Dutasteride
EmergingDual 5α-reductase inhibitor — knocks DHT down ~95%. | Pharmaceutical · Oral
Aliases (4)
▸Brand options4 known
StatusRx (US, prescription only)
▸ Overview TL;DR
Dual 5α-reductase inhibitor — knocks DHT down ~95%. FDA-approved for BPH, off-label hammer for male pattern baldness. Wrong drug for a 20-year-old with no hair loss and an intact HPG axis. PFS risk + 5-week half-life make it a high-stakes commitment. Topical ru58841 is the smarter first-line if MPB ever appears.
▸ Mechanism of action
Dutasteride is a competitive, irreversible inhibitor of both Type 1 and Type 2 5α-reductase, the enzymes that convert testosterone → dihydrotestosterone (DHT).
- Type 1 5α-reductase: skin (sebaceous glands), liver, scalp, brain
- Type 2 5α-reductase: prostate, hair follicles, genitals, brain
- Finasteride inhibits only Type 2 (~70% DHT reduction)
- Dutasteride inhibits both (~95% DHT reduction at 0.5 mg/day, plateauing in 1-2 weeks of dosing but full receptor occupancy in days)
DHT is the dominant androgen in the prostate and miniaturizing hair follicles in genetically susceptible scalps. Suppressing DHT shrinks the prostate (BPH benefit) and halts/reverses follicular miniaturization (MPB benefit).
DHT is also a major neurosteroid precursor — 5α-reductase produces allopregnanolone (ALLO), 3α-androstanediol, and other GABA-A-active metabolites. Cutting central 5α-reductase activity disrupts ALLO biosynthesis, which is the leading mechanistic candidate for the mood/anxiety/cognitive components of post-finasteride syndrome (PFS).
The half-life is ~5 weeks (vs ~6 hours for finasteride). This is a defining feature of dutasteride: any adverse effect persists for months after discontinuation, and steady-state takes ~6 months to fully wash out.
▸ Pharmacokinetics No data
▸Research indications2 use cases
Type 1 5α-reductase
Most effectiveskin (sebaceous glands), liver, scalp, brain
Type 2 5α-reductase
Effectiveprostate, hair follicles, genitals, brain
▸Research protocols4 protocols
| Goal | Dose | Frequency | Solo | Cycle |
|---|---|---|---|---|
| BPH (FDA-approved) | 0.5 mg/day PO | — | — | — |
| MPB (off-label, full dose) | 0.5 mg/day — same as BPH dose | — | — | — |
| MPB (off-label, reduced frequency) | 0.5 mg 2-3×/week — leverages 5-week half-life to maintain DHT suppression with lower cumulative exposure | — | — | — |
| For Dylan | — | — | — | — |
Auto-extracted from dosing notes. For full context including caveats and Dylan-specific protocols, see the Dosing protocols section.
▸Quality indicators4 checks
▸ What to expect Generic
- 1Day 1PK-driven acute peak per administration. Verify dose tolerated.
- 2Week 1Steady-state reached for most daily-dosed pharma.
- 3Week 2-4Therapeutic effect established; titration window if needed.
- 4Long-termPeriodic monitoring per drug class (labs, BP, ECG as applicable).
▸ Side effects + safety
Common (>10% in BPH trials, lower in younger MPB users):
- Decreased libido (3-7% on-drug)
- Erectile dysfunction (4-9% on-drug)
- Decreased ejaculate volume (1-3%)
- Gynecomastia / breast tenderness (1-3%)
Less common (1-10%):
- Depression / depressed mood
- Dizziness
- Hot flashes
- Headache
Rare-serious (<1% but worth knowing):
- Post-Dutasteride Syndrome (PDS): persistent sexual/neurological/physical symptoms after stopping. Reversibility unknown. Higher stakes with dutasteride than finasteride due to long half-life and dual inhibition.
- High-grade prostate cancer risk paradox: REDUCE trial showed reduction in low-grade PCa but slight increase in Gleason 8-10. Clinical significance debated; PSA interpretation altered (multiply by ~2 on dutasteride).
- Severe depression / suicidal ideation — rare but documented.
- Male breast cancer — rare association; FDA label includes warning.
- Birth defects in male fetuses — pregnant women and women of childbearing age should not handle crushed/leaking capsules; teratogenic in offspring exposed in utero. Donor sperm/blood deferral 6 months after last dose.
Specific watch periods:
- First 3 months: peak window for sexual side effects to manifest. Stop immediately if onset.
- First 6 months: any depression/cognitive change → discontinue and seek workup.
- Ongoing: PSA monitoring (×2 multiplier), breast self-exam, mood tracking.
▸Interactions5 compounds
- minoxidilSynergisticStandard MPB combo — minoxidil acts on follicle vascularization/growth phase; dutasteride suppresses the upstream DHT signal. Different mechanisms, additive …
- anastrozoleSynergistic(low-dose): Some users add to manage E2 elevation from T → E2 shunting when DHT is suppressed. Use only with bloodwork confirmation; otherwise avoid.
- finasterideAvoidRedundant — dutasteride already covers Type 2 inhibition and goes further. No additive benefit, additive risk.
- TRT / anabolic steroidsAvoidSuppressing DHT while pushing T creates abnormal androgen ratios. T → E2 conversion increases without DHT to shunt to. Gyno risk amplified.
- enclomiphene / SERMsAvoidMixed signals — enclomiphene raises endogenous T (some of which routes through 5αR); blocking that conversion changes the SERM's downstream profile in ways n…
▸References8 sources
GlaxoSmithKline Avodart prescribing information
FDA label, full PK/AE profile
Olsen EA et al. 2006, J Am Acad Dermatol — Dutasteride vs finasteride for MPB
2006pivotal MPB efficacy trial
Eun HC et al. 2010, J Am Acad Dermatol — Korean MPB trial
2010replication of efficacy in Asian population
REDUCE trial (Andriole 2010, NEJM)
2010prostate cancer prevention with high-grade signal
PFS Foundation
patient-reported PFS/PDS evidence, mechanistic research links
Traish AM 2018, Endocr Connect — 5α-reductase inhibitors and persistent adverse effects review
2018neurosteroid disruption hypothesis
Melcangi RC et al. 2017, J Steroid Biochem Mol Biol — Neuroactive steroids in PFS
2017ALLO and androgen metabolite changes
WADA Prohibited List (current year)
confirm current sport-specific status before competition