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What is/are Norethindrone?

Norethisterone (or norethindrone) (or 19-nor-17α-ethynyltestosterone) is a molecule used in some combined oral contraceptive pills, progestogen only pills and is also available as a stand-alone drug. It is a progestogen and can be used to treat premenstrual syndrome, painful periods, abnormal heavy bleeding, irregular periods, menopausal syndrome (in combination with oestrogen), or to postpone a period. It is also commonly used to help prevent uterine hemorrhage in complicated non-surgical or pre-surgical gynecologic cases. Norethindrone was the first orally highly active progestin to be synthesized. It was synthesized for the first time by chemists Luis Miramontes, Carl Djerassi, and George Rosenkranz at Syntex in Mexico City in 1951.It was the progestin used in one of the first three oral contraceptives. Its related ester, norethisterone acetate, is used for the same indications.

Description: Norethindrone is a synthetic oral progestin. It is used for contraception or to treat such conditions as secondary amenorrhea, abnormal uterine bleeding, and endometriosis. As an oral contraceptive, norethindrone is available as either a single agent or in combination with an estrogen. Progestin-only formulations or "mini-pills" of norethindrone are not widely used because of increased incidence of certain side effects such as irregular, unpredictable spotting and breakthrough bleeding. Progestin-only contraceptives have a higher risk of failure compared to estrogen-progestin combinations because of variable suppression of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) in low-dose progestin-only regimens. Norethindrone was approved by the FDA in 1961. An implant dosage form for contraception is under investigation.
Mechanism of Action: The primary contraceptive effect of progestins involves the suppression of the midcycle surge of LH. The exact mechanism of action, however, is unknown. At the cellular level, progestins diffuse freely into target cells and bind to the progesterone receptor. Target cells include the female reproductive tract, the mammary gland, the hypothalamus, and the pituitary. Once bound to the receptor, progestins slow the frequency of release of gonadotropin releasing hormone (GnRH) from the hypothalamus and blunt the pre-ovulatory LH surge, thereby preventing follicular maturation and ovulation. Overall, progestin-only contraceptives prevent ovulation in 70—80% of cycles, however, the clinical effectiveness ranges 96—98%. This suggests that additional mechanisms may be involved. Other actions of norethindrone include alterations in the endometrium that can impair implantation and an increase in cervical mucus viscosity which inhibits sperm migration into the uterus. The administration of norethindrone to women with adequate estrogen production transforms the uterus from a proliferative to a secretory phase. Norethindrone has minimal estrogenic, androgenic, and anabolic activity.
Pharmacokinetics: Norethindrone is administered orally. Pharmacokinetic parameters for norethindrone are poorly understood. Norethindrone is moderately bound to plasma proteins. It is hepatically metabolized and eliminated in both the urine and the feces. The elimination half-life of norethindrone is about 10 hours.

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