Identification

Name
Finasteride
Accession Number
DB01216  (APRD00632, DB07774)
Type
Small Molecule
Groups
Approved
Description

An orally active testosterone 5-alpha-reductase inhibitor. It is used as a surgical alternative for treatment of benign prostatic hyperplasia. [PubChem]

Structure
Thumb
Synonyms
  • (5alpha,17beta)-(1,1-Dimethylethyl)-3-oxo-4-azaandrost-1-ene-17-carboxamide
  • Finasterida
  • Finasteridum
External IDs
MK-906
Product Images
Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
Accel-finasteride Tablets USPTablet5 mgOralAccel Pharma IncNot applicableNot applicableCanada
Ach-finasterideTablet5 mgOralAccord Healthcare Limited2010-10-04Not applicableCanada
Act FinasterideTablet5 mgOralActavis Pharma Company2010-11-17Not applicableCanada
Ag-finasterideTablet5 mgOralAngita Pharma Inc.Not applicableNot applicableCanada
Auro-finasterideTablet5 mgOralAuro Pharma Inc2013-05-30Not applicableCanada
Auro-finasteride 1mgTablet1 mgOralAuro Pharma Inc2014-11-12Not applicableCanada
Dom-finasterideTablet5 mgOralDominion Pharmacal2013-06-13Not applicableCanada
FinasterideTablet5 mgOralSanis Health Inc2015-10-14Not applicableCanada
FinasterideTablet1 mgOralSanis Health Inc2015-10-14Not applicableCanada
FinasterideTablet5 mgOralSivem Pharmaceuticals Ulc2015-11-25Not applicableCanada
Generic Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing End
Apo-finasterideTablet5 mgOralApotex Corporation2011-11-17Not applicableCanada
FinasterideTablet5 mg/1OralHetero Drugs Ltd.,2010-06-07Not applicableUs
FinasterideTablet, film coated1 mg/1OralAmerincan Health Packaging2015-03-312017-09-30Us31722 0526 90 nlmimage10 cf406793
FinasterideTablet, film coated5 mg/1OralNu Care Pharmaceuticals,inc.2010-05-28Not applicableUs
FinasterideTablet, film coated5 mg/1OralNorth Star Rx Llc2011-05-162016-12-21Us
FinasterideTablet, film coated5 mg/1OralHetero Labs Limited2016-03-04Not applicableUs
FinasterideTablet, film coated5 mg/1OralNu Care Pharmaceuticals,inc.2010-05-28Not applicableUs
FinasterideTablet, film coated5 mg/1OralMylan Institutional2007-10-222016-11-22Us
FinasterideTablet, film coated1 mg/1OralDr Reddy's Laboratories2013-01-02Not applicableUs
FinasterideTablet, film coated5 mg/1OralAv Pak2007-03-28Not applicableUs
International/Other Brands
Finastid / Finpecia
Categories
UNII
57GNO57U7G
CAS number
98319-26-7
Weight
Average: 372.5441
Monoisotopic: 372.277678406
Chemical Formula
C23H36N2O2
InChI Key
DBEPLOCGEIEOCV-WSBQPABSSA-N
InChI
InChI=1S/C23H36N2O2/c1-21(2,3)25-20(27)17-8-7-15-14-6-9-18-23(5,13-11-19(26)24-18)16(14)10-12-22(15,17)4/h11,13-18H,6-10,12H2,1-5H3,(H,24,26)(H,25,27)/t14-,15-,16-,17+,18+,22-,23+/m0/s1
IUPAC Name
(1S,2R,7R,10S,11S,14S,15S)-N-tert-butyl-2,15-dimethyl-5-oxo-6-azatetracyclo[8.7.0.0²,⁷.0¹¹,¹⁵]heptadec-3-ene-14-carboxamide
SMILES

Pharmacology

Indication

For the treatment of symptomatic benign prostatic hyperplasia (BPH) in men with an enlarged prostate to: Improve symptoms, reduce the risk of acute urinary retention, reduce the risk of the need for surgery including transurethral resection of the prostate. Also used for the stimulation of regrowth of hair in men with mild to moderate androgenetic alopecia (male pattern alopecia, hereditary alopecia, common male baldness).

Structured Indications
Pharmacodynamics

Finasteride is a synthetic 4-azasteroid compound. This drug is a competitive and specific inhibitor of Type II 5a-reductase, an intracellular enzyme that converts the androgen testosterone into 5α-dihydrotestosterone (DHT). Two distinct isozymes are found in mice, rats, monkeys, and humans: Type I and II. Each of these isozymes is differentially expressed in tissues and developmental stages. In humans, Type I 5a-reductase is predominant in the sebaceous glands of most regions of skin, including scalp, and liver. Type I 5a-reductase is responsible for approximately one-third of circulating DHT. The Type II 5a-reductase isozyme is primarily found in prostate, seminal vesicles, epididymides, and hair follicles as well as liver, and is responsible for two-thirds of circulating DHT. Although finasteride is 100-fold more selective for type II 5a-reductase than for the type I isoenzyme, chronic treatment with this drug may have some effect on type I 5a-reductase.

Mechanism of action

The mechanism of action of Finasteride is based on its preferential inhibition of Type II 5a-reductase through the formation of a stable complex with the enzyme. Inhibition of Type II 5a-reductase blocks the peripheral conversion of testosterone to DHT, resulting in significant decreases in serum and tissue DHT concentrations, minimal to moderate increase in serum testosterone concentrations, and substantial increases in prostatic testosterone concetrations. As DHT appears to be the principal androgen responsible for stimulation of prostatic growth, a decrease in DHT concentrations will result in a decrease in prostatic volume (approximately 20-30% after 6-24 months of continued therapy). In men with androgenic alopecia, the mechanism of action has not been fully determined, but finasteride has shown to decrease scalp DHT concentration to the levels found in hairy scalp, reduce serum DHT, increase hair regrowth, and slow hair loss.

TargetActionsOrganism
A3-oxo-5-alpha-steroid 4-dehydrogenase 2
inhibitor
Human
U3-oxo-5-alpha-steroid 4-dehydrogenase 1
inhibitor
Human
U3-oxo-5-beta-steroid 4-dehydrogenase
inhibitor
Human
Absorption
Not Available
Volume of distribution
  • 44 to 96 L
Protein binding

Approximately 90%

Metabolism

Drug is extensively metabolized, primarily in the liver via CYP3A4. Two metabolites have been identified with ≤20% of the activity of finasteride.

Route of elimination

Following an oral dose of 14C-finasteride in man (n = 6), a mean of 39% (range, 32 to 46%) of the dose was excreted in the urine in the form of metabolites; 57% (range, 51 to 64%) was excreted in the feces. Urinary excretion of metabolites was decreased in patients with renal impairment. This decrease was associated with an increase in fecal excretion of metabolites.

Half life

4.5 hours (range 3.3-13.4 hours)

Clearance
  • 165 mL/min [healthy young subjects]
Toxicity
Not Available
Affected organisms
  • Humans and other mammals
Pathways
Not Available
Pharmacogenomic Effects/ADRs
Not Available

Interactions

Drug Interactions
DrugInteractionDrug group
AmiodaroneThe metabolism of Finasteride can be decreased when combined with Amiodarone.Approved, Investigational
AprepitantThe serum concentration of Finasteride can be increased when it is combined with Aprepitant.Approved, Investigational
AtazanavirThe metabolism of Finasteride can be decreased when combined with Atazanavir.Approved, Investigational
AtomoxetineThe metabolism of Finasteride can be decreased when combined with Atomoxetine.Approved
BoceprevirThe metabolism of Finasteride can be decreased when combined with Boceprevir.Approved, Withdrawn
BortezomibThe metabolism of Finasteride can be decreased when combined with Bortezomib.Approved, Investigational
BosentanThe serum concentration of Finasteride can be decreased when it is combined with Bosentan.Approved, Investigational
CarbamazepineThe metabolism of Finasteride can be increased when combined with Carbamazepine.Approved, Investigational
CeritinibThe serum concentration of Finasteride can be increased when it is combined with Ceritinib.Approved
ClarithromycinThe metabolism of Finasteride can be decreased when combined with Clarithromycin.Approved
ClemastineThe metabolism of Finasteride can be decreased when combined with Clemastine.Approved
ClotrimazoleThe metabolism of Finasteride can be decreased when combined with Clotrimazole.Approved, Vet Approved
CobicistatThe metabolism of Finasteride can be decreased when combined with Cobicistat.Approved
ConivaptanThe serum concentration of Finasteride can be increased when it is combined with Conivaptan.Approved, Investigational
CrizotinibThe metabolism of Finasteride can be decreased when combined with Crizotinib.Approved
CyclosporineThe metabolism of Finasteride can be decreased when combined with Cyclosporine.Approved, Investigational, Vet Approved
DabrafenibThe serum concentration of Finasteride can be decreased when it is combined with Dabrafenib.Approved
DarunavirThe metabolism of Finasteride can be decreased when combined with Darunavir.Approved
DasatinibThe serum concentration of Finasteride can be increased when it is combined with Dasatinib.Approved, Investigational
DeferasiroxThe serum concentration of Finasteride can be decreased when it is combined with Deferasirox.Approved, Investigational
DelavirdineThe metabolism of Finasteride can be decreased when combined with Delavirdine.Approved
DihydroergotamineThe metabolism of Finasteride can be decreased when combined with Dihydroergotamine.Approved
DiltiazemThe metabolism of Finasteride can be decreased when combined with Diltiazem.Approved
DoxycyclineThe metabolism of Finasteride can be decreased when combined with Doxycycline.Approved, Investigational, Vet Approved
DronedaroneThe metabolism of Finasteride can be decreased when combined with Dronedarone.Approved
EnzalutamideThe serum concentration of Finasteride can be decreased when it is combined with Enzalutamide.Approved
ErythromycinThe metabolism of Finasteride can be decreased when combined with Erythromycin.Approved, Vet Approved
FluconazoleThe metabolism of Finasteride can be decreased when combined with Fluconazole.Approved
FluvoxamineThe metabolism of Finasteride can be decreased when combined with Fluvoxamine.Approved, Investigational
FosamprenavirThe metabolism of Finasteride can be decreased when combined with Fosamprenavir.Approved
FosaprepitantThe serum concentration of Finasteride can be increased when it is combined with Fosaprepitant.Approved
FosphenytoinThe metabolism of Finasteride can be increased when combined with Fosphenytoin.Approved
Fusidic AcidThe serum concentration of Finasteride can be increased when it is combined with Fusidic Acid.Approved
IdelalisibThe serum concentration of Finasteride can be increased when it is combined with Idelalisib.Approved
ImatinibThe metabolism of Finasteride can be decreased when combined with Imatinib.Approved
IndinavirThe metabolism of Finasteride can be decreased when combined with Indinavir.Approved
IsavuconazoniumThe metabolism of Finasteride can be decreased when combined with Isavuconazonium.Approved, Investigational
IsradipineThe metabolism of Finasteride can be decreased when combined with Isradipine.Approved
ItraconazoleThe metabolism of Finasteride can be decreased when combined with Itraconazole.Approved, Investigational
IvacaftorThe serum concentration of Finasteride can be increased when it is combined with Ivacaftor.Approved
KetoconazoleThe metabolism of Finasteride can be decreased when combined with Ketoconazole.Approved, Investigational
LopinavirThe metabolism of Finasteride can be decreased when combined with Lopinavir.Approved
LovastatinThe metabolism of Finasteride can be decreased when combined with Lovastatin.Approved, Investigational
LuliconazoleThe serum concentration of Finasteride can be increased when it is combined with Luliconazole.Approved
LumacaftorThe metabolism of Finasteride can be increased when combined with Lumacaftor.Approved
MifepristoneThe serum concentration of Finasteride can be increased when it is combined with Mifepristone.Approved, Investigational
MitotaneThe serum concentration of Finasteride can be decreased when it is combined with Mitotane.Approved
NefazodoneThe metabolism of Finasteride can be decreased when combined with Nefazodone.Approved, Withdrawn
NelfinavirThe metabolism of Finasteride can be decreased when combined with Nelfinavir.Approved
NetupitantThe serum concentration of Finasteride can be increased when it is combined with Netupitant.Approved
NevirapineThe metabolism of Finasteride can be increased when combined with Nevirapine.Approved
NilotinibThe metabolism of Finasteride can be decreased when combined with Nilotinib.Approved, Investigational
OlaparibThe metabolism of Finasteride can be decreased when combined with Olaparib.Approved
OsimertinibThe serum concentration of Finasteride can be increased when it is combined with Osimertinib.Approved
PalbociclibThe serum concentration of Finasteride can be increased when it is combined with Palbociclib.Approved
PentobarbitalThe metabolism of Finasteride can be increased when combined with Pentobarbital.Approved, Vet Approved
PhenobarbitalThe metabolism of Finasteride can be increased when combined with Phenobarbital.Approved
PhenytoinThe metabolism of Finasteride can be increased when combined with Phenytoin.Approved, Vet Approved
PosaconazoleThe metabolism of Finasteride can be decreased when combined with Posaconazole.Approved, Investigational, Vet Approved
PrimidoneThe metabolism of Finasteride can be increased when combined with Primidone.Approved, Vet Approved
RanolazineThe metabolism of Finasteride can be decreased when combined with Ranolazine.Approved, Investigational
RifabutinThe metabolism of Finasteride can be increased when combined with Rifabutin.Approved
RifampicinThe metabolism of Finasteride can be increased when combined with Rifampicin.Approved
RifapentineThe metabolism of Finasteride can be increased when combined with Rifapentine.Approved
RitonavirThe metabolism of Finasteride can be decreased when combined with Ritonavir.Approved, Investigational
SaquinavirThe metabolism of Finasteride can be decreased when combined with Saquinavir.Approved, Investigational
SildenafilThe metabolism of Finasteride can be decreased when combined with Sildenafil.Approved, Investigational
SiltuximabThe serum concentration of Finasteride can be decreased when it is combined with Siltuximab.Approved
SimeprevirThe serum concentration of Finasteride can be increased when it is combined with Simeprevir.Approved
St. John's WortThe serum concentration of Finasteride can be decreased when it is combined with St. John's Wort.Investigational, Nutraceutical
StiripentolThe serum concentration of Finasteride can be increased when it is combined with Stiripentol.Approved
SulfisoxazoleThe metabolism of Finasteride can be decreased when combined with Sulfisoxazole.Approved, Vet Approved
TelaprevirThe metabolism of Finasteride can be decreased when combined with Telaprevir.Approved, Withdrawn
TelithromycinThe metabolism of Finasteride can be decreased when combined with Telithromycin.Approved
TiclopidineThe metabolism of Finasteride can be decreased when combined with Ticlopidine.Approved
TocilizumabThe serum concentration of Finasteride can be decreased when it is combined with Tocilizumab.Approved
VenlafaxineThe metabolism of Finasteride can be decreased when combined with Venlafaxine.Approved
VerapamilThe metabolism of Finasteride can be decreased when combined with Verapamil.Approved
VoriconazoleThe metabolism of Finasteride can be decreased when combined with Voriconazole.Approved, Investigational
ZiprasidoneThe metabolism of Finasteride can be decreased when combined with Ziprasidone.Approved
Food Interactions
  • Take without regard to meals.

References

Synthesis Reference

Roman Davis, Alan Millar, "Method for preparing finasteride." U.S. Patent US5670643, issued October, 1992.

US5670643
General References
  1. Suzuki R, Satoh H, Ohtani H, Hori S, Sawada Y: Saturable binding of finasteride to steroid 5alpha-reductase as determinant of nonlinear pharmacokinetics. Drug Metab Pharmacokinet. 2010;25(2):208-13. [PubMed:20460827]
  2. 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]
External Links
Human Metabolome Database
HMDB01984
KEGG Drug
D00321
PubChem Compound
57363
PubChem Substance
46507645
ChemSpider
51714
BindingDB
50334788
ChEBI
5062
ChEMBL
CHEMBL710
Therapeutic Targets Database
DAP000045
PharmGKB
PA449627
HET
FIT
RxList
RxList Drug Page
Drugs.com
Drugs.com Drug Page
Wikipedia
Finasteride
ATC Codes
D11AX10 — FinasterideG04CB01 — FinasterideG04CA51 — Alfuzosin and finasteride
AHFS Codes
  • 92:08.00 — 5 Alfa Reductase Inhibitors
  • 84:92.00 — Misc. Skin and Mucous Membrane Agents
PDB Entries
3g1r
FDA label
Download (103 KB)

Clinical Trials

Clinical Trials
PhaseStatusPurposeConditionsCount
1CompletedNot AvailableBenign Prostatic Hyperplasia (BPH)1
1CompletedNot AvailableHealthy Volunteers6
1CompletedTreatmentAndrogenetic Alopecia2
1CompletedTreatmentContraception / Hypogonadism1
1CompletedTreatmentHealthy Volunteers4
1, 2CompletedTreatmentRetinal Diseases2
2CompletedTreatmentAdenocarcinoma of the Prostate / Stage II Prostate Cancer1
2CompletedTreatmentBenign Prostate Hypertrophy / Muscle Wasting / Sarcopenia / Testicular Hypogonadism1
2CompletedTreatmentBenign Prostatic Hyperplasia (BPH) / Enlarged Prostate1
2CompletedTreatmentHealthy Males / Male Contraceptive1
2CompletedTreatmentNODULOCYSTIC ACNE1
2CompletedTreatmentProstate Cancer1
2CompletedTreatmentProstate Cancer / Sexual Dysfunction and Infertility1
2RecruitingSupportive CareCentral Nervous System Diseases / Endocrine System Diseases / Genital Diseases, Male / Gonadal Disorders / Hypogonadism / Nervous System Diseases / Spinal Cord Diseases / Spinal Cord Injuries (SCI) / Trauma, Nervous System / Wounds and Injuries1
2RecruitingTreatmentLung Cancer Non-Small Cell Cancer (NSCLC)1
2TerminatedTreatmentHematospermia / Hematuria1
2TerminatedTreatmentRetinal Diseases1
2Unknown StatusTreatmentHealthy Volunteers1
2WithdrawnTreatmentDetectable Prostate Nodules1
3Active Not RecruitingTreatmentAndrogenetic Alopecia1
3CompletedDiagnosticEnlarged Prostate1
3CompletedTreatmentBenign Prostatic Hyperplasia (BPH) / Enlarged Prostate1
3CompletedTreatmentProstatic Hyperplasia / Prostatic Hypertrophy, Benign1
3TerminatedTreatmentBenign Prostatic Hyperplasia (BPH)2
3WithdrawnTreatmentBenign Prostatic Hyperplasia (BPH)1
3WithdrawnTreatmentErythrocytosis1
4Active Not RecruitingTreatmentBenign Prostatic Hyperplasia (BPH)1
4CompletedScreeningProstate Cancer1
4CompletedTreatmentProstatic Hyperplasia1
4RecruitingOtherElderly Adults / Sleep Apnea Syndrome1
4Unknown StatusTreatmentBenign Prostatic Hyperplasia (BPH)1
4WithdrawnTreatmentFemale Androgenetic Alopecia1
Not AvailableCompletedNot AvailableProstatic Hyperplasia2
Not AvailableCompletedPreventionProstate Cancer1
Not AvailableCompletedTreatmentIdiopathic Hirsutism1
Not AvailableRecruitingTreatmentProstate Cancer1

Pharmacoeconomics

Manufacturers
Not Available
Packagers
Dosage forms
FormRouteStrength
TabletOral1 mg/1
TabletOral5 mg/1
Tablet, coatedOral1 mg/1
Tablet, film coatedOral1 mg/1
Tablet, film coatedOral5 mg/1
TabletOral1 mg
TabletOral5 mg
Prices
Unit descriptionCostUnit
Proscar 5 mg tablet3.64USD tablet
Finasteride 5 mg tablet3.19USD tablet
Propecia 1 mg tablet2.74USD tablet
DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.
Patents
Patent NumberPediatric ExtensionApprovedExpires (estimated)
US6046183No1994-03-202011-03-20Us
CA2173457No1999-03-232014-10-11Canada
CA1331601No1994-08-232011-08-23Canada
US5942519No1998-10-232018-10-23Us

Properties

State
Solid
Experimental Properties
PropertyValueSource
melting point (°C)252-254 °CPhysProp
water solubility11.7 mg/LNot Available
logP3.03HANSCH,C ET AL. (1995)
Predicted Properties
PropertyValueSource
Water Solubility0.00198 mg/mLALOGPS
logP3.53ALOGPS
logP3.07ChemAxon
logS-5.3ALOGPS
pKa (Strongest Acidic)14.53ChemAxon
pKa (Strongest Basic)2.22ChemAxon
Physiological Charge0ChemAxon
Hydrogen Acceptor Count2ChemAxon
Hydrogen Donor Count2ChemAxon
Polar Surface Area58.2 Å2ChemAxon
Rotatable Bond Count2ChemAxon
Refractivity108.2 m3·mol-1ChemAxon
Polarizability43.93 Å3ChemAxon
Number of Rings4ChemAxon
Bioavailability1ChemAxon
Rule of FiveYesChemAxon
Ghose FilterYesChemAxon
Veber's RuleNoChemAxon
MDDR-like RuleNoChemAxon
Predicted ADMET features
PropertyValueProbability
Human Intestinal Absorption+0.9952
Blood Brain Barrier+0.9777
Caco-2 permeable-0.5496
P-glycoprotein substrateSubstrate0.7639
P-glycoprotein inhibitor IInhibitor0.7258
P-glycoprotein inhibitor IINon-inhibitor0.5558
Renal organic cation transporterNon-inhibitor0.7854
CYP450 2C9 substrateNon-substrate0.8062
CYP450 2D6 substrateNon-substrate0.9116
CYP450 3A4 substrateSubstrate0.7407
CYP450 1A2 substrateNon-inhibitor0.9045
CYP450 2C9 inhibitorInhibitor0.8948
CYP450 2D6 inhibitorNon-inhibitor0.923
CYP450 2C19 inhibitorInhibitor0.8994
CYP450 3A4 inhibitorNon-inhibitor0.9176
CYP450 inhibitory promiscuityLow CYP Inhibitory Promiscuity0.7841
Ames testNon AMES toxic0.8581
CarcinogenicityNon-carcinogens0.9436
BiodegradationNot ready biodegradable1.0
Rat acute toxicity2.9188 LD50, mol/kg Not applicable
hERG inhibition (predictor I)Weak inhibitor0.9901
hERG inhibition (predictor II)Non-inhibitor0.8734
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
LC-MS/MS Spectrum - LC-ESI-qTof , PositiveLC-MS/MSNot Available
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-0ab9-1319000000-9f18f09bea4e9168f1df
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-0002-5900000000-3ad6a0d10c51f9892144
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-0a4i-0119000000-f683db304300c01e907a
LC-MS/MS Spectrum - LC-ESI-ITFT , positiveLC-MS/MSsplash10-0a4i-0129000000-a097bfd2187d4d4c97c6
MS/MS Spectrum - , positiveLC-MS/MSsplash10-00xr-0119000000-43c6646bf19d62255966
MS/MS Spectrum - , positiveLC-MS/MSsplash10-01b9-2539000000-c47506144391db372c4b
LC-MS/MS Spectrum - LC-ESI-QFT , positiveLC-MS/MSsplash10-014i-0900000000-a55cf309ee5a976c5e45

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-hydroxysteroids / 4-azasteroids and derivatives / Cyclic carboximidic acids / Propargyl-type 1,3-dipolar organic compounds / Azacyclic compounds / Organopnictogen compounds / Organooxygen compounds / Organonitrogen compounds / Hydrocarbon derivatives
Substituents
20-hydroxysteroid / Androgen-skeleton / 3-hydroxysteroid / Hydroxysteroid / 4-azasteroid / Azasteroid / Cyclic carboximidic acid / Carboximidic acid / Carboximidic acid derivative / Azacycle
Molecular Framework
Aliphatic heteropolycyclic compounds
External Descriptors
3-oxo steroid, aza-steroid (CHEBI:5062)

Targets

Kind
Protein
Organism
Human
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. Bowman CJ, Barlow NJ, Turner KJ, Wallace DG, Foster PM: Effects of in utero exposure to finasteride on androgen-dependent reproductive development in the male rat. Toxicol Sci. 2003 Aug;74(2):393-406. Epub 2003 May 28. [PubMed:12773767]
  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. Ha SJ, Kim JS, Myung JW, Lee HJ, Kim JW: Analysis of genetic polymorphisms of steroid 5alpha-reductase type 1 and 2 genes in Korean men with androgenetic alopecia. J Dermatol Sci. 2003 Apr;31(2):135-41. [PubMed:12670724]
  4. Suzuki R, Satoh H, Ohtani H, Hori S, Sawada Y: Saturable binding of finasteride to steroid 5alpha-reductase as determinant of nonlinear pharmacokinetics. Drug Metab Pharmacokinet. 2010;25(2):208-13. [PubMed:20460827]
  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. Joseph MA, Jayaseelan E, Ganapathi B, Stephen J: Hidradenitis suppurativa treated with finasteride. J Dermatolog Treat. 2005 Apr;16(2):75-8. [PubMed:16019620]
Kind
Protein
Organism
Human
Pharmacological action
Unknown
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. Thigpen AE, Russell DW: Four-amino acid segment in steroid 5 alpha-reductase 1 confers sensitivity to finasteride, a competitive inhibitor. J Biol Chem. 1992 Apr 25;267(12):8577-83. [PubMed:1314830]
  2. Levy MA, Brandt M, Sheedy KM, Holt DA, Heaslip JI, Trill JJ, Ryan PJ, Morris RA, Garrison LM, Bergsma DJ: Cloning, expression and functional characterization of type 1 and type 2 steroid 5 alpha-reductases from Cynomolgus monkey: comparisons with human and rat isoenzymes. J Steroid Biochem Mol Biol. 1995 Apr;52(4):307-19. [PubMed:7734398]
  3. Tian G, Stuart JD, Moss ML, Domanico PL, Bramson HN, Patel IR, Kadwell SH, Overton LK, Kost TA, Mook RA Jr, et al.: 17 beta-(N-tert-butylcarbamoyl)-4-aza-5 alpha-androstan-1-en-3-one is an active site-directed slow time-dependent inhibitor of human steroid 5 alpha-reductase 1. Biochemistry. 1994 Mar 1;33(8):2291-6. [PubMed:8117686]
  4. Suzuki R, Satoh H, Ohtani H, Hori S, Sawada Y: Saturable binding of finasteride to steroid 5alpha-reductase as determinant of nonlinear pharmacokinetics. Drug Metab Pharmacokinet. 2010;25(2):208-13. [PubMed:20460827]
  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]
Kind
Protein
Organism
Human
Pharmacological action
Unknown
Actions
Inhibitor
General Function
Steroid binding
Specific Function
Efficiently catalyzes the reduction of progesterone, androstenedione, 17-alpha-hydroxyprogesterone and testosterone to 5-beta-reduced metabolites. The bile acid intermediates 7-alpha,12-alpha-dihyd...
Gene Name
AKR1D1
Uniprot ID
P51857
Uniprot Name
3-oxo-5-beta-steroid 4-dehydrogenase
Molecular Weight
37376.615 Da
References
  1. Drury JE, Di Costanzo L, Penning TM, Christianson DW: Inhibition of human steroid 5beta-reductase (AKR1D1) by finasteride and structure of the enzyme-inhibitor complex. J Biol Chem. 2009 Jul 24;284(30):19786-90. doi: 10.1074/jbc.C109.016931. Epub 2009 Jun 10. [PubMed:19515843]

Enzymes

Kind
Protein
Organism
Human
Pharmacological action
Unknown
Actions
Substrate
General Function
Vitamin d3 25-hydroxylase activity
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 performs a variety of oxidation react...
Gene Name
CYP3A4
Uniprot ID
P08684
Uniprot Name
Cytochrome P450 3A4
Molecular Weight
57342.67 Da
References
  1. Huskey SW, Dean DC, Miller RR, Rasmusson GH, Chiu SH: Identification of human cytochrome P450 isozymes responsible for the in vitro oxidative metabolism of finasteride. Drug Metab Dispos. 1995 Oct;23(10):1126-35. [PubMed:8654202]
  2. Preissner S, Kroll K, Dunkel M, Senger C, Goldsobel G, Kuzman D, Guenther S, Winnenburg R, Schroeder M, Preissner R: SuperCYP: a comprehensive database on Cytochrome P450 enzymes including a tool for analysis of CYP-drug interactions. Nucleic Acids Res. 2010 Jan;38(Database issue):D237-43. doi: 10.1093/nar/gkp970. Epub 2009 Nov 24. [PubMed:19934256]
  3. Drug Interactions: Cytochrome P450 Drug Interaction Table [Link]
Kind
Protein
Organism
Human
Pharmacological action
Unknown
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. Drug Interactions: Cytochrome P450 Drug Interaction Table [Link]
Kind
Protein
Organism
Human
Pharmacological action
Unknown
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
CYP3A7
Uniprot ID
P24462
Uniprot Name
Cytochrome P450 3A7
Molecular Weight
57525.03 Da
References
  1. Drug Interactions: Cytochrome P450 Drug Interaction Table [Link]

Drug created on June 13, 2005 07:24 / Updated on November 13, 2017 21:49