Pharmaceutical compositions containing 3-beta-hydroxylated 6,7-s

Drug – bio-affecting and body treating compositions – Designated organic active ingredient containing – Cyclopentanohydrophenanthrene ring system doai

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514178, A61K 3156

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active

057634335

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BRIEF SUMMARY
This application is a 371 of PCT/FR93/01029 filed 19 Oct. 1993.
The present invention relates to pharmaceutical compositions containing as active ingredient 7-hydroxylated derivatives of natural steroid hormones optionally possessing a 3-beta hydroxyl function, and their use as a trigger or stimulator of immunity (designated hereafter as "immunity effector"), more particularly of cellular immunity; these pharmaceutical composition may also be used as anti-glucocorticoid agents.
The family of 3-beta-hydroxylated steroid hormones comprises: pregnenolone known as 3-beta-hydroxy-5-pregnen-20-one (designated hereafter by PREG), dehydroepiandrosterone known as 3-beta-hydroxy-5-androsten-17-one (designated hereafter by DHEA), androstenediol known as 5-androstene-3-beta, 17-beta-diol (designated hereafter by 5-DIOL), iosandrosterone or epiandrosterone known as 3-beta-hydroxy-5-alpha-androstan-17-one (designated hereafter by ISOA) and androstanediol known as 5-alpha-androstane-3-beta, 17-beta-diol (designated hereafter by ADIOL).
PREG is known to be the precursor of all of the steroid hormones. PREG is formed irreversibly from cholesterol in tissues and organs like the cortical part of the adrenal glands, the gonads (E. Baulieu, Hormones, Publ. Hermann (1978) and brain (Z. Hu et al., Proc. Nat. Acad. Sci. USA, 84, 8215-8219 (1987)). Formed at a very early age, the circulating quantities of it are high and relatively stable (E. DePeretti and E. Mappus, J. Clin. Endocr. Metab. 57, 550-556, (1983)). It can be converted into progesterone even in the brain (Y. Akwa et al., J. Cell. Biol., 121, 135-143 (1993)) but its irreversible conversion into mineralocorticoid and glucocorticoid hormones only occurs in the adrenocortical glands (E. Baulieu, Hormones, Publ. Hermann (1978)).
DHEA is a 17-ketosteroid which is quantitatively one of the major adrenocortical steroid hormones present in the blood of humans and other mammals. M. E. Windholz, the Merck Index, Ninth Edition (1976); K. Diem and C. Lentner, Geigy Scientific Tables (1975); E. Barret-Connor et al., N.E.J.M. 315, 1519-1524 (1986). Although DHEA seems to serve as intermediate in the synthesis of the steroids of the gonads, its primary physiological function is not clear. It is known however that the plasma concentrations of this hormone, which are maximal in the second decade of life, then decline, ultimately to reach 5% of the original level in elderly people.
In certain cases DHEA exhibits properties of an immunity effector: in R. M. Loria, T. H. Inge, S. S. Cook, A. Z. Szakl and W. Regelson (1988), J. Med. Virol., 26, 301-314, it enables the survival of mice infected by the human viruses Edwards CVB4 or HSV2 to be increased when it is injected by the subcutaneous route in amounts of the order of 1 g/kg 4 hours prior to viral infection. This effect is also observed when DHEA is administered by the oral route (0.4% in the diet) for 16 weeks before infection.
More generally, the same authors in the U.S. Pat. No. 5,077,284 demonstrate a positive effect on patients suffering from AIDS treated with doses of 400 to 2500 mg/day, and recommend the use of DHEA together with an antiviral at doses of 25 mg/kg to 2 g/kg.
The irreversible production of DHEA from PREG is known to occur particularly in adrenocortical tissue and in the gonads (E. Baulieu, Hormones, Publ. Hermann (1978)). Moreover, DHEA is only produced from the time of adrenarche and the circulating amount of it increases with puberty (E. DePeretti and E. Mappus, J. Clin. Endocr. Metab., 57, 550-556 (1983)). Once mature, considerable quantities of DHEA circulate in the blood of adult human and other mammals but these quantities reach a maximum in the second decade of human life then decline to ultimately attain less than 10% of the original level in very old people (N. Orentreich et al., J. Clin. Endocr. Metab., 59, 551-555 (1984)).
5-DIOL is derived directly from DHEA, the 17-ketone function of which is reduced by an oxidoreductase. Its circulating quantities are low compared with those of DHEA since the oxidore

REFERENCES:
patent: 4628052 (1986-12-01), Peat
patent: 4898694 (1990-02-01), Schwartz et al.
patent: 5077284 (1991-12-01), Loria et al.

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