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Dutasteride

MCE China：Dutasteride

Brand：MedChemExpress (MCE)

Cat. No.HY-13613

CAS：164656-23-9

Synonyms：GG 745; GI 198745

Purity：99.83%

Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year

Shipping：Room temperature in continental US; may vary elsewhere.

Description：Dutasteride (GG745) is a potent inhibitor of both 5α-reductase isozymes. Dutasteride may possess off-target effects on the androgen receptor (AR) due to its structural similarity to DHT.

In Vitro：Dutasteride inhibits 3H-T conversion to 3H-DHT and, as anticipated, inhibits T-induced secretion of PSA and proliferation. However the drug also inhibited DHT-induced PSA secretion and cell proliferation (IC50 approximately 1 μM)[1]. Dutasteride competes for binding the LNCaP cell AR with an IC50 approximately 1.5 μM. High concentrations of dutasteride (10-50 μM), but not finasteride, in steroid-free medium, resulted in enhanced cell death, possibly by apoptosis[1]. Dutasteride reduces cell viability and cell proliferation in both cell lines tested (androgen-responsive (LNCaP) and androgen-unresponsive (DU145) human prostate cancer (PCa)) [2].

In Vivo：GG745 has a terminal half-life of approximately 240 hr, and single doses of >10 mg decreased DHT levels significantly more than did single 5-mg doses of finasteride[3].In placebo treated men without prostate cancer there was an 8.3% median increase in PSA at month 24 compared with -59.5% in those who received dutasteride, using doubled values to correct for dutasteride treatment[4]. Toxicity: Dutasteride may affect male fertility and steroid hormone dynamics. Therefore, a 21-day reproduction study was conducted to determine the effects of dutasteride (10, 32 and 100 μg/L) on fish reproduction. Exposure to dutasteride significantly reduced fecundity of fish and affected several aspects of reproductive endocrine functions in both males and females[5].

IC50 & Target：IC50: 5 alpha-reductase[1] In Vitro Dutasteride inhibits 3H-T conversion to 3H-DHT and, as anticipated, inhibits T-induced secretion of PSA and proliferation. However the drug also inhibited DHT-induced PSA secretion and cell proliferation (IC50 approximately 1 μM)[1]. Dutasteride competes for binding the LNCaP cell AR with an IC50 approximately 1.5 μM. High concentrations of dutasteride (10-50 μM), but not finasteride, in steroid-free medium, resulted in enhanced cell death, possibly by apoptosis[1]. Dutasteride reduces cell viability and cell proliferation in both cell lines tested (androgen-responsive (LNCaP) and androgen-unresponsive (DU145) human prostate cancer (PCa)) [2]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> Dutasteride Related Antibodies

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References：

[1]. Lazier CB, et al. Dutasteride, the dual 5alpha-reductase inhibitor, inhibits androgen action and promotes cell death in the LNCaP prostate cancer cell line. Prostate. 2004 Feb 1;58(2):130-44.  [Content Brief]

[2]. Biancolella M, et al. Effects of dutasteride on the expression of genes related to androgen metabolism and related pathway in human prostate cancer cell lines. Invest New Drugs. 2007 Oct;25(5):491-7.  [Content Brief]

[3]. Bramson HN, et al. Unique preclinical characteristics of GG745, a potent dual inhibitor of 5AR. J Pharmacol Exp Ther. 1997 Sep;282(3):1496-502.  [Content Brief]

[4]. Andriole GL, et al. Clinical usefulness of serum prostate specific antigen for the detection of prostate cancer is preserved in men receiving the dual 5alpha-reductase inhibitor dutasteride. J Urol. 2006 May;175(5):1657-62.  [Content Brief]

[5]. Margiotta-Casaluci L, et al. Mode of action of human pharmaceuticals in fish: the effects of the 5-alpha-reductase inhibitor, dutasteride, on reproduction as a case study. Aquat Toxicol. 2013 Mar 15;128-129:113-23.  [Content Brief]