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Last update 08 May 2025

17β-HSD3

Last update 08 May 2025

Basic Info

Synonyms

17-beta-HSD 3, 17-beta-hydroxysteroid dehydrogenase type 3, EDH17B3

+ [7]

Introduction

Catalyzes the conversion of 17-oxosteroids to 17beta-hydroxysteroids (PubMed:16216911, PubMed:26545797, PubMed:27927697, PubMed:8075637). Favors the reduction of androstenedione to testosterone (PubMed:16216911, PubMed:26545797, PubMed:27927697). Testosterone is the key androgen driving male development and function (PubMed:8075637). Uses NADPH while the two other EDH17B enzymes use NADH (PubMed:16216911, PubMed:26545797, PubMed:8075637). Androgens such as epiandrosterone, dehydroepiandrosterone, androsterone and androstanedione are accepted as substrates and reduced at C-17 (PubMed:16216911). Can reduce 11-ketoandrostenedione as well as 11beta-hydroxyandrostenedione at C-17 to the respective testosterone forms (PubMed:16216911, PubMed:27927697).

Drugs associated with 17β-HSD3

STX1383

Target

17β-HSD3

Mechanism

17β-HSD3 inhibitors

Active Org.-

Originator Org.

Sterix Ltd.

Active Indication-

Inactive Indication

Hormone-dependent prostate cancer

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

STX2171

Target

17β-HSD3

Mechanism

17β-HSD3 inhibitors

Active Org.-

Originator Org.

Sterix Ltd.

Active Indication-

Inactive Indication

Hormone-dependent prostate cancer

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

BMS-856

Target

17β-HSD3

Mechanism

17β-HSD3 inhibitors

Active Org.-

Originator Org.

Bristol Myers Squibb Co.

Active Indication-

Inactive Indication

Prostatic Cancer

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with 17β-HSD3

100 Translational Medicine associated with 17β-HSD3

0 Patents (Medical) associated with 17β-HSD3

557

Literatures (Medical) associated with 17β-HSD3

01 Aug 2025·Tissue and Cell

Vitamin D alleviates chronic stress-induced testicular steroidogenesis disruption in Wistar rats

Article

Author: Chaudhary, Rishabh ; Kushwaha, Sapana ; Mishra, Vikas ; Srivastava, Siddhi ; Agarwal, Vipul ; Rehman, Mujeeba ; Kaushik, Arjun Singh ; Srivastava, Sukriti

Stress is associated with various health issues. Research has highlighted the relationship between chronic stress and male reproductive health. One of the primary mechanisms underlying stress-induced male reproductive dysfunction is impaired steroidogenesis. In the present study, we validated a chronic unpredictable stress (CUS) model and investigated testicular dysfunction in CUS rats. The CUS paradigm involved exposing rats to a variety of stressors daily for 8 weeks. Vitamin D (10 µg/kg/twice a week, p.o) was administered to CUS rats starting 2 weeks after the onset of stress exposure and continued until the end of study. The stress in rats was confirmed by the occurrence of anxiety and depressive-like behaviours through elevated plus-maze test & novelty-suppressed feeding test and rise in serum corticosterone levels. Testicular dysfunction in CUS rats was assessed via serum gonadotropins, testosterone, cytokines, oxidative stress, and testis-epididymis-sperm morphology. The reduction in steroidogenesis was confirmed via immunohistochemical analysis of 17β-hydroxysteroid dehydrogenase-3 (17β-HSD3), steroidogenic acute regulatory gene (StAR) and vitamin D receptor (VDR) expression. Further, we studied the role of vitamin D in alleviating stress-induced testicular damage and the potential mechanisms underlying steroidogenic alterations in CUS rats. Notably, vitamin D treatment prevented CUS-induced decline in testicular 17β-HSD3, StAR and VDR expression. Moreover, vitamin D ameliorated the CUS-induced reduction in serum testosterone levels. Histological assessment revealed that vitamin D prevented CUS-induced damage in sperm, testis and epididymis morphology. In conclusion, our findings suggest that CUS exposure induces testicular dysfunction, which can be prevented by vitamin D, potentially through the regulation of steroidogenic pathways.

01 Jul 2025·The Journal of Steroid Biochemistry and Molecular Biology

Production of 11-ketotestosterone in childhood adrenal tumors with virilization or peripheral precocious puberty: Dominant expression of 11β-hydroxysteroid dehydrogenase type 2

Article

Author: Fujisawa, Yasuko ; Sakaguchi, Kimiyoshi ; Murai, Yuki ; Kinjo, Kenichi ; Oyama, Ibuki ; Ogata, Tsutomu ; Ikeda, Maiko ; Tanikawa, Wataru ; Masunaga, Yohei ; Sano, Shinichiro

11-Oxygenated androgens are important components of the androgen pool in humans. Among them, 11-ketotestosterone (11-KT), a potent 11-oxygenated androgen primarily produced in peripheral tissues outside the adrenal glands, has garnered research interest for its crucial role in several diseases associated with androgen excess. This study aimed to investigate the biosynthesis of 11-oxygenated androgens, particularly 11-KT, in childhood adrenocortical tumors (ACTs) presenting with symptoms of androgen excess. This retrospective study included three patients, aged 6 months, 2 years, and 12 years, presenting with symptoms of androgen excess due to childhood ACTs. Multiple androgen metabolites were simultaneously measured using pre- or postoperative serum samples, tumors, and tumor-attached adrenal glands obtained from patients using liquid chromatography-tandem mass spectrometry. The expression of genes involved in androgen synthesis was analyzed using DNA microarray analysis. Serum androgen levels were elevated prior to tumor removal and decreased to within or near reference ranges after tumor removal. Notably, serum 11-KT levels were markedly elevated compared to reference ranges, similar to testosterone (T), and 11-KT was abundant within the tumor tissues. Unique gene expression patterns were observed across the three cases of childhood ACTs, including marked HSD11B2, attenuated HSD11B1, and elevated HSD17B3 expression levels, which are involved in 11-KT biosynthesis. This study confirms the direct production of 11-KT in childhood ACTs; gene expression patterns observed in these cases favored 11-KT biosynthesis, providing insight into their potential role in androgen excess.

01 Jun 2025·General and Comparative Endocrinology

Characterization of a direct role of GnRHs in the control of spermiogenesis and steroidogenesis in the small-spotted catshark Scyliorhinus canicula

Review

Author: Dufour, Sylvie ; Pilet, Stanislas ; Bernay, Benoît ; Delépée, Raphaël ; Lagadu, Stéphanie ; Jeanne, Fabian ; Sourdaine, Pascal

Hypothalamic gonadotropin-releasing hormone (GnRH) regulates the production of gonadotropins, which control reproduction. In elasmobranchs, unlike other gnathostomes, GnRH is released into the systemic circulation to stimulate gonadotrope cells located in the ventral lobe of the pituitary. The aim of this study was to investigate the potential role of systemic GnRH in the regulation of the testis in Scyliorhinus canicula. Phylogeny and synteny analyses identified three GnRHs and four GnRH receptor (ScGnRHR-I1, -IIa1, -IIa2 and -IIb2). In vitro functional hormone-receptor interactions using synthetic ScGnRHs showed that all ScGnRHs were effective at receptors, except ScGnRHRIIa2, at femtomolar to nanomolar concentrations, with lower efficiency for ScGnRH1/ScGnRHRIIb2. Real-time PCR analyses in a wide range of tissues, including male and female reproductive tracts, showed that all three gnrh were expressed mainly in the brain and all four gnrhr were expressed in the testis, particularly during spermiogenesis. Testicular explants containing cysts with spermatids were treated with ScGnRHs and their protein content analyzed by NanoLC-ESI-MS/MS, highlighting 1677 significantly differentially expressed proteins. Among them, the growth hormone receptor (GHR) and proteins involved in cholesterol and steroid metabolism, including several HSD17bs, were upregulated. In situ hybridization showed that ghr, hsd17b3 and hsd17b12 transcripts were localized in Sertoli cells, which are the main testicular steroidogenic cells in S. canicula. Fifteen steroids were assayed in the culture media, using LC-ESI-HRMS/MS, and an increase in 17β-estradiol concentrations was observed, consistent with hsd17b expressions. Furthermore, proteins involved in transcription and DNA structure were downregulated in response to GnRHs. In conclusion, this study showed that ScGnRHs may play a direct role in the regulation of elasmobranch testes by promoting spermiogenesis and modulating steroidogenesis.

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