1. OverView:
Chlormadinone acetate (INN, USAN, BAN, JAN; sold under brand names including Clordion, Gestafortin, Lormin, Non-Ovlon,Normenon, Verton, and many others) (CMA) is a derivative of progesterone (17α-acetoxy-6-chloro-4,6-pregnadiene-3,20-dione), first synthesized in 1961 and is used as an orally effective progestogen in hormone replacement therapy (HRT), and in combination with ethinyl estradiol (EE) in contraception since 1999. Chlormadinone acetate has a strong progestogenic effect — about one-third higher than that of progesterone — and may vary depending on the previous effect of an estrogen, i.e., estrogens may promote the formation of progesterone receptors and proliferation of the endometrium. Like progesterone, it is anti-estrogenic and has no partial androgenic effect (at the doses used for contraception and HRT). In contrast to progesterone, it has a slight glucocorticoid effect, a pronounced anti-androgenic effect and no anti-mineralocorticoid effect. No pregnancy-maintaining effect of CMA has been demonstrated in humans.
The anti-androgenic effect of CMA is presumed to be the result of both its binding to androgen receptors — competitively inhibiting the effect of endogenous testosterone and dihydrotestosterone — and the competitive inhibition of 5α-reductase. In this respect, dosing of CMA is crucial; agonistic effects are observed when doses are increased from those optimal for an antagonistic effect.
2. Applications:
Chlormadinone acetate is a steroidal progestin with additional antiandrogen andantigonadotropic (and thus also antiestrogenic) effects. It is used clinically as a hormonal contraceptive, and in part due to its lowering of estrogen levels, but also for improved effectiveness in contraception, chlormadinone is frequently combinedwith ethinyl estradiol for this purpose.
Chlormadinone acetate has a strong anti-gonadotropic effect, through negative feedback on gonadotropin secretion, and has been used for more than 20 years alone for contraception in arterial risk patients. The clinical and metabolic tolerability of CMA has been demonstrated in numerous clinical studies with duration of treatment of up to 2.5 years.

3. Competitive Advantage:
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