Medroxyprogesteronacetat

less than 1 mg/mL at 73 °F (NTP, 1992)

10mM

Breast Feeding; Lactation; Milk, Human; Contraceptive Agents, Female; Contraceptives, Oral, Synthetic; Hormones; Progesterone Congeners

FDA approved drugs -> Active ingredient

FDA approved drugs -> Active ingredient

Injectable hormonal contraceptives

405 to 408 °F (NTP, 1992)

205-209

This chemical does not meet GHS hazard criteria for 0.6% (1 of 166) of reports.

Danger

H302 (19.3%): Harmful if swallowed [Warning Acute toxicity, oral]

P203, P260, P261, P263, P264, P270, P271, P273, P280, P301+P317, P302+P352, P304+P340, P317, P318, P321, P330, P362+P364, P405, and P501 (click each P-code to see the statement)

Aggregated GHS information provided per 166 reports by companies from 19 notifications to the ECHA C&L Inventory. Each notification may be associated with multiple companies.

Hazard Traits - Carcinogenicity; Developmental Toxicity

Medroxyprogesterone acetate: Does not have an individual approval but may be used under an appropriate group standard

SYMPTOMS: Symptoms of exposure to this compound include breast tenderness, galactorrhea, nervousness, insomnia, somnolence, fatigue, dizziness, thromboembolic phenomena such as thrombophlebitis, pulmonary embolism, pruritus, urticaria, angioneurotic edema, rash, anaphylaxis, alopecia, acne, hirsutism, nausea, jaundice, headache, hyperpyrexia, liver dysfunction, premenstrual-like syndrome, changes in libido, changes in appetite, cystitis-like syndrome, backache, loss of scalp hair, erythema multiforme, erythema nodosum, hemorrhagic eruption, itching, breakthrough bleeding, spotting, amenorrhea, changes in cervical erosion and secretions, melasma or chloasma, mental depression, clitoral hypertrophy, postpartum bleeding (prolonged), postabortal bleeding and missed abortion. Other symptoms include increased intraocular pressure, teratogenic effects such as developmental abnormalities of the urogenital system, and reproductive effects such as spermatogenesis changes, menstrual cycle changes or disorders, postpartum effects, female fertility effects and newborn behavior effects. Exposure may cause edema, candidiasis, cramps and ischemic colitis.

Medroxyprogesterone acetate (MPA) inhibits gonadotropin production, reduces nuclear estrogen receptors and DNA synthesis in epithelial cells of the endometrium, and induces p53 dependant apoptosis in cancer cell lines. MPA oral tablets have a half life of 40-60 hours and other formulations can have half lives that are considerably longer, so the duration of action is long. The therapeutic window is wide as patients may take doses ranging from 5mg orally daily to 1000mg as a depo injection weekly. Long term use of MPA is associated with a reduction in bone density and patients who taking MPA during adolescence may have lower peak bone mass than untreated patients, which can also increase the risk of osteoporosis and fractures in the future.

Medroxyprogesterone acetate (MPA) inhibits the production of gonadotropin, preventing follicular maturation and ovulation, which is responsible for it’s ability to prevent pregnancy. This action also thins the endometrium. MPA reduces nuclear estrogen receptors and DNA synthesis in epithelial cells of the endometrium. MPA can also induce p53 dependant apoptosis in certain cancer cell lines, and inhibit GABA-A receptors.

Oral medroxyprogesterone acetate (MPA) has an absorption half life of 15-30min and a biological half life of 40-60 hours. Intramuscular MPA has an absorption half life of 0.86±0.30 days and an elimination half life of 24.03±21.74 days. Subcutaneous MPA has an absorption half life of 1.05±0.56 days and an elimination half life of 30.90±15.11 days.

Medroxyprogesterone acetate undergoes beta hydroxylation to form the metabolites 6-beta (M-2), 2-beta (M-4), and 1-beta-hydroxymedroxyprogesterone acetate (M-3). M-2 and M-4 are further metabolized to 2-beta,6-beta-dihydroxymedroxyprogesterone (M-1). M-3 is further metabolized to 1,2-dehydromedroxyprogesterone acetate (M-5).