CJC-1295 DAC

Two human studies have given CJC-1295 with its albumin-binding Drug Affinity Complex to healthy adults, and both measured hormones in blood rather than any health outcome. The first was a pair of randomized, double-blind, placebo-controlled trials, one running 28 days and the other 49, in volunteers aged 21 to 61. The second drew blood at 20-minute intervals through the night from healthy men between 20 and 40 years old, first at baseline and again seven days after one injection. Both were published in 2006.

Within those limits the results are clear. One injection raised mean growth hormone 2 to 10 fold for six days or more and mean IGF-I 1.5 to 3 fold for 9 to 11 days, and the compound's estimated half-life came out at 5.8 to 8.1 days. The abstracts do not report how many people took part.

It is not an FDA-approved drug, FDA's published safety concerns about compounded CJC-1295 still stand, and WADA names CJC-1295 on its prohibited list.

CJC-1295 is the first 29 amino acids of human growth hormone-releasing factor with four substitutions, plus a lysine at the end carrying a maleimide reactive group. That reactive group is the Drug Affinity Complex. Once injected, it bonds covalently to cysteine 34 on serum albumin, and the peptide then travels on albumin for days instead of being broken down as quickly as the body's own GHRH.

In the original papers, the name CJC-1295 meant this albumin-binding compound. Jette and colleagues at ConjuChem picked it in 2005 as the best of three maleimide derivatives they built, and every human study cited here used it. The name has since split in two: a 2021 anti-doping study treated "CJC-1295" and "CJC-1295 with drug affinity complex" as separate analytes, which is why the DAC label now has to be spelled out.

A Releasing Signal, Not the Hormone

CJC-1295 works on the GHRH receptor in the anterior pituitary, the same receptor the body's own releasing hormone uses. It contains no growth hormone. It prompts the pituitary to release more of its own, and IGF-I rises downstream. In the 2005 rat work, the albumin conjugates were active in cultured rat anterior pituitary cells and raised plasma GH when injected into normal male rats.

What the Albumin Anchor Changes

The short duration of native GHRH is what limited its use. Bound to albumin in the rat studies, the peptide resisted the enzyme dipeptidylpeptidase-IV in vitro, produced a 4 fold larger GH response over two hours than unmodified GRF(1-29), and was still present in plasma beyond 72 hours. A Western blot found it on the albumin band within 15 minutes and still circulating past 24 hours.

Any constant stimulus raises the question of whether it flattens the pituitary's natural pulsing. In the overnight human study it did not: a week after injection, GH still arrived in bursts of the same number and height. What moved was the floor. Trough GH rose 7.5 fold, mean GH rose 46 percent and IGF-I rose 45 percent. The IGF-I rise did not correlate with any single measure of GH secretion, and the authors pointed to the raised trough as the likely driver.

A hormone curve gets read as a result. Every human number for this compound is a blood level of GH or IGF-I. None of the studies measured muscle, fat, strength, sleep, recovery, ageing or any disease. A raised IGF-I says the pituitary responded. It does not say anything improved.

Seven weeks in healthy people is the whole human record. The longest trial ran 49 days, and every participant was a healthy adult. Nothing here describes older adults with declining GH, people with pituitary disease, or anyone exposed for months.

The other CJC-1295 borrows this file. Because the name is shared, the 2006 results are routinely quoted for products made without the albumin-binding group. Those studies measured a molecule that rides on albumin for about a week. They cannot be transferred to a version that lacks the very feature that produced the multi-day exposure.

An intact pulse is not a clean bill of health. The overnight study found GH pulses preserved one week after a single injection. It did not look at repeated exposure, and even in that study the trough GH level sat 7.5 times above where it started.

In the 2006 placebo-controlled trials, no serious adverse reactions were reported, and the authors described CJC-1295 as safe and relatively well tolerated over 28 and 49 days. The abstract does not list which milder effects occurred or how often.

FDA's compounding safety review covers CJC-1295 as a single entry, with no distinction between forms. Among the problems FDA lists are serious adverse events it has identified with CJC-1295, specifically a systemic vasodilatory reaction and a raised heart rate. It also raises immunogenicity risk for certain routes, complexities with peptide-related impurities and with characterizing the active ingredient, and describes the clinical data available as limited.

CJC-1295 left FDA's Category 2 on or about 22 April 2026 because the nominators withdrew the nomination, not because FDA resolved its safety concerns. Those concerns remain published.

The fair reading is that CJC-1295 with DAC does what its designers set out to do pharmacologically. It is a long-lived GHRH signal, it raised GH and IGF-I in healthy adults for days after one injection, and in one study it did so without erasing the pulse pattern. That is a well-described hormonal effect backed by placebo-controlled human work, which is more than many compounds sold beside it can claim.

The record stops there. Its developers framed it as a potential therapeutic agent, and no published trial cited here went on to test it against a disease or a performance outcome. Anyone citing it for body composition or recovery is reasoning from hormone levels to outcomes nobody measured.

Not growth hormone. It signals the pituitary to release the body's own GH and contains none. The 2006 authors saw its potential use in patients whose pituitary can still secrete GH.

Not interchangeable with CJC-1295 made without DAC. The albumin bond is what produced the six to eight day half-life measured in people. Take it away and the human pharmacology above no longer describes the molecule.

Not approved, and not permitted in tested sport. FDA has not approved it. WADA prohibits it under S2.2.4, naming it among GHRH analogues: "GHRH and its analogues (e.g. CJC-1293, CJC-1295, sermorelin and tesamorelin)".

Not a tested treatment for anything. Its developers called it a potential therapeutic, and no cited trial measured a clinical outcome.

I take this compound more seriously than most of what gets sold next to it, because someone ran placebo-controlled trials in people and published the hormone curves. Those curves are real. A single injection kept GH and IGF-I raised for more than a week, and that is a genuine pharmacological achievement.

I also notice where the trail ends. The newest human study I can point to is from 2006, and no human trial I can cite measured an outcome anyone actually cares about. Meanwhile the name now covers two different molecules, and I would rather be exact about which one the evidence belongs to than let the stronger file prop up the weaker product.

Where I land: measurable, well-characterised endocrine pharmacology in healthy volunteers, and no outcome data at all. I am not going to publish doses, and I am not going to treat a rising IGF-I number as a reason to take it.