CJC-1295 with DAC: The Research, History and Status

DAC stands for drug affinity complex, the platform ConjuChem built to extend the working life of short peptides. In CJC-1295, DAC is a maleimidopropionamide group attached through a lysine at the peptide's C-terminus. Once injected, that maleimide group reacts with a single free thiol group on cysteine 34 (Cys34) of human serum albumin and forms a stable covalent bond.^[1]

Albumin is the most abundant protein in blood plasma. By anchoring itself to that carrier, CJC-1295 with DAC effectively borrows albumin's own circulating life instead of relying on its own. In the rat studies that first identified the compound, the DAC-linked peptide appeared on the albumin band of a blood sample within 15 minutes of dosing, was still circulating after 24 hours, and remained detectable in plasma after 72 hours.^[1]

Those are rodent pharmacokinetic findings, not human ones — the human numbers come from separate clinical trials, covered next. The chemistry also explains why the no-DAC version of CJC-1295 behaves nothing like it: without an albumin anchor, a different pharmacokinetic story applies, one this article does not repeat.

The only published human data on CJC-1295 concern the DAC form. Teichman and colleagues ran two randomised, double-blind, placebo-controlled, ascending-dose trials in healthy adults aged 21 to 61, lasting 28 and 49 days. The first tested four ascending single subcutaneous doses; the second gave two to three weekly or twice-weekly injections.^[2]

A single dose produced dose-dependent increases in mean plasma growth hormone of two- to ten-fold, lasting six days or more, and IGF-1 rose 1.5- to three-fold and stayed elevated for nine to eleven days. The estimated half-life was 5.8 to 8.1 days. With repeated dosing, IGF-1 remained above baseline for up to 28 days.^[2]

The trial authors reported no serious adverse reactions and described the compound as relatively well tolerated. These are the only numbers with a named human trial behind them: a small, short, healthy-volunteer hormone study, not a body-composition or performance trial.^[2]

Growth hormone is not released steadily; the pituitary fires it in overnight pulses. A follow-up study asked what happens to that rhythm when a long-acting GHRH analogue keeps the receptor engaged for days rather than minutes. Ionescu and Frohman sampled blood every 20 minutes overnight in healthy men aged 20 to 40, before and one week after a single 60 or 90 microgram-per-kilogram dose of CJC-1295 with DAC.^[3]

Deconvolution analysis of the overnight GH profile found that pulse frequency and amplitude were unchanged. What moved was the floor between pulses: trough GH rose roughly 7.5-fold and mean GH by about 46%, alongside a rise in IGF-1.^[3]

The authors read this as sustained GHRH-receptor stimulation raising the baseline between pulses rather than replacing the pulsatile pattern — most likely because the counter-regulatory hormone somatostatin keeps suppressing the receptor between pulses regardless. It is a mechanistic finding about one week of exposure in a small group of healthy men, not a description of any longer-term effect.^[3]

CJC-1295 was developed by ConjuChem, a Montreal-based biopharmaceutical company that built the drug affinity complex platform specifically to extend the working life of short peptides like GHRH(1-29). The Teichman healthy-volunteer trials were part of the company's own clinical-pharmacology programme, and ConjuChem went on to sponsor the compound's only registered trial in patients: a multicentre, randomised, double-blind, placebo-controlled Phase 2 study of CJC-1295 in people with HIV-associated visceral obesity.^[1][2][4]

That trial, registered as NCT00267527, is the only CJC-1295 study ever entered on ClinicalTrials.gov. Its record lists 120 participants enrolled, a start in December 2005 and a completion in September 2006, an overall status of terminated, no results ever posted, and no reason for the termination on file. No later-phase trial of CJC-1295, in any form, has been registered since.^[4]

More than two decades after Jetté and colleagues first described the DAC-conjugated molecule, that one terminated trial remains the entire patient-level record. No marketing application for CJC-1295, in either form, is on file with the FDA or the EMA.^[1][5][6]

The controlled human trials reported no serious adverse reactions, in a small number of healthy volunteers followed for at most 49 days. That is a narrow safety record: short duration, a population selected for good health, and hormone measurements rather than long-term outcomes as the endpoint.^[2]

The FDA takes a more cautious public position. Its page on bulk substances that may present significant safety risks in compounding (current as of 22 April 2026) lists CJC-1295 among substances previously in category 2 whose nominations were withdrawn by the nominators, and states that compounded drugs containing CJC-1295 may pose a risk of immunogenicity and raise complexities in characterising peptide-related impurities, and that the FDA has identified serious adverse events associated with CJC-1295, including increased heart rate and a systemic vasodilatory reaction, while noting that available clinical data are limited.^[5]

That FDA listing does not name a specific trial or case report behind those adverse events, and it does not distinguish the DAC form from the no-DAC form — it treats 'CJC-1295' as one entry. Put together, the honest picture is a short, clean safety record in the one controlled trial that exists, next to a regulator's broader caution about compounded peptide use.^[5]

No regulator has approved CJC-1295, in either form, as a medicine. The FDA has approved no CJC-1295 product, and its compounding safety-risk page lists CJC-1295 among nominations previously in category 2 and later withdrawn; a search of the EMA medicines database found no marketing authorisation and no European public assessment report for CJC-1295 (searched 22 September 2026).^[5][6]

In competitive sport the position is explicit. The WADA 2026 Prohibited List, in force since 1 January 2026, names CJC-1295 by name under section S2.2.4, growth hormone releasing factors, alongside CJC-1293, sermorelin and tesamorelin as GHRH analogues. Substances in class S2 are non-specified and prohibited at all times, in and out of competition.^[7]

The List does not distinguish the DAC form from the no-DAC form either; both fall under the same 'CJC-1295' entry and the same GHRH-analogue category.^[7]

Every figure in this article describes the DAC-linked molecule specifically. CJC-1295 without DAC — also called modified GRF(1-29) — is the same substituted GHRH(1-29) backbone without the albumin-binding linker, and it behaves like a different molecule in the body. The point-by-point comparison between the two, and why blends default to the no-DAC form, lives in the CJC-1295 + ipamorelin guide; it is not repeated here.^[1]

Peptyds does not sell CJC-1295 with DAC. The catalogue carries CJC-1295 No DAC as a standalone vial, and CJC-1295 No DAC + Ipamorelin as a blend — both built on the no-DAC peptide described above, supplied as a lyophilised compound for in-vitro laboratory research only, never the long-acting DAC form covered in this article.

Readers comparing CJC-1295 to the rest of its family can find it set against ipamorelin's different receptor pathway in one guide, and against sermorelin and tesamorelin — the one family member currently marketed with an FDA-approved indication — in another.