl-ethoxy)-benzyl]-1H-indol-5-ols which are useful as tissue selective estrogenic agents.
The use of hormone replacement therapy for bone loss prevention in post-menopausal women is well precedented. The normal protocol calls for estrogen supplementation using such formulations containing estrone, estriol, ethynyl estradiol or conjugated estrogens isolated from natural sources (i.e., PREMARIN; conjugated equine estrogens). In some patients, therapy may be contraindicated due to the proliferative effects of unopposed estrogens (estrogens not given in combination with progestins) have on uterine tissue. This proliferation is associated with increased risk for endometriosis and/or endometrial cancer. The effects of unopposed estrogens on breast tissue are less clear, but are of some concern. The need for estrogens which can maintain the bone sparing effect while minimizing the proliferative effects in the uterus and breast is evident. Certain nonsteroidal antiestrogens have been shown to maintain bone mass in the ovariectomized rat model as well as in human clinical trials. Tamoxifen (sold as NOVALDEX, tamoxifen citrate), for example, is a useful palliative for the treatment of breast cancer and has been demonstrated to exert an estrogen agonist-like effect on the bone, in humans. However, it is also a partial agonist in the uterus and this is cause for some concern. EVISTA (raloxifene), a benzothiophene antiestrogen, has been shown to stimulate uterine growth in the ovariectomized rat to a lesser extent than Tamoxifen while maintaining the ability to spare bone. A useful review of tissue selective estrogens is seen in the article “Tissue-Selective Actions Of Estrogen Analogs”,
Bone
Vol. 17, No. 4, October 1995, 181S-190S.
The use of indoles as estrogen antagonists has been reported by Von Angerer, See, J. Med. Chem. 1990, 33, 2635-2640; J. Med. Chem. 1987, 30, 131-136. Also see Ger. Offen., DE 3821148 A1 891228 and WO 96/03375.
WO A 95 17383 (Kar Bio AB) describes indole antiestrogens with long straight chains. Another related patent WO A 93 10741 describes 5-hydroxyindole with a generic descriptor incorporating other side chains. WO 93/23374 (Otsuka Pharmaceuticals, Japan) describes compounds which differ from the present invention; where OR
2
in the present formula I, below, is defined as thioalkyl and the reference discloses no such compounds having chains from the indole nitrogen having the same structure as the ones provided by the present invention. Where the side chain claimed is similar to that described herein, the compounds are amides: Acylated indoles are not claimed in the present invention. Glucuronic acid conjugates of the selective estrogen receptor modulator raloxifene (a benzothiophene) have been reported (EP 683170 A1 951122).
DESCRIPTION OF THE INVENTION
This invention provides compounds of Formula I having the structure
wherein:
R
1
and R
2
are independently, hydrogen, alkyl chain of 1-6 carbon atoms, benzyl, acyl of 2-7 carbon atoms, benzoyl,
X is hydrogen, alkyl of 1-6 carbon atoms, CN, halogen, trifluoromethyl, or thioalkyl of 1-6 carbon atoms;
n=1-3;
with the proviso that at least one of R
1
or R
2
are not hydrogen, alkyl chain of 1-6 carbon atoms, benzyl, acyl of 2-7 carbon atoms, or benzoyl;
or a pharmaceutically acceptable sat thereof which are useful as tissue selective estrogens.
The alkyl moiety of the phenol ether substituent include both straight chain as well as branched moieties. Halogen means bromine, chlorine, fluorine, and iodine.
The pharmaceutically acceptable salts include salts formed from the addition reaction with either inorganic or organic acids. Inorganic acids such as hydrochloric acid, hydrobromic acid, hydroiodic acid, sulfuric acid, phosphoric acid and nitric acid are useful. Organic acids such as acetic acid, propionic acid, citric acid, maleic acid, malic acid, tartaric acid, phthalic acid, succinic acid, methanesulfonic acid, toluenesulfonic acid, napthalenesulfonic acid, camphorsulfonic acid and benzenesulfonic acid are also useful. The pharmaceutically acceptable salts of this invention also include quaternary ammonium salts which can be prepared by quaternizing the basic amine of the compounds of this invention with an electrophilic organic halide, mesylate, tosylate, and the like. Compounds of this invention which contain a carboxylic acid may form pharmaceutically acceptable base addition salts by treating the neutral starting material with a suitable inorganic base such as hydoxides or carbonates of alkali metals-such as lithium, sodium, potassium, cesium, magnesium, calcium or barium. Or, the acid may be treated with an organic base (such as various organic primary (including ammonia), secondary or tertiary amines) to form the ammonium salts.
The compounds of this invention can be synthesized according to the generic methods shown in Scheme 1. The orthogonally protected indole is formed by a modified Bischler protocol wherein the &agr;-bromo-4-pivaloyl protected hydroxypropiophenone or acetophenone 1 is reacted with 4-benzyloxyaniline in DMF in the presence of triethylamine. The reaction is monitored by TLC for consumption of starting materials. The aniline substituted material does not need to be isolated but instead, in the same flask, treated with an additional 1.25-1.5 equivalents of 4-benzyloxyaniline hydrochloride and heated to 120-160° C. until the previous intermediate is completely consumed. The protected indole 2 is subsequently treated with a suitable base such as sodium hydride in DMF and then reacted with an appropriate benzyl chloride of type 3. The indole 4 can then be mono-deprotected by either hydrogenating the benzyl group off at the 5-position of the indole or hydrolyzing the pivaloyl group at the 4′-position of the 2-phenyl group of the indole. The group removed is determined by the position of the glucuronic acid conjugate desired. The removal of the benzyl group or the pivaloyl ester renders compounds of either type 5 or 6, respectively. Reaction of compound 5 or 6 with the trichloroacetimidate CAS# [150607-95-7] of the protected glucopyranoside in the presence of BF
3
etherate in a polar aprotic solvent such as dichloromethane results in the glucopyranisodated compounds 7 or 8. We have found that the reaction of either 7 or 8 with the trichloroacetimidate supra in CH
2
Cl
2
using 3 Å molecular sieves allowed for the synthesis of the glucopyranosides in very good yield. The compounds are exclusively formed as the &bgr;-glucopyranosides (equatorial substituted). The pivaloylated compound 7 can be then treated with LiOH in THF/H
2
O/MeOH (or dioxane/MeOH/H
2
O) to effect the complete deprotection of the compound, to give after workup, the monoglucuronic acid 9. The mono-benzyl ether 8 can be hydrogenated by hydrogen transfer between cyclohexadiene and Pd/C and then hydrolyzed by LiOH in THF/H
2
O/MeOH (or dioxane/MeOH/H
2
O) to yield the mono glucuronic acid 10. More preferable for larger scale hydrogenations are the conditions using a 10% Pd/C catalyst, H
2
and a solvent system consisting of THF/EtOH.
Compounds wherein both phenols are glucuronidated can be prepared according to Scheme 2. The bis-benzyl protected indole 12 is prepared by a modified Bischler reaction analogously to that described for indole 2 in scheme 1. The indole can then be subsequently alkylated with the side chain 3 (same as shown in scheme 1). The substituted indole 13 can then be deprotected by hydrogenation of the benzyl ethers to form the deprotected compound 14. The deprotected compound is then bis-glucuronidated by treatment of the free phenolic containing compound with the trichloroacetimidate of the protected glucopyranoside CAS# [150607-95-7] (same reagent used as in scheme 1) to afford 15. The final deprotected bis-glucuronic acid is obtained by base hydrolysis of precursor 15 to afford product 16. The side chains can be p

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