Identification

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Name
Dutasteride
Accession Number
DB01126  (APRD00385)
Type
Small Molecule
Groups
Approved, Investigational
Description

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

Structure
Thumb
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
Product Images
Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
Act DutasterideCapsuleOralTEVA Canada Limited2014-09-05Not applicableCanada
AvodartCapsule0.5 mgOralGlaxosmithkline Inc2003-11-14Not applicableCanada
AvodartCapsule, liquid filled0.5 mg/1OralAvera McKennan Hospital2015-03-232018-05-22Us69189 071220180907 15195 1tvib44
AvodartCapsule, liquid filled0.5 mg/1OralGlaxoSmithKline LLC2002-12-10Not applicableUs00173 0712 02 nlmimage10 32191978
AvodartCapsule, liquid filled0.5 mg/1OralPreferreed Pharmaceuticals Inc.2002-12-102013-11-30Us
AvodartCapsule, liquid filled0.5 mg/1OralPhysicians Total Care, Inc.2004-07-16Not applicableUs54868 511420180907 15195 1wntyr8
AvodartCapsule, liquid filled0.5 mg/1OralLake Erie Medical &Surgical Supply Dba Quality Care Products Llc2012-03-262016-12-31Us
AvodartCapsule, liquid filled0.5 mg/1OralA-S Medication Solutions2002-12-10Not applicableUs54569 660720180907 15195 z78nd1
DutasterideCapsule0.5 mgOralSanis Health Inc2015-07-21Not applicableCanada
DutasterideCapsule, liquid filled0.5 mg/1OralGlaxoSmithKline LLC2015-02-19Not applicableUs
Additional Data Available
  • Application Number
    Application Number

    A unique ID assigned by the FDA when a product is submitted for approval by the labeller.

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  • Product Code
    Product Code

    A governmentally-recognized ID which uniquely identifies the product within its regulatory market.

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Generic Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
Ag-dutasterideCapsuleOralAngita Pharma Inc.Not applicableNot applicableCanada
Apo-dutasterideCapsuleOralApotex Corporation2014-07-18Not applicableCanada
Auro-dutasterideCapsuleOralAuro Pharma Inc2018-06-04Not applicableCanada
DutasterideCapsule, liquid filled0.5 mg/1OralNucare Pharmaceuticals,inc.2017-11-28Not applicableUs
DutasterideCapsule0.5 mg/1OralA-S Medication Solutions2015-11-02Not applicableUs
DutasterideCapsule, liquid filled0.5 mg/1OralREMEDYREPACK INC.2019-10-23Not applicableUs
DutasterideCapsule, liquid filled0.5 mg/1OralNucare Pharmaceuticals,inc.2015-11-25Not applicableUs
DutasterideCapsule, liquid filled0.5 mg/1OralGolden State Medical Supply Inc.2016-10-24Not applicableUs
DutasterideCapsule, liquid filled0.5 mg/1OralIntergel Pharmaceuticals Inc2002-12-10Not applicableUs
DutasterideCapsule0.5 mg/1OralViona Pharmaceuticals Inc2019-04-15Not applicableUs
Additional Data Available
  • Application Number
    Application Number

    A unique ID assigned by the FDA when a product is submitted for approval by the labeller.

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  • Product Code
    Product Code

    A governmentally-recognized ID which uniquely identifies the product within its regulatory market.

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Mixture Products
NameIngredientsDosageRouteLabellerMarketing StartMarketing End
Bakumokon 5% MinoxidilDutasteride (0.1 mg/100mg) + Minoxidil (5 mg/100mg) + Oxytocin (0.01 mg/100mg)LiquidTopicalDS LABORATORIES, INC.2015-02-092017-10-19Us
Bakumokon 7% Minoxidil SulfateDutasteride (0.1 mg/100mg) + Minoxidil sulfate (7 mg/100mg) + Oxytocin (0.01 mg/100mg)LiquidTopicalDS LABORATORIES, INC.2015-02-092017-10-11Us
Dutasteride and tamsulosin hydrochlorideDutasteride (0.5 mg/1) + Tamsulosin hydrochloride (0.4 mg/1)CapsuleOralCadila Healthcare Limited2018-06-04Not applicableUs
Dutasteride and tamsulosin hydrochlorideDutasteride (0.5 mg/1) + Tamsulosin hydrochloride (0.4 mg/1)CapsuleOralZydus Pharmaceuticals (USA) Inc.2018-06-04Not applicableUs
Dutasteride and tamsulosin hydrochlorideDutasteride (0.5 mg/1) + Tamsulosin hydrochloride (0.4 mg/1)CapsuleOralActavis Pharma, Inc.2016-04-13Not applicableUs
Dutasteride and Tamsulosin HydrochlorideDutasteride (0.5 mg/1) + Tamsulosin hydrochloride (0.4 mg/1)CapsuleOralPar Pharmaceutical, Inc.2015-11-18Not applicableUs
Dutasteride and Tamsulosin HydrochlorideDutasteride (0.5 mg/1) + Tamsulosin hydrochloride (0.4 mg/1)CapsuleOralPrasco Laboratories2016-07-01Not applicableUs
JalynDutasteride (0.5 mg/1) + Tamsulosin hydrochloride (0.4 mg/1)CapsuleOralPhysicians Total Care, Inc.2012-05-02Not applicableUs54868 632820180907 15195 11okuzb
JalynDutasteride (0.5 mg) + Tamsulosin hydrochloride (0.4 mg)Capsule, extended releaseOralGlaxosmithkline Inc2011-11-17Not applicableCanada
JalynDutasteride (0.5 mg/1) + Tamsulosin hydrochloride (0.4 mg/1)CapsuleOralGlaxoSmithKline LLC2010-06-21Not applicableUs00173 0809 61 nlmimage10 d11968cb
Categories
UNII
O0J6XJN02I
CAS number
164656-23-9
Weight
Average: 528.5297
Monoisotopic: 528.221147444
Chemical Formula
C27H30F6N2O2
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
(1S,2R,7R,10S,11S,14S,15S)-N-[2,5-bis(trifluoromethyl)phenyl]-2,15-dimethyl-5-oxo-6-azatetracyclo[8.7.0.0²,⁷.0¹¹,¹⁵]heptadec-3-ene-14-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

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

Associated Conditions
Pharmacodynamics

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

TargetActionsOrganism
A3-oxo-5-alpha-steroid 4-dehydrogenase 2
inhibitor
Humans
A3-oxo-5-alpha-steroid 4-dehydrogenase 1
inhibitor
Humans
Additional Data Available
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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

Toxicity

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

Affected organisms
  • Humans and other mammals
Pathways
Not Available
Pharmacogenomic Effects/ADRs
Not Available

Interactions

Drug Interactions
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.
DrugInteraction
1-benzylimidazoleThe risk or severity of hypertension can be increased when Dutasteride is combined with 1-benzylimidazole.
2,5-Dimethoxy-4-ethylamphetamineThe therapeutic efficacy of Dutasteride can be decreased when used in combination with 2,5-Dimethoxy-4-ethylamphetamine.
2,5-Dimethoxy-4-ethylthioamphetamineThe therapeutic efficacy of Dutasteride can be decreased when used in combination with 2,5-Dimethoxy-4-ethylthioamphetamine.
4-Bromo-2,5-dimethoxyamphetamineThe therapeutic efficacy of Dutasteride can be decreased when used in combination with 4-Bromo-2,5-dimethoxyamphetamine.
4-Bromo-2,5-dimethoxyphenethylamineThe therapeutic efficacy of 4-Bromo-2,5-dimethoxyphenethylamine can be decreased when used in combination with Dutasteride.
4-MethoxyamphetamineThe risk or severity of hypertension can be increased when Dutasteride is combined with 4-Methoxyamphetamine.
5-methoxy-N,N-dimethyltryptamineThe risk or severity of hypertension can be increased when Dutasteride is combined with 5-methoxy-N,N-dimethyltryptamine.
AbataceptThe metabolism of Dutasteride can be increased when combined with Abatacept.
AbediterolThe risk or severity of hypertension can be increased when Dutasteride is combined with Abediterol.
AcalabrutinibThe metabolism of Dutasteride can be decreased when combined with Acalabrutinib.
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    Severity

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Food Interactions
  • Take with or without food. The absorption is unaffected by food.

References

Synthesis Reference

Manne Reddy, "Forms of dutasteride and methods for preparation thereof." U.S. Patent US20040077673, issued April 22, 2004.

US20040077673
General References
  1. Keam SJ, Scott LJ: Dutasteride: a review of its use in the management of prostate disorders. Drugs. 2008;68(4):463-85. [PubMed:18318566]
  2. 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. [PubMed:19091347]
  3. 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. [PubMed:28294070]
  4. 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. [PubMed:27549867]
  5. Evans HC, Goa KL: Dutasteride. Drugs Aging. 2003;20(12):905-16; discussion 917-8. doi: 10.2165/00002512-200320120-00005. [PubMed:14565784]
  6. 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 . [PubMed:15757426]
  7. 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. [PubMed:19707263]
  8. Wilson JD: The pathogenesis of benign prostatic hyperplasia. Am J Med. 1980 May;68(5):745-56. [PubMed:6155068]
  9. Carson C 3rd, Rittmaster R: The role of dihydrotestosterone in benign prostatic hyperplasia. Urology. 2003 Apr;61(4 Suppl 1):2-7. [PubMed:12657354]
  10. 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. [PubMed:10073740]
  11. 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. [PubMed:22500150]
  12. 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. [PubMed:16985831]
  13. 34. (2012). In Rang and Dale's Pharmacology (7th ed., pp. 424). Edinburgh: Elsevier/Churchill Livingstone. [ISBN:978-0-7020-3471-8]
  14. Avodart (dutasteride capsules) - Product Monograph [Link]
  15. AVODART (dutasteride) Capsules - FDA Label [Link]
External Links
Human Metabolome Database
HMDB0015258
KEGG Drug
D03820
PubChem Compound
6918296
PubChem Substance
46504830
ChemSpider
5293502
BindingDB
50340481
RxNav
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
ATC Codes
G04CB02 — DutasterideG04CA52 — Tamsulosin and dutasteride
AHFS Codes
  • 92:08.00 — 5 Alfa Reductase Inhibitors
MSDS
Download (37 KB)

Clinical Trials

Clinical Trials
PhaseStatusPurposeConditionsCount
1CompletedNot AvailableBenign Prostatic Hyperplasia (BPH)1
1CompletedBasic ScienceAging1
1CompletedBasic ScienceBenign Prostatic Hyperplasia (BPH)1
1CompletedOtherAlopecia1
1CompletedOtherUrologic Diseases2
1CompletedPreventionBenign Prostatic Hyperplasia (BPH)1
1CompletedTreatmentBenign Prostatic Hyperplasia (BPH) / Prostatic Hyperplasia1
1CompletedTreatmentDepression / Healthy Volunteers / Premenstrual Syndrome1
1CompletedTreatmentHypogonadism / Testicular Hypogonadism1
1CompletedTreatmentProstatic Hyperplasia8
1RecruitingTreatmentAndrogenetic Alopecia1
1Unknown StatusNot AvailableBenign Prostatic Hyperplasia (BPH) / Healthy Volunteers1
1, 2CompletedTreatmentContraception1
1, 2CompletedTreatmentHealthy Males1
1, 2TerminatedTreatmentProstate Cancer1
2Active Not RecruitingTreatmentErectile Dysfunction / Lower Urinary Tract Symptoms (LUTS) / Prostate Cancer1
2Active Not RecruitingTreatmentProstate Cancer1
2CompletedTreatmentBenign Prostatic Hyperplasia (BPH) / Prostatic Hyperplasia1
2CompletedTreatmentContraception / Hypogonadism1
2CompletedTreatmentHypogonadism / Testicular Hypogonadism1
2CompletedTreatmentKennedy's Disease / Spinal and Bulbar Muscular Atrophy1
2CompletedTreatmentMalignancies / Prostate Neoplasms1
2CompletedTreatmentProstate Cancer5
2CompletedTreatmentProstate Cancer After a Radical Treatment / Prostate Neoplasms1
2TerminatedTreatmentProstate Cancer1
2Unknown StatusTreatmentHealthy Volunteers1
2Unknown StatusTreatmentProstate Cancer1
2WithdrawnTreatmentAdenocarcinoma of the Prostate1
2WithdrawnTreatmentLocalized Prostate Cancer / Prostate Cancer1
2WithdrawnTreatmentPituitary gonadotropin hypofunction1
2, 3CompletedPreventionProstate Cancer1
2, 3CompletedTreatmentHealthy Volunteers1
2, 3RecruitingTreatmentAlcohol Use Disorder (AUD)1
3CompletedDiagnosticProstate Cancer1
3CompletedPreventionProstate Cancer1
3CompletedPreventionProstate Neoplasms1
3CompletedTreatmentAlopecia2
3CompletedTreatmentAlopecia / Androgenetic Alopecia1
3CompletedTreatmentAndrogenetic Alopecia1
3CompletedTreatmentBenign Prostatic Hyperplasia (BPH) / Prostatic Hyperplasia1
3CompletedTreatmentProstate Cancer1
3CompletedTreatmentProstatic Hyperplasia3
3CompletedTreatmentTranssexualism1
3TerminatedTreatmentBenign Prostatic Hyperplasia (BPH)1
3TerminatedTreatmentBenign Prostatic Hyperplasia (BPH) / Chronic Prostatitis (CP)1
4CompletedTreatmentAlcohol Abuse / Alcohol Dependence2
4CompletedTreatmentBenign Prostatic Hyperplasia (BPH)4
4CompletedTreatmentBenign Prostatic Hyperplasia (BPH) / Hypogonadism1
4CompletedTreatmentBenign Prostatic Hyperplasia (BPH) / Prostate Cancer1
4CompletedTreatmentBenign Prostatic Hyperplasia (BPH) / Prostatic Hyperplasia1
4CompletedTreatmentHealthy Volunteers1
4CompletedTreatmentHypogonadism1
4CompletedTreatmentProstate Cancer1
4CompletedTreatmentProstate Cancer / Prostate Neoplasms1
4CompletedTreatmentProstate Neoplasms1
4CompletedTreatmentProstatic Hyperplasia2
4TerminatedTreatmentBenign Prostatic Hyperplasia (BPH)1
4TerminatedTreatmentProstatic Hyperplasia1
4Unknown StatusTreatmentBenign Prostatic Hyperplasia (BPH)1
Not AvailableActive Not RecruitingNot AvailableProstate Cancer1
Not AvailableActive Not RecruitingPreventionLow Grade Prostate Cancer / Prostatic Neoplasms1
Not AvailableActive Not RecruitingTreatmentProstate Cancer1
Not AvailableCompletedNot AvailableAlcohol Abuse / Alcohol Dependence / Alcohol Related Disorders2
Not AvailableCompletedNot AvailableAlopecia1
Not AvailableCompletedNot AvailableBenign Prostatic Hyperplasia (BPH)1
Not AvailableCompletedNot AvailableBenign Prostatic Hyperplasia (BPH) / Malignancies / Prostate Neoplasms1
Not AvailableCompletedNot AvailableBenign Prostatic Hyperplasia (BPH) / Prostatic Hyperplasia1
Not AvailableCompletedNot AvailableProstate Cancer1
Not AvailableCompletedNot AvailableProstate Neoplasms1
Not AvailableCompletedNot AvailableProstatic Hyperplasia6
Not AvailableCompletedDiagnosticNonmalignant Neoplasm / Prostate Cancer1
Not AvailableCompletedTreatmentBenign Prostatic Hyperplasia (BPH) / Urinary Retention1
Not AvailableCompletedTreatmentBenign Prostatic Hypertrophy1
Not AvailableUnknown StatusTreatmentBMI >30 kg/m2 / Insulin Resistance1
Not AvailableUnknown StatusTreatmentBenign Prostatic Hyperplasia (BPH) / Lower Urinary Tract Symptoms (LUTS)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
FormRouteStrength
CapsuleOral0.5 mg
Capsule, liquid filledOral0.5 mg/1
LiquidTopical
CapsuleOral0.5 mg/1
CapsuleOral
Capsule, extended releaseOral
CapsuleOral
Prices
Unit descriptionCostUnit
Avodart 0.5 mg capsule4.12USD capsule
Avodart 0.5 mg softgel4.06USD softgel capsule
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
Patents
Patent NumberPediatric ExtensionApprovedExpires (estimated)
US5846976No1998-12-082013-09-17Us
CA2171329No2004-11-232014-09-16Canada
CA2170047No2004-11-092014-09-16Canada
US5565467No1996-10-152015-11-20Us
Additional Data Available
  • Filed On
    Filed On

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Properties

State
Solid
Experimental Properties
PropertyValueSource
melting point (°C)242-250MSDS, FDA Label
water solubilityInsolubleMSDS
logP6.8Human Metabolome Database
Predicted Properties
PropertyValueSource
Water Solubility0.000908 mg/mLALOGPS
logP5.45ALOGPS
logP5.79ChemAxon
logS-5.8ALOGPS
pKa (Strongest Acidic)12.56ChemAxon
pKa (Strongest Basic)2.17ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count2ChemAxon
Hydrogen Donor Count2ChemAxon
Polar Surface Area58.2 Å2ChemAxon
Rotatable Bond Count4ChemAxon
Refractivity127.9 m3·mol-1ChemAxon
Polarizability50.13 Å3ChemAxon
Number of Rings5ChemAxon
Bioavailability0ChemAxon
Rule of FiveNoChemAxon
Ghose FilterNoChemAxon
Veber's RuleNoChemAxon
MDDR-like RuleNoChemAxon
Predicted ADMET features
PropertyValueProbability
Human Intestinal Absorption+1.0
Blood Brain Barrier+0.9884
Caco-2 permeable-0.5223
P-glycoprotein substrateSubstrate0.747
P-glycoprotein inhibitor IInhibitor0.7278
P-glycoprotein inhibitor IINon-inhibitor0.6085
Renal organic cation transporterNon-inhibitor0.8299
CYP450 2C9 substrateNon-substrate0.8077
CYP450 2D6 substrateNon-substrate0.9117
CYP450 3A4 substrateSubstrate0.7186
CYP450 1A2 substrateNon-inhibitor0.8089
CYP450 2C9 inhibitorInhibitor0.5412
CYP450 2D6 inhibitorNon-inhibitor0.8391
CYP450 2C19 inhibitorInhibitor0.6287
CYP450 3A4 inhibitorNon-inhibitor0.6506
CYP450 inhibitory promiscuityLow CYP Inhibitory Promiscuity0.5913
Ames testNon AMES toxic0.6677
CarcinogenicityNon-carcinogens0.9149
BiodegradationNot ready biodegradable1.0
Rat acute toxicity2.6885 LD50, mol/kg Not applicable
hERG inhibition (predictor I)Weak inhibitor0.9829
hERG inhibition (predictor II)Non-inhibitor0.574
ADMET data is predicted using admetSAR, a free tool for evaluating chemical ADMET properties. (23092397)

Spectra

Mass Spec (NIST)
Not Available
Spectra
SpectrumSpectrum TypeSplash Key
Predicted GC-MS Spectrum - GC-MSPredicted GC-MSNot Available
Predicted MS/MS Spectrum - 10V, Positive (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 20V, Positive (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 40V, Positive (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 10V, Negative (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 20V, Negative (Annotated)Predicted LC-MS/MSNot Available
Predicted MS/MS Spectrum - 40V, Negative (Annotated)Predicted LC-MS/MSNot Available

Taxonomy

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
Androgen-skeleton / 3-oxosteroid / 3-oxo-4-azasteroid / 3-oxo-5-alpha-steroid / Oxosteroid / 4-azasteroid / Azasteroid / Trifluoromethylbenzene / Anilide / N-arylamide
show 21 more
Molecular Framework
Aromatic heteropolycyclic compounds
External Descriptors
delta-lactam, aza-steroid, (trifluoromethyl)benzenes (CHEBI:521033)

Targets

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
  1. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [PubMed:11752352]
  2. Rathnayake D, Sinclair R: Male androgenetic alopecia. Expert Opin Pharmacother. 2010 Jun;11(8):1295-304. doi: 10.1517/14656561003752730. [PubMed:20426708]
  3. 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. [PubMed:19879888]
  4. 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. [PubMed:19707263]
  5. 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. [PubMed:19543428]
  6. Keam SJ, Scott LJ: Dutasteride: a review of its use in the management of prostate disorders. Drugs. 2008;68(4):463-85. [PubMed:18318566]
  7. 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. [PubMed:16818707]
  8. 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. [PubMed:19200641]
  9. 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. [PubMed:19091347]
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
  1. Chen X, Ji ZL, Chen YZ: TTD: Therapeutic Target Database. Nucleic Acids Res. 2002 Jan 1;30(1):412-5. [PubMed:11752352]
  2. 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. [PubMed:16818707]
  3. Rathnayake D, Sinclair R: Male androgenetic alopecia. Expert Opin Pharmacother. 2010 Jun;11(8):1295-304. doi: 10.1517/14656561003752730. [PubMed:20426708]
  4. 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. [PubMed:19879888]
  5. 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. [PubMed:19707263]
  6. 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. [PubMed:19543428]
  7. Keam SJ, Scott LJ: Dutasteride: a review of its use in the management of prostate disorders. Drugs. 2008;68(4):463-85. [PubMed:18318566]
  8. 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. [PubMed:19200641]
  9. 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. [PubMed:19091347]

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
  1. 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
  1. 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. [PubMed:26006269]
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
  1. 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. [PubMed:26006269]

Drug created on June 13, 2005 07:24 / Updated on February 25, 2020 00:12