CJC-1295

CJC-1295 was developed by the Montreal company ConjuChem and described in 2005. It starts from GRF(1-29), the active 29-amino-acid fragment of human GHRH that is also the basis of sermorelin. Four amino acids are substituted (including a D-alanine at position 2) to make the peptide more resistant to enzymatic breakdown, and a reactive maleimide group is attached to an extra lysine at the end. After injection that group binds covalently to albumin, the most abundant protein in blood, which dramatically extends how long the peptide circulates ^[1]. ConjuChem called this approach Drug Affinity Complex, or DAC.

All of the published research on “CJC-1295” refers to this DAC version: the rat study that identified it ^[1], a mouse study ^[2], and the human studies discussed below ^[3][4].

Many suppliers sell two different products under similar names. “CJC-1295 with DAC” is the albumin-binding molecule described above. “CJC-1295 no DAC”, also sold as Modified GRF (1-29) or Mod GRF 1-29, is the four-substituted GRF(1-29) peptide without the maleimide-lysine group. It cannot bind albumin, so it would be expected to behave like a somewhat more stable version of sermorelin, acting for a short time rather than for days.

These are different molecules with different molecular weights and, almost certainly, very different durations of action. The distinction matters because the human evidence for CJC-1295 (a half-life of roughly six to eight days, raised IGF-1 for up to a week or more) comes entirely from the DAC version ^[3][4]. We found no published human pharmacokinetic or clinical study of Modified GRF (1-29) under that name. It appears in the scientific literature mainly in forensic and anti-doping work: Danish customs seizures, for instance, identified glycine-modified versions of “modified GRF 1-29” alongside GHRP analogues ^[5]. A 2026 review of GH-axis peptides also treats CJC-1295 with and without DAC as separate agents with different evidence ^[6].

When comparing products, check the label and the certificate of analysis: the molecular weight reported by mass spectrometry should match the molecule you intend to buy.

Like natural GHRH, CJC-1295 binds the GHRH receptor on pituitary somatotroph cells and stimulates growth hormone (GH) release, which raises insulin-like growth factor 1 (IGF-1). The difference is duration. Native GHRH lasts minutes in the blood; once CJC-1295 is attached to albumin, the complex keeps stimulating the receptor for days.

A key question was whether constant stimulation would flatten the normal pulsing pattern of GH release. In a study of healthy young men, one injection of CJC-1295 increased overall GH secretion and IGF-1 while GH pulses kept their normal frequency and size; the main change was a 7.5-fold rise in the baseline (trough) GH level between pulses ^[4].

CJC-1295 acts on a different receptor from ipamorelin and the GH-releasing peptides (GHRP-2, GHRP-6, hexarelin), which act at the ghrelin receptor. Combining a GHRH analogue with a ghrelin-receptor agonist produces a greater-than-additive GH response in human studies of the older compounds ^[7], which is the rationale behind the popular CJC-1295 and ipamorelin combination. That specific combination has not been studied in any published human trial.

In the original rat experiments, CJC-1295 produced a fourfold greater GH response over two hours than unmodified GRF(1-29), resisted breakdown by the enzyme DPP-4, and was still detectable in plasma beyond 72 hours, bound to albumin ^[1].

In mice genetically unable to make GHRH, 2 µg of CJC-1295 given every 24 hours for five weeks produced normal body weight, length and body composition, and increased pituitary GH content. Dosing every 48 or 72 hours improved growth but did not fully normalise it. The treated mice also showed more GH-producing cells in the pituitary, suggesting that sustained GHRH stimulation can make somatotrophs multiply ^[2]. These are animal results and cannot be translated directly to people.

The main human data come from two randomised, placebo-controlled, double-blind ascending-dose trials in healthy adults aged 21 to 61, published together by Teichman and colleagues in 2006. A single injection raised mean GH levels two- to tenfold for six days or more and IGF-1 levels 1.5- to threefold for nine to eleven days, depending on dose. The estimated half-life was 5.8 to 8.1 days, and with repeated weekly or fortnightly doses IGF-1 stayed above baseline for up to 28 days. No serious adverse reactions were reported ^[3].

The design is worth understanding because it is often over-interpreted. The first trial gave one of four ascending single doses and followed participants for 28 days; the second gave two or three doses at weekly or fortnightly intervals over 49 days. The outcomes were hormone levels and drug pharmacokinetics, not muscle, fat or any clinical measure. The authors saw evidence of a cumulative effect with repeated doses and concluded the data supported developing CJC-1295 as a treatment ^[3], which is a statement about promise rather than proven benefit.

A companion study measured GH every 20 minutes overnight in healthy men before and one week after a single injection. Mean GH rose by 46% and IGF-1 by 45%, with pulsatility preserved. The participants were men aged 20 to 40 given 60 or 90 µg/kg, and the two doses produced no significant difference in response. Interestingly, the rise in IGF-1 did not correlate with any single measure of GH secretion, and the authors suggested that the sustained increase in baseline GH was the main driver ^[4].

ConjuChem then began a phase 2 trial in people with HIV-associated visceral obesity, the same indication later approved for tesamorelin. In July 2006 the company halted the trial after a participant died; at the time the cause and any relationship to the drug were reported as under investigation ^[8]. The registry entry lists the trial as terminated ^[9], and no results have been published. Development of CJC-1295 as a medicine did not resume.

In short, the human evidence is limited to short-term hormone measurements in healthy volunteers. There are no published human trials of CJC-1295 for body composition, fat loss, muscle, recovery, sleep or ageing, and none at all for the no-DAC version.

The human trials dosed CJC-1295 with DAC by body weight. The ascending-dose studies used single subcutaneous injections and then two or three doses given weekly or every two weeks; the authors reported that it was relatively well tolerated “particularly at doses of 30 or 60 µg/kg” ^[3]. The pulsatility study used a single 60 or 90 µg/kg injection ^[4]. In GHRH-deficient mice, the dose was 2 µg per mouse ^[2].

No human dose has been established for Modified GRF (1-29), because it has not been studied clinically. These figures describe what researchers used; they are not recommendations. For laboratory reconstitution arithmetic, see our peptide calculator.

In the phase 1 studies, no serious adverse reactions were reported, and the authors described CJC-1295 as safe and relatively well tolerated over the 28- and 49-day study periods ^[3]. The published abstracts do not give a detailed breakdown of individual side effects, so we have not listed them here.

The unresolved death in the phase 2 programme ^[8], the absence of any long-term data and the sustained elevation of GH and IGF-1 are the main open safety questions. The long half-life also has a practical consequence: unlike short-acting peptides, the effect of a DAC injection cannot be stopped quickly, because the drug remains bound to albumin for days after it is given ^[3][4]. A 2026 clinical review of GH-axis peptides lists fluid retention, joint and muscle pain, changes in glucose, and injection-site reactions among the adverse effects reported with this class, and notes that the composition of unregulated products is uncertain ^[6].

CJC-1295 is not an approved medicine in the UK, US, Canada, Australia or New Zealand, and its clinical development stopped in 2006. It is sold by research-chemical suppliers as a laboratory reagent. How the law treats buying and possessing it varies by country; see our legal status overview and the US page.

CJC-1295 is named on the WADA Prohibited List under S2 (GHRH and its analogues), alongside CJC-1293, sermorelin and tesamorelin, and is banned at all times ^[10]. The no-DAC version falls under the same class wording, which covers GHRH analogues generally rather than only the examples listed.

Both versions are sold as freeze-dried powder. No stability data have been published for research-grade CJC-1295, so handling follows general practice for lyophilised peptides; see our guide to storing peptides.

Because two different molecules share one name, this is a peptide where the certificate of analysis matters more than usual. If a listing says only “CJC-1295”, confirm with the supplier whether it contains the DAC group before comparing prices, since the two products are not interchangeable. Compare prices for the specific version you want, read the COA using our guide on how to read a COA, and prefer third-party tested suppliers.