Minny/Minny 28 Mechanism of Action

Pharmacology: MINNY is an estrogen/progestogen combination oral contraceptive that inhibits ovulation.
Pharmacodynamics: MINNY inhibits ovulation by suppressing the gonadotropins, FSH, and LH. Additionally, alteration in the genital tract, including cervical mucus (which inhibits sperm penetration) and the endometrium (which reduces the likelihood of implantation), may contribute to contraceptive effectiveness.
Ethinylestradiol is a well known synthetic estrogen.
Desogestrel is a synthetic progestogen. After oral administration it has a strong ovulation-inhibiting activity, a strong progestational and anti-estrogenic activity, no estrogenic activity, very weak androgenic/anabolic activity.
Pharmacokinetics: Ethinylestradiol is rapidly absorbed with peak concentrations attained within 2 hours. It undergoes considerable first-pass elimination. Ethinylestradiol is 97% to 98% bound to plasma albumin. Half-life varies from 6 to 20 hours. It is excreted in bile and urine as conjugates and undergoes some enterohepatic recirculation.
Desogestrel is rapidly and completely absorbed and converted into 3-keto-desogestrel, the biologically active metabolite. Relative bioavailability is about 34%.
Maximum concentrations of the metabolite are reached at about 1.4 hours. Desogestrel is bound to albumin and to sex hormone binding globulins. Terminal half-life of desogestrel (metabolite) is 38 ± 20 hours.