CJC-1295 No-DAC (Mod GRF 1-29)

01 · What it is

CJC-1295 No-DAC, also sold as Mod GRF 1-29, is GRF(1-29) carrying four amino acid substitutions — D-alanine at position 2, glutamine at 8, alanine at 15 and leucine at 27 — and nothing else. The substitutions protect the peptide from cleavage by dipeptidyl peptidase-4 and from trypsin-like degradation. It acts on the growth hormone-releasing hormone receptor of anterior pituitary somatotrophs, as every compound in this family does ¹.

This guide is short because the evidence is. No human trial of the no-DAC compound was identified in the indexed literature during preparation of this guide. Every human pharmacokinetic figure attached to the name “CJC-1295” — the estimated half-life of 5.8 to 8.1 days, the IGF-1 elevation sustained for up to 28 days — was generated with the DAC version, a structurally different molecule bearing a maleimidopropionyl group that binds covalently to serum albumin ^3,4. Removing the drug affinity complex removes the mechanism that produced those numbers.

What remains is a stabilised GRF(1-29) with a circulating half-life measured in minutes rather than days. That is a real pharmacological difference, not a technicality. The two compounds share a name, a receptor and a peptide backbone; they do not share a duration of action, a dosing rationale, or an evidence base.

The most rigorous treatment of the distinction in the literature is a 2026 review that lists “CJC-1295 with Drug Affinity Complex (DAC)” and “CJC-1295 without DAC” as separate agents encountered in clinical practice and in online self-administration protocols ¹¹. Analytical chemists studying detection likewise treat them as distinct analytes ⁸.

As of September 2026 neither form holds a marketing authorisation from any regulator.

02 · Evidence at a glance

Evidence grade

Preclinical

Structure

GRF(1-29) with four amino acid substitutions; no albumin-binding complex

Molecular target

Growth hormone-releasing hormone receptor, anterior pituitary ¹

Human trials of the no-DAC compound

None identified

Human pharmacokinetic data for the no-DAC compound

None identified

Approximate duration of action

Minutes to a few hours, by contrast with days for the DAC form ^3,4

Data commonly attributed to it

Belongs to CJC-1295 with DAC ⁴

Randomised controlled trials

None

Toxicology

None identified

Approval status

None, any jurisdiction

Recognised as a distinct agent in the literature

Yes ^8,11

03 · Mechanism of action

The receptor, which is not in dispute

Like every compound in Family B, this one is an agonist at the growth hormone-releasing hormone receptor on anterior pituitary somatotrophs, stimulating synthesis and pulsatile release of endogenous growth hormone and, downstream, hepatic IGF-1 production ¹. Nothing about the receptor pharmacology is contested, and nothing about it is specific to this compound.

What the four substitutions do, and what they do not do

Unmodified GRF(1-29) — sermorelin — is cleaved at the Ala2 position by dipeptidyl peptidase-4 within minutes ². Substituting D-alanine at position 2 blocks that cleavage; the substitutions at positions 8, 15 and 27 address further degradation and aggregation liabilities. The result is a peptide more stable than sermorelin in plasma.

More stable is not long-acting. Blocking enzymatic cleavage extends a half-life from minutes to somewhat longer minutes; it does not produce the multi-day exposure that made the DAC version pharmacologically interesting. That came from covalent attachment to serum albumin, demonstrated in rats as an immunoreactive species migrating with the albumin band from 15 minutes and persisting beyond 24 hours ³. The no-DAC compound has the substitutions and not the conjugation.

The inference nobody has tested

The implicit argument for the no-DAC form is that a shorter-acting GHRH analogue better mimics physiological pulsatile signalling than one that stimulates the receptor continuously for days. That argument has a certain logic. It also has a complication: Ionescu and Frohman showed that pulsatile growth hormone secretion persisted under continuous stimulation by the DAC version, assessed by 20-minute overnight sampling after a single injection ⁵. The pituitary continued to release growth hormone in bursts regardless.

So the main pharmacological argument for preferring the short-acting form addresses a problem that was tested in humans and found not to occur. That does not make the argument wrong — a different pattern of stimulation may still produce different downstream effects — but it does mean the case is untested rather than established.

What has never been measured

No study has reported the plasma half-life of the no-DAC compound in humans. No study has reported its growth hormone or IGF-1 response curve in humans. No study has compared the two forms head to head in any species. Every quantitative statement made about this compound’s duration of action is extrapolated from structure rather than measured.

04 · Key research findings

The compound’s own literature. No clinical trial, no pharmacokinetic study, no animal efficacy study specific to the no-DAC form was identified in the indexed literature for this guide. This is the finding, and it is the reason this guide exists in the form it does.

What the adjacent literature establishes. The albumin-conjugation mechanism was demonstrated in rats for the DAC form ³. The pivotal human pharmacokinetic study — half-life 5.8 to 8.1 days, IGF-1 above baseline for up to 28 days after multiple doses — was conducted with the DAC form in healthy adults ⁴. Persistence of pulsatility under continuous stimulation was demonstrated with the DAC form ⁵. Growth normalisation in GHRH knockout mice used the DAC form at 24-, 48- and 72-hour dosing intervals ⁶.

Four findings, all frequently attributed to “CJC-1295” without qualification, and all generated with the molecule that has the drug affinity complex.

Where the distinction is drawn correctly. A 2026 review of performance-enhancing peptides modulating the GH–IGF1 axis separates CJC-1295 with DAC from CJC-1295 without DAC as distinct agents encountered in clinical practice and self-administration ¹¹. Analytical work on GHRH analogue detection likewise studies the two forms separately, identifying nineteen major in vitro metabolites across the class ⁸.

Two independent literatures — clinical review and doping control — both treat these as different compounds. The commercial literature generally does not.

Detection. Methods developed for GHRH analogues in urine and plasma cover the class ^7,8,9,10,12, with capillary electrophoresis able to separate analogues differing by the chirality of a single amino acid ¹⁰.

A compound can be detectable without being studied; these methods exist to catch GHRH analogues in sport, not to characterise this one’s pharmacology.

How reviews position the class. Recent syntheses in sports medicine, orthopaedics and endocrine practice list CJC-1295 among growth hormone secretagogues with mechanistic rationale and no validated clinical outcomes ^{13,14,15,16,17,18}.

None distinguishes the two forms when reporting outcomes, because there are no outcomes for either form to report.

05 · Evidence overview

06 · Safety profile

Animal data. No acute toxicity, repeat-dose toxicity, genotoxicity, reproductive or developmental toxicity, or carcinogenicity study of the no-DAC compound was identified. The animal work in this family used either the DAC form ^3,6 or unmodified GRF(1-29).

Human data. None exists for this form.

Class liability. Raising growth hormone antagonises insulin action, and reviews of growth hormone secretagogues treat glucose tolerance as the principal metabolic consideration for the class ^7,15. That liability applies to any effective GHRH agonist regardless of duration.

What is genuinely unknown. Whether the four substitutions alter receptor selectivity or downstream signalling relative to sermorelin — never tested. What plasma concentrations are achieved at any dose — never measured. What growth hormone response follows — never measured in humans. Whether repeated short-acting stimulation differs in consequence from sustained stimulation — the question the compound exists to answer, and unaddressed. Immunogenicity of a substituted peptide administered parenterally — unassessed. FDA’s account of why CJC-1295 was placed in category 2 cites immunogenicity risk, peptide-related impurity and characterisation complexity, and serious adverse events including increased heart rate and systemic vasodilatory reaction, with available clinical data described as limited ¹⁹; that entry does not distinguish between the two forms, which is itself a signal about how the two are handled in practice.

07 · US regulatory status

Current as of 6 September 2026. CJC-1295 in either form is not approved as a drug in the United States or any other jurisdiction, and is not a controlled substance.

CJC-1295 appears in FDA’s category 2 bulk drug substances material, in the table of substances nominated for compounding but subsequently withdrawn by the nominators ¹⁹. The entry does not distinguish CJC-1295 with DAC from CJC-1295 without DAC. CJC-1295 was not among the seven substances reviewed by the Pharmacy Compounding Advisory Committee in July 2026 ²⁰.

Under the World Anti-Doping Code, growth hormone-releasing factors and their analogues are prohibited at all times, and detection methods covering GHRH analogues in urine and plasma have been validated ^8,9,12. Competitors should consult the current Prohibited List directly rather than rely on secondary summaries, including this one.

08 · Limitations of the evidence

1. There is no evidence specific to this compound. No human trial, no pharmacokinetic study, no animal efficacy study. Every claim made about it is inferred from a related molecule or from its structure.
2. The data commonly cited belong to a different molecule. The half-life and IGF-1 duration figures come from the DAC form ⁴, whose extended action derives entirely from covalent albumin binding ³ that the no-DAC form does not have. Attributing those numbers to this compound is a category error of the same kind as attributing thymosin β4’s clinical record to TB-500.
3. Its duration of action has never been measured. Not in humans, not in animals, not in any published study. Statements about how long it acts are structural predictions.
4. The pulsatility rationale is untested and partly undercut. The argument for a short-acting GHRH analogue is that it preserves physiological pulsatility — but pulsatility was shown to persist under continuous stimulation by the long-acting form ⁵. The premise of the argument may not hold.
5. Regulatory records do not separate the two forms. FDA’s category 2 entry addresses “CJC-1295” without distinguishing them ¹⁹, so what regulatory attention exists cannot be mapped cleanly onto either.
6. No toxicology exists in any species. Neither acute nor repeat-dose, and no genotoxicity, reproductive or carcinogenicity data.
7. This guide is deliberately thin. The compound is listed separately from CJC-1295 with DAC, so it is documented separately. Consolidating them would produce a better single article and would also obscure the fact that one of the two has human data and the other has none.

09 · References

1. Grossman A, Savage MO, Besser GM. Growth hormone releasing hormone. Clin Endocrinol Metab. 1986;15(3):607–627.

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2. Esposito P, Barbero L, Caccia P, et al. PEGylation of growth hormone-releasing hormone (GRF) analogues. Adv Drug Deliv Rev. 2003;55(10):1279–1291.

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3. Jetté L, Léger R, Thibaudeau K, et al. Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog. Endocrinology. 2005;146(7):3052–3058.

   PMID 15817669 ↗

4. Teichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA. 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. J Clin Endocrinol Metab. 2006;91(3):799–805.

   PMID 16352683 ↗

5. Ionescu M, Frohman LA. Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. J Clin Endocrinol Metab. 2006;91(12):4792–4797.

   PMID 17018654 ↗

6. Alba M, Fintini D, Sagazio A, et al. Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse. Am J Physiol Endocrinol Metab. 2006;291(6):E1290–E1294.

   PMID 16822960 ↗

7. Sinha DK, Balasubramanian A, Tatem AJ, et al. Beyond the androgen receptor: the role of growth hormone secretagogues in the modern management of body composition in hypogonadal males. Transl Androl Urol. 2020;9(Suppl 2):S149–S159.

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8. Memdouh S, Gavrilović I, Ng K, Cowan D, Abbate V. Advances in the detection of growth hormone releasing hormone synthetic analogs. Drug Test Anal. 2021;13(11–12):1871–1887.

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9. Coppieters G, Deventer K, Polet M, Van Eenoo P, Judák P. An antibody-free, ultrafiltration-based assay for the detection of growth hormone-releasing hormones in urine at low pg/mL concentrations using nanoLC-HRMS/MS. J Pharm Biomed Anal. 2022;214:114726.

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10. Otin J, Tran NT, Benoit A, Buisson C, Taverna M. Online large volume sample staking preconcentration and separation of enantiomeric GHRH analogs by capillary electrophoresis. Electrophoresis. 2023;44(9–10):807–817.

    PMID 36787346 ↗

11. Dominikowski A, Rękoś Z, Olejarz M, Szczepanek-Parulska E, Domin R, Ruchała M. The emerging landscape of performance-enhancing peptides modulating the GH-IGF1 axis: bridging the gap between clinical evidence and patient self-administration. Front Endocrinol (Lausanne). 2026;17:1822475.

    PMID 42395176 ↗

12. Uçaktürk E, Nemutlu E. Analysis of growth hormone releasing hormone and its analogs in urine using nano liquid chromatography coupled with quadrupole/orbitrap mass spectrometry. J Pharm Biomed Anal. 2026;268:117207.

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13. Mayfield CK, Bolia IK, Feingold CL, et al. Injectable peptide therapy: a primer for orthopaedic and sports medicine physicians. Am J Sports Med. 2026;54(1):223–229.

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14. Rahman OF, Lee SJ, Seeds WA. Therapeutic peptides in orthopaedics: applications, challenges, and future directions. J Am Acad Orthop Surg Glob Res Rev. 2026;10(1):e25.00236.

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15. Mendias CL, Awan TM. Safety and efficacy of approved and unapproved peptide therapies for musculoskeletal injuries and athletic performance. Sports Med. 2026;56(8):1921–1935.

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16. Coutinho LFD, de Oliveira Neves LF, Camilo RP. A new era of doping? Use of peptide and peptide-analog drugs in recreational and professional sport and bodybuilding: a critical review. J Sports Med Phys Fitness. 2026;66(7):880–885.

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17. Tewari K, Liu TP, Im C, et al. Peptide supplements and their therapeutic applications in sports medicine. Am J Sports Med. 2026; online ahead of print.

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18. Renke G, Chinellato L. Therapeutic peptides in aesthetic, metabolic and endocrine conditions: effects, safety, clinical applications, and future perspectives. Int J Mol Sci. 2026;27(9):3890.

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19. US Food and Drug Administration. Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks. Page current as of 22 April 2026. Regulatory document; no PMID.

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20. US Food and Drug Administration. July 23–24, 2026: Meeting of the Pharmacy Compounding Advisory Committee. Docket FDA-2025-N-6895. Regulatory document; no PMID.

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