5-alpha reductase

Every compound in the sci-wiki that affects 5-alpha reductase; the ones you can source are floated to the front, then the reference-only entries. Tap any for the full entry, mechanism, and outlets.

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Neurosteroid

5α-Dihydroprogesterone

5α-Dihydroprogesterone (5α-DHP) is an endogenous neurosteroid and progestogen formed when the enzyme 5α-reductase reduces progesterone at the A-ring of the steroid nucleus, yielding 5α-pregnane-3,20-dione. It occupies the committed first step of the principal neurosteroid pathway, standing between progesterone and allopregnanolone (its 3α-hydroxylated metabolite and one of the most potent naturally occurring positive modulators of the GABA-A receptor, the brain's main inhibitory ion channel). Unlike allopregnanolone, 5α-DHP is itself a high-affinity agonist of the classical (nuclear) progesterone receptor, driving progesterone-responsive gene transcription; in horses it is a fully biopotent progesterone receptor agonist that sustains the second half of pregnancy after circulating progesterone becomes undetectable. It is synthesized in situ within neurons and glia of the central and peripheral nervous systems, where its production rises after nerve injury and falls under chronic stress.

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Neurosteroid

Allotetrahydrocorticosterone

Allotetrahydrocorticosterone (3α,5α-tetrahydrocorticosterone, or allo-THB) is an endogenous neurosteroid generated by sequential 5α-reduction and 3α-hydroxylation of the adrenal glucocorticoid corticosterone. It is the corticosterone-derived structural counterpart of THDOC (which is formed the same way from deoxycorticosterone) and behaves as a positive allosteric modulator (an enhancer that boosts a receptor's response without activating it directly) of the GABA-A receptor (the brain's principal inhibitory chloride ion channel); the additional 11β-hydroxyl group it carries, however, makes it a considerably weaker potentiator than THDOC or allopregnanolone. Beyond GABA-A it shows an unusually broad ion-channel profile, inhibiting glycine receptors (a second inhibitory chloride channel, prominent in the brainstem and spinal cord) and N-type calcium channels (presynaptic channels that gate neurotransmitter release), opening large-conductance calcium-activated potassium channels (BK or Maxi-K channels) in sensory nerves, and retaining residual glucocorticoid-receptor agonism. Clinically it appears mainly as a minor urinary corticosteroid metabolite that indexes 5α-reductase activity in steroid profiling.

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