CJC-1295

Overview

CJC-1295 is a synthetic analog of growth hormone releasing hormone (GHRH), the hypothalamic signal that tells the pituitary to release growth hormone (GH). It is built on GRF (1-29), the shortest fully active fragment of human GHRH, with four amino acid substitutions that make it more resistant to enzymatic breakdown.

The name covers two different molecules, and keeping them apart is the most important thing to know about this compound.

• CJC-1295 with DAC. The original compound carries a "drug affinity complex," a reactive linker attached to a lysine at the end of the peptide. After it enters the bloodstream, the linker bonds to circulating albumin, which stretches the half-life from minutes to roughly a week. Every published human study of "CJC-1295" used this version.
• CJC-1295 without DAC. Often sold as "modified GRF (1-29)" or "mod GRF," this is the same substituted 29 amino acid backbone without the albumin-binding linker. It is expected to act for a short time, like other GRF (1-29) analogs, and it has almost no published human data of its own.

Prime Core Dynamics supplies both variants as research material, each with its own batch certificate of analysis.

Findings from the DAC studies below should not be read as evidence about the non-DAC molecule. The pharmacology is different by design.

For how CJC-1295 fits alongside tesamorelin, ipamorelin and oral ghrelin mimetics, see our field guide to growth hormone secretagogues.

Research history

Native GHRH is broken down within minutes, largely by the enzyme dipeptidyl peptidase-4, which limited earlier attempts to use it clinically. In the early 2000s the Montreal company ConjuChem was developing a platform that attached peptides to albumin to extend their life in the body.

In 2005, Jetté and colleagues described three albumin-reactive versions of GRF (1-29) and selected the best performer, CJC-1295, after rat studies showed it produced a larger GH response than unmodified GRF (1-29) and remained in plasma beyond 72 hours, bound to albumin (Jetté 2005).

Human studies followed quickly. In 2006, two randomized trials in healthy adults described multi-day increases in GH and IGF-1 (Teichman 2006), and a separate study examined how that stimulation affected the natural pulse pattern of GH release (Ionescu 2006). Published clinical work largely stops after 2009, and the compound never reached approval.

The "without DAC" form entered circulation later, mainly through the research chemical market rather than through a published development program. By 2010 a Norwegian doping laboratory reported identifying a 29 amino acid peptide consistent with the product marketed as CJC-1295 in a seized, unlabeled preparation (Henninge 2010).

What published studies have examined

Animal and laboratory studies (with DAC)

• Rats. The original characterization showed CJC-1295 resisted enzymatic breakdown in vitro, activated GH release from cultured pituitary cells, and bound albumin in circulation (Jetté 2005).
• Mice. In mice lacking the GHRH gene, repeated CJC-1295 given over five weeks normalized body weight and length when given daily but not fully when given less often, and was associated with signs of pituitary somatotroph cell proliferation (Alba 2006). This is a deficiency model and does not tell us about effects in animals with normal GH axes.

Human studies (with DAC only)

• Teichman 2006. Two randomized, placebo-controlled, double-blind, ascending dose trials in healthy adults aged 21 to 61, lasting 28 and 49 days. After a single injection, mean GH rose 2 to 10 fold for six days or more and IGF-1 rose 1.5 to 3 fold for 9 to 11 days. The estimated half-life was 5.8 to 8.1 days. No serious adverse reactions were reported in these short trials.
• Ionescu 2006. Healthy men aged 20 to 40 had overnight GH sampling every 20 minutes before and one week after a single injection. GH pulses kept their normal frequency and size, while baseline (trough) GH rose about 7.5 fold, mean GH about 46 percent and IGF-1 about 45 percent.
• Sackmann-Sala 2009. Blood from 11 healthy young men before and after CJC-1295 was analyzed for protein changes as possible markers of GH activity. Several candidate proteins shifted, but their meaning was not established.

These are small, short studies in healthy volunteers that measured hormone levels, not clinical outcomes, and they share an overlapping group of investigators.

Studies of CJC-1295 without DAC

We found no published randomized human trial specifically of the non-DAC molecule. Its pharmacology is generally inferred from other short-acting GRF (1-29) analogs rather than measured directly.

Open questions

• Which molecule? Product labels and online discussion often say "CJC-1295" without specifying the DAC status. Mass spectrometry is the only reliable way to confirm identity, which our guide to reading a certificate of analysis explains.
• Non-DAC human data. Duration of action, safety and hormonal effects of the non-DAC form in people are largely uncharacterized in the peer-reviewed literature.
• Long-term safety. No published study has followed people on CJC-1295 in either form for more than a few weeks. The effects of sustained GH and IGF-1 elevation, including on glucose regulation, are not established for this compound.
• Outcomes versus biomarkers. Raising GH and IGF-1 is not the same as a functional or clinical benefit, and no trial has tested outcomes such as body composition, strength or recovery.
• Regulatory signals. The FDA's compounding review cited limited clinical data, possible immunogenicity and impurity concerns, and reported adverse events.