CJC-1295 (no DAC): the complete research guide.

CJC-1295 is a 29-amino-acid GHRH analog that tells the pituitary to release growth hormone. The pharmacology is well characterized and the mechanism is real. The human evidence is the problem: we found zero randomized trials testing it for muscle, fat or aging outcomes.

Here's the short version of how CJC-1295 got here. ConjuChem developed it in the early 2000s as a once-weekly treatment for adult growth hormone deficiency. It cleared early human safety studies, and then the program was shelved.

The molecule resurfaced in research supply chains and found two audiences. One is lab researchers who use it to study how growth hormone pulses behave. The other is grey-market users chasing GH-axis effects without a prescription.

This guide is written for the first group. If you're in the second, we'd say plainly that you're swimming upstream of a thin evidence base.

What is CJC-1295?

CJC-1295 is a modified copy of the first 29 amino acids of GHRH, the growth hormone-releasing hormone your hypothalamus already makes. Four amino acids were swapped out to resist enzyme breakdown and stretch the circulating half-life.

Those four swaps give the peptide its other name, “Modified GRF 1-29” or “Mod GRF.” CJC-1295 no DAC and Mod GRF 1-29 are the same molecule. You'll see vendors sell them under both labels.

CJC-1295 works by binding the GHRH receptor on pituitary somatotrophs, the cells that make and release growth hormone. Occupying that receptor triggers a burst of GH through the same cAMP/PKA pathway your own GHRH uses. The difference is stability, not signaling.

A 2026 review by Rahman and colleagues grouped CJC-1295 with sermorelin, tesamorelin, ipamorelin and AOD-9604 as growth-hormone secretagogues. These compounds prompt your body to release its own GH rather than supplying GH from outside.

They share a downstream target, and they differ sharply in half-life, receptor affinity and regulatory standing. Treating them as interchangeable is the most common mistake we see readers make.

“Mechanistically credible, clinically unstudied” is the most accurate one-line summary of CJC-1295 in 2026. We'd stand behind that sentence in front of anyone.

DAC vs no DAC: what's the difference?

DAC is a chemical handle that keeps CJC-1295 in your blood for days instead of minutes. It stands for Drug Affinity Complex. It binds loosely to albumin, the most abundant protein in plasma, and albumin itself circulates for roughly 19 days.

The half-life numbers show the size of the gap. Native GHRH lasts ~7 minutes. CJC-1295 no DAC, which is Mod GRF 1-29, stretches that to approximately 30 minutes on the four substitutions alone.

CJC-1295 DAC circulates for 6 to 8 days by riding albumin. That's roughly a 400-fold difference, from one chemical modification.

For a once-weekly pharmaceutical, DAC is the enabling modification. A 30-minute peptide can't support weekly dosing at all.

For pulsatility research, DAC is a confound. The pituitary evolved to release GH in episodes. Bathing it in continuous GHRH signaling for a week is a pharmacological artifact, not a physiological model.

So research groups studying pulse dynamics use the no-DAC form. A short half-life means each dose produces one pulse that decays before the next, and the episodic pattern survives.

The DAC variant flattens those pulses into sustained elevation. That suits some experimental questions and ruins pulse-fidelity studies.

CJC-1295 (no DAC)

GHRH analog 29 aa No DAC

The same compound cited across the GHRH-analog reviews in this guide. Lab-verified identity and purity, third-party COA per lot.

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Why do researchers prefer CJC-1295 no DAC?

Because the pituitary is a pulse generator, and pulse shape is the signal. Healthy adults release GH in 6 to 10 discrete bursts every 24 hours, and the largest lands in the first hours of slow-wave sleep. Between bursts, circulating GH falls to near-basal.

That pattern isn't incidental. Downstream tissues are calibrated to respond to pulse amplitude, not to the total area under the curve.

Liver IGF-1 output is the clearest example. It tracks GH pulse height. Continuous GH exposure has been shown to blunt IGF-1 output by saturating the receptor and triggering negative feedback, while pulsatile secretion keeps receptor sensitivity intact.

That's why most published GHRH-analog research uses tesamorelin, which also clears in about 30 minutes, in preference to CJC-1295 DAC. No-DAC CJC-1295 sits in the same research niche.

The catch is dosing frequency. Holding meaningful exposure across a full day takes several administrations of the no-DAC form. That inconvenience is why grey-market use has historically leaned toward DAC.

Does stacking CJC-1295 with ipamorelin do anything?

In rodents it did. In people, nobody has run the trial. Ipamorelin is a 5-amino-acid peptide that binds the ghrelin receptor, GHS-R1a, rather than the GHRH receptor, and hitting both receptors at once is the whole rationale.

The two receptors trigger complementary signals inside pituitary somatotrophs, which can produce additive or synergistic GH release. That mirrors the way your own GHRH and ghrelin co-secrete to shape a natural GH pulse.

A 2026 review in the American Journal of Sports Medicine reported the one recent result worth citing. Co-administering CJC-1295 and ipamorelin improved muscle force in a mouse model of steroid-induced muscle wasting, per Mayfield and colleagues.

That's the strongest recent body-composition signal for the pair in the published record. We'd read it carefully, though. The model was pathological muscle atrophy in rodents, not resistance-trained humans.

Where does the human evidence for CJC-1295 stop?

It stops at biomarkers. CJC-1295 has circulated in grey-market channels since roughly 2010, and across the 2020–2026 literature we found no published human efficacy data at all.

What does exist splits into two piles. The first is anti-doping detection methodology. Four groups published validated methods for finding CJC-1295 in athlete urine and blood: Memdouh et al., 2021, Coppieters et al., 2022, Cristea et al., 2023 and Thomas et al., 2024.

That volume of detection work tells you something by itself. Regulators consider misuse common enough to keep funding analytical chemistry against it.

The second pile is narrative reviews and book chapters that discuss CJC-1295 inside broader peptide overviews, including Sinha et al., 2020, Mavrych et al., 2026 and Mendias and Awan, 2026. They place the compound in its class and add no new controlled efficacy data.

No randomized controlled trial of CJC-1295 has been published for muscle accretion, adiposity, aging outcomes, sleep, recovery or cognition. We looked. That gap is the defining fact about where this compound stands.

What has CJC-1295 actually been shown to do?

It raises GH and IGF-1. Everything past that line gets attributed to CJC-1295 in grey-market discourse, so here's what the evidence behind each claim actually amounts to.

• Lean body mass accretion. Theoretical basis: elevated IGF-1 is anabolic in skeletal muscle. No controlled human trials have tested this specifically for CJC-1295.
• Adiposity reduction. The only RCT-backed body-composition data in the GHRH-analog class involves tesamorelin in HIV-related visceral fat redistribution. No equivalent data exist for CJC-1295 in otherwize healthy research subjects.
• Sleep architecture and recovery. Mechanistically plausible: the largest physiological GH pulse occurs during slow-wave sleep onset. No controlled sleep-study data have been published for CJC-1295 specifically.
• GH and IGF-1 biomarker elevation. Supported by older pharmacokinetic studies, primarily for the DAC form. Biomarker shifts do not automatically imply downstream tissue benefit.
• Aging-related outcomes. No human RCT data. The hypothesis derives from the observed age-related decline in GH secretion; whether pharmacological restoration of GH levels reverses aging-related physiology has not been demonstrated in controlled trials.

So the honest summary is a narrow one. Published work confirms CJC-1295 moves GH and IGF-1 as biomarkers, and nothing published tells you whether those shifts become anything you'd notice.

What are the risks of CJC-1295?

The risks are the ones that come with any GH-axis drug, plus a supply-chain risk that has nothing to do with the molecule. Decades of recombinant GH pharmacology document edema, joint pain, paresthesias, carpal tunnel syndrome and worsened insulin sensitivity as class effects.

Whether CJC-1295 reproduces those at investigational doses has never been quantified. No dedicated safety trial has been completed, so the class profile is all you have to reason from.

Two longer-term concerns recur across the GH-axis literature.

• IGF-1 and oncologic risk. Epidemiological studies have observed associations between chronically elevated IGF-1 and increased rates of colorectal, prostate, and breast cancers. This is a class-level concern for GH-axis modulation, not specific to CJC-1295. Whether intermittent, pulse-synchronized IGF-1 elevation carries equivalent risk to continuous elevation has not been established.
• Receptor desensitization. Sustained GHRH receptor stimulation is hypothesized to downregulate somatotroph responsiveness. Older pharmacokinetic data for the DAC form showed declining GH responses over multi-week observation periods. Whether the no-DAC form, with its shorter half-life and interval between doses, avoids this is not established.

A 2026 review in the Journal of Sports Medicine and Physical Fitness by Coutinho and colleagues adds the supply chain itself. It names cardiovascular strain, insulin resistance, dyslipidemia and psychiatric instability as emerging concerns in the literature.

It also flags manufacturing quality and contamination as documented hazards in unregulated channels. That's a hazard of where you bought the vial rather than of the peptide inside it. It's also the only one on this page you can actually check, with a batch-matched certificate of analysis.

CJC-1295 (no DAC)

10 mg ≥99% pure Lyophilized

Modified GRF 1-29, the 29-aa GHRH analog. The same reference compound used across the cited preclinical studies. COA available with each lot.

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What's the regulatory status of CJC-1295?

Unapproved everywhere. The FDA, the EMA and every other major regulator have approved CJC-1295 for nothing, and ConjuChem's clinical development stopped in the late 2000s.

Why it stopped isn't documented anywhere we can verify. A fatal adverse event in a trial of CJC-1131, a different molecule on the same delivery platform, gets repeated as the reason. We couldn't find a primary source for it, and no published CJC-1295 trial reports a death.

No new registered clinical trial has appeared on ClinicalTrials.gov in the last decade either.

In sport, CJC-1295 sits on the WADA Prohibited List under category S2, which covers peptide hormones, growth factors and related substances. Published detection methods work at sub-nanogram-per-milliliter urine concentrations.

The FDA also added CJC-1295 to its list of bulk substances not eligible for 503A compounding. Licensed compounding pharmacies can't legally prepare it for clinical use. That action pushed CJC-1295 out of medical practice and into research-only supply, which is where you find it today.