Finasteride
Propecia · Proscar
Finasteride (Propecia, Proscar) is an oral type II 5-alpha-reductase inhibitor that lowers dihydrotestosterone (DHT), the main androgen driving male-pattern hair loss and prostate growth. It is prescribed at 1 mg/day for androgenetic alopecia and 5 mg/day for benign prostatic hyperplasia (BPH), and was studied at 5 mg/day for prostate cancer prevention. It is not an anabolic steroid and does not build muscle; on this reference it appears as an ancillary sometimes used to counter androgen-driven hair loss. The main risks are not liver or cardiac toxicity but endocrine and neuropsychiatric: dose-independent sexual dysfunction (reduced libido, erectile and ejaculatory dysfunction) that in a subset of men persists after stopping ("post-finasteride syndrome"), increased risk of depression and suicidal ideation, and gynecomastia. In the large prostate-cancer prevention trial it reduced overall prostate cancer but was associated with more high-grade tumors. It is strictly contraindicated around pregnancy because DHT blockade can disrupt development of a male fetus's external genitalia. It also lowers PSA by roughly half, which can mask prostate cancer screening. This is educational information, not medical advice; use requires a prescribing clinician and monitoring.
Mechanism of action
Pharmacokinetics
Short plasma half-life on the order of several hours in adult men (approximately 5-8 h reported in pharmacokinetic literature; longer in older men). Human single-dose studies show rapid oral absorption with peak plasma concentration around 1-2 h.
Pharmacodynamic effect far outlasts plasma levels: near-maximal serum DHT suppression (roughly 70%) is sustained across a 24 h dosing interval, supporting once-daily dosing. After discontinuation, DHT and the drug effect return toward baseline over roughly 2 weeks. PK is documented here for monitoring and washout reasoning, not for evading any test.
Oral (tablet).
Hepatically metabolized (primarily via CYP3A4) to less-active metabolites that are excreted in urine and feces; caution/consideration is warranted in hepatic impairment. Numeric clearance/half-life values derive from human PK and product pharmacology literature.
For monitoring and washout planning, not drug-test evasion.
Physiological & performance effects
- At 1 mg/day, slows progression of male-pattern hair loss and modestly increases scalp hair count over 1-2 years in randomized trials
- Dose-ranging trials found 1 mg/day gave near-maximal hair benefit, similar to 5 mg; doses below ~0.2 mg were progressively less effective
- Lowers serum DHT by roughly 70% and scalp-skin DHT by roughly 60-70% at 1-5 mg/day, with a modest rise in testosterone
- At 5 mg/day reduces prostate volume and urinary symptoms in BPH and lowers PSA by approximately 50%
- In the Prostate Cancer Prevention Trial, 5 mg/day reduced overall prostate cancer prevalence by ~25% over 7 years but was associated with more high-grade (Gleason 7-10) tumors
Adverse effects by system
No consistent human evidence that finasteride is directly cardiotoxic or meaningfully alters blood pressure; unlike anabolic androgens it is not associated with adverse lipid/cardiac remodeling in the reviewed literature. This is an absence of a strong signal, not proof of cardiac safety.
No established pattern of clinically significant hepatotoxicity in the human literature; liver injury is not a recognized common effect. Because it is hepatically metabolized, hepatic impairment is a caution. Routine transaminase elevations are not a characteristic feature.
Central endocrine effect: suppresses DHT by ~70% with a compensatory modest rise in testosterone (and can raise estradiol relative to androgen, contributing to gynecomastia). It does not suppress the HPT axis the way exogenous androgens do (it is not a testosterone-lowering drug); rather it blocks peripheral androgen conversion. Reduced DHT can lower libido and impair erectile/ejaculatory function.
Sexual dysfunction is the hallmark adverse effect — reduced libido, erectile dysfunction, and ejaculatory/orgasmic dysfunction; meta-analysis shows ~1.6-fold increased risk versus placebo. Decreased ejaculate volume and reduced sperm parameters are reported. A subset of men report persistent sexual dysfunction after stopping ('post-finasteride syndrome'). Gynecomastia and breast tenderness are increased. It is also teratogenic: exposure of a pregnant partner (including via handling crushed/broken tablets) can impair development of a male fetus's external genitalia.
Meta-analytic human data associate finasteride with increased depression (pooled odds ratio ~2.1) and increased suicidal ideation/behavior; anxiety and mood changes are also reported, and in a subset may persist after discontinuation. This is a leading, serious hazard.
No significant nephrotoxicity or clinically important renal effects reported in the reviewed human literature; dose adjustment is generally driven by hepatic rather than renal handling.
No known clinically significant effect on blood cell counts (not an erythrocytosis-causing agent). The key lab caveat is not hematologic toxicity but that finasteride lowers PSA by ~50%, which can mask prostate cancer on screening.
As a treatment it improves androgenetic alopecia; reported skin/appendage adverse reports (e.g., rash) are uncommon. Some post-marketing reports describe skin changes as part of the broader persistent-symptom cluster, but controlled dermatologic-toxicity data are limited.
HPTA suppression & recovery
Suppression: Not a classic HPTA-suppressing agent — mechanism differs from anabolic steroids
Finasteride does not shut down endogenous testosterone production the way exogenous androgens do; it blocks conversion of testosterone to DHT peripherally, and serum testosterone typically rises modestly. The recovery concern is different: DHT normalizes over roughly 2 weeks after stopping, but a subset of men report persistent sexual, and sometimes neuropsychiatric, symptoms after discontinuation ('post-finasteride syndrome') that do not reliably resolve. Any concern about persistent hormonal/sexual dysfunction after stopping should be evaluated by an endocrinologist (and, for mood/suicidality, urgent mental-health care). Single-agent framing only; no SERM/multi-drug 'recovery' protocol is recommended here.
Monitoring
Cadence: Clinician-directed: PSA and prostate assessment at baseline then periodically (e.g., annually) for men of screening age; mood monitoring on starting and whenever new psychiatric symptoms appear; reassess sexual function at follow-up visits.
- New or worsening depression, anxiety, or any suicidal thoughts — seek urgent medical/mental-health care
- Persistent sexual dysfunction (low libido, erectile/ejaculatory problems) that does not resolve, including after stopping
- Breast lumps, breast pain, tenderness, enlargement, or nipple discharge — evaluate to exclude male breast pathology
- A rising PSA while on finasteride (concerning given the drug normally lowers it)
- Any pregnancy exposure in a partner
Contraindications
- Pregnancy and women who are or may become pregnant — risk of abnormal development of a male fetus's external genitalia (DHT-dependent); pregnant/potentially pregnant persons should not take it or handle crushed or broken tablets
- Known hypersensitivity to finasteride
- Use in women of childbearing potential and in children is generally not indicated
- Caution in significant hepatic impairment (hepatic metabolism)
- Relative caution / informed discussion in men with personal or family history of depression or suicidality given the psychiatric signal
- Men being screened or monitored for prostate cancer must have clinicians account for the ~50% PSA reduction; not a substitute contraindication but a critical monitoring caveat
Interaction profile
- ModerateWith another 5α-reductase inhibitor: Hormonal
- ContraindicatedWith DNP: Additive cardiovascular strain
Check a specific combination in the interaction checker.
Reducing harm & when to stop
- This is educational information, not medical advice, and does not create a doctor-patient relationship; finasteride is a prescription drug that should be used only under a clinician's supervision. 21+.
- Pregnant people or those who may become pregnant must not take finasteride or handle crushed/broken tablets, because DHT suppression can disrupt male fetal genital development; store securely away from pregnant partners.
- Because finasteride is associated with depression and suicidal ideation, anyone who develops new low mood, hopelessness, or suicidal thoughts should seek urgent medical/mental-health care and discuss stopping the drug with a clinician.
- Sexual side effects (low libido, erectile/ejaculatory dysfunction) are a recognized risk; if they occur, discuss discontinuation with a prescriber. Be aware a subset of men report symptoms persisting after stopping — this uncertainty should be part of an informed decision before starting.
- Report any breast lump, pain, enlargement, or nipple discharge promptly to exclude male breast disease.
- Tell any clinician you take finasteride so PSA results are interpreted correctly (it roughly halves PSA); a rising PSA on treatment needs evaluation and should never be dismissed.
- Questions about persistent hormonal or sexual symptoms after stopping should be directed to an endocrinologist; this monograph does not endorse any self-managed drug 'recovery' protocol.
- Nothing here is about maximizing results or obtaining the drug; the goal is safety, monitoring, and knowing when to stop and seek care.
Citations (13)
Every clinical claim above is tied to a primary source. Overall evidence grade A — graded to the best available evidence for its core claims.
- 01
Finasteride is a type II 5-alpha-reductase inhibitor that lowers serum and scalp DHT and, at 1 mg/day, slows hair loss and increases scalp hair count over 1-2 years in randomized double-blind placebo-controlled trials.
- 02
Dose-ranging RCT: efficacy for male-pattern hair loss was seen at 0.2 mg/day and above, with 1 mg and 5 mg giving similar, near-maximal benefit; 1 mg/day was selected as the alopecia dose.
- 03
Finasteride lowered serum DHT by roughly 70% (and scalp-skin DHT ~60-70%) at 1-5 mg/day in men with androgenetic alopecia.
- 04
In the Prostate Cancer Prevention Trial (18,882 men, 5 mg/day, 7 years), finasteride reduced overall prostate cancer prevalence by ~24.8% but was associated with more high-grade (Gleason 7-10) tumors; sexual side effects were more common than placebo.
- 05
Review of the PCPT confirming ~24.8% reduction in prostate cancer prevalence alongside an increased incidence of high-grade disease, requiring individualized risk discussion.
ReviewPMID 16061372 ↗
- 06
Meta-analysis of 15 RCTs (4,495 men): 5-alpha-reductase inhibitors carried a 1.57-fold risk of sexual dysfunction; for finasteride the relative risk was 1.66.
Meta-analysisPMID 30206635 ↗
- 07
Meta-analysis: finasteride associated with increased depression (odds ratio ~2.14) and increased suicidal ideation/behavior, with high rates of sustained sexual dysfunction.
Meta-analysisPMID 33814544 ↗
- 08
A subset of men develop persistent sexual, neurological, and psychiatric symptoms ('post-finasteride syndrome') that continue after discontinuation; sexual dysfunction persisting in a subset is a consistent finding, though controlled data are limited.
ReviewPost-finasteride syndrome: a surmountable challenge for cliniciansPMID 32033719 ↗
- 09
Review evaluating the plausibility of persistent 5-alpha-reductase-inhibitor sexual dysfunction and mood changes, noting symptoms including decreased libido, erectile dysfunction, gynecomastia, and depression/suicidal ideation.
ReviewPMID 28232919 ↗
- 10
Meta-analysis of RCTs: finasteride significantly increased gynecomastia and breast tenderness versus placebo in men treated for BPH; breast cancer risk was not clearly increased.
Meta-analysisPMID 31126837 ↗
- 11
Cohort with nested case-control (UK CPRD): 5-alpha-reductase inhibitors increased gynecomastia risk about 3.5-fold but did not significantly increase male breast cancer risk.
CohortPMID 28228662 ↗
- 12
Human single-dose pharmacokinetic study: finasteride is orally absorbed with peak plasma concentration around 1-2 hours; used here to characterize absorption and washout, not test evasion.
- 13
Inherited type II 5-alpha-reductase deficiency causes males to be born with underdeveloped/female-appearing external genitalia, establishing that DHT via this enzyme is required for normal male external genital development — the mechanistic basis for finasteride's pregnancy/teratogenic contraindication.
CohortPMID 1522235 ↗
Last reviewed 2026-07-06 · Verified against PubMed · Educational, not medical advice