CJC-1295: research overview

The short version

CJC-1295 is a laboratory-made copy of a hormone the brain uses to tell the pituitary gland to release growth hormone. The natural signal is called GHRH, for growth-hormone-releasing hormone. CJC-1295 copies the working front end of it and adds changes that stop the body breaking it down quickly.

Unlike the two compounds before it in this hub, CJC-1295 is not an approved medicine anywhere. It is sold for laboratory research use only, its original development programme was discontinued, and the published human evidence amounts to a handful of early pharmacology studies.

The naming lesson here is the sharpest on the site, and it is a safety lesson too. Two versions circulate. One, the DAC form, is engineered to latch permanently onto a blood protein and stays active for days. The other, sold as no-DAC or Modified GRF 1-29, lacks that attachment and lasts minutes to hours. The names look almost the same. The molecules do not behave the same way at all.

What it is: a code that never became a name

The label CJC-1295 is a company development code of exactly the form described on the home page: a letter group identifying the originating organisation, followed by digits identifying the compound within that organisation's programme. The record for this compound names ConjuChem as the company behind the original long-acting programme, which was discontinued.

That discontinuation is why the code is still the name. An international nonproprietary name is assigned to compounds moving through the regulatory system; a molecule whose development halts keeps whatever internal identifier it had when the music stopped. So CJC-1295 has no generic name, not because of any oversight, but because the process that would have conferred one never ran to completion. A code where a reader expects a generic name is therefore a genuine signal — usually that the compound did not finish the approval path.

Structurally, it is built on the first 29 residues of human growth-hormone-releasing factor, written hGRF(1-29) — itself a naming convention worth decoding, since the parenthetical is a residue range specifying which fragment of the parent hormone is in play. Four amino-acid substitutions (D-Ala at position 2, Gln at 8, Ala at 15, Leu at 27) stabilise the helix and block enzymatic cleavage, deamidation and oxidation, which is why the corpus also records it as tetrasubstituted GRF(1-29).

Then comes the fork. In the DAC variant — DAC standing for Drug Affinity Complex — a C-terminal lysine carries a linker that reacts with a free thiol on cysteine 34 of circulating serum albumin, forming a covalent peptide-albumin conjugate and stretching the plasma half-life toward that of albumin itself. The no-DAC form keeps the four substitutions but has no albumin-binding moiety, and is consequently short-acting.

The synonym list is where the trouble starts: CJC-1295 DAC, CJC-1295 with DAC, DAC:GRF, DAC GRF, hGRF(1-29)-albumin bioconjugate, Modified GRF 1-29, Mod GRF 1-29, CJC-1295 no-DAC, tetrasubstituted GRF(1-29), long-acting GHRH analog. Ten labels for what are, pharmacokinetically, two different things — and no convention anywhere in that list makes the division obvious to a newcomer.

How it works

CJC-1295 binds the growth-hormone-releasing hormone receptor on somatotroph cells of the anterior pituitary, activating Gs/cAMP/PKA signalling that stimulates the synthesis and pulsatile release of growth hormone, which in turn raises hepatic IGF-1. The protease-resistant substitutions and, in the DAC variant, the covalent albumin bond give it a multi-day half-life, so a single dose can elevate growth hormone and IGF-1 for days.

A 2025 review in the endocrinology literature synthesises the pharmacology of GHRH and its synthetic analogues as a class — receptor signalling, the design rationale for long-acting analogues, and the therapeutic and investigational landscape — and provides the current framing for where this compound sits ^[12].

One mechanistic detail matters more than it first appears: the pulsatile pattern of growth-hormone release is preserved. In healthy men aged 20 to 40, a single subcutaneous dose raised trough growth hormone approximately 7.5-fold and mean growth hormone by about 46%, with IGF-1 up about 45% a week later, while the frequency and magnitude of pulsatile secretion were unaltered ^[16]. Continuous stimulation by a long-acting analogue did not flatten the body's own rhythm.

What the research shows

The human evidence base is small, early, and almost entirely pharmacological rather than clinical. It establishes that the compound does what it is designed to do to hormone levels; it does not establish that this produces any benefit.

Pharmacokinetics and hormone response. In healthy adults aged 21 to 61, single subcutaneous doses of 30 or 60 micrograms per kilogram produced dose-dependent 2- to 10-fold increases in mean plasma growth hormone lasting six days or more, and 1.5- to 3-fold increases in IGF-1 lasting nine to eleven days. After multiple doses IGF-1 remained above baseline for up to 28 days. The estimated half-life was 5.8 to 8.1 days ^[15].

Pulsatility. The companion study in healthy men aged 20 to 40 established the preserved pulsatility described above, at single doses of 60 or 90 micrograms per kilogram ^[16].

Biomarkers. In 11 healthy young adult men, administration shifted the serum proteome — apolipoprotein A1 and a transthyretin isoform decreased, while a C-terminal albumin fragment and immunoglobulin and beta-haemoglobin species increased — and the immunoglobulin and albumin-fragment signal correlated linearly with IGF-1, identifying candidate biomarkers of activation of the growth-hormone axis ^[14].

Detection. CJC-1295 was structurally identified by high-resolution mass spectrometry as the active ingredient in an unknown preparation labelled only as GHRH, seized in an anti-doping context ^[13]. That study is a naming story in miniature: a product whose label named a hormone class turned out to contain a specific engineered analogue, and only laboratory analysis could establish which.

What is absent from this list is as informative as what is in it. There are no large trials, no long-term trials, and no controlled evidence of benefit in healthy adults. Most dosing protocols circulating online are not derived from controlled human trials at all.

Reported effects, cautions and safety

Everything in this first part is anecdotal, not clinical evidence — self-reported accounts from research-use communities, recorded here without doses, and unsupported by controlled human data.

Deeper and more restful sleep is the single most commonly reported effect, and users often say it is the first thing they notice. It at least fits the known biology, since growth hormone is released chiefly during deep sleep. Faster recovery between hard training sessions and less lingering soreness are frequently described, though such reports are easily confused with better sleep or ordinary training adaptation. Gradual fat loss around the midsection over several weeks, a leaner look with better muscle retention while dieting, more daytime energy, sharper focus, and firmer-feeling skin and connective tissue are all reported, generally as slow and subtle rather than dramatic changes.

The most commonly reported downside is fluid retention — mild bloating, puffiness in the hands and face, a heavier feeling. Communities widely note this is more pronounced with the long-acting DAC form than with the short-acting no-DAC form, which is exactly what the pharmacology would predict. Tingling or numbness in the fingers, often compared to mild carpal tunnel and attributed to that same fluid pressing on nerves at the wrist, is frequently reported and described as reversible at lower exposure. Injection-site reactions are common. Brief flushing or a warm head rush shortly after a dose is reported more with the short-acting form. Fatigue and drowsiness, mild headaches, and — mainly when the compound is combined with ipamorelin rather than used alone — increased hunger all appear. A smaller number of users, and at least one widely discussed self-experiment, report that sustained growth-hormone elevation nudged blood sugar upward.

Documented cautions. The foremost is that CJC-1295 is not approved for human use anywhere and is sold only as a research chemical; published human evidence is limited to a small number of early pharmacology studies, with no large or long-term trials of safety or efficacy in healthy adults ^[15]. Sustained elevation of IGF-1 raises a mechanism-based concern for anyone with a personal or family history of cancer or an active or undiagnosed tumour, since population data link higher circulating IGF-1 to modestly increased risk of certain cancers — an association, not proof that this compound causes cancer. Growth hormone promotes renal retention of sodium and water, which is the likely basis of the reported swelling and nerve-compression effects, and a real concern for anyone prone to oedema, high blood pressure or cardiac strain. Growth hormone is also glucose-sparing, so sustained stimulation of the axis can reduce insulin sensitivity, with the clearest implications for people with diabetes, prediabetes or insulin resistance. Immunogenicity — the risk of an immune response to the peptide itself — was cited in 2024 regulatory briefing materials among the concerns behind the decision not to recommend CJC-1295 for the 503A compounding bulks list, and the current pharmacology review reinforces that long-acting albumin-binding designs carry such considerations ^[12]. The original DAC programme ran a phase 2 trial that was discontinued, and a patient death from the development era is frequently cited alongside it; the public record does not establish that CJC-1295 caused that death, so it stands as unresolved history rather than proof of harm. The compound is prohibited in sport at all times under section S2 of the anti-doping list, and detection assays are well established.

Where it fits in Research Peptide Fundamentals

CJC-1295 is the hub's clearest evidence that naming is not merely a filing problem.

Its own safety record states the case directly: marketing and forums routinely treat CJC-1295 DAC and Modified GRF 1-29 as the same thing when they are pharmacokinetically very different, one persisting for days and the other for minutes to hours. That confusion has consequences, because the duration of the DAC form is what drives more sustained fluid retention, blood-sugar effects and IGF-1 exposure. Establishing which form is actually in hand is a precondition for interpreting any reported effect at all — a claim that a compound caused puffiness or did not is close to meaningless without it.

Two naming failures compound each other here. The first is the absence of a generic name, which removes the one label that a standards body would have made unambiguous. The second is that the distinguishing suffix, DAC, is a three-letter abbreviation for a proprietary conjugation technology rather than a pharmacological descriptor — so unlike -glutide on the semaglutide page, it encodes nothing a reader could decode without being told.

The next page turns to a third possibility: a name that is neither a company code nor a generic name, but a description — one that states outright what its discoverers believed the molecule did.