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Abstract
Chlormadinone acetate (CMA) is a derivative of naturally secreted progesterone that shows high affinity and activity at the progesterone receptor. It has an anti-estrogenic effect and, in contrast to natural progesterone, shows moderate anti-androgenic properties. CMA acts by blocking androgen receptors in target organs and by reducing the activity of skin 5α-reductase. It suppresses gonadotropin secretion and thereby reduces ovarian and adrenal androgen production. CMA shows high contraceptive efficacy by inhibiting ovulation due to its ability to suppress or disrupt endogenous gonadotropin secretion and, by this, inhibits follicular growth and maturation. In addition, it suppresses endometrial thickness and increases the viscosity of cervical mucus. Pharmacokinetic studies have shown rapid and almost complete absorption after oral administration, and CMA is being bound to albumin rather than SHBG (Sex-Hormone-Binding-Globulin). Multiple dosing studies have demonstrated that steady state is reached by day 7 after oral administration with peak plasma concentrations in the region of 2 ng/ml. After a single dose of CMA the half-life time is around 34 hours and after multiple dose administration approximately 38 hours. Safety studies have indicated that CMA has no clinically relevant effect on a wide range of metabolic parameters in normal subjects. Further studies in groups at high thromboembolic risk have shown that CMA alone produces a relative risk of 0.8 which is not considered significant. These results indicated the potential for CMA to be combined with ethinylestradiol in an oral contraceptive which provides highly effective contraception and excellent cycle control.