Prednicarbate is a corticosteroid used topically for its glucocorticoid activity in the treatment of various skin disorders. Prednicarbate is deesterified to form prednisolone-17-ethylcarbonate and prednisone. Being a topical preparation the systemic exposure is probably insignificant. As for prednisolone and prednisone conclusive pharmacokinetic evidence not compatible with CYP-inducing capacity in clinical use. Being ligand to glucocorticoid nuclear receptor giving rise to endogenous protective glucose production. Feedback inhibition of adrenal androgen production will add to a protective effect. No reports of porphyrogenic side effects in clinical use of prednisolone, but well documented evidence of tolerance in acute porphyria.

11β,17,21-Trihydroxypregna-1,4-diene-3,20-dione 17-(ethyl carbonate) 21-propionate (M=488.6).

Prednicarbate may be useful as a topical corticosteroid for the treatment of steroid-responsive dermatoses. However, since it is non-halogenated and is rapidly deesterified following topical absorption, it is much less likely to cause adverse local effects (skin atrophy) and systemic effects (adrenal suppression). Prednicarbate may be particularly advantageous for patients requiring long-term therapy, those at greater risk for adverse reactions, and pediatric patients who are more susceptible to the systemic effects of topical glucocorticoids.

Irrelevant.

In animals, prednicarbate is deesterified to form prednisolone-17-ethylcarbonate and prednisone. As a ligand to glucocorticoid nuclear receptor, prednisolon may participate in PXR activation and subsequent ALAS1 induction. Inducer of gluconeogenetic enzymes. Substrate of CYP3A4, the metabolism affected by CYP-inducers as well as by CYP3A4 inhibitors. No effects on the elimination rate of other CYP-metabolized drugs.