Misoprostol (DB00929): A Comprehensive Pharmacological and Clinical Monograph

Executive Summary

Misoprostol is a synthetic prostaglandin E1 (PGE1) analogue, a small molecule drug with a remarkable and complex dual identity in modern medicine.[1] Originally developed and granted FDA approval in 1988 for a narrow indication—the prevention of gastric ulcers induced by nonsteroidal anti-inflammatory drugs (NSAIDs)—its clinical profile has been profoundly reshaped by its extensive and potent off-label applications in obstetrics and gynecology.[3] This report provides an exhaustive analysis of misoprostol, synthesizing its chemical properties, pharmacological mechanisms, multifaceted clinical uses, and critical safety considerations.

The drug's primary mechanism for its approved indication involves acting as a prostaglandin agonist on gastric parietal cells, where it inhibits acid secretion and provides a cytoprotective effect by enhancing the secretion of mucus and bicarbonate.[3] This directly counteracts the mucosal damage caused by NSAIDs. Concurrently, misoprostol exerts powerful uterotonic effects by binding to prostaglandin receptors in the myometrium and cervix, leading to increased uterine contractility and cervical ripening.[1] This second mechanism forms the basis for its widespread off-label use in labor induction, medical termination of pregnancy, management of miscarriage, and prevention and treatment of postpartum hemorrhage.[3]

A defining feature of misoprostol is the critical influence of the administration route on its pharmacokinetic profile. Oral and sublingual routes provide rapid peak plasma concentrations ideal for acute interventions, whereas vaginal and rectal administration result in slower absorption and sustained action, suitable for applications like labor induction.[3] This deliberate manipulation of pharmacokinetics is a cornerstone of its versatile clinical application.