Norethindrone acetate is a female progestin approved by FDA for the treatment of endometriosis, uterine bleeding caused by abnormal hormone levels, and secondary amenorrhea.
Norethindrone acetate could be a cost-effective alternative with relatively mild side effects in the treatment of symptomatic endometriosis. Subjects treated with norethindrone acetate obtain dysmenorrhea and noncyclic pelvic pain relief[1]. Norethindrone acetate alone is a well-tolerated, effective option to manage pain and bleeding for all stages of endometriosis. Post-Norethindrone acetate bleeding scores are improved regardless of prior hormonal regimen, and post-Norethindrone acetate pain scores improved in all patients except for those previously prescribed GnRH-agonist plus add-back[2]. Norethindrone acetate shows low acute toxicity in experimental animals and is consistent with the lack of toxicity seen in humans. Administration of norethindrone acetate alone to rodents at several multiples of the human dose results in no treatment related mortality, hematological changes, behavioral changes, or organ pathology[3]. Norethindrone acetate administration leads to significant and proportional reductions of the concentrations of triglycerides, cholesterol and phospholipids of plasma lipoproteins of density <1.006 of rats fed a high carbohydrate diet. Norethindrone acetate (0.1 mM) also significantly inhibits the incorporation of both palmitate and glycerol into triglycerides of isolated hepatocytes from fed rats[4].
References:
[1]. Muneyyirci-Delale O, et al. Effect of norethindrone acetate in the treatment of symptomatic endometriosis. Int J Fertil Womens Med. 1998 Jan-Feb;43(1):24-7.
[2]. Kaser DJ, et al. Use of norethindrone acetate alone for postoperative suppression of endometriosis symptoms. J Pediatr Adolesc Gynecol. 2012 Apr;25(2):105-8.
[3]. Maier WE, et al. Pharmacology and toxicology of ethinyl estradiol and norethindrone acetate in experimental animals. Regul Toxicol Pharmacol. 2001 Aug;34(1):53-61.
[4]. Cheng DC, et al. Norethindrone acetate inhibition of triglyceride synthesis and release by rat hepatocytes. Atherosclerosis. 1983 Jan;46(1):41-8.