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Dutasteride

Emerging

Dual 5α-reductase inhibitor — knocks DHT down ~95%. | Pharmaceutical · Oral

Aliases (4)
Avodart · Jalyn · GG745 · Duagen
TYPICAL DOSE
BPH (FDA-approved): 0.5 mg/day PO
ROUTE
Oral (tablet)
CYCLE
Continuous use (BPH), continuous or 2-3×/wk (MPB)
STORAGE
Room temp; original container
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Brand options4 known
AvodartJalynGG745Duagen

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
Pharmacokinetics data not available for this compound.
No half-life mentions found in the source notes.
Research indications2 use cases

Type 1 5α-reductase

Most effective

skin (sebaceous glands), liver, scalp, brain

Type 2 5α-reductase

Effective

prostate, hair follicles, genitals, brain

Research protocols4 protocols
GoalDoseFrequencySoloCycle
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
FDA-approved manufacturer
NDC code on the bottle matches FDA registration. Generic OK; backyard not OK.
Brand vs generic listed
Pharmacy fills should disclose substitution. AB-rated generics are bioequivalent.
Tamper-evident packaging
Pharmacy seal intact, lot number + expiry visible on the bottle and the box.
!
Schedule labeling correct
C-II / C-IV warnings on label match the medication; report any mismatch to the pharmacist.
What to expect Generic
  1. 1
    Day 1
    PK-driven acute peak per administration. Verify dose tolerated.
  2. 2
    Week 1
    Steady-state reached for most daily-dosed pharma.
  3. 3
    Week 2-4
    Therapeutic effect established; titration window if needed.
  4. 4
    Long-term
    Periodic 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
  • minoxidilSynergistic
    Standard 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.
  • finasterideAvoid
    Redundant — dutasteride already covers Type 2 inhibition and goes further. No additive benefit, additive risk.
  • TRT / anabolic steroidsAvoid
    Suppressing DHT while pushing T creates abnormal androgen ratios. T → E2 conversion increases without DHT to shunt to. Gyno risk amplified.
  • enclomiphene / SERMsAvoid
    Mixed 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
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