CJC-1295 without DAC (modified GRF 1-29)
mod GRF (1-29), modified GRF 1-29, CJC-1295 no DAC, tetrasubstituted GRF(1-29), MOD GRF
Modified GRF (1-29), sold as CJC-1295 without DAC, is the 29-amino-acid GHRH fragment carrying the same four protective amino acid substitutions as CJC-1295, but without the albumin-binding linker that gives that compound its week-long half-life. It is therefore a short-acting GHRH receptor agonist. This is the thinnest evidence file in the entire GH secretagogue class: no clinical trial of this exact molecule has ever been published, in humans or in animals.
Mechanism
Modified GRF (1-29) is an agonist at the GHRH receptor on pituitary somatotrophs. Binding couples to Gs, elevates cAMP, activates protein kinase A and CREB, and triggers release of stored growth hormone alongside GH1 gene transcription. Its behaviour is that of a brief pharmacological pulse: it amplifies a growth hormone secretory episode if one is already being permitted by the hypothalamus, but cannot force secretion against a somatostatin trough, and cannot exceed the pituitary's stored capacity. This dependence on prevailing somatostatin tone is the pharmacological basis of the usual claim that short-acting GHRH analogues produce a 'more physiological' pattern than long-acting ones, a plausible argument that has never been tested against a clinical endpoint.
The four substitutions relative to native GRF(1-29) are D-Ala2, Gln8, Ala15 and Leu27. D-Ala2 is the important one for duration of action: it blocks dipeptidyl peptidase-4 from clipping the N-terminal dipeptide, which is the principal route by which native GHRH is inactivated within minutes in plasma. The other three address chemical and conformational liabilities rather than metabolic ones: Gln8 replaces a deamidation-prone asparagine, Leu27 an oxidation-prone methionine, and Ala15 replaces glycine in a way that stabilises the peptide's helical conformation. Critically, none of these substitutions extends the half-life the way the drug affinity complex does. Removing the albumin-binding lysine from CJC-1295 does not produce a slightly shorter-acting version of the same drug; it produces a fundamentally different pharmacology, from continuous receptor tone measured in days back down to a single secretory episode measured in tens of minutes.
What the research shows
There is no published clinical trial of modified GRF (1-29). Not a randomised trial, not an open-label study, not a pharmacokinetic study. A search of PubMed and ClinicalTrials.gov identifies nothing in the peer-reviewed literature examining this precise molecule in humans, and no published animal study of it either. This point is routinely obscured by marketing that cites the Teichman and Ionescu trials, both of which studied CJC-1295 with the drug affinity complex attached: a molecule with a vastly longer half-life and an entirely different exposure profile. Those two papers are not evidence for this compound.
What can reasonably be inferred comes from adjacent molecules. Sermorelin, the unmodified GRF(1-29) parent, held FDA approval and has a genuine trial record in children with growth hormone deficiency and small open-label studies in older adults, so the receptor pharmacology of a short-acting GHRH fragment in humans is characterised in general terms. The tetrasubstituted backbone itself was developed as an intermediate in the CJC-1295 chemistry programme rather than as a drug candidate in its own right, and no sponsor has ever taken it into a clinical trial. Everything else circulating about this peptide (the specific half-life figures, the claims about superior pulsatility, the assertions about synergy when combined with a ghrelin-receptor agonist) is extrapolation, anecdote, or vendor copy. A reader should treat this compound as pharmacologically plausible and clinically unstudied, which is not the same thing as safe or effective.
Evidence assessment
Preclinical only
No study of this exact molecule has been identified in humans or animals; its properties are inferred entirely from sermorelin and from the CJC-1295 chemistry programme, so it sits at the floor of the scale: 'preclinical' overstates it, since there is not even a published animal study.
Tiers are applied consistently across the library and re-checked when new trials read out. Read the grading method.
Key studies
Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults Limited evidence
Establishes the pharmacology of the tetrasubstituted GRF(1-29) backbone, but only as an albumin-conjugated bioconjugate; the exposure profile does not transfer to the unconjugated peptide.
Sermorelin: a review of its use in the diagnosis and treatment of children with idiopathic growth hormone deficiency Limited evidence
Provides the closest human evidence base available, showing that a short-acting GRF(1-29) fragment can raise growth velocity in children with growth hormone deficiency.
Safety
No safety data of any kind exist for this molecule. Nothing has been formally studied: not in a phase 1 trial, not in a published animal toxicology package. Assumed risks are those of GHRH-receptor agonism generally: fluid retention, joint pain, carpal tunnel symptoms, impaired glucose tolerance, and a theoretical neoplasia concern from repeated IGF-1 elevation. In practice, the more immediate hazard for anyone encountering this peptide is the supply chain: unregulated products have no verified identity or purity, no endotoxin testing, no sterility assurance and no accountability for residual solvents or synthesis by-products. A compound with zero published human exposure data, obtained from an unregulated source, is not a low-risk proposition simply because the molecule is small and short-acting.
Regulatory status
| Jurisdiction | Status |
|---|---|
| United Kingdom | No UK marketing authorisation. Supply for human use is unlawful under the Human Medicines Regulations 2012. Legal to sell and possess only as a laboratory research chemical, and the MHRA treats the provision of dosing or administration instructions as evidence of marketing an unlicensed medicine. |
| United States | Not approved by the FDA for any indication, and never submitted for approval. It is not on Category 1 of the FDA's interim 503A bulk drug substances list, so it cannot lawfully be compounded for human use in the US. Sold online under a 'for research use only' label, a designation that reflects no regulatory review of identity, purity or safety and functions chiefly to permit the sale of an unapproved drug to consumers. |
| WADA (sport) | Prohibited at all times under section S2.2.4 of the WADA Prohibited List. The list names CJC-1295 and covers GHRH and its analogues as a class, which captures modified GRF (1-29) regardless of the naming convention a supplier uses. |
Questions
No. They are distinct molecules with radically different pharmacology. CJC-1295 with DAC carries a maleimidopropionyl-lysine that binds covalently to albumin, giving a half-life of roughly a week. Removing it leaves a short-acting peptide that produces a single growth hormone episode. The published human trials of CJC-1295 used the DAC version and do not apply to this one.
Yes. The two names describe the same molecule: human GRF(1-29) with four amino acid substitutions at positions 2, 8, 15 and 27. The 'CJC-1295 without DAC' naming came from the supplement and research-chemical market rather than from the pharmaceutical literature, where the compound has no development code of its own.
None that has been published. There is no clinical trial, no published pharmacokinetic study, and no published animal study of this exact molecule. Its half-life, its dose-response, and its effects on any clinical endpoint are all unmeasured. Sources presenting specific half-life figures for it are repeating a vendor claim, not citing data.
The rationale is real pharmacology: GHRH and ghrelin-receptor agonists act on different receptors and act synergistically on acute growth hormone release, which was demonstrated in humans by Bowers and colleagues in 1990 using GHRH plus GHRP-6. But that synergy was shown for other molecules on an acute biomarker, and no trial has tested any such combination against a clinical outcome.