General
Preferred name
finasteride
Synonyms
CHEMBL710 ()
Finasteride (acetate) ()
MK-906 acetate ()
MK-906 ()
FINASTERIDE98319-26-7 ()
NSC-741485 ()
Aindeem ()
Finasterida ()
Propecia ()
NSC-759318 ()
Prostide ()
Proscar ()
Finasteride-d9 ()
P&D ID
PD002995
CAS
98319-26-7
140375-21-9
1131342-85-2
Tags
available
drug
probe
Approved by
FDA
First approval
1992
Drug indication
Benign prostatic hyperplasia
Inhibitor (alpha reductase)
Drug Status
approved
Max Phase
4.0
Probe info
Probe type
calculated probe
Probe sources
Probe Miner (suitable probes)
Tool Compound Set
Probe targets
[[ compound.targets[t].gene_name ]]
Probe control
Orthogonal probes
0
No orthogonal probes found
Similar probes
0
No structurally similar probes found
Structure
P&D probe-likeness score
Structure formats
[[ format ]]
[[ compound[format === 'MOL' ? 'molblock' : format.toLowerCase()] ]]
Description
(extracted from source data)
PHARMACODYNAMICS
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.[Label] 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. [label] 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.[A2132] It is expected that DHT levels return to normal within 14 days upon discontinuation of the drug.[L6244] 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.[label] While finasteride reduces the size of the prostate gland by 20%, this may not correlate well with improvement in symptoms.[A178273] 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.[A2132]; ; 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.[A178222] The incidences of these effects in treatment groups were significantly higher than that of the group receiving a placebo.[A178222] 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.[A178195] 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.[A178195]. There is evidence from early clinical observations and controlled studies that finasteride may reduce bleeding of prostatic origin.[A178183]
ROE
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.[label]
INDICATION
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.; ; Indicated for the treatment of male pattern hair loss (androgenetic alopecia, hereditary alopecia, or common male baldness) in male patients.
TOXICITY
**LD50**; ; Oral LD50 is about 418 mg/kg in rats[MSDS] 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.[label] ; ; **Nonclinical toxicology**; ; In a 24-month rat study, there were no signs of the tumorigenic potential of finasteride.[L6235] 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.[L6235] _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.[L6235] ; ; **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.[L6235] As there have been no cases of overdose or clinically significant toxicity with finasteride, there are no specific recommendations in case of an overdose.[label]; ; **Significant adverse events**; ; Common reproductive adverse events seen with finasteride therapy include erectile dysfunction, ejaculatory dysfunction, and loss of libido.[A178195] 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.[A178195]; ; **Special populations**; ; Finasteride can be safely used in elderly patients or those with renal impairment with no specific dosing adjustment recommendations.[label] 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.[L6235]
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.[A178195,Label] Theses metabolites retain less than 20% of the pharmacological activity of the parent compound.[Label]
HALF-LIFE
In healthy young subjects receiving finasteride, the mean elimination half-life in plasma was 6 hours ranging from 3 to 16 hours.[label] In elderly patients over the age of 70 years, the half-life is prolonged to 8 hours.
ABSORPTION
Finasteride is well absorbed following oral administration [T28] 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.[L6235,Label] It is reported that food intake does not affect the oral bioavailability of the drug.[A178195] The peak plasma concentrations (Cmax) averaged 37 ng/mL (range, 27-49 ng/mL) and was reached 1-2 hours post administration.[label] The AUC(0-24 hr) was 53 ngxhr/mL (range, 20-154 ngxhr/mL).[L6235] The plasma concentrations and AUC are reported to be higher in elderly male patients aged 70 years or older.[L6235]
DESCRIPTION
Inhibits steroid 5-alpha-reductase 2
(GtoPdb)
DESCRIPTION
Non-nucleoside DNA methyltransferase inhibitor
(Tocris Bioactive Compound Library)
[[ p.pathway_name ]]
[[ compound.targets[tid].gene_name ]]
Cell lines
4
Organisms
1
Compound Sets
31
AdooQ Bioactive Compound Library
Axon Medchem Screening Library
ChEMBL Approved Drugs
ChEMBL Drugs
CZ-OPENSCREEN Bioactive Library
Drug Repurposing Hub
DrugBank
DrugBank Approved Drugs
DrugCentral
DrugCentral Approved Drugs
DrugMAP
DrugMAP Approved Drugs
Enamine BioReference Compounds
EU-OPENSCREEN Bioactive Compound Library
Guide to Pharmacology
LSP-MoA library (Laboratory of Systems Pharmacology)
MedChem Express Bioactive Compound Library
NCATS Inxight Approved Drugs
NIH Clinical Collections (NCC)
Novartis Chemogenetic Library (NIBR MoA Box)
NPC Screening Collection
Other bioactive compounds
Prestwick Chemical Library
Probe Miner (suitable probes)
ReFrame library
Selleckchem Bioactive Compound Library
TargetMol Bioactive Compound Library
Tocris Bioactive Compound Library
Tool Compound Set
ZINC Tool Compounds
[[ a.name ]]
[[ ligand_id ]]
free of charge
External IDs
52
Molecular Weight
372.28
Hydrogen Bond Acceptors
2
Hydrogen Bond Donors
2
Rotatable Bonds
1
Ring Count
4
Aromatic Ring Count
0
cLogP
3.81
TPSA
58.2
Fraction CSP3
0.83
Chiral centers
7.0
Largest ring
6.0
QED
0.74
Structural alerts
0
No structural alerts detected
Related compounds
Custom attributes
(extracted from source data)
Target
5 alpha Reductase
Steroid 5-alpha-reductase 2
5-?? reductase
AKR1D1, SRD5A1, SRD5A2
5a-reductase inhibitor
5-alpha Reductase
Pathway
Metabolic Enzyme/Protease
Endocrinology/Hormones
Metabolism
Primary Target
Other Reductases
MOA
Inhibitor
Steroid 5alpha-Reductase Inhibitors
5 alpha reductase inhibitor
Member status
member
Indication
androgenetic alopecia
Therapeutic Class
Antihyperplasia Agents
Source data
