CJC-1295: Two forms, one research record, fourteen years of citations — here is what the studies actually measured.
A peer-reviewed digest of the GHRH analog CJC-1295 — mechanism, pharmacokinetics, the with-DAC vs no-DAC distinction, and the ipamorelin stack.
What the CJC-1295 Literature Has Demonstrated
CJC-1295 is a synthetic 29-amino-acid analog of human growth hormone-releasing hormone (GHRH). A single subcutaneous injection of the with-DAC form elevated mean plasma GH concentrations 2- to 10-fold in healthy adults and sustained that elevation for six days or more; IGF-1 rose 1.5- to 3-fold for nine to eleven days.[1] That finding — one injection, nearly two weeks of measurable hormonal response — is the result of a maleimide–Cys34 thioether bond that tethers the peptide to circulating albumin after injection, extending half-life from roughly thirty minutes (no-DAC form) to 5.8–8.1 days (with-DAC).[3]
The two forms share a 29-residue GHRH backbone with four amino-acid substitutions that confer resistance to dipeptidyl peptidase-IV (DPP-IV) cleavage. The with-DAC form carries an additional C-terminal Drug Affinity Complex (DAC) extension — the structural difference that produces a 250-fold difference in half-life and fundamentally distinct dosing architectures. Understanding this distinction is the starting point for reading the CJC-1295 literature.[14]
The human evidence base is modest: two randomized, placebo-controlled, double-blind trials conducted by Teichman et al. (2006) and Ionescu and Frohman (2006) in a combined n=24 healthy adults, with a maximum duration of 49 days.[1][2] No peer-reviewed human pharmacokinetic data exists for the no-DAC form (Mod GRF 1-29). Rodent studies extend the picture — GHRH-knockout mice normalized body weight, bone length, and GH mRNA expression with once-daily CJC-1295 over five weeks[4] — but species translation is not established. The site records what was measured; the limits of the data are part of that record.
What the Research Says: CJC-1295 Benefits
The downstream findings across the CJC-1295 literature cluster around two axes: GH/IGF-1 elevation and the downstream physiology that follows from it.
In the Teichman 2006 trial, mean GH rose 2- to 10-fold dose-dependently at doses of 30, 60, 90, and 125 μg/kg SC; IGF-1 followed, rising 1.5- to 3-fold and remaining elevated for nine to eleven days.[1] The Ionescu and Frohman 2006 sub-study confirmed that pulsatile GH secretion is preserved during continuous CJC-1295 administration — trough GH rose 7.5-fold above baseline (P<0.0001) and mean GH rose 46%, but pulse frequency and amplitude remained intact.[2] This is a mechanistically important distinction from exogenous GH, which suppresses endogenous pulsatile output via negative feedback.
For body composition, the most rigorous human evidence in the GHRH analog class comes from tesamorelin, an FDA-approved GHRH analog. In randomized controlled trials, tesamorelin reduced visceral adipose tissue by 10.9% at six months and approximately 18% at twelve months in HIV-associated lipodystrophy;[9] a 2026 meta-analysis of GHRH analog RCTs confirmed the class effect.[21] CJC-1295 and tesamorelin are distinct compounds; the tesamorelin data is cited here as mechanistic context for the GHRH compound class, not as direct CJC-1295 evidence.
Ipamorelin, the predominant co-studied partner, counteracted glucocorticoid-induced decreases in bone formation in rats — periosteal bone formation rate was four times higher in the ipamorelin group[10] — and counteracted prednisolone-induced catabolism in a seven-day rat model, improving whole-body nitrogen balance comparably to exogenous GH.[11] These ipamorelin findings are relevant to understanding the stacking rationale covered on the CJC-1295 ipamorelin stack page.
What Is CJC-1295? (Peptide, Not Steroid)
CJC-1295 is a peptide — a short chain of amino acids — not a steroid. It has no steroidal ring structure and does not directly bind androgen, estrogen, or glucocorticoid receptors. It acts exclusively on pituitary somatotroph GHRH receptors (GHRH-R) via a Gαs-coupled adenylyl cyclase cascade that elevates intracellular cAMP, activates protein kinase A (PKA), and drives both GH exocytosis and GH gene transcription.[12] The structural category is relevant because the compound is sometimes conflated with anabolic steroids in community literature; the mechanisms are entirely distinct.
CJC-1295 is not FDA-approved for any indication. It was reviewed by the FDA Pharmacy Compounding Advisory Committee in December 2024 for potential 503A bulk-drug compounding inclusion (docket FDA-2024-N-4777); the FDA identified potential immunogenicity concerns related to aggregation in injectable compounded formulations.[16] Its WADA status is prohibited under Section S2. This site documents the research record only.
What Does CJC-1295 Do?
CJC-1295 is a synthetic GHRH analog that binds pituitary somatotroph GHRH receptors, stimulating pulsatile or sustained growth hormone secretion depending on whether the DAC extension is present. The GHRH-R activation cascade — Gαs coupling → adenylyl cyclase → cAMP elevation → PKA → CREB phosphorylation → GH gene transcription, plus voltage-dependent calcium-channel opening for acute GH exocytosis — is comprehensively reviewed in a 2025 paper by Halmos et al.[12]
Downstream, elevated GH drives hepatic IGF-1 synthesis. GH also stimulates sodium reabsorption in the distal nephron via a mechanism that prevents pressure natriuresis,[8] explaining the water retention reported at higher doses in the Teichman trial.[13] For further detail on observed downstream effects, see the CJC-1295 dosage in research protocols and CJC-1295 side effects pages.
With DAC: 5.8–8.1 days
Without DAC: ~30 minutes
2 published RCTs, n=24 total, max 49 days duration
GHRH receptor agonist → Gαs/cAMP/PKA → GH secretion