Finasteride is an oral drug that blocks type II 5α-reductase, the enzyme that turns testosterone into the more potent androgen dihydrotestosterone (DHT). It is FDA-approved at 5 mg/day as Proscar for an enlarged prostate (benign prostatic hyperplasia, BPH) and at 1 mg/day as Propecia for male pattern hair loss.
In the context of anabolic steroids, it is used to try to limit DHT-driven effects of testosterone, mainly scalp hair loss and prostate growth. It does not lower testosterone, and it has no effect on steroids that are already 5α-reduced. The single most important fact for most readers: the labels list sexual side effects, depression and suicidal ideation, and sexual problems that persisted after stopping have been reported after marketing.
This page summarizes what the FDA labels, the major randomized trials and large observational studies report. It is for education only and is not medical advice.
| Property | Detail |
|---|---|
| Drug class | 5α-reductase inhibitor (4-azasteroid) |
| Brands / approval | Proscar 5 mg (NDA 020180, approved June 1992); Propecia 1 mg (NDA 020788, approved December 1997); generics available |
| Route | Oral film-coated tablet |
| Labeled doses | 5 mg once daily (BPH); 1 mg once daily (male pattern hair loss) |
| Half-life (label) | About 6 h in adults up to 60; about 8 h in men 70 and older |
| Key mechanism | About 100-fold more selective for type II than type I 5α-reductase; enzyme complex turns over with a half-life of about 30 days |
| Effect on serum DHT | About 70% lower on 5 mg/day; 65% lower within 24 h of a 1 mg dose |
| US status | Prescription only; not a scheduled anabolic steroid |
| WADA status | Not named on the 2026 Prohibited List |
What it is
Finasteride is a synthetic 4-azasteroid with the formula C₂₃H₃₆N₂O₂ and a molecular weight of 372.55 (Proscar label). It is not a hormone. It has no affinity for the androgen receptor and no androgenic, antiandrogenic, estrogenic or progestational activity of its own (Propecia label).
Humans have two main 5α-reductase isozymes, and finasteride blocks them unequally (Propecia label):
| Isozyme | Main locations | Share of circulating DHT | Finasteride IC50 (native tissue) |
|---|---|---|---|
| Type I | Sebaceous glands of most skin, including scalp; liver | About one-third | 500 nM |
| Type II | Prostate, seminal vesicles, epididymis, hair follicles; liver | About two-thirds | 4.2 nM |
IC50 is the concentration needed to block half the enzyme’s activity, so a lower number means stronger inhibition. Finasteride forms a stable complex with the enzyme that breaks down very slowly, with a half-life of about 30 days for type II and 14 days for type I. This is why DHT stays suppressed across the 24-hour dosing interval despite the drug’s short plasma half-life.
Men born with a genetic type II 5α-reductase deficiency have low DHT, a small prostate throughout life and do not develop BPH. Apart from genital differences present at birth, no other clinical abnormalities have been linked to the deficiency (Proscar label). This observation was part of the rationale for developing the drug.
Pharmacokinetics
From the Proscar and Propecia labels:
| Parameter | Value |
|---|---|
| Oral bioavailability | 63% (range 34–108%) for 5 mg; 65% for 1 mg; not affected by food |
| Peak concentration | 37 ng/mL at 1–2 h after a single 5 mg dose; 9.2 ng/mL at 1.3 h on 1 mg/day |
| Protein binding | About 90% |
| Volume of distribution | 76 L |
| Metabolism | Extensive, in the liver, mainly by CYP3A4; two metabolites keep no more than 20% of the parent’s activity |
| Elimination half-life | 6.0 h at ages 45–60 and 8.2 h at 70 or older (5 mg, first dose); 4.5 h in men 19–42 on 1 mg |
| Excretion | 39% in urine and 57% in feces, as metabolites |
Finasteride crosses the blood-brain barrier but does not concentrate in cerebrospinal fluid. After a 14-day course in healthy men, DHT returned to pretreatment levels about 2 weeks after stopping (Proscar label).
Hormonal effects
| Measure | Finasteride 5 mg/day | Finasteride 1 mg/day |
|---|---|---|
| Serum DHT | About 70% lower (up to 4 years of dosing) | 65% lower within 24 h |
| Serum testosterone | Median about 10–20% higher, within normal range | About 15% higher, within normal range |
| Serum estradiol | Not stated | About 15% higher, within normal range |
| LH and FSH | About 10% higher, within normal range | No clinically meaningful change |
| Prostate tissue (1–100 mg/day for 7–10 days before surgery) | About 80% lower DHT; testosterone up to 10 times higher | — |
A placebo-controlled study in 20 healthy men gave 5 mg/day for 28 days (Rittmaster et al., JCEM 1992). Serum DHT fell from 1.1 to 0.15 nmol/L, while basal and GnRH-stimulated LH and FSH did not change. In other words, finasteride lowers DHT without shutting down the body’s own testosterone production.
The dose-response curve flattens early. In 249 men with hair loss given 0.01–5 mg/day for 42 days, the drop in serum and scalp DHT was nearly maximal from 0.2 mg/day upward (Drake et al., JAAD 1999):
| Daily dose | Scalp DHT change | Serum DHT change |
|---|---|---|
| Placebo | −13.0% | — |
| 0.05 mg | −61.6% | −49.5% |
| 0.2 mg | −56.5% | −68.6% |
| 1 mg | −64.1% | −71.4% |
| 5 mg | −69.4% | −72.2% |
Approved medical use
| Product | Indication | Labeled dose |
|---|---|---|
| Proscar 5 mg | Symptomatic BPH in men with an enlarged prostate, to improve symptoms and lower the risk of acute urinary retention and surgery; also with doxazosin to lower the risk of symptom progression | 5 mg once daily |
| Propecia 1 mg | Male pattern hair loss (androgenetic alopecia), men only | 1 mg once daily |
Both labels state that finasteride is not indicated for women or children. The Proscar label also states that it is not approved to prevent prostate cancer. For hair loss, the Propecia label says that 3 months or more of daily use is generally needed before any benefit appears, and that stopping reverses the effect within 12 months. Efficacy for receding temples (bitemporal recession) has not been established.
What the research shows
Benign prostatic hyperplasia
The first large trial randomized 895 men with BPH to finasteride 1 mg, 5 mg or placebo for 12 months (Gormley et al., NEJM 1992). On 5 mg, peak urinary flow rose by 1.6 mL/s (22%) and prostate volume fell by 19%, with a significant drop in symptom scores. The 1 mg dose shrank the prostate by 18% but did not significantly improve symptoms.
The 4-year PLESS trial randomized 3,040 men with moderate-to-severe symptoms and an enlarged prostate to 5 mg/day or placebo (McConnell et al., NEJM 1998; Proscar label):
| Outcome over 4 years | Placebo | Finasteride 5 mg |
|---|---|---|
| Surgery for BPH | 10.1% | 4.6% (55% risk reduction) |
| Acute urinary retention | 6.6% | 2.8% (57% risk reduction) |
| Symptom score change (0–34 scale) | −1.3 | −3.3 |
| Prostate volume change | +14.1% | −17.9% |
The MTOPS trial followed 3,047 men for a mean of 4.5 years on placebo, doxazosin (an alpha-blocker), finasteride or both (McConnell et al., NEJM 2003). Compared with placebo, the risk of overall clinical progression fell by 34% with finasteride, 39% with doxazosin and 66% with the combination. Only finasteride and the combination lowered the long-term risk of acute urinary retention and invasive therapy.
Male pattern hair loss
Two 1-year trials randomized 1,553 men aged 18–41 with mild-to-moderate vertex (crown) hair loss to 1 mg/day or placebo, and 1,215 continued into a blinded second year (Kaufman et al., JAAD 1998). Hair was counted in a 1-inch circle (5.1 cm²) of balding scalp, with a baseline of about 876 hairs. The Propecia label reports the extension results through 5 years:
| Time point | Hair-count difference vs placebo | Men with further hair loss: placebo | Men with further hair loss: finasteride |
|---|---|---|---|
| 1 year | +107 hairs | 58% | 14% |
| 2 years | +138 hairs | 72% | 17% |
| 5 years | +277 hairs | 100% | 35% |
Two caveats come with these numbers. In the finasteride group, hair counts peaked during the first 2 years and then declined slowly while staying above baseline; the gap widened mainly because the placebo group kept losing hair. Also, very few men stayed on placebo for 5 years (15 men in the 5-year count), so the late comparisons rest on small control groups. Men switched from finasteride to placebo after 1 year lost the gain within the following 12 months.
Prostate cancer prevention
The Prostate Cancer Prevention Trial (PCPT) randomized 18,882 men aged 55 or older with a normal rectal exam and PSA (prostate-specific antigen) of 3.0 ng/mL or lower to finasteride 5 mg/day or placebo for 7 years (Thompson et al., NEJM 2003):
| Outcome | Placebo | Finasteride |
|---|---|---|
| Prostate cancer prevalence over 7 years | 24.4% | 18.4% (24.8% relative reduction, 95% CI 18.6–30.6) |
| Gleason 7–10 tumors, share of all cancers found | 22.2% | 37.0% |
| Gleason 7–10 tumors, share of men analyzed | 5.1% | 6.4% |
| Gleason 8–10 tumors (label) | 1.1% | 1.8% |
The Gleason score grades how aggressive a prostate cancer looks under the microscope; 8–10 is high grade. The excess of high-grade tumors led to the warning now on both labels.
Follow-up for up to 18 years confirmed about one-third fewer prostate cancers (10.5% vs 14.9%; relative risk 0.70, 95% CI 0.65–0.76). High-grade cancer remained slightly more common (3.5% vs 3.0%; relative risk 1.17, 95% CI 1.00–1.37). Overall survival did not differ: 78.0% vs 78.2% at 15 years, hazard ratio for death 1.02 (95% CI 0.97–1.08) (Thompson et al., NEJM 2013). Despite the lower cancer rate, the FDA has not approved finasteride for prevention.
Use alongside testosterone and other anabolic steroids
The question most relevant to this library is whether blocking DHT takes away the muscle and bone benefits of testosterone. One randomized trial addressed this directly. Seventy men aged 65 or older with low testosterone received testosterone enanthate 200 mg IM every 2 weeks plus placebo pills, the same testosterone plus finasteride 5 mg/day, or double placebo for 36 months; 50 men finished (Page et al., JCEM 2005; Amory et al., JCEM 2004):
| Outcome at 36 months | Placebo | Testosterone only | Testosterone + finasteride |
|---|---|---|---|
| Lean body mass | −0.21 kg | +3.77 kg | +3.64 kg |
| Timed physical performance | −5.6% | +4.3% | +3.8% |
| Lumbar spine bone density | +1.3% | +10.2% | +9.3% |
| Hip bone density | −0.2% | +2.7% | +2.2% |
| PSA | — | Rose significantly from baseline | — |
| Prostate volume | Increased | Increased | Increased significantly less than the other two groups |
The authors concluded that high DHT levels are not essential for testosterone’s effects on muscle, strength or bone, and that adding finasteride blunted testosterone’s effect on prostate size and PSA. This was a small trial in older hypogonadal men at replacement doses. It does not show what happens at higher, non-medical doses, and no trial has tested whether finasteride prevents hair loss caused by anabolic steroids.
Two mechanistic limits are worth knowing:
- Already 5α-reduced steroids. DHT and steroids built on the DHT skeleton, such as oxandrolone, do not pass through the 5α-reductase step, so finasteride has no mechanism to reduce their androgenic effects.
- Nandrolone works the other way. In rat tissue and cell studies, 5α-reduction raised testosterone’s binding to the androgen receptor but lowered nandrolone’s, because nandrolone is converted to the weaker dihydronandrolone (Bergink et al., J Steroid Biochem 1985). Blocking the enzyme could therefore leave more active nandrolone in tissues such as the prostate and skin. No human study has tested finasteride together with nandrolone, so this remains theoretical.
Side effects and risks
Sexual side effects
These are the most frequently reported adverse effects in the trials. The rates are higher in older men with BPH than in young men with hair loss, and in both groups the excess over placebo was concentrated in the first year.
| Drug-related event | Propecia 1 mg, year 1 (n = 945) | Placebo (n = 934) | Proscar 5 mg, PLESS year 1 (n = 1,524) | Placebo (n = 1,516) |
|---|---|---|---|---|
| Decreased libido | 1.8% | 1.3% | 6.4% | 3.4% |
| Erectile dysfunction | 1.3% | 0.7% | 8.1% | 3.7% |
| Ejaculation disorder or decreased ejaculate volume | 1.2% | 0.7% | 3.7% (volume) | 0.8% |
In the hair-loss trials, 3.8% of men on finasteride reported at least one of these effects, compared with 2.1% on placebo (p = 0.04). The labels state that these resolved in men who stopped and in most who continued, and that their incidence fell to 0.3% or less by the fifth year. In PLESS, years 2–4 showed no significant difference from placebo in impotence, libido or ejaculation disorders (Propecia label; Proscar label).
Meta-analyses of randomized trials reach slightly different conclusions for hair-loss doses:
- Across 17 trials, the pooled risk of sexual dysfunction was clearly raised in men with BPH (RR 2.56, 95% CI 1.48–4.42), but not significantly raised in men with hair loss (RR 1.21, 95% CI 0.85–1.72) (Liu et al., J Sex Med 2016).
- A later meta-analysis of 15 hair-loss trials found a significant increase for finasteride 1 mg (RR 1.66, 95% CI 1.20–2.30) (Lee et al., Acta Derm Venereol 2019).
Persistent symptoms after stopping
Both labels list, from postmarketing reports, sexual dysfunction that continued after the drug was stopped. This includes erectile dysfunction, libido and ejaculation disorders and orgasm disorders. The Proscar label adds that most such reports in BPH patients came from older men on other medicines or with other conditions, and that the independent role of finasteride is unknown. Because these are voluntary reports, their true frequency cannot be estimated.
Depression and suicidality
Depression, suicidal ideation and suicidal behavior are listed as postmarketing reactions on the Propecia label. Large studies give a mixed picture:
| Study | Population | Depression | Suicide |
|---|---|---|---|
| Welk et al., JAMA Intern Med 2017 | 93,197 Ontario men aged 66 or older starting a 5α-reductase inhibitor, matched to non-users | HR 1.94 (95% CI 1.73–2.16) in the first 18 months; HR 1.22 (1.08–1.37) afterward | HR 0.88 (0.53–1.45), not significant; self-harm HR 1.88 (1.34–2.64) in the first 18 months |
| Garcia-Argibay et al., JAMA Netw Open 2022 | 2,236,876 Swedish men aged 50–90 | Finasteride HR 1.61 (1.48–1.75), constant over time | Finasteride HR 1.22 (0.99–1.49), not significant |
In the Ontario study, the absolute increases were 17 self-harm events and 237 depression diagnoses per 100,000 patient-years. Both studies were in older men, mostly treated for the prostate.
For younger men taking finasteride for hair loss, the main data come from a WHO pharmacovigilance database (Nguyen et al., JAMA Dermatol 2021). It found a disproportionate share of suicidality reports with finasteride (reporting odds ratio 1.63, 95% CI 1.47–1.81), concentrated in men under 45 using it for hair loss and not seen in older men with BPH. Reports rose sharply after 2012, and the authors noted that heightened publicity (“stimulated reporting”) may explain part of the signal. This design can flag a possible risk but cannot measure how often it happens.
High-grade prostate cancer and PSA
Both labels warn that 5α-reductase inhibitors may increase the risk of high-grade prostate cancer, based on PCPT (Gleason 8–10: 1.8% vs 1.1%) and a similar dutasteride trial. Finasteride also lowers PSA by about 50% within 6 months in men with BPH, and from 0.7 to 0.5 ng/mL at 12 months in young men on 1 mg. It can lower PSA even when prostate cancer is present, which can mask a rising value.
Breast changes
Breast enlargement and tenderness are listed adverse reactions. In PLESS years 2–4, breast enlargement occurred in 1.8% on finasteride vs 1.1% on placebo. Male breast cancer has been reported:
- MTOPS: 4 cases in men on finasteride, none in men not on finasteride.
- PLESS: no cases on finasteride, 2 on placebo.
- PCPT: 1 case in each group.
The Proscar label states that the relationship between long-term finasteride use and male breast cancer is currently unknown.
Semen and fertility
On 5 mg/day for 24 weeks, healthy men had a median 0.6 mL (22.1%) drop in ejaculate volume, with no clinically meaningful change in sperm concentration, motility or morphology. These changes reversed after stopping, with an average return to baseline of 84 weeks. On 1 mg/day for 48 weeks, ejaculate volume fell by a median 0.3 mL (−11%) compared with 0.2 mL (−8%) on placebo. Postmarketing reports include male infertility or poor semen quality, which improved in some men after stopping.
Pregnancy and exposure of women
Finasteride is contraindicated in women who are or may become pregnant. Blocking DHT can cause abnormal development of the external genitals of a male fetus, as seen in rat and monkey studies and in boys born with genetic 5α-reductase deficiency. Pregnant women should not handle crushed or broken tablets; intact coated tablets prevent skin contact. The Proscar label estimates that the amount of finasteride reaching a partner through semen is 50–100 times lower than a 5 µg dose that had no effect on DHT in men.
Interactions and other cautions
- Drug interactions. No clinically important interactions have been identified. Antipyrine, digoxin, propranolol, theophylline and warfarin were tested in humans without meaningful effects.
- Liver. Because finasteride is extensively metabolized in the liver, the label advises caution in men with liver function abnormalities. Its effect in hepatic impairment has not been studied.
- Kidneys. No dose adjustment is needed in renal impairment.
- Lipids and bone. No clinically meaningful effect on cholesterol, triglycerides or bone mineral density was seen.
- Overdose. Single doses up to 400 mg and 80 mg/day for 3 months were given without adverse effects.
Monitoring
The Proscar label gives specific rules for reading PSA on finasteride:
| Situation | Label guidance |
|---|---|
| Starting treatment | Set a new PSA baseline at least 6 months after starting |
| Single PSA value after 6 or more months on treatment | Double it before comparing with normal ranges for untreated men |
| Any confirmed rise from the lowest on-treatment value | Evaluate for prostate cancer, even if still in the normal range |
| Percent free PSA | No adjustment needed |
| Missed doses | Can affect PSA results, so tell the doctor |
Legal status and use outside medicine
In the US, finasteride is a prescription-only drug, with brand and generic tablets listed on Drugs@FDA. It is not named in Schedule III (21 CFR 1308.13), where anabolic steroids are listed.
Finasteride and other 5α-reductase inhibitors are not named on the WADA 2026 Prohibited List. Anti-doping laboratories still treat them as possible confounders of the urinary steroid profile. A small study in 3 volunteers found that finasteride altered the metabolism of testosterone and of a nandrolone precursor, and shifted the carbon-isotope values used to confirm steroid doping (Iannella et al., Drug Test Anal 2021).
Key takeaways
- It lowers DHT, not testosterone. Finasteride cuts serum DHT by about 65–70% and slightly raises testosterone, without suppressing LH or FSH.
- Proven for BPH and male pattern hair loss. At 5 mg it cut the 4-year risk of BPH surgery and urinary retention by more than half; at 1 mg it preserved and partly regrew crown hair, but only while taken.
- Muscle and bone gains from testosterone appear intact. In older men on replacement-dose testosterone, adding finasteride did not reduce lean mass or bone gains and limited prostate growth. No data exist at higher doses.
- No effect on DHT-derived steroids, and theory suggests it may strengthen nandrolone. The nandrolone point rests on rat and in-vitro data only.
- Sexual and mood effects are the main concerns. Sexual side effects exceeded placebo by a few percentage points in the first year. Depression risk was raised in large cohorts, and persistent symptoms after stopping have been reported.
- It changes prostate cancer screening. PSA roughly halves, so values must be adjusted, and high-grade tumors were somewhat more common in PCPT, with no difference in survival.
Sources
- Organon. Proscar (finasteride) tablets, prescribing information, March 2026. DailyMed; Drugs@FDA, NDA 020180.
- Organon. Propecia (finasteride) tablets, prescribing information, October 2024. DailyMed; Drugs@FDA, NDA 020788.
- Rittmaster RS, Lemay A, Zwicker H, et al. Effect of finasteride, a 5 alpha-reductase inhibitor, on serum gonadotropins in normal men. J Clin Endocrinol Metab. 1992;75(2):484–488. PubMed.
- Drake L, Hordinsky M, Fiedler V, et al. The effects of finasteride on scalp skin and serum androgen levels in men with androgenetic alopecia. J Am Acad Dermatol. 1999;41(4):550–554. PubMed.
- Gormley GJ, Stoner E, Bruskewitz RC, et al. The effect of finasteride in men with benign prostatic hyperplasia. The Finasteride Study Group. N Engl J Med. 1992;327(17):1185–1191. PubMed.
- McConnell JD, Bruskewitz R, Walsh P, et al. The effect of finasteride on the risk of acute urinary retention and the need for surgical treatment among men with benign prostatic hyperplasia. Finasteride Long-Term Efficacy and Safety Study Group. N Engl J Med. 1998;338(9):557–563. PubMed.
- McConnell JD, Roehrborn CG, Bautista OM, et al. The long-term effect of doxazosin, finasteride, and combination therapy on the clinical progression of benign prostatic hyperplasia. N Engl J Med. 2003;349(25):2387–2398. PubMed.
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- Thompson IM, Goodman PJ, Tangen CM, et al. The influence of finasteride on the development of prostate cancer. N Engl J Med. 2003;349(3):215–224. PubMed.
- Thompson IM Jr, Goodman PJ, Tangen CM, et al. Long-term survival of participants in the prostate cancer prevention trial. N Engl J Med. 2013;369(7):603–610. PubMed.
- Page ST, Amory JK, Bowman FD, et al. Exogenous testosterone (T) alone or with finasteride increases physical performance, grip strength, and lean body mass in older men with low serum T. J Clin Endocrinol Metab. 2005;90(3):1502–1510. PubMed.
- Amory JK, Watts NB, Easley KA, et al. Exogenous testosterone or testosterone with finasteride increases bone mineral density in older men with low serum testosterone. J Clin Endocrinol Metab. 2004;89(2):503–510. PubMed.
- Bergink EW, Janssen PS, Turpijn EW, van der Vies J. Comparison of the receptor binding properties of nandrolone and testosterone under in vitro and in vivo conditions. J Steroid Biochem. 1985;22(6):831–836. PubMed.
- Liu L, Zhao S, Li F, et al. Effect of 5α-reductase inhibitors on sexual function: a meta-analysis and systematic review of randomized controlled trials. J Sex Med. 2016;13(9):1297–1310. PubMed.
- Lee S, Lee YB, Choe SJ, Lee WS. Adverse sexual effects of treatment with finasteride or dutasteride for male androgenetic alopecia: a systematic review and meta-analysis. Acta Derm Venereol. 2019;99(1):12–17. PubMed.
- Welk B, McArthur E, Ordon M, et al. Association of suicidality and depression with 5α-reductase inhibitors. JAMA Intern Med. 2017;177(5):683–691. PubMed.
- Garcia-Argibay M, Hiyoshi A, Fall K, Montgomery S. Association of 5α-reductase inhibitors with dementia, depression, and suicide. JAMA Netw Open. 2022;5(12):e2248135. PubMed.
- Nguyen DD, Marchese M, Cone EB, et al. Investigation of suicidality and psychological adverse events in patients treated with finasteride. JAMA Dermatol. 2021;157(1):35–42. PubMed.
- Iannella L, Colamonici C, Curcio D, et al. 5α-reductase inhibitors: evaluation of their potential confounding effect on GC-C-IRMS doping analysis. Drug Test Anal. 2021;13(11-12):1852–1861. PubMed.
- US Code of Federal Regulations. 21 CFR 1308.13, Schedule III. eCFR.
- World Anti-Doping Agency. The 2026 Prohibited List. WADA.