CJC-1295 with DAC

01 · What it is

CJC-1295 with DAC is a 30-amino-acid analogue of GRF(1-29) carrying four amino acid substitutions and, at its C-terminus, a maleimidopropionyl group — the drug affinity complex, or DAC. That linker forms a covalent bond with cysteine-34 of circulating serum albumin, converting a peptide with a half-life of minutes into one with a half-life of days ³.

The bioconjugation was demonstrated directly. In rats, Western blot analysis of plasma after injection showed a CJC-1295 immunoreactive species migrating with serum albumin, appearing within 15 minutes and still present beyond 24 hours ³. It is an elegant piece of protein engineering, and it worked.

In the published literature, “CJC-1295” means this compound. The pharmacokinetic figures that circulate under that name — the multi-day half-life, IGF-1 elevated for weeks — were generated with the albumin-conjugated version, not the version sold without DAC. That distinction is covered in the separate no-DAC guide and is the single most important thing a reader of either can know.

What this compound has is one unusually clean phase 1 result. In healthy adults, the estimated half-life was 5.8 to 8.1 days, and after multiple doses mean IGF-1 remained above baseline for up to 28 days ⁴. What it does not have is anything after that. There is no phase 2, no phase 3, no efficacy trial in any disease, and no development programme. Twenty years after the pivotal human study concluded that the data supported the compound’s potential utility as a therapeutic agent ⁴, that potential remains untested.

As of September 2026 CJC-1295 holds no marketing authorisation from any regulator.

02 · Evidence at a glance

Evidence grade

Early Clinical

Structure

GRF(1-29) with four substitutions plus a C-terminal maleimidopropionyl drug affinity complex; 30 residues ^3,13

Mechanism of extended action

Covalent conjugation to serum albumin in circulation ³

Molecular target

Growth hormone-releasing hormone receptor, anterior pituitary ¹

Published human studies

2 ^4,7, plus a pulsatility substudy ⁶

Estimated half-life in humans

5.8–8.1 days ⁴

Duration of IGF-1 elevation after multiple doses

Up to 28 days ⁴

Phase 2 trials

None

Phase 3 trials

None

Efficacy trials in any disease

None

Human safety database

Limited to the phase 1 programme

Approval status

None, any jurisdiction

Detection

Established in human and equine matrices ^{8,10,11,13,14,15}

03 · Mechanism of action

Albumin conjugation, and why it changes everything

The central problem for every GHRH analogue is dipeptidyl peptidase-4, which cleaves GRF(1-29) at the Ala2 position within minutes — a liability the field has approached in several ways, including PEGylation of GRF analogues ². CJC-1295 with DAC addresses this twice over: four amino acid substitutions reduce enzymatic susceptibility, and the maleimidopropionyl group at the C-terminus reacts with a free thiol on serum albumin to form a covalent adduct ³. Albumin has a circulating half-life of around nineteen days, so a peptide covalently attached to it inherits a pharmacokinetic profile it could never achieve alone.

The demonstration is direct rather than inferred. Injected into rats, the compound appeared as an albumin-associated immunoreactive band within 15 minutes and persisted beyond 24 hours, and the bioconjugate activated the GRF receptor on the anterior pituitary ³.

This is the most cleanly demonstrated delivery mechanism of any compound covered on this site.

GHRH receptor agonism

Once bound to albumin, the peptide remains available to act on the growth hormone-releasing hormone receptor of anterior pituitary somatotrophs, stimulating growth hormone synthesis and release, which drives hepatic IGF-1 production ^1,4. The receptor pharmacology is that of the GHRH class and is not in dispute.

Pulsatility under continuous stimulation — the important human finding

The obvious objection to a GHRH analogue with a multi-day half-life is that it converts a pulsatile signal into a continuous one, which would be pharmacologically undesirable. Ionescu and Frohman tested this directly: growth hormone pulsatility was assessed by 20-minute blood sampling during an overnight period after a single injection of CJC-1295, and pulsatile secretion persisted despite continuous receptor stimulation ⁶. They also examined which secretion parameters correlated with the rise in IGF-1.

This is a genuinely good experiment and it answers a question that matters. Continuous stimulation did not abolish pulsatility — the pituitary continued to release growth hormone in bursts, presumably because somatostatin tone still governs the timing. It is the strongest mechanistic result in this compound’s file and it deserves to be better known than the half-life figure.

Downstream protein effects

Analysis of sera from 11 healthy young adult men before and one week after CJC-1295 injection, by two-dimensional gel electrophoresis, identified changes in the serum protein profile consequent to GH–IGF1 axis activation ⁷.

A small study, and one of the few attempts to characterise what activating this axis does beyond measuring the axis itself.

Proof of concept in a genetic model

In GHRH knockout mice, three groups treated for five weeks with 2 µg of CJC-1295 at intervals of 24, 48 and 72 hours showed normalised growth ⁵.

A clean demonstration that receptor activation at extended dosing intervals is sufficient to restore a growth phenotype in an animal lacking the native ligand.

04 · Key research findings

The pivotal human study. Teichman and colleagues administered CJC-1295 to healthy adults and reported an estimated half-life of 5.8 to 8.1 days, with mean IGF-1 levels remaining above baseline for up to 28 days after multiple doses. The authors concluded that the data supported the potential utility of CJC-1295 as a therapeutic agent ⁴.

One phase 1 study, in healthy volunteers, with pharmacokinetic and biomarker endpoints. Everything asserted about this compound rests on it.

Pulsatility preserved. After a single injection, overnight 20-minute sampling showed that pulsatile growth hormone secretion persisted under continuous stimulation, and the analysis identified which secretion parameters correlated with IGF-1 production ⁶.

The answer to the most serious pharmacological objection to the compound, and it came out in the compound’s favour.

Serum proteomics. Two-dimensional gel electrophoresis of sera from 11 healthy young men, before and one week after injection, showed changes in serum protein profile associated with GH–IGF1 axis activation ⁷.

Eleven subjects, exploratory, and the only look at systemic consequences beyond the axis itself.

Animal proof of concept. Once-daily and less frequent administration normalised growth in the GHRH knockout mouse ⁵.

Establishes that the extended half-life translates into sustained biological effect at practical dosing intervals.

Where the development went. Nowhere. No phase 2 study, no efficacy trial in growth hormone deficiency or any other indication, and no regulatory filing appears in the indexed literature. The compound instead surfaces in a doping laboratory’s identification of an unknown pharmaceutical preparation, where the sequence was matched to the peptide then being marketed as CJC-1295 and noted as prohibited under Section S2 of the WADA Prohibited List ⁸.

A compound that reached a promising phase 1 in 2006 and whose next literature appearance is a forensic identification in an unlabelled vial is telling a story about drug development that the pharmacology alone does not.

The detection literature. Immuno-polymerase chain reaction screening and confirmatory LC-MS/MS methods were developed for equine plasma ^10,11; in vitro metabolism and detection were characterised for CJC-1295 alongside CJC-1295 with DAC, sermorelin and tesamorelin, identifying nineteen major metabolites ¹³; and antibody-free ultrafiltration assays now detect GHRH analogues in urine at low picogram-per-millilitre concentrations ^14,15.

As with several compounds in this roadmap, the most active modern research programme is the one trying to detect it.

What the use literature documents. A netnographic study analysed 96 bodybuilding website hits referencing CJC-1295 to characterise patterns of female use ⁹. Reviews of growth hormone secretagogues in body composition management ¹², of peptide use in sport ¹⁸, and of performance-enhancing peptides modulating the GH–IGF1 axis ²⁰ all describe CJC-1295 as encountered in self-administration protocols.

Every one of these documents behaviour. None reports an outcome trial, because none exists.

How reviews position it. Recent syntheses in sports medicine, orthopaedics, aesthetic and gerontological medicine consistently list CJC-1295 among peptides with mechanistic rationale and absent clinical validation ^{16,17,19,21,22,23}.

Independent reviewers reach the same conclusion this guide does.

05 · Evidence overview

06 · Safety profile

Human data. The phase 1 programme in healthy adults established the pharmacokinetic profile and the IGF-1 response ⁴, with the pulsatility substudy ⁶ and serum proteomic analysis ⁷ adding observations in small numbers of subjects. That is the entire human safety database: healthy volunteers, short duration, phase 1 scale, twenty years ago.

Animal data. The GHRH knockout mouse work assessed growth normalisation over five weeks ⁵, and the rat bioconjugation work characterised albumin binding over 24 hours ³. Neither was a toxicology study, and no acute, repeat-dose, genotoxicity, reproductive or carcinogenicity programme for CJC-1295 was identified in the indexed literature.

Class liability. Sustained elevation of growth hormone and IGF-1 antagonises insulin action, and reviews of growth hormone secretagogues treat glucose tolerance as the principal metabolic consideration for the class ^12,19.

What is genuinely unknown, and the specific risk this compound creates. No repeat-dose data beyond the phase 1 exposure. No reproductive, developmental or carcinogenicity data in any species. No immunogenicity assessment. But the distinctive unknown here follows from the mechanism rather than from the missing studies: a compound with a 5.8-to-8.1-day half-life that keeps IGF-1 elevated for 28 days after dosing stops ⁴ cannot be titrated or withdrawn quickly. With a short-acting GHRH analogue, stopping ends the exposure within hours. With this one, a decision to stop is followed by weeks of continuing effect, and nothing in the published literature characterises what sustained IGF-1 elevation over months does in a person with a normal axis.

07 · US regulatory status

Current as of 6 September 2026. CJC-1295 with DAC is not approved as a drug in the United States or any other jurisdiction, and is not a controlled substance. No regulatory filing appears in the indexed literature, and development did not proceed past phase 1.

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, with FDA citing immunogenicity risk for certain routes of administration, complexity regarding peptide-related impurities and active ingredient characterisation, and identified serious adverse events including increased heart rate and systemic vasodilatory reaction, with available clinical data described as limited ²⁴. CJC-1295 was not among the seven substances reviewed by the Pharmacy Compounding Advisory Committee in July 2026 ²⁵.

Under the World Anti-Doping Code, growth hormone-releasing factors and their analogues are prohibited at all times; a doping laboratory identifying CJC-1295 in an unlabelled preparation in 2010 recorded it as prohibited under Section S2 ⁸. Validated detection methods exist for human urine and equine plasma ^10,11,14,15. Competitors should consult the current Prohibited List directly rather than rely on secondary summaries, including this one.

08 · Limitations of the evidence

1. Everything rests on one phase 1 study. A single trial in healthy adults, with pharmacokinetic and biomarker endpoints ⁴, is the foundation for every claim made about this compound. Phase 1 establishes exposure and tolerability at the doses tested. It does not establish that anything beneficial happens.
2. IGF-1 is a biomarker, not an outcome. Raising IGF-1 for 28 days ⁴ demonstrates that the compound engages its axis. It does not demonstrate improved body composition, recovery, function or any clinical endpoint, none of which has been measured in a trial.
3. No efficacy trial exists in any indication. Not a failed one — none was conducted. The development programme stopped after phase 1 and the published record does not explain why.
4. The long half-life is a liability as well as a feature. Effects persisting for weeks after dosing stops ⁴ mean exposure cannot be adjusted quickly, and no study has characterised sustained IGF-1 elevation over months in people with a normal axis.
5. Clinical authorship is concentrated. The pivotal study, the pulsatility substudy and the proteomic analysis share investigators ^4,6,7. There is no independent human replication of the pharmacokinetic finding.
6. Safety data are twenty years old and phase 1 in scale. No toxicology programme, no immunogenicity assessment, and no pharmacovigilance stream, because there has never been an approved product.
7. Regulatory review identified adverse events not visible in the trial literature. Increased heart rate and systemic vasodilatory reaction appear in FDA’s account of why the substance was placed in category 2 ²⁴. Those observations are not in the indexed clinical papers, which is itself a limitation of relying on a two-study literature.

09 · References

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

   PMID 2429796 ↗

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.

   PMID 14499707 ↗

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. 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 ↗

6. 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 ↗

7. Sackmann-Sala L, Ding J, Frohman LA, Kopchick JJ. Activation of the GH/IGF-1 axis by CJC-1295, a long-acting GHRH analog, results in serum protein profile changes in normal adult subjects. Growth Horm IGF Res. 2009;19(6):471–477.

   PMID 19386527 ↗

8. Henninge J, Pepaj M, Hullstein I, Hemmersbach P. Identification of CJC-1295, a growth-hormone-releasing peptide, in an unknown pharmaceutical preparation. Drug Test Anal. 2010;2(11–12):647–650.

   PMID 21204297 ↗

9. Van Hout MC, Hearne E. Netnography of female use of the synthetic growth hormone CJC-1295: pulses and potions. Subst Use Misuse. 2016;51(1):73–84.

   PMID 26771670 ↗

10. Timms M, Ganio K, Forbes G, Bailey S, Steel R. An immuno polymerase chain reaction screen for the detection of CJC-1295 and other growth-hormone-releasing hormone analogs in equine plasma. Drug Test Anal. 2019;11(6):804–812.

    PMID 30489688 ↗

11. Timms M, Ganio K, Steel R. A method for confirming CJC-1295 abuse in equine plasma samples by LC-MS/MS. Drug Test Anal. 2019;11(8):1248–1257.

    PMID 30938069 ↗

12. 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.

    PMID 32257855 ↗

13. 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.

    PMID 34665524 ↗

14. 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.

    PMID 35298973 ↗

15. 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.

    PMID 41138283 ↗

16. 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.

    PMID 41476424 ↗

17. 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.

    PMID 41490200 ↗

18. 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.

    PMID 41880199 ↗

19. 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.

    PMID 41966639 ↗

20. 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 ↗

21. 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.

    PMID 42578445 ↗

22. 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.

    PMID 42123471 ↗

23. Mavrych V, Shypilova I, Bolgova O. Therapeutic peptides in gerontology: mechanisms and applications for healthy aging. Front Aging. 2026;7:1790247.

    PMID 42021992 ↗

24. 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.

    Source ↗

25. 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.

    Source ↗