Comparative Pharmacology
Head-to-head clinical analysis: ACTHAR GEL versus ACTHAR GEL AUTOINJECTOR.
Peer-Reviewed Evidence
Head-to-head clinical analysis: ACTHAR GEL versus ACTHAR GEL AUTOINJECTOR.
ACTHAR GEL vs ACTHAR GEL (AUTOINJECTOR)
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Stimulates adrenal cortex to secrete cortisol, corticosterone, and aldosterone; also exerts extra-adrenal effects via melanocortin receptors.
ACTHAR Gel (repository corticotropin injection) acts primarily by stimulating the adrenal cortex to secrete corticosteroids (cortisol, corticosterone, and aldosterone), which exert anti-inflammatory, immunosuppressive, and antiproliferative effects. The exact mechanism in specific indications (e.g., infantile spasms) is not fully understood but may involve modulation of the hypothalamic-pituitary-adrenal axis and direct effects on the central nervous system.
Initial: 40-80 Units intramuscularly or subcutaneously every 24-48 hours; maintenance: 40 Units intramuscularly or subcutaneously every 24-72 hours.
Initial: 40-80 units intramuscularly or subcutaneously every 24-48 hours; maintenance: 20-40 units intramuscularly or subcutaneously every 48 hours. Titrate based on response.
None Documented
None Documented
Terminal elimination half-life approximately 2–3 hours for corticotropin component; repository formulation (gel) extends to 15–20 hours due to slow absorption.
The terminal half-life of exogenously administered ACTH is approximately 15 minutes; however, the duration of adrenal cortisol stimulation persists for 6-12 hours after IM administration due to prolonged absorption from the gel formulation.
Renal metabolism and excretion (primarily as inactive metabolites); <5% unchanged in urine. Biliary/fecal excretion negligible.
ACTH (corticotropin) is metabolized by tissue peptidases; renal excretion accounts for <5% of unchanged drug. Biliary/fecal elimination is negligible.
Category C
Category C
Corticotropin
Corticotropin