Medrogeston

Warning

H361 (100%): Suspected of damaging fertility or the unborn child [Warning Reproductive toxicity]

P203, P280, P318, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 43 reports by companies from 2 notifications to the ECHA C&L Inventory.

G - Genito urinary system and sex hormones

QG - Genito urinary system and sex hormones

Medrogestone, as presented for all progestogens, is highly bound to plasma proteins. It is mainly bound to albumin but it also binds to other plasma proteins like sex hormone binding globulin or corticosteroid-binding globulin. The pharmacokinetics of medrogestone will depend on the degree of plasma protein bindind which makes this characteristic the main regulator of the tissue availability of medrogestone.

Medrogestone was created as a more potent and orally active option of progesterone. In pre-clinical trials, medrogestone was proven to have four times more progestational activity than progesterone with a similar duration effect than the one found for 17-hydroxyprogesterone. Medrogestone was also able to maintain pregnancy and prevented ovulation in ovariectomized rats. Administration of medrogestone, alone or with premarin, prevented pregnancy, as well as it suppressed ovarian weight increase by nearly 100% of the tested individuals. Medrogestone does not produce any androgenic effect but it presented a marked anti-androgenic effect. It did not present an oestrogenic effect, nor changes in organ weight or histological appearance in adrenal glands or thymus and it does not present any anti-inflammatory effects.

Medrogestone is a progestogen, thus its action is done under the same profile. These type of molecules are steroid hormones that bind and activate the progesterone receptor. Its action may involve the suppression of gonadotropic hormones from the anterior portion of the pituitary gland and secondary suppression of testosterone. Medrogestone presents structural similarities to testosterone which allows it to compete for the androgen-receptor-protein receptor sites in prostatic cells. Administration of medrogestone diminishes the response to endogenous hormones in tumor cells due to a reduction in hormone steroid receptors; this effect will translate into cytotoxic or antiproliferative effects.