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Comparison

CJC-1295 With DAC vs Without DAC (Mod GRF 1-29): How the Research Compares

CJC-1295 with DAC and CJC-1295 without DAC share the same tetrasubstituted, 29-amino-acid GHRH backbone; only the DAC version carries an extra lysine with a maleimide group that bonds to serum albumin, stretching its half-life in people to about a week1,2. The published human studies of CJC-1295 all used the DAC compound. The version without DAC, also sold as Mod GRF (1-29), has a much thinner literature, and the two have never been compared head to head.

Two molecules under one name

CJC-1295 was introduced in a 2005 paper from ConjuChem as a tetrasubstituted form of human GRF(1-29) with an N-epsilon-3-maleimidopropionamide derivative of lysine added at the C terminus. That reactive lysine is the drug affinity complex, or DAC1. Strictly speaking, then, CJC-1295 is the DAC compound.

In the research market the name split in two. CJC-1295 with DAC refers to the original molecule. CJC-1295 without DAC, also sold as Mod GRF (1-29) or modified GRF 1-29, is the tetrasubstituted 29-residue peptide alone. When a Norwegian doping-control laboratory analyzed an unidentified preparation in 2009, it found a 29-amino-acid amide, with no added lysine, whose sequence matched the peptide then marketed as CJC-12955. Anti-doping laboratories now test for CJC-1295 and CJC-1295 with DAC as separate analytes6, and a 2026 clinical review lists them as distinct GHRH analogues7.

What is CJC-1295 without DAC (Mod GRF 1-29)?

Native human GHRH is a 44-amino-acid peptide8, and it is inactivated quickly in plasma. Dipeptidyl peptidase IV (DPP-IV) cuts it between residues 2 and 3, leaving a fragment with under one-thousandth of the original activity, and intact GHRH(1-44) had a half-life of about 6.8 minutes after intravenous administration in people9. The 1-29 fragment, which is sermorelin, is cleaved the same way10.

Mod GRF (1-29) keeps the 29-residue length but changes four positions: D-alanine at 2, glutamine at 8, alanine at 15 and leucine at 27. Each targets a known weakness. A D-amino acid at position 2 blocks DPP-IV cleavage10; asparagine 8 is prone to rearrangement in solution and methionine 27 to oxidation, and alanine at 15 had been linked to stronger receptor binding4. In earlier analogue work built on the same logic, combined substitutions produced peptides that were more stable in plasma and several-fold more potent than native GHRH in rat pituitary cells and in pigs4.

Like native GHRH, the peptide acts at the GHRH receptor, a G protein-coupled receptor found predominantly in the anterior pituitary that signals through cyclic AMP11.

What is CJC-1295 with DAC?

The DAC version adds a lysine after residue 29 whose maleimide group reacts with the free thiol of cysteine 34 on serum albumin. ConjuChem made three such maleimido derivatives; their albumin conjugates resisted DPP-IV and released GH from cultured rat pituitary cells. The lead compound, CJC-1295, gave a fourfold larger GH area under the curve than GRF(1-29) over two hours in rats, appeared bound at the albumin band within 15 minutes, and remained in plasma beyond 72 hours1.

In GHRH-knockout mice, five weeks of daily CJC-1295 normalized body weight and length, while the same amount given every 48 or 72 hours improved growth without normalizing it; treated pituitaries showed more GH mRNA and signs of somatotroph proliferation12.

CJC-1295 DAC vs no DAC: side-by-side

CJC-1295 without DAC (Mod GRF 1-29)CJC-1295 with DAC
Also sold asMod GRF (1-29), modified GRF 1-29, CJC-1295 no DACCJC-1295 DAC, DAC:GRF
OriginSynthetic analogue of human GHRH(1-29); the peptide portion of CJC-1295Synthetic GHRH analogue developed at ConjuChem1
Structure29 residues, C-terminal amide; D-Ala2, Gln8, Ala15 and Leu27 substitutionsThe same 29 residues plus a C-terminal lysine carrying a maleimidopropionyl group1
Approximate molecular weightAbout 3,368 Da (C152H252N44O42)About 3,647 Da (C165H269N47O46)
Albumin bindingNoneCovalent, to cysteine 34 of serum albumin1
ReceptorGHRH receptor on pituitary somatotrophs11GHRH receptor; activity shown in rat pituitary cells and in vivo1
Half-life evidenceNo published measurement; native GHRH(1-44) lasts about 6.8 minutes in people9Estimated 5.8 to 8.1 days in healthy adults2
Main research modelsStability and receptor rationale from related analogues4; anti-doping metabolism and detection6Rats1, GHRH-knockout mice12, healthy adult volunteers2,3
Key findingsSubstitutions target DPP-IV cleavage, asparagine rearrangement and methionine oxidation10,4Sustained GH and IGF-I rises; GH pulses preserved with higher trough GH2,3
Regulatory statusNot an approved medicine; prohibited in sport6Reached early clinical trials, never approved; prohibited in sport5

What the human studies measured, and which compound they used

The three published human studies of CJC-1295 that we found all used the DAC compound. The first comprised two randomized, placebo-controlled, double-blind trials in healthy adults aged 21 to 61, lasting 28 and 49 days. After a single administration, mean GH rose 2- to 10-fold for six days or more and mean IGF-I 1.5- to 3-fold for 9 to 11 days, scaling with the amount given; with repeated administration, IGF-I stayed above baseline for up to 28 days. The estimated half-life was 5.8 to 8.1 days, and no serious adverse reactions were reported2.

The second sampled GH every 20 minutes overnight in healthy men aged 20 to 40, before and one week after a single administration3. The third analyzed serum from 11 healthy young men before and one week after administration and reported changes in apolipoprotein A1, transthyretin and albumin-fragment spots as candidate biomarkers of GH and IGF-I action13.

None of these papers tested the 29-residue peptide without DAC. Claims about the no-DAC version's half-life, pulse shape or IGF-I response that cite them are borrowing data from a different molecule.

The pulsatility question

GH is normally released in pulses, a pattern considered important for many of its physiological effects3. A common argument in the research market is that the short-acting no-DAC peptide mimics natural, pulsatile GHRH signaling while the DAC compound produces a constant, unnatural signal. The data are more nuanced.

In the overnight sampling study, continuous stimulation by CJC-1295 with DAC left the frequency and magnitude of GH pulses unchanged. What changed was the baseline between pulses: trough GH rose about 7.5-fold, mean GH 46% and IGF-I 45%, and the IGF-I increase did not correlate with any measure of pulsatile secretion. The authors concluded that the rise in trough GH may be important for the IGF-I response3.

Two caveats apply. That was one study, in young men, measured one week after a single administration. And no study has measured GH pulsatility during exposure to the no-DAC peptide, so the claim that it better preserves physiological pulsatility is a hypothesis, not a finding. In GHRH-knockout mice, the interval between administrations of the long-acting compound did affect growth12, a reminder that exposure pattern is a variable worth studying directly.

Limitations and open questions

  • No head-to-head study compares the two versions on pharmacokinetics, GH output or IGF-I.
  • We found no published pharmacokinetic study of CJC-1295 without DAC in people or animals; its stability is inferred from related analogues and enzyme studies10,4.
  • Human data on the DAC compound come from a few short studies in healthy volunteers2,3,13; there are no long-term safety data.
  • A 2026 clinical review stressed uncertainty about the composition of GH-axis peptides sold outside regulated channels7; with two molecules sharing one name, mislabeling is a specific risk.
  • Neither compound is an approved medicine, and both are prohibited in sport5,6.

How to tell which one you have

Because the two molecules share a backbone, the label is the only thing that separates them unless the material is tested. Mass spectrometry distinguishes them easily: the DAC lysine and its maleimidopropionyl group add about 279 daltons, so the expected mass is roughly 3,368 Da for the no-DAC peptide and roughly 3,647 Da for the DAC compound. HPLC purity tells you how much of the vial is the target peptide; mass-spec identity tells you which peptide it is.

Every Peptides Only lot ships with a lot-matched certificate of analysis (HPLC purity and mass-spec identity) from an independent lab, published at our COA library. Our guide How to read a peptide COA explains what to check. The two forms are listed separately as CJC-1295 with DAC and CJC-1295 without DAC; the CJC-1295 + Ipamorelin blend uses the version without DAC.

Frequently asked questions

Is Mod GRF 1-29 the same as CJC-1295 without DAC?

In current usage, yes. Both names refer to the tetrasubstituted GHRH(1-29) amide that forms the backbone of CJC-12951, without the albumin-binding lysine.

Which lasts longer, CJC-1295 with DAC or without DAC?

The DAC version, by design. Its estimated half-life in healthy adults was 5.8 to 8.1 days2. No published study has measured the half-life of the no-DAC peptide; native GHRH lasts minutes9, and the no-DAC substitutions are meant to slow its breakdown, not to bind albumin.

Which version was used in the CJC-1295 clinical studies?

The DAC version. The randomized trials in healthy adults2, the pulsatility study3 and the serum proteomics study13 all used the long-acting, albumin-binding compound.

Does CJC-1295 with DAC stop natural GH pulses?

Not in the study that measured it: pulse frequency and size were unchanged, while trough and mean GH rose3.

Is CJC-1295 approved by the FDA?

No. Neither version is an approved medicine. The DAC compound reached early clinical trials2, and GHRH analogues are prohibited by the World Anti-Doping Agency6. Peptides Only supplies both for laboratory research only.

Which version is in the CJC-1295 + Ipamorelin blend?

The version without DAC, combined 1:1 with ipamorelin; see CJC-1295 + Ipamorelin.

Research use only. This article summarizes published laboratory and clinical literature for researchers. It is not medical advice, and nothing sold by Peptides Only is for human or veterinary use. We do not provide dosing or usage information.

References

  1. Jetté L, Léger R, 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):3052-8. PubMed 15817669
  2. Teichman SL, Neale A, et al. 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. PubMed 16352683
  3. 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):4792-7. PubMed 17018654
  4. Campbell RM, Stricker P, et al. Enhanced stability and potency of novel growth hormone-releasing factor (GRF) analogues derived from rodent and human GRF sequences. Peptides. 1994;15(3):489-95. PubMed 7937325
  5. Henninge J, Pepaj M, et al. Identification of CJC-1295, a growth-hormone-releasing peptide, in an unknown pharmaceutical preparation. Drug Test Anal. 2010;2(11-12):647-50. PubMed 21204297
  6. Memdouh S, Gavrilović I, et al. Advances in the detection of growth hormone releasing hormone synthetic analogs. Drug Test Anal. 2021;13(11-12):1871-1887. PubMed 34665524
  7. Dominikowski A, Rękoś Z, et al. The emerging landscape of performance-enhancing peptides modulating GH-IGF1 axis: bridging the gap between clinical evidence and patient self-administration. Front Endocrinol (Lausanne). 2026;17:1822475. PubMed 42395176
  8. Guillemin R, Brazeau P, et al. Growth hormone-releasing factor from a human pancreatic tumor that caused acromegaly. Science. 1982;218(4572):585-7. PubMed 6812220
  9. Frohman LA, Downs TR, et al. Rapid enzymatic degradation of growth hormone-releasing hormone by plasma in vitro and in vivo to a biologically inactive product cleaved at the NH2 terminus. J Clin Invest. 1986;78(4):906-13. PubMed 3093533
  10. Frohman LA, Downs TR, et al. Dipeptidylpeptidase IV and trypsin-like enzymatic degradation of human growth hormone-releasing hormone in plasma. J Clin Invest. 1989;83(5):1533-40. PubMed 2565342
  11. Mayo KE. Molecular cloning and expression of a pituitary-specific receptor for growth hormone-releasing hormone. Mol Endocrinol. 1992;6(10):1734-44. PubMed 1333056
  12. Alba M, Fintini D, 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):E1290-4. PubMed 16822960
  13. Sackmann-Sala L, Ding J, et al. 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):471-7. PubMed 19386527
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CJC-1295 (With DAC) 5 mg — Peptides Only, research use onlyBuy One Get One
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CJC-1295 (With DAC)

GHRH analogue with a drug affinity complex, for extended half-life GH-axis research.

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GHRH (1-29) analogue for pituitary-axis research.

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Stabilised GHRH analogue used in visceral-adiposity research.

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