Finasteride — Type II 5α-reductase inhibitor

Post-Finasteride Syndrome (PFS) remains a polarizing topic in dermatology and urology; while the FDA added persistent sexual side effects to the label, high-quality RCT evidence specifically for PFS is lacking. Clinically, DHT suppression can also affect neurosteroids (allopregnanolone), potentially explaining mood-related side effects. For hair loss, finasteride is most effective at vertex (crown) and mid-scalp thinning; it is less effective for frontal recession. Combination with minoxidil is synergistic. PSA monitoring in older men on finasteride requires 'doubling' the measured value to assess prostate cancer risk correctly.

Overview

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Compound Class

Type II 5α-reductase inhibitor

Mechanism of Action

Irreversibly binds and inhibits Type II 5α-reductase — the enzyme that converts testosterone to DHT (dihydrotestosterone) in the scalp, prostate, liver, and skin. DHT is 5x more potent than testosterone at androgen receptors and is the primary driver of androgenetic alopecia via miniaturization of hair follicles. Finasteride reduces serum DHT by ~70% and scalp DHT by ~60-80%. Type II is the dominant isoenzyme in hair follicles and prostate. Dutasteride inhibits BOTH Type I and II isoenzymes, reducing serum DHT by ~90%, but is not FDA-approved for hair loss. Key pharmacokinetic point: 1mg/day (Propecia for AGA) vs 5mg/day (Proscar for BPH) — both approved.

Regulatory Status

FDA approved — Propecia 1997 (1mg AGA), Proscar 1992 (5mg BPH)

Evidence Level

High — PLESS trial (n=3040 for BPH), multiple RCTs for AGA; FDA-approved 1992 (BPH) and 1997 (AGA)