<?xml version="1.0" encoding="UTF-8"?>
<compound>
  <id type="integer">4875</id>
  <title>T3D4820</title>
  <common-name>Finasteride</common-name>
  <description>An orally active testosterone 5-alpha-reductase inhibitor. It is used as a surgical alternative for treatment of benign prostatic hyperplasia. </description>
  <cas>98319-26-7</cas>
  <pubchem-id>57363</pubchem-id>
  <chemical-formula>C23H36N2O2</chemical-formula>
  <weight nil="true"/>
  <appearance>White powder.</appearance>
  <melting-point>252-254°C</melting-point>
  <boiling-point nil="true"/>
  <density nil="true"/>
  <solubility>11.7 mg/L</solubility>
  <specific-gravity nil="true"/>
  <flash-point nil="true"/>
  <vapour-pressure nil="true"/>
  <route-of-exposure nil="true"/>
  <target nil="true"/>
  <mechanism-of-toxicity>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.</mechanism-of-toxicity>
  <metabolism>Drug is extensively metabolized, primarily in the liver via CYP3A4. Two metabolites have been identified with дЉ_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)</metabolism>
  <toxicity nil="true"/>
  <lethaldose nil="true"/>
  <carcinogenicity>No indication of carcinogenicity to humans (not listed by IARC).</carcinogenicity>
  <use-source>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).</use-source>
  <min-risk-level nil="true"/>
  <health-effects nil="true"/>
  <symptoms nil="true"/>
  <treatment nil="true"/>
  <created-at type="dateTime">2014-09-11T05:18:00Z</created-at>
  <updated-at type="dateTime">2026-03-31T19:50:06Z</updated-at>
  <interacting-proteins nil="true"/>
  <wikipedia>Finasteride</wikipedia>
  <uniprot-id nil="true"/>
  <kegg-compound-id nil="true"/>
  <omim-id nil="true"/>
  <chebi-id>5062</chebi-id>
  <biocyc-id nil="true"/>
  <ctd-id nil="true"/>
  <stitch-id nil="true"/>
  <drugbank-id>DB01216</drugbank-id>
  <pdb-id nil="true"/>
  <actor-id nil="true"/>
  <organism nil="true"/>
  <export type="boolean">true</export>
  <metabolizing-proteins nil="true"/>
  <transporting-proteins nil="true"/>
  <moldb-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</moldb-smiles>
  <moldb-formula>C23H36N2O2</moldb-formula>
  <moldb-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</moldb-inchi>
  <moldb-inchikey>DBEPLOCGEIEOCV-WSBQPABSSA-N</moldb-inchikey>
  <moldb-average-mass type="decimal">372.5441</moldb-average-mass>
  <moldb-mono-mass type="decimal">372.277678406</moldb-mono-mass>
  <origin>Exogenous</origin>
  <state>Solid</state>
  <logp>3.03</logp>
  <hmdb-id>HMDB01984</hmdb-id>
  <chembl-id>CHEMBL710</chembl-id>
  <chemspider-id>51714</chemspider-id>
  <structure-image-file-name nil="true"/>
  <structure-image-content-type nil="true"/>
  <structure-image-file-size type="integer" nil="true"/>
  <structure-image-updated-at type="dateTime" nil="true"/>
  <biodb-id nil="true"/>
  <synthesis-reference>&lt;p&gt;Roman Davis, Alan Millar, &amp;#8220;Method for preparing finasteride.&amp;#8221; U.S. Patent US5670643, issued October, 1992.&lt;/p&gt;</synthesis-reference>
  <structure-image-caption nil="true"/>
  <chemdb-id>CHEM003777</chemdb-id>
  <dsstox-id>DTXSID3020625</dsstox-id>
  <toxcast-id nil="true"/>
  <stoff-ident-origin nil="true"/>
  <stoff-ident-id nil="true"/>
  <susdat-id>NS00010893</susdat-id>
  <iupac>(1S,2R,7R,10S,11S,14S,15S)-N-tert-butyl-2,15-dimethyl-5-oxo-6-azatetracyclo[8.7.0.0^{2,7}.0^{11,15}]heptadec-3-ene-14-carboxamide</iupac>
</compound>
