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PrecisePep/Peptide Library/CJC-1295 (no DAC)
Growth Hormone & Anabolic Support
Mod GRF(1-29) · Modified GRF 1-29 · tetrasubstituted GRF(1-29) · CJC-1295 without DAC
A GHRH fragment with four amino-acid substitutions for enzymatic stability — engineered to last long enough to work and short enough to still produce a pulse. The "no DAC" in the name does all the pharmacological work.
The naming around this compound is a mess, and the mess matters. "CJC-1295" strictly refers to a GHRH analogue bearing a drug affinity complex (DAC) — a maleimide group that binds serum albumin and extends the half-life to six to eight days. "CJC-1295 no DAC" is really Mod GRF(1-29): the same tetrasubstituted GHRH(1-29) fragment without that group, with a half-life around thirty minutes.
The four substitutions to native GHRH(1-29) confer resistance to dipeptidyl peptidase-IV, which otherwise degrades the peptide within minutes. That gets it from "unusable" to "usable as a pulse" — which is the design target, because GH signalling is pulse-sensitive.
The DAC version is a different drug in effect. Sustained multi-day elevation of GH and IGF-1 flattens the physiological pulse architecture that the GHRH-analogue approach is supposed to preserve, and it drives higher cumulative IGF-1 exposure. Every pulsatility argument made for this compound applies only to the no-DAC form, and vendors are not consistently clear about which they are selling.
The DAC and no-DAC forms look identical in a vial and are frequently sold under the same name. They have half-lives that differ by a factor of roughly three hundred. If a supplier cannot tell you which it is, they cannot tell you what the dosing schedule should be either.
GHRH receptor agonism. Binds the GHRH receptor on pituitary somatotrophs, driving cAMP-mediated GH synthesis and release. Because it acts upstream, GH secretion remains pulsatile and subject to somatostatin negative feedback.
DPP-IV resistance. The four substitutions protect the cleavage site that destroys native GHRH within minutes, extending the useful window to roughly half an hour — long enough to generate a full pulse, short enough that the pulse ends.
Why it is paired with a ghrelin mimetic. GHRH agonism presses the accelerator; GHS-R1a agonism releases the somatostatin brake. Two receptors, two mechanisms, a greater combined response than either alone. This is established endocrine pharmacology and the reason the ipamorelin pairing is near-universal.[2]
Downstream IGF-1. Sustained use raises IGF-1, which is the practical monitoring marker and the variable carrying the long-term risk.
Fasted timing. Insulin suppresses GH release, so administering in a fed state works directly against the mechanism.
Effects that have been reported. A study-tier entry means a result was published — not that the effect is established, reproducible, or transferable from a rodent to a person.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Clinical pharmacology work on CJC-1295 demonstrated sustained increases in GH and IGF-1 in healthy adults. Note that most of this data concerns the DAC form, where sustained elevation is the design objective.
GHRH-analogue stimulation retains physiological pulse architecture and feedback control, unlike exogenous GH administration.
Co-stimulation of the GHRH receptor and GHS-R1a produces a greater response than either alone — the strongest evidence supporting any combination on this site.
CJC-1295 never reached an approved indication. There is no phase 3 dataset, no label and no long-term safety characterisation.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
The dominant use case. A larger GH pulse is documented; translation into measurable body-composition change in non-GH-deficient adults is not.
GH secretion and slow-wave sleep are coupled bidirectionally. The most consistently reported subjective effect and the least studied.
From GH-driven collagen synthesis in GH-deficiency literature. Inferred for healthy adults.
Preserved pulsatility and intact feedback should protect against receptor downregulation in principle. Uncharacterised over long horizons.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The most consistent report, as with every GH-axis compound.
Near-universal, transient, and often used as an informal confirmation the product is active.
Dose-related, usually settling within weeks.
Consistently reported, and consistent with the two-receptor pharmacology.
Users frequently discover mid-protocol that they have the wrong form, usually because effects persist longer than expected.
Adverse effects, contraindications and unknowns. The grey-market tier is where under-reporting is worst: uncontrolled use produces no systematic safety surveillance at all, so absence of a reported harm is not evidence of safety.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Sustained GH and IGF-1 elevation produces insulin resistance, fluid retention, arthralgia and carpal tunnel symptoms regardless of the upstream stimulus.
Development was not completed. There is no chronic-use safety dataset for either form.
The DAC programme was reported to have encountered safety issues during development, which is part of why it did not proceed. Details in the public literature are limited.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
The standard concern with sustained GH-axis stimulation, and worse with the DAC form because exposure is continuous rather than pulsatile.
Directly relevant when combined with a glucagon-receptor agonist in a metabolic stack.
Dosing the DAC form on a no-DAC schedule produces continuous, accumulating elevation rather than nightly pulses.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The most common complaint.
The recognisable GH-excess signal at higher doses.
Transient and near-universal.
Generally mild.
Figures below are documented, not recommended. Study ranges come from published protocols in the stated model; grey-market ranges are what the research community reports using and carry no safety validation of any kind.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
CJC-1295 never reached approval. Clinical pharmacology studies used defined doses to measure GH and IGF-1 response, not to establish a therapeutic regimen.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Insulin suppresses GH release and the largest physiological pulse occurs early in slow-wave sleep. The coherent design.
The two-receptor argument is the one thing here with real pharmacological support.
The meaningful exposure variable, and measurable.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The standard figure, and half of the "100/100" convention when paired with ipamorelin.
Pulse-mimicking approach with higher total exposure.
Higher community range; ceiling effects make the additional gain questionable.
Common cycling pattern, not derived from any finding.
| Approach | Dose | Frequency | Timing |
|---|---|---|---|
| Standard (with ipamorelin) | 100 mcg | Nightly | Fasted, pre-sleep |
| Multi-pulse | 100 mcg | 2–3× daily | Fasted windows |
| Higher-end | 200 – 300 mcg | Nightly | Fasted, pre-sleep |
Combination effects. Almost no peptide combination has been studied as a combination in humans; stack logic is overwhelmingly mechanistic inference and community practice. Each linked compound has its own page.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Established endocrine pharmacology and the best-supported combination claim documented anywhere on this site.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
The canonical pairing, with matched short half-lives producing a single amplified pulse.
All three are GHRH analogues competing for the same receptor. Combining them is a higher GHRH dose, not a new mechanism.
The most consequential and most easily avoided antagonism.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
Standalone use is uncommon and reported as noticeably weaker.
The most likely GHRH arm in an undisclosed three-secretagogue vial.
Whole schedules — dosing, titration, cycle length, and off-time — as documented in trials, as proposed from mechanism, and as circulated in the research community. Reproduced for study and comparison only.
Highest confidenceReported in peer-reviewed literature, registered clinical trials, or regulatory filings. Note the model: much peptide literature is in vitro or rodent work, not human trial data.
Development did not complete for any GH indication.
Unproven — inference onlyExtrapolated from a known mechanism, receptor profile, or adjacent compound class. Biologically plausible but not directly demonstrated for this compound in this context.
Directly transferable from how approved GH-axis drugs are monitored.
DAC and no-DAC require completely different dosing frequencies.
Uncontrolled reportsAggregated from research-community logs, forums, vendor literature and self-reported experience. Uncontrolled, unverified, subject to placebo, polypharmacy and product-purity confounds. Lowest evidentiary weight.
The standard circulating pattern.
Grouped with ipamorelin in that matrix.
There is one question worth answering on this page and it is not a condition. It is whether the version you have carries the Drug Affinity Complex — because that single modification changes the pharmacology from a pulse into a plateau, and a plateau is what the pathological state of this axis actually looks like.
CJC-1295 is not approved anywhere, in either form. No controlled human trial supports any condition below. "CJC-1295" is used in the market to mean both the DAC and no-DAC versions, which are pharmacologically different compounds sold under one name.
Pathophysiology
The pituitary responds to the pattern of GHRH exposure, not merely to its presence. Somatostatin feedback shapes GH into pulses, and the pulsatile pattern is what the downstream tissue is adapted to.
Mechanistic rationale
No-DAC CJC-1295 — often sold as modified GRF(1–29) — has a short half-life and produces a pulse. The DAC version binds albumin and extends the half-life to days, producing a continuous elevation sometimes called a "bleed". Continuous exposure to a GHRH signal is closer to the acromegaly pattern than to the physiological one, and it is why the no-DAC form is generally preferred despite requiring more frequent injection. Leuprolide is the clearest demonstration of the same principle in an approved drug: continuous GnRH exposure shuts an axis down that pulsatile exposure switches on.
Community reports
DAC users report more fluid retention, more carpal tunnel symptoms and more lethargy — consistent with sustained rather than pulsed exposure. Many report better results after switching to the no-DAC form despite the extra injections.
Components carrying the argument: The DAC modification, or its absence
Pathophysiology
Adult GH deficiency follows pituitary disease and is diagnosed on a provocative test.
Mechanistic rationale
A GHRH analogue requires a pituitary capable of responding. In genuine GH deficiency the pituitary is the lesion, so recombinant GH is the treatment. Where the axis is merely quieter with age, a GHRH analogue is at least acting on an intact system — which is the honest version of the argument for it.
Community reports
Widely used on the basis of symptoms rather than a diagnosis.
Components carrying the argument: GHRH receptor — requires a functioning pituitary
Pathophysiology
Lean mass, visceral fat, sleep and bone are GH-responsive to varying degrees.
Mechanistic rationale
Every claim and every caveat is set out on the Ipamorelin + CJC-1295 page, including the ROMANA result separating mass from function, the diabetogenic effect of GH, and the thyroid lab interaction. The one addition specific to this compound is that a DAC-driven plateau makes the glucose effect more likely to persist, because the exposure does.
Community reports
As across the class — sleep and fullness reported most, strength least.
Components carrying the argument: Downstream GH and IGF-1
Pathophysiology
Acromegaly is sustained GH excess and causes cardiomyopathy, hypertension, sleep apnoea, insulin resistance, arthropathy and increased colorectal neoplasia.
Mechanistic rationale
A DAC-modified GHRH analogue producing a continuous elevation is, in kind if not in degree, the pattern acromegaly is defined by. Octreotide exists to suppress it. Reading the two pages together is the fastest way to understand why pulsatility is the whole argument here.
Community reports
Not raised in community discussion, where DAC is usually presented purely as a convenience feature.
Components carrying the argument: Sustained GHRH signalling
| Question | No-DAC (mod GRF 1-29) | DAC |
|---|---|---|
| Half-life | Minutes | Days |
| Exposure pattern | Pulse | Continuous plateau |
| Injection frequency | Daily or more | Weekly or twice weekly |
| Feedback preserved? | Largely yes | Largely no |
| Resembles the physiological state? | Yes | No — closer to the acromegaly pattern |
| Reported fluid retention | Less | More |
For diagnosed GH deficiency: recombinant human GH under endocrinology supervision after a provocative test.
For the age-related decline: resistance training, adequate protein, sleep, and treatment of obstructive sleep apnoea, which is common, missed, and independently degrades both GH secretion and daytime function.
Physical-chemistry reference for laboratory handling of the lyophilised material. Reproduced so that stability and concentration mathematics can be studied — see the calculator for the arithmetic and the reconstitution guide for sterile technique.
Supplied lyophilised, commonly 10 mg per vial, or pre-blended with ipamorelin. At 100 mcg nightly a 10 mg vial is over three months — a long in-use period worth planning around.
Lyophilised: −20 °C. Reconstituted: 2–8 °C, protected from light.
Commonly 10 mg lyophilised vials; also supplied pre-blended with ipamorelin at 10 mg total.
Nothing in the vial distinguishes the DAC from the no-DAC form. The certificate of analysis, if supplied, should.
Regulatory status changes and differs by country. This is a summary for orientation, not legal advice — check your own jurisdiction.
Not approved for human use anywhere. Clinical development did not proceed to approval. Sold as a research chemical.
CJC-1295 was among the peptides affected by the FDA's April 2026 restructuring of the Section 503A compounding categories. It was not among the seven substances reviewed at the July 2026 advisory committee meeting, and no listing decision has been made for it.
On 4 December 2024 the FDA's Pharmacy Compounding Advisory Committee voted unanimously against including CJC-1295 on the Section 503A Bulks List. The committee cited a lack of evidence for clinical effectiveness and safety in the uses under review.
This was an earlier and separate round from the July 2026 meeting, and it is the part of the story that the coverage of that meeting almost entirely omits. Across two sittings in October and December 2024, PCAC considered seven substances — including ipamorelin, kisspeptin-10, AOD-9604, CJC-1295 and thymosin alpha-1 — and rejected every one of them. In July 2026 the same committee recommended six of the seven it looked at. What changed between the two rounds was the FDA's April 2026 restructuring of the Category 2 list and the set of substances nominated, not the arrival of new efficacy trials for anything on this page.
A negative advisory vote is not a ban and is not binding. It does mean there is no current 503A compounding pathway for this substance, and that a committee reviewing the evidence was not persuaded by it.
Regulatory and trial claims re-checked against primary sources on 16 August 2026. Checked: PCAC rejected it unanimously on 4 December 2024; no 503A pathway. Approvals, trial readouts and compounding decisions move faster than anything else on this page — a date here means someone looked, not that nothing has changed since.
GHRH analogues are explicitly named on the WADA Prohibited List under S2. Prohibited at all times, in and out of competition.
Links resolve to PubMed records, trial registries, publisher pages or primary documents. Where a body of work rather than a single paper is cited, the link opens a PubMed query so the full result set — including newer papers than this page — can be reviewed. Verify every claim against the primary source before relying on it.
For educational and research reference only. Nothing on this site is medical advice, a recommendation, or an instruction to administer any substance to a human being. Every figure on this page is a record of what has been reported, not a recommendation. Full disclaimer.
