Identification
- Summary
Dutasteride is an antiandrogenic compound that is used for the treatment of symptomatic benign prostatic hyperplasia (BPH) in adult males by inhibiting 5-alpha reductase.
- Brand Names
- Avodart, Jalyn
- Generic Name
- Dutasteride
- DrugBank Accession Number
- DB01126
- Background
Dutasteride is an oral synthetic 4-azasteroid commonly marketed under the trade name Avodart. It is a novel dual 5α-reductase inhibitor that works by blocking both isoforms of 5α-reductase enzymes in a potent, selective, and irreversible manner.1 Type I and II 5α-reductase enzymes convert testosterone into dihydrotestosterone (DHT), a primary hormonal mediator that plays a role in the development and enlargement of the prostate gland. Dutasteride was approved by the FDA in 2001 for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men as monotherapy or in combination with the α-adrenergic antagonist tamsulosin to enhance the therapeutic response. Its clinical efficacy against benign prostate hyperplasia in male patients is comparable to that of finasteride, a specific type II 5α-reductase inhibitor. However, unlike finasteride, dutasteride is not yet indicated for the treatment of androgenic alopecia although it was demonstrated to be effective in several randomized, double-blind, placebo-controlled trials in androgenetic alopecia.3,4
- Type
- Small Molecule
- Groups
- Approved, Investigational
- Structure
Structure for Dutasteride (DB01126)
- Weight
- Average: 528.5297
Monoisotopic: 528.221147444 - Chemical Formula
- C27H30F6N2O2
- Synonyms
- (5α,17β)-N-(2,5-bis(trifluoromethyl)phenyl)-3-oxo-4-azaandrost-1-ene-17-carboxamide
- Dutasterida
- Dutasteride
- α,α,α,α',α',α'-hexafluoro-3-oxo-4-aza-5α-androst-1-ene-17β-carboxy-2',5'-xylidide
- External IDs
- GG-745
- GI 198745
- GI-198745
Pharmacology
- Indication
Indicated for the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate gland to improve symptoms, and reduce the risk of acute urinary retention and the need for BPH-related surgery alone or in combination with tamsulosin.15
Reduce drug development failure ratesBuild, train, & validate machine-learning modelswith evidence-based and structured datasets.Build, train, & validate predictive machine-learning models with structured datasets.- Associated Conditions
Indication Type Indication Combined Product Details Approval Level Age Group Patient Characteristics Dose Form Management of Benign prostatic hyperplasia •••••••••••• Used in combination to manage Symptomatic benign prostatic hyperplasia Combination Product in combination with: Tamsulosin (DB00706) •••••••••••• •••••••• •••••••• - Contraindications & Blackbox Warnings
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Dutasteride is a synthetic 4-azasteroid compound that selectively inhibits both the type I and type II isoforms of steroid 5α-reductase, an intracellular enzyme that converts testosterone to 5α-dihydrotestosterone (DHT). Dutasteride works by reducing the levels of circulating DHT. It was also shown to reduce the size of the prostate gland, improve urinary flow, and symptoms of benign prostatic hyperplasia alone or in combination with tamsulosin.14 The effect of the reduction of DHT by dutasteride is dose-dependent, with the maximum effect observed within 1-2 weeks following initial administration.15
After 1 and 2 weeks of daily dosing with dutasteride 0.5 mg, median serum DHT concentrations were reduced by 85% and 90%, respectively.15 The serum concentrations of DHT were maintained to be decreased by more than 90% in 85% of patients following 1 years' administration of oral dutasteride 0.5 mg/day.5 As evident from the clinical studies, dutasteride may also cause decreases in serum PSA in the presence of prostate cancer.15
- Mechanism of action
The 5α-reductase is a nuclear-bound steroid intracellular enzyme primarily located in the prostatic stromal cell that converts the androgen testosterone into the more active metabolite, 5α-dihydrotestosterone (DHT).7 DHT is considered to be the primary androgen playing a role in the initial development and subsequent enlargement of the prostate gland. It serves as the hormonal mediator for the hyperplasia upon accumulation within the prostate gland.8 DHT displays a higher affinity towards androgen receptors in the prostate gland compared to testosterone13 and by acting on the androgen receptors, DHT modulates genes that are responsible for cell proliferation.9 Responsible for the synthesis of approximately one-third of circulating DHT, type I 5α-reductase is predominant in the sebaceous glands of most regions of skin, including the scalp, and liver. The type II 5a-reductase isozyme is primarily found in the prostate, seminal vesicles, epididymides, and hair follicles as well as liver, and is responsible for two-thirds of circulating DHT.15 Due to its dual inhibition of both isoenzymes of 5α-reductase, dutasteride causes a near-complete suppression of DHT.6 Compared to a 70% reduction of serum DHT levels caused by finasteride, a near-complete suppression of serum DHT-more than 90% is seen with dutasteride.12
By forming a stable complex with both type II and type II 5α-reductase, dutasteride inhibits its enzymatic action of converting testosterone to 5α-dihydrotestosterone (DHT), which is the androgen primarily responsible for the initial development and subsequent enlargement of the prostate gland. It is proposed that DHT is the principal androgen responsible for prostatic growth in later life-normal masculinization of the external genitalia and maturation of the prostate gland during development-thus reducing the serum DHT levels results in reduced prostatic volume and increased epithelial apoptosis.11 Dutasteride is a competitive and specific inhibitor of both Type I and Type II 5α-reductase isoenzymes and when evaluated under in vitro and in vivo conditions, the dissociation of the drug from the drug-enzyme complex is reported to be extremely slow.15 Dutasteride does not bind to the human androgen receptor.15
Target Actions Organism A3-oxo-5-alpha-steroid 4-dehydrogenase 1 inhibitorHumans A3-oxo-5-alpha-steroid 4-dehydrogenase 2 inhibitorHumans - Absorption
Following oral administration of a single dose of 0.5 mg dutasteride, the peak serum concentrations were reached within 2 to 3 hours. Following daily oral administration of 0.5 mg dutasteride, the steady-state concentration of 40 ng/mL is expected to be achieved at 6 months following initial administration. In healthy subjects, the absolute bioavailability was 60%, ranging from 40% to 94%. While food intake reduced the maximum serum concentrations by 10 to 15%, food intake is reported to have a negligible effect on the bioavailability of the drug.15
- Volume of distribution
Dutasteride displays a large volume of distribution ranging from 300 to 500 L. Following daily oral administration of 0.5 mg dutasteride healthy subjects for 12 months, the semen dutasteride concentrations averaged 3.4 ng/mL (range: 0.4 to 14 ng/mL) with 11.5% of serum dutasteride concentrations being partitioned into semen.15
- Protein binding
Dutasteride is about 99% bound to albumin and 96.6% bound to α-1 acid glycoprotein in the serum.15
- Metabolism
Dutasteride undergoes extensive hepatic metabolism mediated by CYP3A4 and CYP3A5. 4′-hydroxydutasteride, 6-hydroxydutasteride, 6,4′-dihydroxydutasteride, 1,2-dihydrodutasteride, and 15-hydroxydutasteride metabolites are formed. 2 minor metabolites - 6,4′-dihydroxydutasteride and 15-hydroxydutasteride - can also be detected. According to in vitro studies, 4′-hydroxydutasteride and 1,2-dihydrodutasteride mediated inhibitory actions against both isoforms of 5α-reductase but with lower potency when compared to the parent drug. The activity of 6β-hydroxydutasteride is comparable to that of dutasteride.15
- Route of elimination
Dutasteride and its metabolites mainly undergo fecal excretion. About 1-15% of the dose is excreted as the unchanged parent compound, while 2-90% of the total dose is excreted in the form of dutasteride-related metabolites in the feces. Trace amounts of unchanged dutasteride, with less than 1%, can also be detected in the urine. Therefore, on average, the dose unaccounted for approximated 55%, with a range between 5% and 97%.15
- Half-life
The terminal elimination half-life of dutasteride is approximately 5 weeks at steady state. This long half-life accounts for the serum concentrations remaining detectable for up to 4 to 6 months after discontinuation of treatment.15
- Clearance
In a study of healthy volunteers receiving single oral doses of dutasteride ranging from 0.01 to 40 mg, dutasteride displayed a low linear clearance of 0.58 L/h. The estimated inter-individual variability for the linear clearance was high.10
- Adverse Effects
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LD50 values
The estimated dermal LD50 of dutasteride in rabbits is > 2,000 mg/kg.14
Overdose
In studies of volunteers receiving single doses of dutasteride up to 40 mg (which is 80 times the therapeutic dose) for 7 days, there were no reports of clinically significant adverse events.15 Low incidences of impotence, reduced libido, gynecomastia, and ejaculation disorder occurred significantly more often in dutasteride than placebo recipients.5 There are no known antidotes for dutasteride. In case of overdose, appropriate symptomatic and supportive treatment should be given.15
Nonclinical Toxicology
In a 2-year carcinogenicity mouse study, there was an increased incidence of benign hepatocellular adenomas in female mice receiving 250 mg/kg/day.15 An increased incidence of Leydig cell hyperplasia was observed in male rats receiving doses of 7.5 mg/kg/day and greater. At tumorogenic doses, the luteinizing hormone (LH) levels in rats were increased by 167%. There was no demonstrated a genotoxic potential of dutasteride or its metabolites in a bacterial mutagenesis assay, a chromosomal aberration assay in CHO cells, and a micronucleus assay in rats.15 At much higher doses than the maximum recommended human dose (MRHD) in sexually mature male rats, dutasteride caused a dose- and time-dependent decrease in fertility, reduced cauda epididymal (absolute) sperm counts but not sperm concentration (at 50 and 500 mg/kg/day), reduced weights of the epididymis, prostate, and seminal vesicles, and microscopic changes in the male reproductive organs.15 At exposures 425- and 315-fold the expected clinical exposure of dutasteride in rats and dogs, respectively, there were some signs of non-specific, reversible, centrally-mediated toxicity without associated histopathological changes. 15
Pregnancy and Lactation
As DHT is a necessary hormone for the development of male genitalia, exposure to dutasteride in pregnant women bearing male fetuses may cause fetal harm.15 In animal reproduction and developmental toxicity studies, dutasteride inhibited normal development of external genitalia in male fetuses.15 Although it is not known whether dutasteride is excreted in human milk, the use of dutasteride in women of childbearing potential, including nursing women.15 In elderly patients, the half-life of dutasteride may increase. As the renal elimination of dutasteride is very minimal, the use of dutasteride in patients renal insufficiency is reported to be safe.14 There are no specific dosage adjustment recommendations for use in elderly patients or patients with renal impairment.15
- Pathways
- Not Available
- Pharmacogenomic Effects/ADRs Browse all" title="About SNP Mediated Effects/ADRs" id="snp-actions-info" class="drug-info-popup" href="javascript:void(0);">
- Not Available
Interactions
- Drug Interactions Learn More" title="About Drug Interactions" id="structured-interactions-info" class="drug-info-popup" href="javascript:void(0);">
- This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.
Drug Interaction Integrate drug-drug
interactions in your softwareAbatacept The metabolism of Dutasteride can be increased when combined with Abatacept. Acalabrutinib The metabolism of Dutasteride can be decreased when combined with Acalabrutinib. Acebutolol Dutasteride may decrease the antihypertensive activities of Acebutolol. Aceclofenac The risk or severity of hypertension can be increased when Dutasteride is combined with Aceclofenac. Acemetacin The risk or severity of hypertension can be increased when Dutasteride is combined with Acemetacin. - Food Interactions
- Take with or without food. The absorption is unaffected by food.
Products
Drug product information from 10+ global regionsOur datasets provide approved product information including:dosage, form, labeller, route of administration, and marketing period.Access drug product information from over 10 global regions.- Product Images
- Brand Name Prescription Products
Name Dosage Strength Route Labeller Marketing Start Marketing End Region Image Act Dutasteride Capsule 0.5 mg Oral TEVA Canada Limited 2014-09-05 Not applicable Canada 
Avodart Capsule, liquid filled 0.5 mg/1 Oral Preferreed Pharmaceuticals Inc. 2002-12-10 2013-11-30 US 
Avodart Capsule, liquid filled 0.5 mg/1 Oral GlaxoSmithKline LLC 2002-12-10 2023-06-30 US 
Avodart Capsule, liquid filled 0.5 mg/1 Oral Woodward Pharma Services Llc 2022-12-15 Not applicable US Avodart Capsule 0.5 mg Oral Glaxosmithkline Inc 2003-11-14 Not applicable Canada - Generic Prescription Products
Name Dosage Strength Route Labeller Marketing Start Marketing End Region Image Ag-dutasteride Capsule 0.5 mg Oral Angita Pharma Inc. Not applicable Not applicable Canada Apo-dutasteride Capsule 0.5 mg Oral Apotex Corporation 2014-07-18 Not applicable Canada Auro-dutasteride Capsule 0.5 mg Oral Auro Pharma Inc 2018-06-04 Not applicable Canada Dutasteride Capsule, liquid filled 0.5 mg/1 Oral Golden State Medical Supply 2015-11-24 Not applicable US Dutasteride Capsule 0.5 mg/1 Oral Vensun Pharmaceuticals, Inc. 2018-06-29 Not applicable US - Mixture Products
Name Ingredients Dosage Route Labeller Marketing Start Marketing End Region Image Aglandin comp. 0,5 mg/0,4 mg-Hartkapseln Dutasteride (0.5 mg) + Tamsulosin hydrochloride (0.4 mg) Capsule Oral G.L. Pharma Gmb H 2019-01-16 Not applicable Austria 
Bakumokon 5% Minoxidil Dutasteride (0.1 mg/100mg) + Minoxidil (5 mg/100mg) + Oxytocin (0.01 mg/100mg) Liquid Topical DS LABORATORIES, INC. 2015-02-09 2017-10-19 US Bakumokon 7% Minoxidil Sulfate Dutasteride (0.1 mg/100mg) + Minoxidil sulfate (7 mg/100mg) + Oxytocin (0.01 mg/100mg) Liquid Topical DS LABORATORIES, INC. 2015-02-09 2017-10-11 US DUODART Dutasteride (0.5 MG) + Tamsulosin (0.4 MG) Capsule Oral บริษัท แกล็กโซสมิทไคล์น (ประเทศไทย) จำกัด 2018-09-24 Not applicable Thailand 
DUODART 0,5 MG/0,4 MG KAPSÜL,30 KAPSÜL Dutasteride (0.5 mg) + Tamsulosin hydrochloride (0.4 mg) Capsule Oral GLAXOSMİTHKLİNE İLAÇLARI SAN. VE TİC. A.Ş. 2020-08-14 2020-05-22 Turkey 
Categories
- ATC Codes
- G04CB02 — Dutasteride
- G04CB — Testosterone-5-alpha reductase inhibitors
- G04C — DRUGS USED IN BENIGN PROSTATIC HYPERTROPHY
- G04 — UROLOGICALS
- G — GENITO URINARY SYSTEM AND SEX HORMONES
- Drug Categories
- 5-alpha Reductase Inhibitors
- Adrenergic alpha-Antagonists
- Adrenergic Antagonists
- Agents that produce hypertension
- Azasteroids
- Cytochrome P-450 CYP3A Substrates
- Cytochrome P-450 CYP3A5 Substrates
- Cytochrome P-450 Substrates
- Drugs Used in Benign Prostatic Hypertrophy
- Enzyme Inhibitors
- Fused-Ring Compounds
- Genito Urinary System and Sex Hormones
- Hormone Antagonists
- Hormones, Hormone Substitutes, and Hormone Antagonists
- Steroid Synthesis Inhibitors
- Steroids
- Urologicals
- Chemical TaxonomyProvided by Classyfire
- Description
- This compound belongs to the class of organic compounds known as androgens and derivatives. These are 3-hydroxylated C19 steroid hormones. They are known to favor the development of masculine characteristics. They also show profound effects on scalp and body hair in humans.
- Kingdom
- Organic compounds
- Super Class
- Lipids and lipid-like molecules
- Class
- Steroids and steroid derivatives
- Sub Class
- Androstane steroids
- Direct Parent
- Androgens and derivatives
- Alternative Parents
- 3-oxo-5-alpha-steroids / 3-oxo-4-azasteroids / 4-azasteroids and derivatives / Trifluoromethylbenzenes / Anilides / N-arylamides / Secondary carboxylic acid amides / Lactams / Azacyclic compounds / Organopnictogen compounds show 5 more
- Substituents
- 3-oxo-4-azasteroid / 3-oxo-5-alpha-steroid / 3-oxosteroid / 4-azasteroid / Alkyl fluoride / Alkyl halide / Androgen-skeleton / Anilide / Aromatic heteropolycyclic compound / Azacycle show 21 more
- Molecular Framework
- Aromatic heteropolycyclic compounds
- External Descriptors
- delta-lactam, aza-steroid, (trifluoromethyl)benzenes (CHEBI:521033)
- Affected organisms
- Humans and other mammals
Chemical Identifiers
- UNII
- O0J6XJN02I
- CAS number
- 164656-23-9
- InChI Key
- JWJOTENAMICLJG-QWBYCMEYSA-N
- InChI
- InChI=1S/C27H30F6N2O2/c1-24-11-9-17-15(4-8-21-25(17,2)12-10-22(36)35-21)16(24)6-7-19(24)23(37)34-20-13-14(26(28,29)30)3-5-18(20)27(31,32)33/h3,5,10,12-13,15-17,19,21H,4,6-9,11H2,1-2H3,(H,34,37)(H,35,36)/t15-,16-,17-,19+,21+,24-,25+/m0/s1
- IUPAC Name
- (4aR,4bS,6aS,7S,9aS,9bS,11aR)-N-[2,5-bis(trifluoromethyl)phenyl]-4a,6a-dimethyl-2-oxo-1H,2H,4aH,4bH,5H,6H,6aH,7H,8H,9H,9aH,9bH,10H,11H,11aH-indeno[5,4-f]quinoline-7-carboxamide
- SMILES
- [H][C@@]1(CC[C@@]2([H])[C@]3([H])CC[C@@]4([H])NC(=O)C=C[C@]4(C)[C@@]3([H])CC[C@]12C)C(=O)NC1=CC(=CC=C1C(F)(F)F)C(F)(F)F
References
- Synthesis Reference
Manne Reddy, "Forms of dutasteride and methods for preparation thereof." U.S. Patent US20040077673, issued April 22, 2004.
US20040077673- General References
- Keam SJ, Scott LJ: Dutasteride: a review of its use in the management of prostate disorders. Drugs. 2008;68(4):463-85. [Article]
- Shah SK, Trump DL, Sartor O, Tan W, Wilding GE, Mohler JL: Phase II study of Dutasteride for recurrent prostate cancer during androgen deprivation therapy. J Urol. 2009 Feb;181(2):621-6. doi: 10.1016/j.juro.2008.10.014. Epub 2008 Dec 16. [Article]
- Arif T, Dorjay K, Adil M, Sami M: Dutasteride in Androgenetic Alopecia: An Update. Curr Clin Pharmacol. 2017;12(1):31-35. doi: 10.2174/1574884712666170310111125. [Article]
- Shanshanwal SJ, Dhurat RS: Superiority of dutasteride over finasteride in hair regrowth and reversal of miniaturization in men with androgenetic alopecia: A randomized controlled open-label, evaluator-blinded study. Indian J Dermatol Venereol Leprol. 2017 Jan-Feb;83(1):47-54. doi: 10.4103/0378-6323.188652. [Article]
- Evans HC, Goa KL: Dutasteride. Drugs Aging. 2003;20(12):905-16; discussion 917-8. doi: 10.2165/00002512-200320120-00005. [Article]
- Djavan B, Milani S, Fong YK: Dutasteride: a novel dual inhibitor of 5alpha-reductase for benign prostatic hyperplasia. Expert Opin Pharmacother. 2005 Feb;6(2):311-7. doi: 10.1517/14656566.6.2.311 . [Article]
- Smith AB, Carson CC: Finasteride in the treatment of patients with benign prostatic hyperplasia: a review. Ther Clin Risk Manag. 2009 Jun;5(3):535-45. Epub 2009 Jul 12. [Article]
- Wilson JD: The pathogenesis of benign prostatic hyperplasia. Am J Med. 1980 May;68(5):745-56. [Article]
- Carson C 3rd, Rittmaster R: The role of dihydrotestosterone in benign prostatic hyperplasia. Urology. 2003 Apr;61(4 Suppl 1):2-7. [Article]
- Gisleskog PO, Hermann D, Hammarlund-Udenaes M, Karlsson MO: The pharmacokinetic modelling of GI198745 (dutasteride), a compound with parallel linear and nonlinear elimination. Br J Clin Pharmacol. 1999 Jan;47(1):53-8. [Article]
- Thomson A: Dutasteride: an evidence-based review of its clinical impact in the treatment of benign prostatic hyperplasia. Core Evid. 2005;1(2):143-56. Epub 2005 Jun 30. [Article]
- Marihart S, Harik M, Djavan B: Dutasteride: a review of current data on a novel dual inhibitor of 5alpha reductase. Rev Urol. 2005 Fall;7(4):203-10. [Article]
- 34. (2012). In Rang and Dale's Pharmacology (7th ed., pp. 424). Edinburgh: Elsevier/Churchill Livingstone. [ISBN:978-0-7020-3471-8]
- Avodart (dutasteride capsules) - Product Monograph [Link]
- FDA Approved Drug Products: AVODART (dutasteride) capsules [Link]
- FDA Approved Drug Products: JALYN (dutasteride and tamsulosin hydrochloride) capsules [Link]
- External Links
- Human Metabolome Database
- HMDB0015258
- KEGG Drug
- D03820
- PubChem Compound
- 6918296
- PubChem Substance
- 46504830
- ChemSpider
- 5293502
- BindingDB
- 50340481
- 228790
- ChEBI
- 521033
- ChEMBL
- CHEMBL1200969
- ZINC
- ZINC000003932831
- Therapeutic Targets Database
- DAP000044
- PharmGKB
- PA164749300
- RxList
- RxList Drug Page
- Drugs.com
- Drugs.com Drug Page
- Wikipedia
- Dutasteride
- MSDS
- Download (37 KB)
Clinical Trials
- Clinical Trials Learn More" title="About Clinical Trials" id="clinical-trials-info" class="drug-info-popup" href="javascript:void(0);">
Phase Status Purpose Conditions Count 4 Completed Treatment Alcohol Abuse / Alcohol Dependency 2 4 Completed Treatment Benign Prostatic Hyperplasia (BPH) 4 4 Completed Treatment Benign Prostatic Hyperplasia (BPH) / Hypogonadism 1 4 Completed Treatment Benign Prostatic Hyperplasia (BPH) / Prostate Cancer 1 4 Completed Treatment Healthy Subjects (HS) 1
Pharmacoeconomics
- Manufacturers
- Not Available
- Packagers
- Catalent Pharma Solutions
- GlaxoSmithKline Inc.
- Letco Medical Inc.
- Murfreesboro Pharmaceutical Nursing Supply
- Physicians Total Care Inc.
- Preferred Pharmaceuticals Inc.
- Resource Optimization and Innovation LLC
- Santec Chemicals Corp.
- Dosage Forms
Form Route Strength Capsule Oral 0.500 mg Capsule, liquid filled Oral 0.5 mg/1 Liquid Topical Capsule Oral Capsule Oral 0.5 mg/1 Capsule, gelatin coated Oral 0.5 mg Capsule, liquid filled Oral 0.5 mg Capsule Oral Capsule, extended release Oral Capsule Oral 0.4 MG Capsule, delayed release pellets Oral Capsule, coated Oral Capsule Oral 0.500 mg Capsule Oral 0.5 mg - Prices
Unit description Cost Unit Avodart 0.5 mg capsule 4.12USD capsule Avodart 0.5 mg softgel 4.06USD softgel capsule DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.- Patents
Patent Number Pediatric Extension Approved Expires (estimated) Region US5846976 No 1998-12-08 2013-09-17 US CA2171329 No 2004-11-23 2014-09-16 Canada CA2170047 No 2004-11-09 2014-09-16 Canada US5565467 No 1996-10-15 2015-11-20 US
Properties
- State
- Solid
- Experimental Properties
Property Value Source melting point (°C) 242-250 MSDS, FDA Label water solubility Insoluble MSDS logP 6.8 Human Metabolome Database - Predicted Properties
Property Value Source Water Solubility 0.000908 mg/mL ALOGPS logP 5.45 ALOGPS logP 5.79 Chemaxon logS -5.8 ALOGPS pKa (Strongest Acidic) 12.56 Chemaxon pKa (Strongest Basic) -0.16 Chemaxon Physiological Charge 0 Chemaxon Hydrogen Acceptor Count 2 Chemaxon Hydrogen Donor Count 2 Chemaxon Polar Surface Area 58.2 Å2 Chemaxon Rotatable Bond Count 4 Chemaxon Refractivity 127.9 m3·mol-1 Chemaxon Polarizability 49.92 Å3 Chemaxon Number of Rings 5 Chemaxon Bioavailability 0 Chemaxon Rule of Five No Chemaxon Ghose Filter No Chemaxon Veber's Rule No Chemaxon MDDR-like Rule No Chemaxon - Predicted ADMET Features
Property Value Probability Human Intestinal Absorption + 1.0 Blood Brain Barrier + 0.9884 Caco-2 permeable - 0.5223 P-glycoprotein substrate Substrate 0.747 P-glycoprotein inhibitor I Inhibitor 0.7278 P-glycoprotein inhibitor II Non-inhibitor 0.6085 Renal organic cation transporter Non-inhibitor 0.8299 CYP450 2C9 substrate Non-substrate 0.8077 CYP450 2D6 substrate Non-substrate 0.9117 CYP450 3A4 substrate Substrate 0.7186 CYP450 1A2 substrate Non-inhibitor 0.8089 CYP450 2C9 inhibitor Inhibitor 0.5412 CYP450 2D6 inhibitor Non-inhibitor 0.8391 CYP450 2C19 inhibitor Inhibitor 0.6287 CYP450 3A4 inhibitor Non-inhibitor 0.6506 CYP450 inhibitory promiscuity Low CYP Inhibitory Promiscuity 0.5913 Ames test Non AMES toxic 0.6677 Carcinogenicity Non-carcinogens 0.9149 Biodegradation Not ready biodegradable 1.0 Rat acute toxicity 2.6885 LD50, mol/kg Not applicable hERG inhibition (predictor I) Weak inhibitor 0.9829 hERG inhibition (predictor II) Non-inhibitor 0.574
Spectra
- Mass Spec (NIST)
- Not Available
- Spectra
- Chromatographic Properties
Collision Cross Sections (CCS)
Adduct CCS Value (Å2) Source type Source [M-H]- 222.2239267 predictedDarkChem Lite v0.1.0 [M-H]- 215.29892 predictedDeepCCS 1.0 (2019) [M+H]+ 220.9456267 predictedDarkChem Lite v0.1.0 [M+H]+ 217.19432 predictedDeepCCS 1.0 (2019) [M+Na]+ 219.5823267 predictedDarkChem Lite v0.1.0 [M+Na]+ 223.18266 predictedDeepCCS 1.0 (2019)
Targets
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Inhibitor
- General Function
- Electron carrier activity
- Specific Function
- Converts testosterone into 5-alpha-dihydrotestosterone and progesterone or corticosterone into their corresponding 5-alpha-3-oxosteroids. It plays a central role in sexual differentiation and andro...
- Gene Name
- SRD5A1
- Uniprot ID
- P18405
- Uniprot Name
- 3-oxo-5-alpha-steroid 4-dehydrogenase 1
- Molecular Weight
- 29458.18 Da
References
- Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [Article]
- Xu Y, Dalrymple SL, Becker RE, Denmeade SR, Isaacs JT: Pharmacologic basis for the enhanced efficacy of dutasteride against prostatic cancers. Clin Cancer Res. 2006 Jul 1;12(13):4072-9. [Article]
- Rathnayake D, Sinclair R: Male androgenetic alopecia. Expert Opin Pharmacother. 2010 Jun;11(8):1295-304. doi: 10.1517/14656561003752730. [Article]
- Aggarwal S, Thareja S, Verma A, Bhardwaj TR, Kumar M: An overview on 5alpha-reductase inhibitors. Steroids. 2010 Feb;75(2):109-53. doi: 10.1016/j.steroids.2009.10.005. Epub 2009 Oct 30. [Article]
- Smith AB, Carson CC: Finasteride in the treatment of patients with benign prostatic hyperplasia: a review. Ther Clin Risk Manag. 2009 Jun;5(3):535-45. Epub 2009 Jul 12. [Article]
- Goldenberg L, So A, Fleshner N, Rendon R, Drachenberg D, Elhilali M: The role of 5-alpha reductase inhibitors in prostate pathophysiology: Is there an additional advantage to inhibition of type 1 isoenzyme? Can Urol Assoc J. 2009 Jun;3(3 Suppl 2):S109-14. [Article]
- Keam SJ, Scott LJ: Dutasteride: a review of its use in the management of prostate disorders. Drugs. 2008;68(4):463-85. [Article]
- Rittmaster RS, Fleshner NE, Thompson IM: Pharmacological approaches to reducing the risk of prostate cancer. Eur Urol. 2009 May;55(5):1064-73. doi: 10.1016/j.eururo.2009.01.037. Epub 2009 Feb 5. [Article]
- Shah SK, Trump DL, Sartor O, Tan W, Wilding GE, Mohler JL: Phase II study of Dutasteride for recurrent prostate cancer during androgen deprivation therapy. J Urol. 2009 Feb;181(2):621-6. doi: 10.1016/j.juro.2008.10.014. Epub 2008 Dec 16. [Article]
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- Yes
- Actions
- Inhibitor
- General Function
- Sterol 5-alpha reductase activity
- Specific Function
- Converts testosterone (T) into 5-alpha-dihydrotestosterone (DHT) and progesterone or corticosterone into their corresponding 5-alpha-3-oxosteroids. It plays a central role in sexual differentiation...
- Gene Name
- SRD5A2
- Uniprot ID
- P31213
- Uniprot Name
- 3-oxo-5-alpha-steroid 4-dehydrogenase 2
- Molecular Weight
- 28393.015 Da
References
- Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [Article]
- Rathnayake D, Sinclair R: Male androgenetic alopecia. Expert Opin Pharmacother. 2010 Jun;11(8):1295-304. doi: 10.1517/14656561003752730. [Article]
- Aggarwal S, Thareja S, Verma A, Bhardwaj TR, Kumar M: An overview on 5alpha-reductase inhibitors. Steroids. 2010 Feb;75(2):109-53. doi: 10.1016/j.steroids.2009.10.005. Epub 2009 Oct 30. [Article]
- Smith AB, Carson CC: Finasteride in the treatment of patients with benign prostatic hyperplasia: a review. Ther Clin Risk Manag. 2009 Jun;5(3):535-45. Epub 2009 Jul 12. [Article]
- Goldenberg L, So A, Fleshner N, Rendon R, Drachenberg D, Elhilali M: The role of 5-alpha reductase inhibitors in prostate pathophysiology: Is there an additional advantage to inhibition of type 1 isoenzyme? Can Urol Assoc J. 2009 Jun;3(3 Suppl 2):S109-14. [Article]
- Keam SJ, Scott LJ: Dutasteride: a review of its use in the management of prostate disorders. Drugs. 2008;68(4):463-85. [Article]
- Xu Y, Dalrymple SL, Becker RE, Denmeade SR, Isaacs JT: Pharmacologic basis for the enhanced efficacy of dutasteride against prostatic cancers. Clin Cancer Res. 2006 Jul 1;12(13):4072-9. [Article]
- Rittmaster RS, Fleshner NE, Thompson IM: Pharmacological approaches to reducing the risk of prostate cancer. Eur Urol. 2009 May;55(5):1064-73. doi: 10.1016/j.eururo.2009.01.037. Epub 2009 Feb 5. [Article]
- Shah SK, Trump DL, Sartor O, Tan W, Wilding GE, Mohler JL: Phase II study of Dutasteride for recurrent prostate cancer during androgen deprivation therapy. J Urol. 2009 Feb;181(2):621-6. doi: 10.1016/j.juro.2008.10.014. Epub 2008 Dec 16. [Article]
Enzymes
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- No
- Actions
- Substrate
- General Function
- Oxygen binding
- Specific Function
- Cytochromes P450 are a group of heme-thiolate monooxygenases. In liver microsomes, this enzyme is involved in an NADPH-dependent electron transport pathway. It oxidizes a variety of structurally un...
- Gene Name
- CYP3A5
- Uniprot ID
- P20815
- Uniprot Name
- Cytochrome P450 3A5
- Molecular Weight
- 57108.065 Da
References
- Avodart (dutasteride capsules) - Product Monograph [Link]
Carriers
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- No
- Actions
- Binder
- General Function
- Toxic substance binding
- Specific Function
- Serum albumin, the main protein of plasma, has a good binding capacity for water, Ca(2+), Na(+), K(+), fatty acids, hormones, bilirubin and drugs. Its main function is the regulation of the colloid...
- Gene Name
- ALB
- Uniprot ID
- P02768
- Uniprot Name
- Serum albumin
- Molecular Weight
- 69365.94 Da
- Kind
- Protein
- Organism
- Humans
- Pharmacological action
- No
- Actions
- Binder
- General Function
- Not Available
- Specific Function
- Functions as transport protein in the blood stream. Binds various ligands in the interior of its beta-barrel domain. Also binds synthetic drugs and influences their distribution and availability in...
- Gene Name
- ORM1
- Uniprot ID
- P02763
- Uniprot Name
- Alpha-1-acid glycoprotein 1
- Molecular Weight
- 23511.38 Da
Transporters
- Kind
- Protein
- Organism
- Mouse
- Pharmacological action
- Unknown
- Actions
- Binder
- General Function
- Amine transporter. Terminates the action of dopamine by its high affinity sodium-dependent reuptake into presynaptic terminals.
- Specific Function
- Dopamine binding
- Gene Name
- Slc6a3
- Uniprot ID
- Q61327
- Uniprot Name
- Sodium-dependent dopamine transporter
- Molecular Weight
- 68804.71 Da
References
- Litim N, Bourque M, Al Sweidi S, Morissette M, Di Paolo T: The 5alpha-reductase inhibitor Dutasteride but not Finasteride protects dopamine neurons in the MPTP mouse model of Parkinson's disease. Neuropharmacology. 2015 Oct;97:86-94. doi: 10.1016/j.neuropharm.2015.05.015. Epub 2015 May 23. [Article]
- Kind
- Protein
- Organism
- Mouse
- Pharmacological action
- Unknown
- Actions
- Binder
- General Function
- Involved in the ATP-dependent vesicular transport of biogenic amine neurotransmitters. Pumps cytosolic monoamines including dopamine, norepinephrine, serotonin, and histamine into synaptic vesicles. Requisite for vesicular amine storage prior to secretion via exocytosis (By similarity).
- Specific Function
- Amine transmembrane transporter activity
- Gene Name
- Slc18a2
- Uniprot ID
- Q8BRU6
- Uniprot Name
- Synaptic vesicular amine transporter
- Molecular Weight
- 55753.05 Da
References
- Litim N, Bourque M, Al Sweidi S, Morissette M, Di Paolo T: The 5alpha-reductase inhibitor Dutasteride but not Finasteride protects dopamine neurons in the MPTP mouse model of Parkinson's disease. Neuropharmacology. 2015 Oct;97:86-94. doi: 10.1016/j.neuropharm.2015.05.015. Epub 2015 May 23. [Article]
Drug created at June 13, 2005 13:24 / Updated at February 20, 2024 23:55