CJC-1295 is a GHRH analog engineered to bind albumin, and in healthy adults it kept GH and IGF-1 raised for days while preserving the natural GH pulse. Its clinical program stopped in 2006 and never reached phase 3. In the United States it has no lawful compounding pathway in any form.
Key points
- CJC-1295 is GHRH(1-29) with four substitutions and a lysine carrying a maleimide group that, after injection, binds covalently to albumin [1][4].
- In healthy adults, a single dose was associated with GH 2- to 10-fold higher for 6 days or more and IGF-1 1.5- to 3-fold higher for 9 to 11 days, with an estimated half-life of 5.8 to 8.1 days [2].
- GH kept its pulsatile secretion. Pulse frequency and magnitude did not change, while basal GH rose 7.5-fold [3].
- “CJC-1295 without DAC” (Mod GRF 1-29) is a different molecule. It lacks the albumin anchor and has no published controlled clinical studies in humans [8][9].
- The phase 2 trial in HIV-associated lipodystrophy, with 192 participants, was stopped in July 2006 after a participant died. The link to the drug was then under investigation [10][11].
US status (October 2026): Not FDA-approved and no compounding pathway with or without DAC; FDA’s advisory committee voted against all five forms in December 2024, and MDside providers do not prescribe it. See the CJC-1295 status page.
The DAC design ties the peptide to albumin
Natural GHRH stimulates the pituitary to release growth hormone (GH), but its half-life is so short that it limits therapeutic use [3]. In the early 2000s, chemists at the Canadian company ConjuChem tried a chemical fix: add to the peptide a reactive group that, once in the blood, binds the free thiol of cysteine 34 on serum albumin. They called it the drug affinity complex (DAC) [1].
Of three maleimido derivatives of GHRH(1-29), the best was CJC-1295: a tetrasubstituted form of hGRF(1-29) with an added C-terminal lysine carrying the maleimidopropionamide group. In rats it produced a 4-fold larger GH area under the curve than hGRF(1-29) over 2 hours, remained in plasma beyond 72 hours, and appeared on the albumin band 15 minutes after injection [1]. The four substitutions increase resistance to proteolytic degradation [9].
In healthy adults, one dose raised GH and IGF-1 for days
The core human evidence comes from two randomized, double-blind, placebo-controlled ascending-dose trials in healthy adults aged 21 to 61, lasting 28 and 49 days. After a single subcutaneous injection there were dose-dependent increases in plasma GH of 2- to 10-fold for 6 days or more and in IGF-1 of 1.5- to 3-fold for 9 to 11 days. The estimated half-life was 5.8 to 8.1 days [2].
With multiple doses, mean IGF-1 stayed above baseline for up to 28 days, with evidence of a cumulative effect. No serious adverse reactions were reported, and the authors described the compound as safe and relatively well tolerated, particularly at doses of 30 or 60 µg/kg [2]. A later proteomic analysis in 11 healthy young men, before and one week after injection, identified serum protein changes that could serve as biomarkers of GH and IGF-1 action [5].
- 5.8 to 8.1 days: estimated half-life of CJC-1295 in healthy adults [2]
- 7.5-fold: rise in basal (trough) GH with pulses preserved [3]
- 28 days: IGF-1 above baseline after multiple doses [2]
GH pulsatility survived continuous stimulation
Pulsatile GH secretion is considered important for many of the hormone’s physiological effects, and continuous stimulation could in theory flatten it. Ionescu and Frohman measured it with sampling every 20 minutes over 12 overnight hours in healthy men aged 20 to 40, before and one week after an injection. The frequency and magnitude of GH pulses did not change. What rose was basal GH between pulses, 7.5-fold (P < 0.0001), with mean GH up 46% and IGF-1 up 45% [3].
> “Long-acting GHRH preparations may have clinical utility in patients with intact pituitary GH secretory capability.” (Ionescu and Frohman, J Clin Endocrinol Metab 2006 [3])
In mice lacking the GHRH gene, daily CJC-1295 for 5 weeks normalized body weight and length. At 48- or 72-hour intervals the effect was smaller and did not reach full normalization [4]. The nuance matters: a long half-life in humans does not guarantee that any dosing interval reproduces physiology.
With DAC and without DAC are two molecules under one name
Two variants circulate under the name CJC-1295: the version with DAC and the “no-DAC” version, also called Mod GRF 1-29 [9]. In 2009 a Norwegian anti-doping laboratory analyzed, at the request of Norwegian police and customs, an unknown preparation containing a 29-amino-acid peptide with a C-terminal amide, marketed as CJC-1295 [8]. That peptide lacked the extra lysine that carries the albumin anchor [1].
The difference is pharmacological. The Teichman and Ionescu data belong to the DAC molecule [2][3]. A 2026 review placed CJC-1295 without DAC in the lowest evidence tier, with no published human studies, and noted that its claimed effects are extrapolated from related compounds, chiefly GHRH(1-29), which is sermorelin [9]. If a supplier pitches “no DAC” as the safer or permitted version, the FDA committee record on the status page answers that directly.
The same albumin logic later reached semaglutide
ConjuChem also applied the DAC platform to GLP-1. CJC-1131, a DPP-IV-resistant DAC:GLP-1 compound that conjugates to albumin, activated the GLP-1 receptor and lowered glucose in mice [6]. Using albumin as a carrier to prolong a peptide is the idea that, with different chemistry, underpins liraglutide and semaglutide. In those drugs albumin binding is reversible, through an optimized fatty acid and linker. DAC binding is covalent [7]. The full history of that strategy is in A century of peptide therapeutics.
The phase 2 trial stopped in 2006
CJC-1295 advanced to a multicenter, randomized, double-blind, placebo-controlled phase 2 trial in HIV-associated visceral obesity, with 192 participants in North and South America and weekly injections. ConjuChem stopped the study on July 17, 2006 after a participant died at a site in Argentina. At the time, the cause and its relationship to the drug were under investigation [10]. In August 2006 the company posted the findings of that investigation, and the event cost it half of its share value [11].
The same indication did succeed with another GHRH analog. Tesamorelin, a once-daily GHRH(1-44), reduced visceral adipose tissue by 15.4% versus placebo in 806 patients with HIV, with no clinically meaningful changes in glucose at 26 and 52 weeks [12]. Stimulating the patient’s own pituitary to reduce visceral fat was validated. The weekly version never was.
The evidence ends at short-term pharmacology
- The published human data are pharmacokinetic and pharmacodynamic, in healthy adults and short term. There are no controlled efficacy data on body composition or clinical outcomes [2][9].
- There are no long-term safety data. Concern about the mitogenic signal of raised IGF-1 remains theoretical, neither confirmed nor ruled out [9].
- The clinical program was interrupted in 2006, so the molecule never completed a phase 3 [10].
- The no-DAC version has no human studies of its own [9].
What this means for you
CJC-1295 is a case of elegant design: it showed in humans that an albumin-anchored GHRH analog keeps GH and IGF-1 raised for days without losing the pulsatile pattern [2][3]. Elegant pharmacology is not a lawful supply. Take CJC-1295 off the menu in every form, including the ipamorelin stack. For a growth hormone axis option, look at the sermorelin status page and our peptide programs. The comparative picture of secretagogues, including ipamorelin and MK-677, is in CJC-1295, ipamorelin and MK-677.
References
- Jetté L, et al. Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog. Endocrinology. 2005;146(7):3052-8. PMID 15817669. Link
- Teichman SL, et al. Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults. J Clin Endocrinol Metab. 2006;91(3):799-805. PMID 16352683. Link
- Ionescu M, Frohman LA. Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. J Clin Endocrinol Metab. 2006;91(12):4792-7. PMID 17018654. Link
- Alba M, et al. Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse. Am J Physiol Endocrinol Metab. 2006;291(6):E1290-4. PMID 16822960. Link
- Sackmann-Sala L, et al. Activation of the GH/IGF-1 axis by CJC-1295, a long-acting GHRH analog, results in serum protein profile changes in normal adult subjects. Growth Horm IGF Res. 2009;19(6):471-7. PMID 19386527. Link
- Kim JG, et al. Development and characterization of a glucagon-like peptide 1-albumin conjugate: the ability to activate the glucagon-like peptide 1 receptor in vivo. Diabetes. 2003;52(3):751-9. PMID 12606517. Link
- Knudsen LB, Lau J. The discovery and development of liraglutide and semaglutide. Front Endocrinol (Lausanne). 2019;10:155. PMID 31031702. Link
- Henninge J, et al. Identification of CJC-1295, a growth-hormone-releasing peptide, in an unknown pharmaceutical preparation. Drug Test Anal. 2010;2(11-12):647-50. PMID 21204297. Link
- Dominikowski A, et al. The emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis: bridging the gap between clinical evidence and patient self-administration. Front Endocrinol (Lausanne). 2026;17:1822475. PMID 42395176. Link
- Bernard EJ. Lipodystrophy study halted after patient death. aidsmap. July 31, 2006. Link
- FDAnews. ConjuChem reveals findings of patient death investigation. August 10, 2006 (archived copy). Link
- Falutz J, et al. Effects of tesamorelin (TH9507), a growth hormone-releasing factor analog, in human immunodeficiency virus-infected patients with excess abdominal fat: a pooled analysis of two multicenter, double-blind placebo-controlled phase 3 trials with safety extension data. J Clin Endocrinol Metab. 2010;95(9):4291-304. PMID 20554713. Link
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