CJC-1295
Also known as: CJC-1295 DAC, CJC-1295 Without DAC, Mod GRF 1-29
Molecular Formula
Molecular Weight
3,367.9 Da (Non-DAC Free Base; DAC Free Base C165H269N47O46 ~3,647.28 Da)
Half-Life
5.4–9.2 days (for DAC form in healthy volunteers; human PK for non-DAC form unestablished)
Sequence
Tyr-D-Ala-Asp-Ala-Ile-Phe-Thr-Gln-Ser-Tyr-Arg-Lys-Val-Leu-Ala-Gln-Leu-Ser-Ala-Arg-Lys-Leu-Leu-Gln-Asp-Ile-Leu-Ser-Arg-NH2
Clinical Applications & Evidence
Mechanism of Action
CJC-1295 acts as an agonist at the GHRH receptor on anterior pituitary somatotrophs, activating Gs protein–adenylyl cyclase–cAMP signaling to stimulate growth hormone (GH) secretion and downstream hepatic IGF-1 synthesis. The DAC form produces sustained GH-axis stimulation with elevated trough GH levels rather than simple physiological pulses. Nonclinical mouse studies observed DNA-damage signals after prolonged GHRH analog stimulation, raising unquantified theoretical concerns for pituitary hyperplasia.
Investigated Uses
- Pituitary GH & IGF-1 stimulation (Healthy adult volunteer single- & multiple-dose PK/PD trials for DAC form)
- Growth hormone deficiency (Unproven in clinical trials; requires functional pituitary somatotrophs)
- HIV-associated visceral obesity (Historical Phase 2 trial NCT00267527; terminated following a participant death from coronary artery disease)
- Body composition & tissue recovery (Preclinical animal models; unproven in human clinical trials)
Regulatory & Safety Status
FDA Status
Research OnlyWADA / Athletic Status
Prohibited at All Times (WADA S4.4.1)Known Side Effects
Contraindications
- WADA-tested athletes (Prohibited at all times under S2.2.4 Growth Hormone-Releasing Factors)
- Active malignancy or history of cancer (Precautionary exclusion due to GH/IGF-1 axis stimulation)
- Pregnancy and lactation (Unstudied safety profile)
- Severe cardiovascular disease or baseline hypotension (Precautionary exclusion due to vasodilatory reactions)
Drug Interactions
- Exogenous growth hormone or GH secretagogues (Theoretical additive GH/IGF-1 elevation)
- Glucocorticoids (Theoretical blunting of GHRH-mediated GH response)