CJC-1295: What It Is, the Evidence, and Its Legal Status

CJC-1295 is a laboratory-engineered version of GHRH built on the first 29 amino acids of the natural hormone, with four substitutions added to slow how quickly the body breaks it down. It was created in the early 2000s by ConjuChem Biotechnologies, a Montreal biotech that licensed the underlying chemistry from researchers at the University of Saskatchewan. The compound carries the CAS number 446262-90-4 and the alternative name DAC:GRF.

The single most important thing to understand about CJC-1295 is that it exists in two distinct forms, and they are not interchangeable. The version ConjuChem actually developed and tested in humans includes a “drug affinity complex” (DAC), a small chemical handle that latches onto albumin in the bloodstream. That tether dramatically extends how long the molecule survives in circulation, pushing its half-life out to roughly eight days. The second form, sold widely under the label “CJC-1295 without DAC” (and more accurately called Modified GRF 1-29), lacks that handle and clears far faster. Crucially, the no-DAC form has never been the subject of a published clinical study, despite being the version most commonly sold by research-chemical suppliers.

The bottom line: CJC-1295 is an unapproved experimental GHRH analogue, sold in two distinct forms, only one of which has ever been studied in people.

CJC-1295 works by binding to GHRH receptors on somatotroph cells in the anterior pituitary gland, the same docking sites the body’s own GHRH uses, which signals those cells to secrete growth hormone. The released GH then travels to the liver and other tissues, where it drives production of insulin-like growth factor 1 (IGF-1), the downstream messenger responsible for most of GH’s effects on muscle, fat and tissue repair.

What sets the DAC version apart from natural GHRH is duration. The body releases GHRH in brief bursts that are cleared within minutes, producing the pulsatile rhythm the pituitary is wired to expect. By anchoring to albumin, CJC-1295 with DAC keeps GHRH-like signalling switched on for days at a time. Researchers have flagged this as a double-edged property: the convenience of infrequent administration comes at the cost of overriding the natural pulse pattern, and the long-term consequences of holding that signal open continuously have never been characterised in humans.

The bottom line: CJC-1295 amplifies the body’s own GH release rather than supplying GH directly, but the DAC form replaces the natural pulse with sustained stimulation of uncertain long-term effect.

The clinical evidence for CJC-1295 is unusually thin for a compound this widely sold, and the development programme ended in a way that should give any reader pause. There are essentially two data points worth knowing, and both concern the DAC form only.

The published Phase 1 study

The foundational trial was published by Teichman and colleagues in the Journal of Clinical Endocrinology and Metabolism in 2006. It enrolled 21 healthy adults aged 21 to 61 and tested single subcutaneous doses across a range from 30 to 250 micrograms per kilogram. The study confirmed that the molecule raised GH and IGF-1 levels and that the effect was prolonged, which is what established the “long-acting” reputation. This is short-term, early-phase pharmacology in a small healthy cohort, not evidence of safety or benefit over months of use.

The Phase 2 trial that was halted

ConjuChem’s larger study (registered as NCT00267527) enrolled 192 people with HIV-associated lipodystrophy to test whether the peptide could correct the abnormal fat distribution caused by older antiretroviral drugs. In July 2006 the company stopped the trial after a participant at an Argentine study site died roughly two hours after receiving an eleventh weekly injection. The attending physician attributed the death to pre-existing coronary artery disease with plaque rupture and judged it unlikely to be caused by the drug, but the sponsor terminated the programme as a precaution. The full results were never published, and ConjuChem filed for bankruptcy in 2010. No company has since taken the molecule back into clinical development.

Evidence Source	Evidence Tier	What It Showed
Teichman et al. (JCEM)	Phase 1, small healthy cohort	Single doses raised GH and IGF-1 with a prolonged effect
HIV lipodystrophy trial (NCT00267527)	Phase 2, terminated early	Stopped after a participant death; results never released
CJC-1295 without DAC (Mod GRF 1-29)	No published human trial	Body-composition and recovery claims rest on user reports only

The bottom line: The entire clinical record for CJC-1295 is one small Phase 1 study and one Phase 2 trial that was abandoned after a death, with no controlled evidence at all for the no-DAC form most people buy.

CJC-1295 holds no marketing authorisation anywhere in the world. Its status differs by jurisdiction mainly in how each regulator treats the gap between “not a controlled substance” and “not legal to supply for human use.”

Country	Approval	Practical Status
United States	None	Not compoundable; sold only as “research” material
United Kingdom	None	Unlicensed; unlawful to supply for human use
Australia	None	Prescription-only class; import tightly restricted

CJC-1295 sat on the FDA’s Category 2 restricted compounding list from September 2023 until late September 2024, when its nominators withdrew their nominations and it was removed. It then went before the Pharmacy Compounding Advisory Committee, which in December 2024 voted against recommending it for the 503A Bulks List. The committee pointed to cardiac safety concerns – informed in part by the participant death during the halted Phase 2 trial – and insufficient human data to support compounding use. CJC-1295 cannot currently be legally compounded in the United States. For how the category system works, see our explainer on the FDA’s compounding categories. Whether CJC-1295 might be swept into the broader reclassification effort announced in early 2026 remains genuinely uncertain; we track the moving pieces in our peptide reclassification tracker.

In the UK, the MHRA has granted no authorisation for CJC-1295, and supplying it as an unlicensed prescription-only medicine is unlawful under the Human Medicines Regulations 2012; the wider framework is set out in our guide to how UK law treats research peptides. Australia’s TGA treats GHRH-class peptides as prescription-only substances and applies strict import controls, detailed in our overview of Australian peptide regulation. For the full US picture, see our breakdown of peptide legality in the United States.

For athletes there is no ambiguity. The World Anti-Doping Agency lists CJC-1295 under category S2, meaning it is prohibited in tested sport at all times, and modern testing can detect GHRH analogues at picogram concentrations.

The bottom line: CJC-1295 is unapproved everywhere, was rejected for US compounding by the FDA’s advisory committee, and is banned in competitive sport.

The honest answer on CJC-1295 safety is that the long-term picture is unknown, because no study has ever followed people taking it over an extended period. The short-term effects reported in the early trials and in user accounts are largely those associated with elevated GH and IGF-1: injection-site redness or swelling, transient facial flushing, fluid retention, tingling or numbness in the hands, and headaches.

Two structural concerns deserve more weight than the everyday side-effect list. The first is the long half-life of the DAC form. Sustaining GH signalling for days at a time departs sharply from the body’s pulsatile design, and the theoretical risks of chronically elevated GH and IGF-1, which include insulin resistance and tissue overgrowth, have not been measured in long-term use of this molecule in people. The second is the simple fact that the largest trial was halted following a death. Although that death was formally attributed to underlying heart disease rather than the drug, the absence of any completed safety study means the question was never properly answered.

The bottom line: The everyday side effects are mild and GH-related, but the genuine safety unknowns are the consequences of sustained signalling and the unregulated supply chain.

CJC-1295 sits within a family of GH-axis compounds that are frequently discussed, and sometimes combined, together. A few points of orientation help place it.

• Sermorelin is the parent fragment CJC-1295 is built on, but with a very different regulatory history: it was once an FDA-approved drug. The two are set side by side in our head-to-head comparison of the two GHRH analogues.
• Ipamorelin works through a different receptor entirely and is the compound most often paired with CJC-1295 in unregulated products; our ipamorelin guide owns the detail on how GH-axis compounds are stacked.
• Tesamorelin (brand name Egrifta) is worth knowing as the only GHRH analogue that ever reached and held FDA approval, cleared in 2010 for HIV-related abdominal fat; we cover it in our guide to the approved GHRH drug.