Finasteride
Propecia / Proscar
Finasteride (Propecia / Proscar) is a hormonal & sexual research compound. Inhibits 5-alpha-reductase type 2, cutting conversion of testosterone to DHT by roughly 65–70% at 1mg. Follicles miniaturize under DHT, so lowering it halts the process in most men.
Finasteride quick facts
| Reported research dose | 1mg daily (hair) or 5mg daily (BPH) |
| Route | Oral |
| Frequency | 1x |
| Half-life | ~6–8 hours, but the enzyme inhibition far outlasts the drug. |
| Forms | Oral |
| Evidence level | Large RCTs for androgenetic alopecia and BPH |
The most effective oral for male pattern hair loss and the most argued-about drug in this space. ⚠️ Sexual side effects occur in a minority in trials; post-finasteride syndrome — persistent symptoms after stopping — is reported, contested, and not well understood, and anyone considering this should know that going in rather than after. It lowers PSA by about half, which will mask a rising PSA unless your doctor doubles it. Contraindicated in women of childbearing potential.
How Finasteride works
Inhibits 5-alpha-reductase type 2, cutting conversion of testosterone to DHT by roughly 65–70% at 1mg. Follicles miniaturize under DHT, so lowering it halts the process in most men.
Proposed benefits
Scalp DHT reduction for pattern hair loss, and prostate volume in BPH — a 5-alpha-reductase inhibitor. Sexual side effects are the documented concern and are covered on the page.
Where to get Finasteride
Buy Finasteride at AlgoRx →The evidence for Finasteride
Graded by what exists behind each claim.
✅ Clinically validated
- Large randomized trials support it for androgenetic alopecia and benign prostatic hyperplasia. The PCPT trial in over 18,000 men found reduced overall prostate cancer incidence with an apparent increase in high-grade disease — later analyses attributed much of that to detection bias in smaller prostates.
- Post-finasteride syndrome is the live controversy. Persistent sexual and neurological symptoms after discontinuation are reported in the literature and acknowledged on the label in several countries; whether it is a distinct entity and how common it is remain genuinely unsettled.
📊 Correlative data
- Very heavy real-world use with a bimodal reported experience — the large majority report no issues, a minority report significant and sometimes persistent effects. Both of those are true at once and neither cancels the other.
- It halves PSA, so any PSA result must be doubled and the prescriber told.
🧪 Theoretical / extrapolated
- A 5-alpha-reductase type 2 inhibitor, blocking conversion of testosterone to DHT — the androgen driving both follicular miniaturization and prostate growth.
- 5-alpha-reductase also produces neurosteroids such as allopregnanolone, which act on GABA-A receptors. That is the most plausible mechanistic account of the mood and cognitive symptoms a minority report, and it is why the topical route is of interest — less systemic enzyme inhibition.
How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →
What Finasteride actually does
Finasteride does not lower testosterone. It blocks one enzyme that converts testosterone into something more potent, and the whole clinical picture — benefit and harm together — comes from which isoform of that enzyme it blocks and which tissues carry it.
The enzyme and its two isoforms. Steroid 5-alpha-reductase reduces testosterone to dihydrotestosterone. DHT binds the androgen receptor with several-fold higher affinity than testosterone and dissociates more slowly, so it is the more powerful ligand at the same concentration. There are two isoforms. Type 1 predominates in sebaceous glands, liver and much of the skin. Type 2 predominates in the prostate, seminal vesicles, epididymis and the hair follicle of the scalp. Finasteride is selective for type 2. Dutasteride inhibits both, which is the entire pharmacological difference between them Roehrborn 2002 Nickel 2004.
What that selectivity buys and what it costs, as a number. The label states that finasteride produces a rapid fall in serum DHT, reaching 65% suppression within 24 hours of a single 1 mg tablet Propecia label 2022. Sixty-five percent, not ninety-five: the type 1 enzyme is still running. The residual DHT is the price of isoform selectivity, and the isoform selectivity is the reason the drug is tolerated at all.
Why the effect outlasts the drug, which the card gestures at and never explains. The label reports a plasma half-life of about 4.5 hours (range 3.3–13.4), roughly 5–6 hours in men aged 18 to 60, with bioavailability near 65% and about 90% plasma protein binding Propecia label 2022. A drug cleared in hours holds DHT down across a whole day because it is a mechanism-based inhibitor: the enzyme itself reduces finasteride to a dihydro species that stays bound in the active site, so the enzyme molecule that processes the drug is the enzyme molecule that is taken out of service. The pharmacodynamic half-life is a property of enzyme turnover, not of drug clearance, and this is why a missed dose matters less than the plasma numbers suggest.
The scalp argument, and its limit. Follicular miniaturization in androgenetic alopecia is androgen-driven and the follicle carries type 2 enzyme, so a type 2 inhibitor should slow it. It does — but so does minoxidil by a completely different route, and a comparison of their relative efficacy is its own paper Gupta 2022. Finasteride does not regrow a follicle that has already gone; it changes the rate of an ongoing process, which is why the drug is judged on what it prevents rather than on what it restores Landells 2025.
Cell, rodent, human — and where it stops
Step one, enzymology and pharmacokinetics: settled and old. The clinical pharmacokinetics and pharmacodynamics of finasteride were characterized in the 1990s Steiner 1996, and the isoform selectivity difference against dutasteride has its own comparative literature Nickel 2004 Almudimeegh 2024.
Step two, the twelve-month randomized adverse-event table, which is the number this argument is actually about. The Propecia label prints it directly, from 945 men on drug and 934 on placebo over twelve months Propecia label 2022:
Decreased libido 1.8% against 1.3%. Erectile dysfunction 1.3% against 0.7%. Ejaculation disorder 1.2% against 0.7%. Decreased ejaculate volume 0.8% against 0.4%.
Both halves of that table are informative and most writing quotes only one. The absolute rates are low — between one and two people in a hundred. The placebo rates are not zero, which means roughly half of the reported events in the drug arm occur without the drug. And the drug arm is consistently higher on all four measures, which means the effect is real.
Step three, the pooled picture, which is larger than the label's. A systematic review and meta-analysis of 5-alpha-reductase inhibitors covering 34 studies from 28 articles reports a 1.89-fold risk of sexual adverse effects (95% CI 1.74–2.05) and a 1.87-fold risk of post-finasteride-syndrome-like adverse effects (95% CI 1.64–2.14) Zhang 2022. A relative risk of 1.89 on a base rate of about 1% is roughly one extra affected person per hundred treated, and stating the relative risk without the base rate is how the same data is used to argue both sides.
Step four, the part the label puts in postmarketing rather than in the trial table. Sexual dysfunction that continued after discontinuation has been reported, including erectile dysfunction and ejaculation disorders Propecia label 2022. Postmarketing reports have no denominator, so they cannot give a rate; that is exactly why they sit in a different section of the label from the randomized table. They are the reason the meta-analysis above measured a PFS-like category at all, and they are neither proof nor dismissal.
Step five, the routes being tried to keep the follicle and drop the systemic exposure. A phase III, multicenter, randomized, double-blind, placebo-controlled study of a topical finasteride spray solution has been run in Chinese men with androgenetic alopecia Zhou 2025. The entire rationale of a topical is that the adverse-event table above is systemic and the target is not — and whether topical dosing actually escapes systemic DHT suppression is the question that determines whether it works as intended.
Where the chain breaks. (1) A twelve-month table cannot describe a drug taken for twenty years. (2) The trials were in men with androgenetic alopecia or benign prostatic hyperplasia, populations with their own baseline sexual-function rates. (3) The association between 5-alpha-reductase inhibitors and mood outcomes has been examined and is contested Garcia-Argibay 2022. (4) Nocebo is a real and measurable effect in this specific literature — the placebo arm reported all four events — and no trial has separated it from pharmacology by blinding people to the drug's identity and reputation.
What would have to be true, and how you would know it was not
Three predictions. The first says whether the enzyme is blocked, the second is the one that could kill somebody if it is not understood, and the third cuts against the drug.
1. If the enzyme is inhibited, DHT falls and testosterone does not. The mechanism predicts a specific pattern: DHT down by roughly two-thirds Propecia label 2022, total testosterone unchanged or slightly up, free testosterone unchanged, estradiol flat or marginally higher because more substrate is available to aromatase. Measure DHT and total testosterone at baseline and 12 weeks. If DHT has not fallen, the drug is not being taken, not being absorbed, or is not what it claims to be — and that is a question worth answering before attributing anything else to it.
2. The PSA rule, which is the most consequential thing on this page. 5-alpha-reductase inhibition lowers PSA. The label warns that any confirmed increase from the lowest PSA value reached on treatment may signal prostate cancer and should be evaluated even if the value is still inside the normal reference range Propecia label 2022. The failure mode is a cancer hidden by a number that looks normal. The practical version: record a PSA before starting, record the nadir on treatment, and tell any clinician who ever orders a PSA that you take this drug. That single sentence is worth more than everything else here.
3. The falsification test for the sexual adverse-effect argument, and it has to be prospective. The events are common enough on placebo Propecia label 2022 that memory is not evidence. Score the IIEF before the first dose, then at 12 weeks and at 6 months. If the score was already reduced at baseline, the drug did not cause it. If it falls after starting and recovers within weeks of stopping, that is a within-person time course — the strongest evidence one individual can generate about themselves, and the thing no meta-analysis can supply.
What nobody has tested yet
Four experiments nobody has run, and the first is the one the entire public argument turns on.
Nobody has run a prospective study of persistent symptoms with a pre-treatment baseline. Persistent sexual dysfunction after discontinuation appears in postmarketing reports Propecia label 2022 and is captured as a category in meta-analysis Zhang 2022, but every serious version of the question requires validated sexual and hormonal measurements before the first tablet in a large cohort, followed through treatment and after stopping. Without a baseline there is no way to distinguish a drug effect from an attribution, and that study has never been funded.
Nobody has genotyped the responders or the sufferers. The androgen receptor carries a polymorphic CAG repeat that sets receptor sensitivity, and 5-alpha-reductase type 2 has its own coding variants. Whether the small minority with marked symptoms differ genetically from the majority who report nothing is a cheap question with a clean design and no published answer.
Nobody has established whether topical dosing escapes the systemic effect. The phase III topical trial exists Zhou 2025. The measurement that settles the rationale is serum DHT on topical against oral at equivalent scalp efficacy. If serum DHT falls the same amount, the topical is an oral drug with extra steps.
Nobody has separated nocebo from pharmacology. All four adverse events occur in the placebo arm Propecia label 2022. A randomized trial in which participants are blinded not only to allocation but to the drug's identity and public reputation would measure how much of the reported burden is the molecule. It is ethically awkward, it is methodologically possible, and it has not been done.
Finasteride — its own safety story, not its class's
Finasteride is a prescription medicine with a full label. Here is what is specific, in the order that a person deciding about it needs it.
Sexual adverse effects are the known concern and they belong here as rates. Over twelve months against placebo: decreased libido 1.8% vs 1.3%, erectile dysfunction 1.3% vs 0.7%, ejaculation disorder 1.2% vs 0.7%, decreased ejaculate volume 0.8% vs 0.4% Propecia label 2022; pooled across 34 studies, a 1.89-fold relative risk of sexual adverse effects Zhang 2022. Uncommon, real, and larger than zero — all three of those at once is the honest description, and any page that gives you only one of the three is arguing rather than informing.
Persistence after stopping is reported and unquantified. The label records it under postmarketing experience Propecia label 2022. Postmarketing reports have no denominator and therefore no rate. This page will not tell you it is common and will not tell you it does not happen.
Pregnancy is the absolute one and it is not about the person taking the drug. DHT drives development of the external male genitalia in a male fetus. A 5-alpha-reductase inhibitor is therefore contraindicated in women who are or may become pregnant, and crushed or broken tablets must not be handled by them, because the coating is what prevents contact with the active ingredient.
Breast changes get their own line. Breast tenderness, enlargement or a lump should be evaluated rather than watched. The mechanistic reason is on this page already: blocking conversion to DHT leaves more testosterone available to aromatase.
Mood outcomes are contested, not settled. An association between 5-alpha-reductase inhibitors and depression, dementia and suicide has been examined in a large database study Garcia-Argibay 2022. Database studies of this kind carry confounding by indication, so the honest statement is that the question is open and that a new low mood starting after this drug is worth raising with a clinician rather than dismissing.
What this page will not do. Recommend a dose, or minimize either side of the argument. It is a licensed drug with a small, measured excess of sexual adverse effects, a real effect on hair loss, and a PSA interaction that a person must tell their clinician about for the rest of the time they take it.
Sources read for this page
- U.S. Food and Drug Administration. PROPECIA (finasteride) tablets, 1 mg — full prescribing information, including the twelve-month adverse experience table and the postmarketing report of persistent sexual dysfunction. DailyMed, U.S. National Library of Medicine; label revised 2022
- Zhang JJ, et al. Sexual, physical, and overall adverse effects in patients treated with 5alpha-reductase inhibitors: a systematic review and meta-analysis. Asian Journal of Andrology 2022 · PMID 34747724
- Zhou C, et al. Efficacy and safety of topical finasteride spray solution in the treatment of Chinese men with androgenetic alopecia: A phase III, multicenter, randomized, double-blind, placebo-controlled study. Chinese Medical Journal 2025 · PMID 40090937
Finasteride — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- These block 5-alpha-reductase, the enzyme converting testosterone to DHT. That is the point — DHT drives androgenetic hair loss and prostate growth — and it is also the mechanism behind every predicted problem, because DHT is not only a hair hormone.
- DHT contributes to libido, erectile function and mood. Suppressing it systemically predicts reduced libido, erectile difficulty and mood changes in a minority of users.
- Topical formulations (RU58841, topical finasteride) exist specifically to reduce systemic exposure. They are not exposure-free — measurable systemic absorption happens — but the argument for them is a real one rather than marketing.
What has actually been reported
- Sexual side effects are on the label and reported in trials at low single-digit percentages, typically resolving on discontinuation.
- Post-finasteride syndrome — persistent symptoms after stopping — is reported by a subset of users and remains genuinely contested. Its mechanism is not established, and dismissing it and asserting it are both overstating what is known.
- Finasteride and dutasteride roughly HALVE PSA. A 'normal' PSA of 2.0 on finasteride is effectively 4.0.
How to reduce the risk
Same mechanism as the prediction.
- Get a baseline PSA before starting, or a later reading has nothing to be compared against and the halving effect hides a real rise.
- Start topical rather than oral if the concern is systemic exposure. Dutasteride inhibits both isoenzymes and has a much longer half-life than finasteride — it is the harder one to reverse quickly.
- Stop at the first sign of persistent sexual or mood change rather than waiting to see whether it settles.
What it does to your bloodwork
A fact about the assay.
- PSA before starting and periodically after — and remember to double the reading for interpretation. Total testosterone, DHT if you want to confirm the drug is doing what you think.
Don't run this if
- You are or may become pregnant, or you are a woman of childbearing potential — these are teratogenic and the risk is to a male fetus. Do not handle crushed or broken tablets.
- You are actively trying to conceive; effects on semen parameters are documented.
The honest unknown
- Whether persistent post-treatment symptoms represent a distinct syndrome, and who is susceptible, is unresolved.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Finasteride — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Finasteride moves on your bloodwork
Expected direction, not a measured one.
- Complete Blood Count (CBC) with Differential — ↑ expected to rise
Hematocrit and hemoglobin rise — androgens stimulate erythropoiesis. This is the most reliably predictable movement of any compound in the Vault.
What to do: This is the number that decides whether you keep going. Baseline and every 3 months. Dehydration on the draw day inflates it, so hydrate normally or you will chase a false reading. - Total Testosterone — ↑ expected to rise
Expected. Trough vs peak matters enormously — the same protocol reads completely differently depending on when you drew.
What to do: Draw at the same point in the cycle every time or the trend is noise. - LH & FSH — ↓ expected to fall
Suppressed by negative feedback. This is the mechanism, not a side effect — and it is why exogenous androgen shuts down your own production.
What to do: Relevant if fertility matters to you. Worth knowing before, not after. - Estradiol, Sensitive (LC/MS-MS) — ↑ expected to rise
Aromatization converts a fraction to estradiol, and it rises with the androgen. Use the sensitive (LC-MS/MS) assay — the standard immunoassay is unreliable in men and produces numbers people then medicate.
What to do: If you are reading estradiol in a man, the assay choice matters more than the result. - SHBG (Sex Hormone-Binding Globulin) — ↓ expected to fall
Falls with androgen exposure, which raises the free fraction — so free testosterone can climb faster than total.
What to do: Read total and SHBG together; total alone understates what changed. - Lipid Panel (Cholesterol, HDL, LDL, Triglycerides) — ↓ expected to worsen
HDL falls, sometimes markedly. Oral 17-alpha-alkylated compounds do this far more aggressively than injectable esters.
What to do: Baseline and 12 weeks. ApoB is the better long-term read than LDL-C. - PSA (Total + Free + % Free) — ↑ expected to rise
Androgens can raise PSA modestly. It does not create prostate cancer that wasn't there, but it can unmask it.
What to do: Baseline before starting matters — without it, a later number has nothing to be compared against.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Finasteride in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Finasteride
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| Total Testosterone | The baseline you can't reconstruct later |
| Free Testosterone | The fraction that does anything — total alone misleads |
| SHBG (Sex Hormone-Binding Globulin) | Explains a normal total sitting on top of a low free |
| Estradiol, Sensitive (LC/MS-MS) | The other half of the ratio, and the source of most symptoms |
| LH & FSH | Separates a testicular problem from a pituitary one |
The “Low T? Rule Out the Reversible Causes First” panel covers these in one order — 11 markers, $211.50 with the discount applied.
Check results you already have → · All 103 markers A–Z
Finasteride — frequently asked questions
What is Finasteride?
Finasteride (Propecia / Proscar) is a hormonal & sexual research compound. Inhibits 5-alpha-reductase type 2, cutting conversion of testosterone to DHT by roughly 65–70% at 1mg. Follicles miniaturize under DHT, so lowering it halts the process in most men.
Is the full Finasteride protocol on this page?
The reported research dose is on this page, along with how Finasteride works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of Finasteride?
Finasteride has an approximate half-life of ~6–8 hours, but the enzyme inhibition far outlasts the drug., which is part of what determines how often it's dosed.
What's the evidence behind Finasteride?
Current evidence level: Large RCTs for androgenetic alopecia and BPH. Finasteride is offered for research purposes only and is not an approved medicine.
Finasteride inside a finished plan
One arm of 2 Protocol Blueprints, free to read in full.
What Finasteride is used for
Finasteride appears under 2 goals in the goal router.
Related Hormonal & Sexual compounds
Where this goes next
Finasteride is the dht & hair arm of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.