CJC-1295 (No DAC): What the Research Actually Says

Research use only. Not for human consumption.

What it is

CJC-1295 is a synthetic analog of growth hormone–releasing hormone (GHRH). It’s built on the first 29 amino acids of GHRH — the active fragment — with a handful of substitutions that make it more stable than the natural hormone, which the body breaks down in minutes.

Here’s where it splits into two very different compounds, and where most of the confusion starts. CJC-1295 comes in two forms:

• CJC-1295 with DAC (Drug Affinity Complex) carries an extra chemical linker that latches onto albumin in the blood. That anchor stretches its half-life to roughly 6–8 days, producing continuous, sustained GHRH signaling — what’s sometimes called a “GH bleed.”
• CJC-1295 No DAC — also called Modified GRF 1-29 (Mod GRF 1-29) — has no albumin anchor. Its half-life is about 30 minutes, so it produces a short, pulse-like signal that more closely resembles the body’s own rhythm. This is the version most often discussed alongside ipamorelin.

They share a backbone, but pharmacologically they behave like two different drugs. Keep that distinction in mind — it’s the whole story here.

Animal data

The foundational preclinical work was done on the albumin-binding (DAC) construct. Jetté and colleagues (2005, Endocrinology) showed that GRF(1-29)–albumin bioconjugates activated the GRF receptor on the anterior pituitary in rats and drove GH release. Alba and colleagues (2006, American Journal of Physiology) reported that once-daily CJC-1295 normalized growth in GHRH-knockout mice. The mechanism — a stabilized GHRH analog reaching the pituitary and triggering GH — is well supported in rodents.

Worth flagging: even much of the animal literature was generated on the DAC form. Direct preclinical work isolating the No DAC / Mod GRF 1-29 version on its own is thin.

Human data

This is the section that matters most, because it’s where the citation everyone uses doesn’t say what people think it says.

The headline human study is Teichman et al. (2006, Journal of Clinical Endocrinology & Metabolism) — two randomized, placebo-controlled, double-blind ascending-dose trials in healthy adults aged 21–61. A single subcutaneous dose produced mean GH increases of roughly 2- to 10-fold lasting 6+ days, and IGF-1 increases of about 1.5- to 3-fold lasting 9–11 days. The authors described it as “safe and relatively well tolerated” over the study periods. A companion paper (Ionescu & Frohman, 2006, JCEM) found that GH secretion stayed pulsatile even under continuous stimulation.

The catch: both of those human trials studied CJC-1295 with DAC — the long-acting, albumin-binding version. Those “GH elevated for six days from one shot” numbers are only possible because of the DAC anchor. They are not measurements of the No DAC / Mod GRF 1-29 compound.

So when you see the No DAC version marketed with the classic “2–10x growth hormone” figures, those numbers are borrowed from a different molecule. To date there is no published human clinical trial of the No DAC version on its own. Its case rests on GHRH physiology in general and on extrapolation from its long-acting cousin — not on direct human evidence for the specific compound being sold.

Promising vs. overhyped

Genuinely promising: Unlike some peptides in this series, CJC-1295 has real human pharmacology behind the family. The GHRH-analog mechanism is proven in people — the DAC trials clearly raised GH and IGF-1 in a controlled setting. The physiological logic of the No DAC form (short, pulsatile signaling that mimics natural GH release, often paired with ipamorelin) is reasonable and well-articulated.

Overhyped: The specific product most people buy — No DAC / Mod GRF 1-29 — has no dedicated human trial. There are no human outcome studies for either version showing changes in body composition, recovery, injury healing, or anything a buyer is actually hoping for; the human data is pharmacokinetic (it moves GH and IGF-1), not clinical outcomes. Development was abandoned nearly two decades ago. And the “same numbers as the DAC studies” framing quietly swaps one molecule for another.

Regulatory reality

CJC-1295 has never been FDA-approved for any indication. Its clinical development (by ConjuChem) reached a Phase 2 trial in HIV-associated lipodystrophy in 2006, which was halted after a participant died — a cardiovascular death that was attributed to pre-existing disease rather than the drug, but the program was never restarted and no drug application was ever filed.

The compounding picture is unsettled as of mid-2026. CJC-1295 sat in the FDA’s 503A Category 2 (barred from pharmacy compounding), and in December 2024 the Pharmacy Compounding Advisory Committee voted against adding it to the permitted list, citing nonclinical toxicity signals (including DNA damage in pituitary cells and injection-site necrosis), the unresolved 2006 cardiac signal, and immunogenicity concerns. On April 15, 2026, the FDA removed it from Category 2 — but did not move it to Category 1, leaving it in a classification gap pending further committee review. Translation: there’s currently no clear lawful compounding lane for it.

In sport, there’s no ambiguity: CJC-1295 is on the WADA Prohibited List at all times, in and out of competition, as a GHRH analog / GH secretagogue (Section S2). It is not a federally scheduled controlled substance in the U.S. Products in the research market are sold labeled for laboratory research only — not for human consumption.

Hype vs. Evidence rating: 3/5

CJC-1295 earns a 3/5 — a step above BPC-157 and TB-500, and here’s the honest reasoning. The GHRH-analog mechanism is genuinely established in humans, which is more than most research peptides can claim. But the human data belongs to the DAC version, while the No DAC form sold in stacks has no trial of its own; there are no human outcome studies for either; development was shelved 20 years ago; and there’s a real (if disputed) safety signal plus an unsettled regulatory status. Real mechanism, real GH effect — riding on its long-acting cousin’s data, with no outcome evidence for the specific compound.

Research use only. Not for human consumption. This content is educational and does not constitute medical advice or dosing guidance.