Gestagens in the treatment of endometriosis

Т. А. Федотчева, Nikolai L. Shimanovskiy
In: Problems of Endocrinology · 2018 · vol. 64(1) , pp. 54–61 · doi:10.14341/probl201864154-61 · W4236886273
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⚙ AI-generated summary by claude@2026-06, 2026-06-07 ⓘ

This review examines gestagens, particularly the drug Gestobutanoil, for endometriosis treatment by discussing pathogenic mechanisms, progesterone resistance, and the drug's high gestagenic and antiproliferative activities.

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⚙ AI-generated deep summary by claude@2026-06, 2026-06-07 ⓘ

This paper is a review of the mechanisms underlying endometriosis and the role of progestins/gestagens in its pathogenesis and treatment, linking genetic and epigenetic alterations that contribute to resistance to endogenous progesterone. It summarizes how progestins act via progesterone receptors (including modulation of gene transcription), promote decidualization and secretory transformation of endometrial/ectopic tissue, shift estrogen metabolism via activation of 17β-HSD2, and inhibit prostaglandin E2 pathways, and it highlights the review’s caveat that individual treatment selection is said to require molecular-genetic characterization of a patient’s endometriotic tissue. It also discusses the first-line status of gestagens in major guidelines (with level of evidence Ia) and provides specific examples of oral and parenteral progestins, including a focus on the investigational oral gestagen Gestobutanoyl and its reported anti-proliferative activity in preclinical assays, noting a need for safer and more effective progesterone analogs. This paper is centrally about endometriosis — it specifically reviews gestagens’ molecular and clinical rationale as first-line therapy for endometriosis.

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Abstract

Endometriosis occurs in 10% of females of reproductive age and ranks third among gynecological diseases, being one of the causes of infertility. The success of endometriosis treatment depends on individually selected therapy based on molecular-genetic characterization of the patient endometrial tissue. The review addresses the mechanisms of endometriosis development and the role of gestagens in the pathogenesis of this disease. We describe the genetic and epigenetic mechanisms of endometriosis development, which lead to resistance to endogenous progesterone, a key link in the pathogenesis of endometriosis. Because gestagen monotherapy is considered as first-line treatment, we analyze the gestagen properties that underlie the indications for their use in endometriosis. In particular, gestagen should have high gestagenic activity and an antiproliferative effect on target cells. An original domestic drug, an oral gestagen Gestobutanoil based on 17a-acetoxy-3b-butanoyloxy-6-methyl-pregna-4,6-dien-20-one (AMP-17), is promising for clinical use. The gestagenic activity of AMP-17 in the Clauberg-McPhail test is 102-fold higher than that of progesterone. AMP-17 has a pronounced antiproliferative effect on estrogen-dependent targets, such as breast cancer cells, cervical cancer cells, etc.

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Condition tags

endometriosisinfertility

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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