CJC-1295: Long Half-Life, Thin Human File

The short version

CJC-1295 is a synthetic analog of the first 29 residues of human GHRH, engineered for extended activity. It carries four amino-acid substitutions that block the main enzymes that would degrade it, and in its DAC (Drug Affinity Complex) variant, a reactive linker that forms a covalent bond with albumin in the bloodstream — the body's long-lived carrier protein. The result is a GHRH analog with a plasma half-life of 5-8 days; a single dose can keep GH and IGF-1 elevated for over a week ^[15].

Here is the honest picture. CJC-1295 has never been approved for human use anywhere. Its human evidence is limited to two early pharmacokinetic studies in healthy adults that showed sustained GH/IGF-1 elevation and preserved pulsatility ^[15][16]. It was reviewed (and not recommended for the 503A compounding list) by the FDA Pharmacy Compounding Advisory Committee in 2024. It is prohibited in sport. Popular dosing protocols circulating online are not derived from controlled human trials. This page summarizes what was published; it provides no dose recommendations.

What it is

CJC-1295 is built on hGRF(1-29) — the first 29 residues of human growth hormone-releasing factor — with four amino-acid substitutions: D-Ala at position 2 (blocks DPP-IV cleavage), Gln at position 8, Ala at position 15, and Leu at position 27 (the last three stabilize the alpha-helix and block oxidation and deamidation). This four-substitution scaffold is sometimes sold under the name "Modified GRF 1-29" or "Mod GRF 1-29" and is short-acting.

The DAC variant adds a C-terminal lysine functionalized with a maleimidopropionyl (MPA) linker that undergoes a Michael addition reaction with the free thiol on Cys34 of circulating serum albumin, forming a covalent peptide-albumin conjugate. Albumin has a half-life of roughly 19 days; CJC-1295 DAC's observed half-life in humans is 5.8-8.1 days ^[15]. The two variants — DAC and no-DAC — are pharmacokinetically very different, a distinction frequently blurred in commercial and community sources.

How it works

CJC-1295 binds the GHRH receptor on anterior-pituitary somatotrophs, activating Gs/cAMP/PKA signaling that stimulates synthesis and pulsatile secretion of GH, which in turn drives hepatic IGF-1 production. The mechanism is the same as sermorelin and tesamorelin; the engineering difference is duration.

A key finding from a 2006 study in healthy men: despite continuous stimulation by CJC-1295, the pulsatile pattern of GH secretion was preserved. Basal GH rose approximately 7.5-fold, mean GH by ~46%, and IGF-1 by ~45% one week after dosing, but the frequency and magnitude of individual GH pulses were unaltered ^[16]. This indicates that continuous GHRH-receptor stimulation does not collapse pulsatility — the pituitary's own secretory machinery continues to operate. The albumin conjugation is a pharmacokinetic strategy, not a receptor modification ^[1].

What the research shows

Pharmacokinetics and sustained GH/IGF-1 elevation. The pivotal PK study in healthy adults aged 21-61 found that single subcutaneous doses of 30 or 60 mcg/kg CJC-1295 produced dose-dependent 2- to 10-fold increases in mean plasma GH lasting 6 days or more, and 1.5- to 3-fold increases in IGF-1 lasting 9-11 days. After multiple doses, IGF-1 remained above baseline up to 28 days; estimated half-life was 5.8-8.1 days ^[15].

Preserved pulsatility. In healthy 20- to 40-year-old men, a single subcutaneous dose of CJC-1295 (60 or 90 mcg/kg) produced the elevations described above while leaving GH pulse frequency and magnitude unchanged, confirming physiologic pulsatility persists under continuous GHRH-analog stimulation ^[16].

Serum proteomics. In 11 healthy young men, CJC-1295 administration shifted the serum proteome in a reproducible pattern — decreased apolipoprotein A1 and a transthyretin isoform, increased albumin-fragment and immunoglobulin species — with the immunoglobulin/albumin-fragment signal correlating linearly with IGF-1. These shifts were identified as candidate biomarkers of GH/IGF-1 axis activation ^[14].

Anti-doping identification. CJC-1295 was positively identified by high-resolution LC-MS/MS as the active ingredient in an unknown "GHRH" pharmaceutical preparation seized in an anti-doping context, confirming the compound is used and detectable outside formal trials ^[13].

Class context. The 2025 Nature Reviews Endocrinology review frames CJC-1295 alongside sermorelin and tesamorelin in the therapeutic and investigational landscape of GHRH analogs ^[1].

Reported effects, cautions and safety

The cautions below are drawn from the cited literature.

• No regulatory approval. CJC-1295 has never been approved by the FDA or any major regulator for human use. It is sold and handled as a research chemical.
• Reviewed unfavorably for compounding. FDA briefing materials for the 2024 Pharmacy Compounding Advisory Committee cited immunogenicity and other safety concerns for GH secretagogues including CJC-1295; it was not recommended for the 503A bulk drugs list.
• Sustained GH/IGF-1 elevation: theoretical concerns. Sustained elevation of IGF-1 raises theoretical questions: epidemiologic data link higher circulating IGF-1 to modestly increased risk of certain cancers, and GH-axis stimulation can cause fluid retention, edema, and effects on insulin sensitivity ^[1].
• DAC vs no-DAC conflation. Community sources routinely conflate the long-acting albumin-conjugate (CJC-1295 DAC) with the short-acting no-DAC variant; they are pharmacokinetically very different and should not be treated as equivalent.
• Human evidence is early-phase and limited. Published human data are confined to early PK studies; there are no controlled efficacy trials, no long-term safety data, and no approved indication for any population.
• WADA prohibition. CJC-1295 is prohibited at all times under WADA Section S2 (Peptide Hormones, Growth Factors, Related Substances and Mimetics). Detection assays using LC-MS/MS and immuno-PCR are well established.

Where it fits in GH-axis research

CJC-1295 is the furthest-engineered and least-regulated of the three. Where sermorelin has decades of clinical history and a former approval, and tesamorelin has current FDA approval for a specific indication, CJC-1295 occupies a research-only position: a pharmacokinetically interesting molecule with early human PK data and no clinical approval. The multi-day half-life is its defining technical feature, but it comes at the regulatory cost of having no approved pathway and an unfavorable 2024 compounding review. It is the clearest illustration on this desk of an engineering advance that has not (yet) translated into clinical approval. See the comparison page.