Finasteride is an antiandrogenic compound that is used for the treatment of symptomatic benign prostatic hyperplasia (BPH) and male pattern hair loss in adult males by inhibiting Type II 5-alpha reductase.

Brand Names
Entadfi, Propecia, Proscar
Generic Name
DrugBank Accession Number

Finasteride is a synthetic 4-azasteroid compound 13 and specific inhibitor of steroid Type II 5α-reductase, which is an intracellular enzyme that converts the androgen testosterone into 5α-dihydrotestosterone (DHT). It works in a similar fashion as dutasteride, which is another 5-alpha-reductase inhibitor, by exerting antiandrogenic effects. Finasteride is an orally active drug that was first approved by the FDA in 1992 for the treatment of benign prostatic hyperplasia to improve symptoms and reduce the risk for acute urinary retention or the need for surgical procedures.12,13 In 1998, it was approved by the FDA to treat male pattern hair loss.12 Finasteride is commonly marketed under the brand names Propecia and Proscar to be used aloneo or in combination with doxazosin, an alpha-blocker.

Both benign prostatic hyperplasia and androgenic alopecia are androgen-dependent disorders that are characterized by in situ high levels of DHT.2 In the treatment of benign prostate hyperplasia, alpha-blockers such as tamsulosin and terazosin are also used. Compared to alpha-blockers that focus on providing the rapid relief of symptoms, 5α-reductase inhibitors aim to target the underlying disease by blocking the effects of the primary androgen involved in benign prostate hyperplasia and androgenic alopecia, thus reducing the risk for secondary complications while providing symptom control.1

Small Molecule
Average: 372.5441
Monoisotopic: 372.277678406
Chemical Formula
  • (5alpha,17beta)-(1,1-Dimethylethyl)-3-oxo-4-azaandrost-1-ene-17-carboxamide
  • Finasterida
  • Finasteride
  • Finasteridum
External IDs
  • MK-906



Finasteride is indicated 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, and reduce the risk of the need for surgery including transurethral resection of the prostate (TURP) and prostatectomy.13 A combination product with tadalafil is also used for the symptomatic treatment of BPH for up to 26 weeks.14

Finasteride is also indicated for the treatment of male pattern hair loss (androgenetic alopecia, hereditary alopecia, or common male baldness) in male patients.11

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Associated Conditions
Indication TypeIndicationCombined Product DetailsApproval LevelAge GroupPatient CharacteristicsDose Form
Management ofAndrogenetic alopecia••••••••••••
Used in combination to treatBenign prostatic hyperplasia (bph)Combination Product in combination with: Tadalafil (DB00820)•••••••••••••••••••
Management ofHirsutism••• •••••
Management ofHirsutism••• •••••
Used in combination to manageSymptomatic benign prostatic hyperplasiaRegimen in combination with: Doxazosin (DB00590)••••••••••••••••••••••••• ••••••••• • ••••••••• •• ••••• •••••••• •• ••• ••••••• •••••
Contraindications & Blackbox Warnings
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Finasteride is an antiandrogenic compound that works by suppressing the production of serum and intraprostatic dihydrotestosterone (DHT) in men via inhibiting the enzyme responsible for the biosynthesis of DHT. The maximum effect of a rapid reduction in serum DHT concentration is expected to be observed 8 hours following administration of the first dose.13 In a single man receiving a single oral dose of 5 mg finasteride for up to 4 years, there was a reduction in the serum DHT concentrations by approximately 70% and the median circulating level of testosterone increased by approximately 10-20% within the physiologic range. 13 In a double-blind, placebo-controlled study, finasteride reduced intraprostatic DHT level by 91.4% but finasteride is not expected to decrease the DHT levels to castrate levels since circulating testosterone is also converted to DHT by the type 1 isoenzyme expressed in other tissues.1 It is expected that DHT levels return to normal within 14 days upon discontinuation of the drug.12 In a study of male patients with benign prostatic hyperplasia prior to prostatectomy, the treatment with finasteride resulted in an approximate 80% lower DHT content was measured in prostatic tissue removed at surgery compared to placebo.13 While finasteride reduces the size of the prostate gland by 20%, this may not correlate well with improvement in symptoms.8 The effects of finasteride are reported to be more pronounced in male patients with enlarged prostates (>25 mL) who are at the greatest risk of disease progression.1

In phase III clinical studies, oral administration of finasteride in male patients with male pattern hair loss promoted hair growth and prevented further hair loss by 66% and 83% of the subjects, respectively, which lasted during two years' treatment.6 The incidences of these effects in treatment groups were significantly higher than that of the group receiving a placebo.6 Following finasteride administration, the levels of DHT in the scalp skin was shown to be reduced by more than 60%, indicating that the DHT found in scalp is derived from both local DHT production and circulating DHT.5 The effect of finasteride on scalp DHT is likely seen because of its effect on both local follicular DHT levels as well as serum DHT levels.5. There is evidence from early clinical observations and controlled studies that finasteride may reduce bleeding of prostatic origin.3

Mechanism of action

Finasteride acts as a competitive and specific inhibitor of Type II 5α-reductase, 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).1 DHT is considered to be the primary androgen playing a role in the development and enlargement of the prostate gland. It serves as the hormonal mediator for the hyperplasia upon accumulation within the prostate gland.7 DHT displays a higher affinity towards androgen receptors in the prostate gland compared to testosterone10 and by acting on the androgen receptors, DHT modulates genes that are responsible for cell proliferation.9 Responsible for the production of DHT together with type I 5α-reductase, the type II 5α-reductase isozyme is primarily found in the prostate, seminal vesicles, epididymides, and hair follicles as well as liver.11 Although finasteride is 100-fold more selective for type II 5α-reductase than for the type I isoenzyme,3 chronic treatment with this drug may have some effect on type I 5α-reductase, which is predominantly expressed in sebaceous glands of most regions of skin, including the scalp, and liver. It is proposed that the type I 5α-reductase and type II 5α-reductase is responsible for the production of one-third and two-thirds of circulating DHT, respectively.

The mechanism of action of Finasteride is based on its preferential inhibition of Type II 5α-reductase through the formation of a stable complex with the enzyme in vitro and in vivo.13 Finasteride works selectively, where it preferentially displays a 100-fold selectivity for the human Type II 5α-reductase over type I enzyme.11 Inhibition of Type II 5α-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 concentrations. 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). It is suggested that increased levels of DHT can lead to potentiated transcription of prostaglandin D2, which promotes the proliferation of prostate cancer cells.4 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 the hairy scalp, reduce serum DHT, increase hair regrowth, and slow hair loss. Another study suggests that finasteride may work to reduce bleeding of prostatic origin by inhibiting vascular endothelial growth factor (VEGF) in the prostate, leading to atrophy and programmed cell death.3 This may bestow the drug therapeutic benefits in patients idiopathic prostatic bleeding, bleeding during anticoagulation, or bleeding after instrumentation.3

A3-oxo-5-alpha-steroid 4-dehydrogenase 2
U3-oxo-5-alpha-steroid 4-dehydrogenase 1
U3-oxo-5-beta-steroid 4-dehydrogenase

Finasteride is well absorbed following oral administration 10 and displays a slow accumulation phase after multiple dosing.[lablel] In healthy male subjects receiving oral finasteride, the mean oral bioavailability was 65% for 1 mg finasteride and 63% for 5 mg finasteride, and the values ranged from 26 to 170% for 1 mg dose and from 34 to 108% for 5 mg dose, respectively.11,13 It is reported that food intake does not affect the oral bioavailability of the drug.5 The peak plasma concentrations (Cmax) averaged 37 ng/mL (range, 27-49 ng/mL) and was reached 1-2 hours post administration.13 The AUC(0-24 hr) was 53 ngxhr/mL (range, 20-154 ngxhr/mL).11 The plasma concentrations and AUC are reported to be higher in elderly male patients aged 70 years or older.11

Volume of distribution

The volume of distribution is 76 L at steady state, ranging from 44 to 96 L. Finasteride has been shown to cross the blood brain barrier but does not appear to distribute preferentially to the CSF.13 It is not known whether finasteride is excreted in human milk.11

Protein binding

Approximately 90% of circulating finasteride is bound to plasma proteins.13


Finasteride undergoes extensive hepatic metabolism predominantly mediated by the cytochrome P450 3A4 (CYP3A4) enzyme to form the t-butyl side chain monohydroxylated and monocarboxylic acid metabolites.5,13 Theses metabolites retain less than 20% of the pharmacological activity of the parent compound.13

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Route of elimination

In healthy subjects, about 32-46% of total oral dose of finasteride was excreted in the urine in the form of metabolites while about 51-64% of the dose was excreted in the feces. In patients with renal impairment, the extent of urinary excretion of finasteride is expected to be decreased while the fecal excretion is increased.13


In healthy young subjects receiving finasteride, the mean elimination half-life in plasma was 6 hours ranging from 3 to 16 hours. In elderly patients over the age of 70 years, the half-life is prolonged to 8 hours.13


In healthy young subjects (n=15), the mean plasma clearance of finasteride was 165 mL/min with the range between 70 and 279 mL/min.13

Adverse Effects
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Oral LD50 is about 418 mg/kg in ratsMSDS and there have been cases of lethality in rats receiving a single oral dose of 400 mg/kg in males and 1000 mg/kg in females.13

Nonclinical toxicology

In a 24-month rat study, there were no signs of the tumorigenic potential of finasteride.11 In a 19-month carcinogenicity study in CD-1 mice, high doses of finasteride, at 1824 times the human exposure (250 mg/kg/day), resulted in an increase in the incidence of testicular Leydig cell adenomas and an increase in serum LH levels.11 In vitro mutagenesis assays demonstrated no evidence of mutagenicity. In an in vitro chromosome aberration assay, using Chinese hamster ovary cells, there was a slight increase in chromosome aberrations with much higher doses of finasteride.11


There were no reported significant adverse events in clinical trials of male patients receiving single oral doses of finasteride up to 400 mg and multiple doses of finasteride up to 80 mg/day for three months.11 As there have been no cases of overdose or clinically significant toxicity with finasteride, there are no specific recommendations in case of an overdose.13

Significant adverse events

Common reproductive adverse events seen with finasteride therapy include erectile dysfunction, ejaculatory dysfunction, and loss of libido.5 These adverse events tend to disappear after discontinuation or chronic use of the drug. Only causal adverse event occurring at the male reproductive system that is caused by finasteride is decreased ejaculatory volume because of the predominant action of DHT on the prostate.5

Special populations

Finasteride can be safely used in elderly patients or those with renal impairment with no specific dosing adjustment recommendations.13 Finasteride is indicated for male patients only, and it is advised that exposure to finasteride is avoided in pregnant women carrying male fetuses as it may lead to abnormal development of external genitalia in male fetuses.11

Not Available
Pharmacogenomic Effects/ADRs
Not Available


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.
AbametapirThe serum concentration of Finasteride can be increased when it is combined with Abametapir.
AbataceptThe metabolism of Finasteride can be increased when combined with Abatacept.
AcalabrutinibThe metabolism of Finasteride can be decreased when combined with Acalabrutinib.
AcebutololFinasteride may decrease the antihypertensive activities of Acebutolol.
AceclofenacThe risk or severity of hypertension can be increased when Finasteride is combined with Aceclofenac.
Food Interactions
  • Take with or without food. The absorption is unaffected by food.


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Product Images
International/Other Brands
Finastid / Finpecia
Brand Name Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing EndRegionImage
Act FinasterideTablet5 mgOralActavis Pharma Company2010-11-172019-07-08Canada flag
FinasterideTablet1 mgOralSivem Pharmaceuticals Ulc2015-11-25Not applicableCanada flag
FinasterideTablet5 mgOralSanis Health Inc2015-10-14Not applicableCanada flag
FinasterideTablet5 mgOralPro Doc Limitee2010-04-29Not applicableCanada flag
FinasterideTablet1 mgOralSanis Health Inc2015-10-14Not applicableCanada flag
Generic Prescription Products
NameDosageStrengthRouteLabellerMarketing StartMarketing EndRegionImage
Accel-finasteride Tablets USPTablet5 mgOralAccel Pharma IncNot applicableNot applicableCanada flag
Ach-finasterideTablet5 mgOralAccord Healthcare Inc2010-10-04Not applicableCanada flag
Ag-finasterideTablet5 mgOralAngita Pharma Inc.2020-01-20Not applicableCanada flag
Apo-finasterideTablet5 mgOralApotex Corporation2011-11-17Not applicableCanada flag
Auro-finasterideTablet5 mgOralAuro Pharma Inc2013-05-30Not applicableCanada flag
Mixture Products
NameIngredientsDosageRouteLabellerMarketing StartMarketing EndRegionImage
EntadfiFinasteride (5 mg/1) + Tadalafil (5 mg/1)CapsuleOralVeru Inc.2021-12-12Not applicableUS flag
Unapproved/Other Products
NameIngredientsDosageRouteLabellerMarketing StartMarketing EndRegionImage
Dexamethasone Sodium Phosphate 0.1% / Finasteride 0.1% / Minoxidil 5%Finasteride (0.1 g/100g) + Dexamethasone sodium phosphate (0.1 g/100g) + Minoxidil (5 g/100g)SolutionTopicalSincerus Florida, LLC2019-05-09Not applicableUS flag
Dexamethasone Sodium Phosphate 0.1% / Finasteride 0.1% / Minoxidil 5% / Tretinoin 0.025%Finasteride (0.1 g/100g) + Dexamethasone sodium phosphate (0.1 g/100g) + Minoxidil (5 g/100g) + Tretinoin (0.025 g/100g)SolutionTopicalSincerus Florida2019-05-09Not applicableUS flag
Finasteride 0.1% / Minoxidil 5%Finasteride (0.1 g/100g) + Minoxidil (5 g/100g)SolutionTopicalSincerus Florida, LLC2019-05-09Not applicableUS flag
Finasteride 0.1% / Minoxidil 7%Finasteride (0.1 g/100g) + Minoxidil (7 g/100g)SolutionTopicalSincerus Florida, LLC2019-05-01Not applicableUS flag
Finasteride 0.1% / Minoxidil 7% / Tretinoin 0.025%Finasteride (0.1 g/100g) + Minoxidil (7 g/100g) + Tretinoin (0.025 g/100g)SolutionTopicalSincerus Florida, LLC2019-05-11Not applicableUS flag


ATC Codes
D11AX10 — FinasterideG04CA55 — Doxazosin and finasterideG04CA51 — Alfuzosin and finasterideG04CB51 — Finasteride and tadalafilG04CB01 — Finasteride
Drug Categories
Chemical TaxonomyProvided by Classyfire
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.
Organic compounds
Super Class
Lipids and lipid-like molecules
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
20-hydroxysteroid / 3-hydroxysteroid / 4-azasteroid / Aliphatic heteropolycyclic compound / Androgen-skeleton / Azacycle / Azasteroid / Carboximidic acid / Carboximidic acid derivative / Cyclic carboximidic acid
Molecular Framework
Aliphatic heteropolycyclic compounds
External Descriptors
3-oxo steroid, aza-steroid (CHEBI:5062)
Affected organisms
  • Humans and other mammals

Chemical Identifiers

CAS number
InChI Key


Synthesis Reference

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

General References
  1. 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]
  2. Agamia NF, Abou Youssif T, El-Hadidy A, El-Abd A: Benign prostatic hyperplasia, metabolic syndrome and androgenic alopecia: Is there a possible relationship? Arab J Urol. 2016 Feb 23;14(2):157-62. doi: 10.1016/j.aju.2016.01.003. eCollection 2016 Jun. [Article]
  3. Vaughan ED: Long-Term Experience with 5-alpha-Reductase Inhibitors. Rev Urol. 2003;5 Suppl 4:S28-33. [Article]
  4. Bhargava S: Increased DHT levels in androgenic alopecia have been selected for to protect men from prostate cancer. Med Hypotheses. 2014 Apr;82(4):428-32. doi: 10.1016/j.mehy.2014.01.016. Epub 2014 Jan 26. [Article]
  5. Mysore V: Finasteride and sexual side effects. Indian Dermatol Online J. 2012 Jan;3(1):62-5. doi: 10.4103/2229-5178.93496. [Article]
  6. McClellan KJ, Markham A: Finasteride: a review of its use in male pattern hair loss. Drugs. 1999 Jan;57(1):111-26. doi: 10.2165/00003495-199957010-00014. [Article]
  7. Wilson JD: The pathogenesis of benign prostatic hyperplasia. Am J Med. 1980 May;68(5):745-56. [Article]
  8. Steiner JF: Clinical pharmacokinetics and pharmacodynamics of finasteride. Clin Pharmacokinet. 1996 Jan;30(1):16-27. doi: 10.2165/00003088-199630010-00002. [Article]
  9. Carson C 3rd, Rittmaster R: The role of dihydrotestosterone in benign prostatic hyperplasia. Urology. 2003 Apr;61(4 Suppl 1):2-7. [Article]
  10. 34. (2012). In Rang and Dale's Pharmacology (7th ed., pp. 424). Edinburgh: Elsevier/Churchill Livingstone. [ISBN:978-0-7020-3471-8]
  11. FDA Approved Drug Products: PROPECIA (finasteride) tablets [Link]
  12. Finasteride - StatPearls - NCBI Bookshelf [Link]
  13. FDA Approved Drug Products: PROSCAR (finasteride) tablets [Link]
  14. FDA Approved Drug Products: Entadfi (finasteride/tadalafil) capsules for oral use [Link]
Human Metabolome Database
PubChem Compound
PubChem Substance
Therapeutic Targets Database
PDBe Ligand
RxList Drug Page Drug Page
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Clinical Trials

Clinical Trials
Clinical Trial & Rare Diseases Add-on Data Package
Explore 4,000+ rare diseases, orphan drugs & condition pairs, clinical trial why stopped data, & more. Preview package
PhaseStatusPurposeConditionsCountStart DateWhy Stopped100+ additional columns
4CompletedBasic ScienceTranssexualism1somestatusstop reasonjust information to hide
4CompletedScreeningProstate Cancer1somestatusstop reasonjust information to hide
4CompletedTreatmentProstatic Hyperplasia1somestatusstop reasonjust information to hide
4RecruitingOtherElderly Adults / Sleep Apnea1somestatusstop reasonjust information to hide
4RecruitingOtherProstate Cancer / Prostatic Hyperplasia1somestatusstop reasonjust information to hide


Not Available
  • Accord Healthcare
  • Actavis Group
  • Advanced Pharmaceutical Services Inc.
  • Amerisource Health Services Corp.
  • AQ Pharmaceuticals Inc.
  • A-S Medication Solutions LLC
  • Atlantic Biologicals Corporation
  • Aurobindo Pharma Ltd.
  • Barr Pharmaceuticals
  • Cardinal Health
  • Chemical Works Of Gedeon Richter Ltd.
  • Cipla Ltd.
  • Diversified Healthcare Services Inc.
  • Doctor Reddys Laboratories Ltd.
  • Greenstone LLC
  • Intas Pharmaceuticals Ltd.
  • Kansas City Vaccine Co.
  • Merck & Co.
  • Murfreesboro Pharmaceutical Nursing Supply
  • Mylan
  • Northstar Rx LLC
  • Nucare Pharmaceuticals Inc.
  • PD-Rx Pharmaceuticals Inc.
  • Physicians Total Care Inc.
  • Prepackage Specialists
  • Resource Optimization and Innovation LLC
  • Southwood Pharmaceuticals
  • Teva Pharmaceutical Industries Ltd.
  • UDL Laboratories
Dosage Forms
Capsule5 MG
Tablet, film coatedOral1.000 mg
TabletOral5.000 mg
Tablet, film coatedOral5.00 mg
Tablet, coatedOral100000 mg
TabletOral1 mg/1
TabletOral5 mg/1
Tablet, coatedOral1 mg/1
Tablet, film coatedOral5 mg/1
TabletOral1 mg
Tablet, film coatedOral
Capsule, liquid filledOral1 mg
Tablet, film coatedOral1.05 mg
Capsule, liquid filledOral5 mg
TabletOral1.000 mg
TabletOral5.0000 mg
Tablet, film coatedOral1 mg/1
TabletOral5 mg
TabletOral5.0 mg
Tablet, film coatedOral1.00 mg
Tablet, coatedOral5 mg
Tablet, film coatedOral1 mg
Tablet, coatedOral1 mg
Tablet, film coatedOral5 mg
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.
Patent NumberPediatric ExtensionApprovedExpires (estimated)Region
US6046183No2000-04-042011-03-20US flag
CA2173457No1999-03-232014-10-11Canada flag
CA1331601No1994-08-232011-08-23Canada flag
US5942519No1999-08-242018-10-23US flag


Experimental Properties
melting point (°C)252-254 °CMSDS
water solubilitySlightly solubleMSDS
logP3.03HANSCH,C ET AL. (1995)
Predicted Properties
Water Solubility0.00198 mg/mLALOGPS
pKa (Strongest Acidic)14.53Chemaxon
pKa (Strongest Basic)0.33Chemaxon
Physiological Charge0Chemaxon
Hydrogen Acceptor Count2Chemaxon
Hydrogen Donor Count2Chemaxon
Polar Surface Area58.2 Å2Chemaxon
Rotatable Bond Count2Chemaxon
Refractivity108.2 m3·mol-1Chemaxon
Polarizability43.96 Å3Chemaxon
Number of Rings4Chemaxon
Rule of FiveYesChemaxon
Ghose FilterYesChemaxon
Veber's RuleNoChemaxon
MDDR-like RuleNoChemaxon
Predicted ADMET Features
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
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)


Mass Spec (NIST)
Not Available
SpectrumSpectrum TypeSplash Key
Predicted GC-MS Spectrum - GC-MSPredicted GC-MSsplash10-0a4i-1579000000-3a73a92e1d34b87c3e4c
LC-MS/MS Spectrum - LC-ESI-qTof , PositiveLC-MS/MSsplash10-0a4i-5910000000-7dd7b7fbb29b6ae08f4c
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
Predicted MS/MS Spectrum - 10V, Positive (Annotated)Predicted LC-MS/MSsplash10-00di-0039000000-1df9bbb04a3c8e9e1bf6
Predicted MS/MS Spectrum - 10V, Negative (Annotated)Predicted LC-MS/MSsplash10-00di-0009000000-d9d2ea04867c343155e2
Predicted MS/MS Spectrum - 20V, Negative (Annotated)Predicted LC-MS/MSsplash10-00di-1039000000-409286a4747b0c6a7813
Predicted MS/MS Spectrum - 20V, Positive (Annotated)Predicted LC-MS/MSsplash10-00di-3295000000-5a7ec65ea6dc79519bad
Predicted MS/MS Spectrum - 40V, Negative (Annotated)Predicted LC-MS/MSsplash10-0596-2169000000-423ba8427da409bc238b
Predicted MS/MS Spectrum - 40V, Positive (Annotated)Predicted LC-MS/MSsplash10-00di-0391000000-6aaf33f710640acc3bec
Predicted 1H NMR Spectrum1D NMRNot Applicable
Predicted 13C NMR Spectrum1D NMRNot Applicable
Chromatographic Properties
Collision Cross Sections (CCS)
AdductCCS Value (Å2)Source typeSource
DarkChem Lite v0.1.0
DarkChem Lite v0.1.0
DarkChem Lite v0.1.0
DeepCCS 1.0 (2019)
DarkChem Lite v0.1.0
DarkChem Lite v0.1.0
DarkChem Lite v0.1.0
DeepCCS 1.0 (2019)
DarkChem Lite v0.1.0
DarkChem Lite v0.1.0
DarkChem Lite v0.1.0
DeepCCS 1.0 (2019)


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Pharmacological action
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
Uniprot ID
Uniprot Name
3-oxo-5-alpha-steroid 4-dehydrogenase 2
Molecular Weight
28393.015 Da
  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. [Article]
  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. [Article]
  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. [Article]
  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. [Article]
  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. [Article]
  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. [Article]
  7. Joseph MA, Jayaseelan E, Ganapathi B, Stephen J: Hidradenitis suppurativa treated with finasteride. J Dermatolog Treat. 2005 Apr;16(2):75-8. [Article]
Pharmacological action
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
Uniprot ID
Uniprot Name
3-oxo-5-alpha-steroid 4-dehydrogenase 1
Molecular Weight
29458.18 Da
  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. [Article]
  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. [Article]
  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. [Article]
  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. [Article]
  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. [Article]
Pharmacological action
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
Uniprot ID
Uniprot Name
3-oxo-5-beta-steroid 4-dehydrogenase
Molecular Weight
37376.615 Da
  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. [Article]


Pharmacological action
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
Uniprot ID
Uniprot Name
Cytochrome P450 3A4
Molecular Weight
57342.67 Da
  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. [Article]
  2. Hulin-Curtis SL, Petit D, Figg WD, Hsing AW, Reichardt JK: Finasteride metabolism and pharmacogenetics: new approaches to personalized prevention of prostate cancer. Future Oncol. 2010 Dec;6(12):1897-913. doi: 10.2217/fon.10.149. [Article]
  3. Flockhart Table of Drug Interactions [Link]
Pharmacological action
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
Uniprot ID
Uniprot Name
Cytochrome P450 3A5
Molecular Weight
57108.065 Da
  1. Flockhart Table of Drug Interactions [Link]
Pharmacological action
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
Uniprot ID
Uniprot Name
Cytochrome P450 3A7
Molecular Weight
57525.03 Da
  1. Flockhart Table of Drug Interactions [Link]


Pharmacological action
General Function
Mediates electroneutral potassium-chloride cotransport in mature neurons and is required for neuronal Cl(-) homeostasis. As major extruder of intracellular chloride, it establishes the low neuronal Cl(-) levels required for chloride influx after binding of GABA-A and glycine to their receptors, with subsequent hyperpolarization and neuronal inhibition. Involved in the regulation of dendritic spine formation and maturation.
Specific Function
Ammonium transmembrane transporter activity
Gene Name
Uniprot ID
Uniprot Name
Solute carrier family 12 member 5
Molecular Weight
126269.555 Da
  1. Modol L, Casas C, Llido A, Navarro X, Pallares M, Darbra S: Neonatal allopregnanolone or finasteride administration modifies hippocampal K(+) Cl(-) co-transporter expression during early development in male rats. J Steroid Biochem Mol Biol. 2014 Sep;143:343-7. doi: 10.1016/j.jsbmb.2014.05.002. Epub 2014 May 23. [Article]

Drug created at June 13, 2005 13:24 / Updated at July 22, 2024 03:26