ACTH (1-39)
Aliases: Corticotropin · Adrenocorticotropic hormone · Acthar · Repository corticotropin
Last verified: 2026-09-24
The short version
ACTH is paradoxically present on gray lists: it is a 1952 drug with a strong evidence base — but what is now sold as 'ACTH 1-39' to the community is an odd purchase. A hormone whose only sensible goal is raising cortisol is being used in contexts (training, recovery) where higher cortisol is precisely what people try to avoid. Part of the story comes from the old bodybuilding theory that 'ACTH stimulates androgens via adrenal androgens' — a pharmacologically negligible pathway in adult men. Conclusion: a serious drug, serious indications, no sense at all as a gray substance.
Identity & type
- Molecular type
- hormone
- Sequence / structure
- 39 aa, ~4.5 kDa
- Molecular weight
- ~4.5 kDa
- Origin
- Human pituitary hormone; Acthar gel = natural porcine ACTH(1-39) in repository formulation; cosyntropin = synthetic (1-24).
Mechanism of action
The endogenous 39-amino-acid pituitary hormone; binds the melanocortin-2 receptor (MC2R) in the adrenal cortex → stimulation of cortisol synthesis and secretion (plus androgens, and aldosterone at higher doses); the long-acting repository gel provides prolonged pulsatile stimulation.
Dosing & routes
Official / clinical context
Official documents: FDA approval 1952, Acthar gel prescribing information; cosyntropin as a diagnostic test in all standard endocrine guidelines.
Regulator-approved labeling and published study designs — never a recommendation.
Community-reported practice
Occasionally appears in 'hormone stacks' with a myth of 'natural corticosteroid support'; doses are copied arbitrarily, without understanding that the repository gel has a completely different profile from a solution. Serious endocrine specialist supervision is mandatory for approved indications — for gray purposes there is none.
Unverified self-reports. Not medical advice. Not endorsement.
Protocol — official vs community
Official / label
H.P. Acthar Gel (repository corticotropin; infantile spasms and a set of autoimmune/allergic indications): dosing is indication-specific and supervised — infantile spasms uses weight/surface-area-based twice-daily IM courses with a defined 2-week taper after the treatment phase; other labeled indications use 40–80 IU IM every 24–72 h.
- 01Infantile spasms: twice-daily IM course per label, then a supervised stepwise taper over ~2 weeks
- 02Other indications: 40–80 IU IM every 24–72 h, individualized to response
Duration: Course-defined in infantile spasms (treatment plus taper, ≈4 weeks); intermittent in other indications.
Carries the full glucocorticoid-equivalent adverse-effect profile: hypertension, hyperglycemia, immunosuppression, HPA-axis disturbance — plus, uniquely, injection-site reactions from the gel vehicle. WADA S2 prohibited. A gray 'ACTH' research vial is not the repository gel; the formulation is the pharmacokinetics.
Community (anecdotal)
Structured protocol data for this entry is coming.
Human evidence
Very strong for approved indications — decades of clinical use and RCTs. Outside those indications ('cortisol doping', anabolic myths) — there is no sensible goal.
Preclinical evidence
Basic endocrinology — one of the best understood peptide pathways in existence.
Known risks
- All corticosteroid complications: infections, hyperglycemia, hypertension, osteoporosischaracterized
- Suppression of the native HPA axis with longer usecharacterized
Teal: characterized in clinical/labeling contexts. Amber: theoretical or reported outside controlled settings.
Unknowns & evidence gaps
- No clinical 'unknowns' for the indications; gray use is itself an unknown
Frequently asked questions
References
- H.P. Acthar Gel (repository corticotropin) — FDA prescribing information
- Infantile spasms treatment guidelines — ACTH first-line evidence
- WADA Prohibited List — S2 Peptide Hormones