Identification
- Summary
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
- Finasteride
- DrugBank Accession Number
- DB01216
- Background
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
- Type
- Small Molecule
- Groups
- Approved
- Structure
Structure for Finasteride (DB01216)
- Weight
- Average: 372.5441
Monoisotopic: 372.277678406 - Chemical Formula
- C23H36N2O2
- Synonyms
- (5alpha,17beta)-(1,1-Dimethylethyl)-3-oxo-4-azaandrost-1-ene-17-carboxamide
- Finasterida
- Finasteride
- Finasteridum
- External IDs
- MK-906
Pharmacology
- Indication
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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Indication Type Indication Combined Product Details Approval Level Age Group Patient Characteristics Dose Form Management of Androgenetic alopecia •••••••••••• Used in combination to treat Benign prostatic hyperplasia (bph) Combination Product in combination with: Tadalafil (DB00820) •••••••••••• ••••••• Management of Hirsutism ••• ••••• Management of Hirsutism ••• ••••• Used in combination to manage Symptomatic benign prostatic hyperplasia Regimen 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
Target Actions Organism A3-oxo-5-alpha-steroid 4-dehydrogenase 2 inhibitorHumans U3-oxo-5-alpha-steroid 4-dehydrogenase 1 inhibitorHumans U3-oxo-5-beta-steroid 4-dehydrogenase inhibitorHumans - Absorption
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
- Metabolism
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
- Half-life
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
- Clearance
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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LD50
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
Overdose
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
- Pathways
- Not Available
- Pharmacogenomic Effects/ADRs Browse all" title="About SNP Mediated Effects/ADRs" id="snp-actions-info" class="drug-info-popup" href="javascript:void(0);">
- Not Available
Interactions
- Drug Interactions Learn More" title="About Drug Interactions" id="structured-interactions-info" class="drug-info-popup" href="javascript:void(0);">
- This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.
Drug Interaction Integrate drug-drug
interactions in your softwareAbametapir The serum concentration of Finasteride can be increased when it is combined with Abametapir. Abatacept The metabolism of Finasteride can be increased when combined with Abatacept. Acalabrutinib The metabolism of Finasteride can be decreased when combined with Acalabrutinib. Acebutolol Finasteride may decrease the antihypertensive activities of Acebutolol. Aceclofenac The 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.
Products
Drug product information from 10+ global regionsOur datasets provide approved product information including:dosage, form, labeller, route of administration, and marketing period.Access drug product information from over 10 global regions.- Product Images
- International/Other Brands
- Finastid / Finpecia
- Brand Name Prescription Products
Name Dosage Strength Route Labeller Marketing Start Marketing End Region Image Act Finasteride Tablet 5 mg Oral Actavis Pharma Company 2010-11-17 2019-07-08 Canada 
Finasteride Tablet 5 mg Oral Sivem Pharmaceuticals Ulc 2015-11-25 Not applicable Canada Finasteride Tablet, film coated 5 mg/1 Oral Mylan Pharmaceuticals Inc. 2007-04-27 2007-04-27 US 
Finasteride Tablet 1 mg Oral Sivem Pharmaceuticals Ulc 2015-11-25 Not applicable Canada Finasteride Tablet 5 mg Oral Sanis Health Inc 2015-10-14 Not applicable Canada - Generic Prescription Products
Name Dosage Strength Route Labeller Marketing Start Marketing End Region Image Accel-finasteride Tablets USP Tablet 5 mg Oral Accel Pharma Inc Not applicable Not applicable Canada Ach-finasteride Tablet 5 mg Oral Accord Healthcare Inc 2010-10-04 Not applicable Canada Ag-finasteride Tablet 5 mg Oral Angita Pharma Inc. 2020-01-20 Not applicable Canada Apo-finasteride Tablet 5 mg Oral Apotex Corporation 2011-11-17 Not applicable Canada Auro-finasteride Tablet 5 mg Oral Auro Pharma Inc 2013-05-30 Not applicable Canada - Mixture Products
Name Ingredients Dosage Route Labeller Marketing Start Marketing End Region Image Entadfi Finasteride (5 mg/1) + Tadalafil (5 mg/1) Capsule Oral Veru Inc. 2021-12-12 Not applicable US - Unapproved/Other Products
Name Ingredients Dosage Route Labeller Marketing Start Marketing End Region Image 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) Solution Topical Sincerus Florida, LLC 2019-05-09 Not applicable US 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) Solution Topical Sincerus Florida 2019-05-09 Not applicable US Finasteride 0.1% / Minoxidil 5% Finasteride (0.1 g/100g) + Minoxidil (5 g/100g) Solution Topical Sincerus Florida, LLC 2019-05-09 Not applicable US Finasteride 0.1% / Minoxidil 7% Finasteride (0.1 g/100g) + Minoxidil (7 g/100g) Solution Topical Sincerus Florida, LLC 2019-05-01 Not applicable US Finasteride 0.1% / Minoxidil 7% / Tretinoin 0.025% Finasteride (0.1 g/100g) + Minoxidil (7 g/100g) + Tretinoin (0.025 g/100g) Solution Topical Sincerus Florida, LLC 2019-05-11 Not applicable US
Categories
- ATC Codes
- D11AX10 — Finasteride
- D11AX — Other dermatologicals
- D11A — OTHER DERMATOLOGICAL PREPARATIONS
- D11 — OTHER DERMATOLOGICAL PREPARATIONS
- D — DERMATOLOGICALS
- G04CA — Alpha-adrenoreceptor antagonists
- G04C — DRUGS USED IN BENIGN PROSTATIC HYPERTROPHY
- G04 — UROLOGICALS
- G — GENITO URINARY SYSTEM AND SEX HORMONES
- G04CA — Alpha-adrenoreceptor antagonists
- G04C — DRUGS USED IN BENIGN PROSTATIC HYPERTROPHY
- G04 — UROLOGICALS
- G — GENITO URINARY SYSTEM AND SEX HORMONES
- G04CB — Testosterone-5-alpha reductase inhibitors
- G04C — DRUGS USED IN BENIGN PROSTATIC HYPERTROPHY
- G04 — UROLOGICALS
- G — GENITO URINARY SYSTEM AND SEX HORMONES
- Drug Categories
- 5-alpha Reductase Inhibitors
- Adrenergic alpha-Antagonists
- Adrenergic Antagonists
- Agents that produce hypertension
- Androstanes
- Androstenes
- Azasteroids
- Cytochrome P-450 CYP3A Substrates
- Cytochrome P-450 CYP3A4 Substrates
- Cytochrome P-450 CYP3A5 Substrates
- Cytochrome P-450 CYP3A7 Substrates
- Cytochrome P-450 Substrates
- Dermatologicals
- Drugs Used in Benign Prostatic Hypertrophy
- Enzyme Inhibitors
- Fused-Ring Compounds
- Genito Urinary System and Sex Hormones
- Genitourinary Agents
- Hormone Antagonists
- Hormones, Hormone Substitutes, and Hormone Antagonists
- Misc. Skin and Mucous Membrane Agents
- Steroid Synthesis Inhibitors
- Steroids
- Urological Agents
- Urologicals
- Chemical TaxonomyProvided by Classyfire
- Description
- This compound belongs to the class of organic compounds known as androgens and derivatives. These are 3-hydroxylated C19 steroid hormones. They are known to favor the development of masculine characteristics. They also show profound effects on scalp and body hair in humans.
- Kingdom
- Organic compounds
- Super Class
- Lipids and lipid-like molecules
- Class
- Steroids and steroid derivatives
- Sub Class
- Androstane steroids
- Direct Parent
- Androgens and derivatives
- Alternative Parents
- 3-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 / 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
- UNII
- 57GNO57U7G
- CAS number
- 98319-26-7
- 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
- (4aR,4bS,6aS,7S,9aS,9bS,11aR)-N-tert-butyl-4a,6a-dimethyl-2-oxo-1H,2H,4aH,4bH,5H,6H,6aH,7H,8H,9H,9aH,9bH,10H,11H,11aH-indeno[5,4-f]quinoline-7-carboxamide
- SMILES
- [H][C@@]12CC[C@H](C(=O)NC(C)(C)C)[C@@]1(C)CC[C@@]1([H])[C@@]2([H])CC[C@@]2([H])NC(=O)C=C[C@]12C
References
- Synthesis Reference
Roman Davis, Alan Millar, "Method for preparing finasteride." U.S. Patent US5670643, issued October, 1992.
US5670643- General References
- 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]
- 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]
- Vaughan ED: Long-Term Experience with 5-alpha-Reductase Inhibitors. Rev Urol. 2003;5 Suppl 4:S28-33. [Article]
- 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]
- Mysore V: Finasteride and sexual side effects. Indian Dermatol Online J. 2012 Jan;3(1):62-5. doi: 10.4103/2229-5178.93496. [Article]
- 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]
- Wilson JD: The pathogenesis of benign prostatic hyperplasia. Am J Med. 1980 May;68(5):745-56. [Article]
- Steiner JF: Clinical pharmacokinetics and pharmacodynamics of finasteride. Clin Pharmacokinet. 1996 Jan;30(1):16-27. doi: 10.2165/00003088-199630010-00002. [Article]
- Carson C 3rd, Rittmaster R: The role of dihydrotestosterone in benign prostatic hyperplasia. Urology. 2003 Apr;61(4 Suppl 1):2-7. [Article]
- 34. (2012). In Rang and Dale's Pharmacology (7th ed., pp. 424). Edinburgh: Elsevier/Churchill Livingstone. [ISBN:978-0-7020-3471-8]
- FDA Approved Drug Products: PROPECIA (finasteride) tablets [Link]
- Finasteride - StatPearls - NCBI Bookshelf [Link]
- FDA Approved Drug Products: PROSCAR (finasteride) tablets [Link]
- FDA Approved Drug Products: Entadfi (finasteride/tadalafil) capsules for oral use [Link]
- External Links
- Human Metabolome Database
- HMDB0001984
- KEGG Drug
- D00321
- PubChem Compound
- 57363
- PubChem Substance
- 46507645
- ChemSpider
- 51714
- BindingDB
- 50334788
- 25025
- ChEBI
- 5062
- ChEMBL
- CHEMBL710
- ZINC
- ZINC000003782599
- Therapeutic Targets Database
- DAP000045
- PharmGKB
- PA449627
- PDBe Ligand
- FIT
- RxList
- RxList Drug Page
- Drugs.com
- Drugs.com Drug Page
- Wikipedia
- Finasteride
- MSDS
- Download (42.2 KB)
Clinical Trials
- Clinical Trials Learn More" title="About Clinical Trials" id="clinical-trials-info" class="drug-info-popup" href="javascript:void(0);">
Phase Status Purpose Conditions Count 4 Completed Basic Science Transsexualism 1 4 Completed Screening Prostate Cancer 1 4 Completed Treatment Prostatic Hyperplasia 1 4 Recruiting Other Elderly Adults / Sleep Apnea 1 4 Recruiting Other Prostate Cancer / Prostatic Hyperplasia 1
Pharmacoeconomics
- Manufacturers
- Not Available
- Packagers
- 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
Form Route Strength Capsule 5 MG Tablet, film coated Oral 1.000 mg Tablet Oral 5.000 mg Spray Cutaneous Capsule Oral Tablet, film coated Oral 5.00 mg Tablet Oral Tablet, coated Oral 100000 mg Tablet Oral 1 mg/1 Tablet Oral 5 mg/1 Tablet, coated Oral 1 mg/1 Tablet, film coated Oral 5 mg/1 Solution Topical Tablet Oral 1 mg Tablet, film coated Oral Capsule, liquid filled Oral 1 mg Tablet, film coated Oral 1.05 mg Capsule, liquid filled Oral 5 mg Tablet Oral 1.000 mg Tablet Oral 5.0000 mg Tablet, film coated Oral 1 mg/1 Tablet Oral 5 mg Tablet Oral 5.0 mg Tablet, film coated Oral 1.00 mg Tablet, coated Oral 5 mg Tablet, film coated Oral 1 mg Tablet, coated Oral 1 mg Tablet, film coated Oral 5 mg - Prices
Unit description Cost Unit Proscar 5 mg tablet 3.64USD tablet Finasteride 5 mg tablet 3.19USD tablet Propecia 1 mg tablet 2.74USD tablet DrugBank does not sell nor buy drugs. Pricing information is supplied for informational purposes only.- Patents
Patent Number Pediatric Extension Approved Expires (estimated) Region US6046183 No 2000-04-04 2011-03-20 US CA2173457 No 1999-03-23 2014-10-11 Canada CA1331601 No 1994-08-23 2011-08-23 Canada US5942519 No 1999-08-24 2018-10-23 US
Properties
- State
- Solid
- Experimental Properties
Property Value Source melting point (°C) 252-254 °C MSDS water solubility Slightly soluble MSDS logP 3.03 HANSCH,C ET AL. (1995) - Predicted Properties
Property Value Source Water Solubility 0.00198 mg/mL ALOGPS logP 3.53 ALOGPS logP 3.07 Chemaxon logS -5.3 ALOGPS pKa (Strongest Acidic) 14.53 Chemaxon pKa (Strongest Basic) 0.33 Chemaxon Physiological Charge 0 Chemaxon Hydrogen Acceptor Count 2 Chemaxon Hydrogen Donor Count 2 Chemaxon Polar Surface Area 58.2 Å2 Chemaxon Rotatable Bond Count 2 Chemaxon Refractivity 108.2 m3·mol-1 Chemaxon Polarizability 43.96 Å3 Chemaxon Number of Rings 4 Chemaxon Bioavailability 1 Chemaxon Rule of Five Yes Chemaxon Ghose Filter Yes Chemaxon Veber's Rule No Chemaxon MDDR-like Rule No Chemaxon - Predicted ADMET Features
Property Value Probability Human Intestinal Absorption + 0.9952 Blood Brain Barrier + 0.9777 Caco-2 permeable - 0.5496 P-glycoprotein substrate Substrate 0.7639 P-glycoprotein inhibitor I Inhibitor 0.7258 P-glycoprotein inhibitor II Non-inhibitor 0.5558 Renal organic cation transporter Non-inhibitor 0.7854 CYP450 2C9 substrate Non-substrate 0.8062 CYP450 2D6 substrate Non-substrate 0.9116 CYP450 3A4 substrate Substrate 0.7407 CYP450 1A2 substrate Non-inhibitor 0.9045 CYP450 2C9 inhibitor Inhibitor 0.8948 CYP450 2D6 inhibitor Non-inhibitor 0.923 CYP450 2C19 inhibitor Inhibitor 0.8994 CYP450 3A4 inhibitor Non-inhibitor 0.9176 CYP450 inhibitory promiscuity Low CYP Inhibitory Promiscuity 0.7841 Ames test Non AMES toxic 0.8581 Carcinogenicity Non-carcinogens 0.9436 Biodegradation Not ready biodegradable 1.0 Rat acute toxicity 2.9188 LD50, mol/kg Not applicable hERG inhibition (predictor I) Weak inhibitor 0.9901 hERG inhibition (predictor II) Non-inhibitor 0.8734
Spectra
- Mass Spec (NIST)
- Not Available
- Spectra
- Chromatographic Properties
Collision Cross Sections (CCS)
Adduct CCS Value (Å2) Source type Source [M-H]- 205.413338 predictedDarkChem Lite v0.1.0 [M-H]- 200.849638 predictedDarkChem Lite v0.1.0 [M-H]- 206.493338 predictedDarkChem Lite v0.1.0 [M-H]- 192.66881 predictedDeepCCS 1.0 (2019) [M+H]+ 200.450938 predictedDarkChem Lite v0.1.0 [M+H]+ 199.134538 predictedDarkChem Lite v0.1.0 [M+H]+ 202.123438 predictedDarkChem Lite v0.1.0 [M+H]+ 194.56421 predictedDeepCCS 1.0 (2019) [M+Na]+ 200.160338 predictedDarkChem Lite v0.1.0 [M+Na]+ 205.5294772 predictedDarkChem Lite v0.1.0 [M+Na]+ 201.833138 predictedDarkChem Lite v0.1.0 [M+Na]+ 201.09972 predictedDeepCCS 1.0 (2019)
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
- 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]
- 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]
- 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]
- 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]
- Smith AB, Carson CC: Finasteride in the treatment of patients with benign prostatic hyperplasia: a review. Ther Clin Risk Manag. 2009 Jun;5(3):535-45. Epub 2009 Jul 12. [Article]
- Goldenberg L, So A, Fleshner N, Rendon R, Drachenberg D, Elhilali M: The role of 5-alpha reductase inhibitors in prostate pathophysiology: Is there an additional advantage to inhibition of type 1 isoenzyme? Can Urol Assoc J. 2009 Jun;3(3 Suppl 2):S109-14. [Article]
- Joseph MA, Jayaseelan E, Ganapathi B, Stephen J: Hidradenitis suppurativa treated with finasteride. J Dermatolog Treat. 2005 Apr;16(2):75-8. [Article]
- Kind
- Protein
- Organism
- Humans
- 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
- 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]
- 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]
- 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]
- 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]
- 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]
- Kind
- Protein
- Organism
- Humans
- 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
- 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]
Enzymes
- Kind
- Protein
- Organism
- Humans
- 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
- 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]
- 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]
- Flockhart Table of Drug Interactions [Link]
- Kind
- Protein
- Organism
- Humans
- 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
- Flockhart Table of Drug Interactions [Link]
- Kind
- Protein
- Organism
- Humans
- 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
- Flockhart Table of Drug Interactions [Link]
Transporters
- Kind
- Protein
- Organism
- Mouse
- Pharmacological action
- Unknown
- Actions
- Modulator
- 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
- Slc12a5
- Uniprot ID
- Q91V14
- Uniprot Name
- Solute carrier family 12 member 5
- Molecular Weight
- 126269.555 Da
References
- 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 February 20, 2024 23:55