EmergingResearch compound

Finasteride (Propecia / Proscar)

Selective type-II 5α-reductase inhibitor. FDA-approved (Proscar 1992 BPH 5 mg, Propecia 1997 AGA 1 mg). In AAS: scalp DHT suppression to slow hair loss in genetically predisposed users. Type-I 5AR not inhibited.

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Finasteride (Propecia / Proscar) vial

WHAT IS FINASTERIDE (PROPECIA / PROSCAR)?

Detailed overview

Finasteride (Propecia 1 mg, Proscar 5 mg) is a 4-aza-steroid selective type-II 5α-reductase inhibitor developed by Merck and FDA-approved in 1992 as Proscar 5 mg for benign prostatic hyperplasia (BPH), then in 1997 as Propecia 1 mg for androgenetic alopecia (AGA, male-pattern hair loss). Kaufman 1998 (PMID 9821414) 5-year prospective trial documented that 1 mg/day finasteride slows male-pattern hair loss progression by ~83% and generates regrowth in ~48% (more effective on the vertex than on the frontal hairline). In AAS context, finasteride primarily inhibits the secondary DHT conversion from testosterone elevation (~70% scalp DHT suppression at 1 mg/day) – in genetically predisposed AGA-risk users, hair-loss acceleration can be mitigated. **DOES NOT** help with trenbolone-driven hair-loss acceleration (Tren is NOT a 5AR substrate) or with Anadrol (also not). Type-I 5AR (skin/sebum DHT) is **not** inhibited – dutasteride dual-inhibitor is needed for that. WADA listing: under S5 (hormone modulator) – competition-banned but TUE possible in clinical indications. Post-finasteride syndrome (PFS) is controversial at ~1-2% incidence (Irwig 2012, PMID 22366892).

Mechanism

Selective type-II 5α-reductase inhibitor, ~70% scalp DHT suppression at 1 mg/day

Dosing (AAS hair-loss prevention)

1 mg/day (Propecia) continuous during cycle

Half-life

~6 h parent, pharmacodynamic effect 24+ h enzyme inhibition

Onset

DHT reduction measurable 24 h, hair stabilization 3-6 months

Legal status

FDA + EMA Rx, HU + PL approved, WADA allowed (not 5AR-banned)

Data console

Lab data

/lab/molecular-data.jsonLIVE
> Androgenic:AnabolicN/A (not AAS, 5AR inhibitor)
> AR bindingType-II 5AR Ki ~5 nM (competitive), Type-I 5AR ~100× less p…
> Active half-life~6 h (parent), but 24+ h enzyme inhibition reversal depends on new synthesis
> Detection windowPreviously listed as 5AR masking agent; removed from WADA list 2009 – now allowed.
> AromatizationDoes not aromatize – competitive type-II 5α-reductase inhibitor; inhibits DHT conversion, does NOT directly affect the estrogen axis (but secondary E2 elevation may follow testosterone rise).
> HepatotoxicityLow – non-steroidal in mechanism but 4-aza-steroid structure. Rare cholestasis case reports (FDA Propecia label). Post-finasteride syndrome (PFS) – controversial neurosteroid-mediated mood/sexual dysfunction long-term sequela ~1-2% incidence (Irwig 2012 PMID 22366892).

Safety

Side effects, stop signs, contraindications

Side effects · 7

  • Sexual dysfunction: reduced libido, erectile dysfunction, decreased ejaculate volume (about 2–8%, dose-dependent, most common adverse effect).
  • Post-finasteride syndrome (PFS): sexual, mood and cognitive symptoms persisting even after discontinuation (about 1–2%, neurosteroid-mediated, controversial but growing evidence).
  • Mood disturbance: depression, anxiety, anhedonia, rarely suicidal ideation (FDA label warning).
  • Gynecomastia and breast tenderness: due to the testosterone→estrogen shift from DHT blockade (rare but documented; any new breast lump must be evaluated to rule out breast cancer).
  • Roughly 50% reduction in PSA level: can mask prostate cancer screening, the PSA value requires correction in clinical interpretation.
  • Initial shedding (telogen effluvium): a paradoxical transient increase in hair loss may occur in the first 4–8 weeks of therapy.
  • Rare cholestasis / liver enzyme elevation and hypersensitivity reactions (rash, pruritus, angioedema) reported in isolated cases.

Contraindications · 7

  • Pregnancy and pregnant (or potentially pregnant) partner: Pregnancy Category X – DHT suppression can cause malformation of the fetal male external genitalia. A pregnant woman must NOT handle the tablets (especially broken/crushed ones).
  • Women (of childbearing potential) and children: not indicated; teratogenic risk and no proven benefit.
  • History of depression or other mood disorder: relative contraindication due to increased risk of mood side effects and PFS.
  • Known hypersensitivity to finasteride or other 5α-reductase inhibitors (e.g. dutasteride).
  • Adolescents (<18 years): 5AR blockade during development is not indicated.
  • Severe hepatic impairment: finasteride is metabolized in the liver (CYP3A4), caution / monitoring is required with reduced function.
  • Family history of androgen insensitivity syndrome (AIS) or AR mutation: further reduction of androgen signaling should be avoided.

Related Performance Compounds

Same therapeutic category

Studies

Related research and clinical findings

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MolekulaX Editorial Team·Source-verified · PubMed · FDA · EMA
Updated: June 19, 2026

The information here is for educational and scientific purposes only. Performance-enhancing compounds (AAS, prohormones, stimulants, doping agents) are illegal without prescription in Hungary and most of the EU, and carry serious health and legal risks. WADA bans them in competitive sport. This is NOT a usage guide, and we do not encourage any illegal use. If you do use them, medical supervision and regular bloodwork are ESSENTIAL. Severe endocrine, cardiovascular, hepatic and psychiatric side effects are possible.