Finasteride
The most effective single agent for halting male-pattern loss, and the one that acts furthest upstream.
AStrong evidence in men · limited/caution in women
Oral finasteride lowers scalp DHT and halts progression in most men, with regrowth in a meaningful minority. It addresses the driver of miniaturization, but removing a brake is not the same as pressing the accelerator, which is why it pairs so naturally with growth-side approaches.
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Mechanism
Finasteride blocks the type-II 5α-reductase enzyme that converts testosterone to DHT, the androgen that shortens anagen in sensitive follicles. Less DHT means slower miniaturization. It does nothing to restart follicles that have already gone quiet, that requires a growth signal, not the removal of an inhibitory one.
What the trials show
Large, replicated RCTs in men, the basis of the A.
Safety & who it's for
Most men tolerate it well; a minority report sexual side effects that typically resolve on discontinuation. It requires a prescription and medical oversight. It is not for women who may become pregnant, and its evidence in female-pattern loss is far weaker and situation-dependent.
Read honestly: finasteride is one of the two Grade-A pillars. Its ceiling is that it defends rather than rebuilds, which is exactly the gap the growth-factor frontier is trying to close.
