Corticotropin Other names: ACTH Adrenocorticotropin

The mechanism of action of corticotropin in the treatment of infantile spasms is unknown.

Corticotropin and endogenous ACTH stimulate the adrenal cortex to secrete cortisol, corticosterone, aldosterone, and a number of weakly androgenic substances. Prolonged administration of large doses of corticotropin induces hyperplasia and hypertrophy of the adrenal cortex and continuous high output of cortisol, corticosterone and weak androgens. The release of endogenous ACTH is under the influence of the nervous system via the regulatory hormone released from the hypothalamus and by a negative corticosteroid feedback mechanism. Elevated plasma cortisol suppresses ACTH release.

Corticotropin is also reported to bind to melanocortin receptors.

The trophic effects of endogenous ACTH and corticotropin on the adrenal cortex are not well understood beyond the fact that they appear to be mediated by cyclic AMP.

Corticotropin rapidly disappears from the circulation following its intravenous administration; in people, the plasma half-life is about 15 minutes. The pharmacokinetics of corticotropin have not been adequately characterized.

The maximal effects of a trophic hormone on a target organ are achieved when optimal amounts of hormone are acting continuously. Thus, a fixed dose of corticotropin will demonstrate a linear increase in adrenocortical secretion with increasing duration for the infusion.