Catalog No.S1202 Synonyms: GI198745, GG-745
Molecular Weight(MW): 528.53
Dutasteride is a dual 5-α reductase inhibitor that inhibits conversion of testosterone to dihydrotestosterone (DHT).
Purity & Quality Control
Choose Selective 5-alpha Reductase Inhibitors
|Description||Dutasteride is a dual 5-α reductase inhibitor that inhibits conversion of testosterone to dihydrotestosterone (DHT).|
Dutasteride inhibits type-1 5AR and type-2 5AR with IC50 of 6 nM and 7 nM, respectively. Dutasteride is 60-fold more potent than Finasteride in its initial Ki versus type 1 5AR and ~5-fold more rapid in inactivating the enzyme.  Dutasteride inhibits (3)H-T conversion to (3)H-DHT and, as anticipated, inhibits T-induced secretion of PSA and proliferation in LNCaP cells. Dutasteride also inhibits DHT-induced PSA secretion and cell proliferation with IC50 of 1 μM in LNCaP cells. Dutasteride competes for binding the LNCaP cell AR with an IC50 of 1.5 μM. Dutasteride (10–50 μM) results in enhanced cell death, possibly by apoptosis, in steroid-free medium.  Dutasteride reduces cell viability and cell proliferation in androgen-responsive (LNCaP) and androgen-unresponsive (DU145) human prostate cancer(PCa) cell lines. Dutasteride results in overexpressed genes included genes encoding for proteins involved in biosynthesis and metabolism of androgen (HSD17B1;HSD17B3;CYP11B2), androgen receptor and androgen receptor co-regulators (AR;CCND1), and signal transduction(ERBB2; V-CAM; SOS1) whereas, underexpressed genes (KLK3; KLK2; DHCR24) are androgen-regulated genes (ARGs) in androgen-responsive (LNCaP) cell.  Dutasteride inhibits FASN mRNA, protein expression and enzymatic activity in prostate cancer cells. 
|In vivo||Dutasteride (100 mg/kg/day) has prostates about half as large as those in intact male rats treated with vehicle alone. Dutasteride is orally bioavailable and because of its mechanism of action it easily overcomes the potential liability of being >99% plasma protein bound. |
|In vitro||DMSO||62 mg/mL (117.3 mM)|
|Ethanol||6 mg/mL (11.35 mM)|
|In vivo||Add solvents to the product individually and in order:
2% DMSO+30% PEG 300+2% Tween 80+ddH2O
For best results, use promptly after mixing.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
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Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT00082043||Completed||Premenstrual Syndrome|PMS|Healthy|Depression||National Institute of Mental Health (NIMH)|National Institutes of Health Clinical Center (CC)||March 31, 2004||Phase 1|
|NCT02147964||Not yet recruiting||Gonadotropin Deficiency||University of Washington||January 2017||Phase 2|
|NCT02839122||Enrolling by invitation||Benign Prostate Hyperplasia||Yuyu Pharma, Inc.||May 2016||Phase 1|
|NCT02578953||Completed||Prostatic Hyperplasia||GlaxoSmithKline||September 2015||Phase 1|
|NCT02509104||Completed||Prostatic Hyperplasia||GlaxoSmithKline||July 2015||Phase 1|
|NCT02159690||Withdrawn||Prostate Cancer|Localized Prostate Cancer||Kenneth Pienta, MD|Prostate Cancer Foundation Norway|Johns Hopkins University||September 2014||Phase 2|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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