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Comparison · 8 min

CJC-1295 with DAC vs without DAC: half-life, research data and key differences

Uuendatud 2026-09-29See artikkel on kuvatud inglise keeles - tõlge on ettevalmistamisel.
Peamine
  • Both forms share the same modified 29-amino-acid GHRH backbone. The only structural difference is the DAC: a lysine-linked maleimide group that makes the peptide bind blood albumin.
  • CJC-1295 with DAC had an estimated half-life of 5.8-8.1 days in healthy adults and raised GH 2- to 10-fold for 6 days or more and IGF-1 1.5- to 3-fold (Teichman et al., 2006).
  • CJC-1295 without DAC (Modified GRF 1-29) has no albumin anchor, so it acts briefly and produces pulse-like GH release that is closer to the body's own rhythm.
  • The no-DAC form is usually researched with ipamorelin because the two act on different pituitary receptors, both act briefly, and GHRH plus a ghrelin-receptor agonist released GH synergistically in humans (Bowers 1990).

The short answer

CJC-1295 with DAC and CJC-1295 without DAC are two versions of the same stabilised GHRH analogue. The DAC version carries a chemical hook that attaches it to albumin in the blood, which stretches its action from minutes to about a week and produces a continuous rise in growth hormone and IGF-1. The no-DAC version has no hook, so it works in short bursts, which makes it the preferred tool when researchers want to study pulsatile GH release. Almost all published human data are for the DAC form; the no-DAC form is mainly studied preclinically and through its close relatives sermorelin and CJC-1295 with DAC.

What the two molecules have in common

Both start from GRF(1-29), the first 29 amino acids of human growth hormone-releasing hormone and the shortest fragment that keeps full biological activity. Native GRF(1-29), known as sermorelin, is cut apart within minutes in plasma by the enzyme DPP-4. CJC-1295 fixes this with four substitutions: D-alanine at position 2 (blocks DPP-4), glutamine at 8 (prevents deamidation), alanine at 15 (improves receptor binding) and leucine at 27 (removes an oxidation-prone methionine). This tetrasubstituted peptide is what is often called Modified GRF(1-29), and it is the version without DAC.

Both forms bind the GHRH receptor on somatotroph cells of the anterior pituitary. This raises cAMP, activates protein kinase A and CREB, and triggers the synthesis and release of growth hormone. The liver then responds to GH by producing IGF-1.

What the DAC changes

DAC stands for Drug Affinity Complex, a technology from the Canadian company ConjuChem. In CJC-1295 with DAC, an extra lysine with a maleimidopropionamide group is attached to the C-terminus. In the bloodstream, this group forms a covalent bond with the free thiol on cysteine 34 of serum albumin, so the peptide travels on albumin and is protected from clearance.

Jetté et al. introduced CJC-1295 in Endocrinology in 2005. In rats, it gave a 4-fold larger growth hormone response (area under the curve over two hours) than native hGRF(1-29) and was still present in plasma beyond 72 hours, bound to albumin. In a 2006 study in GHRH knockout mice, repeated CJC-1295 treatment normalised body weight and length and increased pituitary GH mRNA (Alba et al.).

Human data: Teichman 2006 and Ionescu 2006

The key human paper is Teichman et al. (Journal of Clinical Endocrinology and Metabolism, 2006): two randomised, placebo-controlled, double-blind trials lasting 28 and 49 days in healthy adults aged 21-61. After a single dose of CJC-1295 with DAC, mean GH rose 2- to 10-fold for 6 days or more and mean IGF-1 rose 1.5- to 3-fold for 9-11 days. The estimated half-life was 5.8-8.1 days, and after repeated administration IGF-1 stayed above baseline for up to 28 days. No serious adverse reactions were reported in these trials.

A common worry with continuous stimulation is that it flattens the natural GH rhythm. Ionescu and Frohman (2006) tested this with 20-minute overnight sampling in healthy men aged 20-40. One week after CJC-1295 with DAC, GH pulses kept their normal frequency and size, but trough GH was 7.5-fold higher, mean GH rose 46 % and IGF-1 rose 45 %. In other words, the DAC form lifted the baseline under an intact pulse pattern.

Clinical development stopped in 2006. A phase 2 trial of CJC-1295 in HIV-associated visceral obesity (192 participants) was halted in July 2006 after a participant died of a heart attack; the investigator's stated most likely cause was pre-existing coronary artery disease, but ConjuChem did not take the compound further. CJC-1295 is not an approved medicine in the EU or US.

Why researchers use the no-DAC form

Without the albumin anchor, Modified GRF(1-29) is cleared much faster than the DAC form. Its half-life is often quoted at around 30 minutes, but no peer-reviewed human pharmacokinetic study of the no-DAC form has been published, so that number should be treated as an estimate. What matters for research is the shape of the signal: a short burst of GHRH-receptor activation followed by a return to baseline, instead of a week-long elevated floor.

  • It models physiology: the pituitary normally releases GH in discrete pulses, most prominently during sleep.
  • It allows timed experiments: a short-acting agonist can be matched to a sampling window, then washes out.
  • It separates pulsatile from continuous signalling: comparing no-DAC with DAC data isolates the effect of exposure pattern on the same receptor.
  • It pairs cleanly with other short-acting secretagogues such as ipamorelin.

CJC-1295 with DAC vs without DAC: comparison table

Human half-life and GH data for the DAC form are from Teichman 2006 and Ionescu and Frohman 2006.
CJC-1295 with DACCJC-1295 no DAC
Other namesDAC:GRFModified GRF(1-29), Mod GRF 1-29
BackboneTetrasubstituted GRF(1-29)Tetrasubstituted GRF(1-29)
Extra groupLys-maleimide (DAC)None
Binds albuminYes, covalentlyNo
Half-life5.8-8.1 days (humans)Minutes; ~30 min often quoted
GH patternRaised baseline, pulses keptShort, pulse-like bursts
Human dataPhase 1 and 2 trials (2006)No dedicated trials
Typical research useSustained GH / IGF-1 elevationPulsatile GH, combined secretagogue models
Sold by CryopeptNoYes (10 mg; 5+5 mg blend)

Why CJC-1295 no DAC is often paired with ipamorelin

Growth hormone release is controlled by two stimulatory receptors on the same pituitary cells. CJC-1295 acts on the GHRH receptor through cAMP. Ipamorelin, a pentapeptide developed by Novo Nordisk, acts on the ghrelin receptor (GHS-R1a), mainly through calcium signalling. Because the two pathways are independent, stimulating both at once releases more GH than either alone. Bowers et al. showed this in 18 healthy men in 1990: sub-maximal amounts of a GH-releasing peptide combined with GHRH released GH synergistically.

Ipamorelin is the preferred partner in research for its selectivity. In Raun et al. (European Journal of Endocrinology, 1998), ipamorelin released GH in rats and swine with potency similar to GHRP-6, but unlike GHRP-6 and GHRP-2 it did not raise ACTH or cortisol above the levels seen with GHRH, even at doses more than 200 times its effective dose for GH release. Pairing it with the short-acting no-DAC form keeps both signals brief, so the combined model stays pulsatile. Cryopept's CJC-1295 no DAC + Ipamorelin blend contains 5 mg of each peptide in one vial.

Where tesamorelin fits

Tesamorelin is a different GHRH analogue: the full 44-amino-acid GHRH chain with a trans-3-hexenoyl group added at the N-terminus for stability. Unlike CJC-1295, it reached approval: the FDA approved it in 2010 (Egrifta) to reduce excess abdominal fat in people with HIV-associated lipodystrophy. It is therefore the GHRH analogue with the most human data, while CJC-1295 no DAC is the more compact, research-only tool.

Cryopept productWhat it isPrice
CJC-1295 no DACMod GRF(1-29), 10 mg€40
CJC-1295 no DAC + Ipamorelin5 mg + 5 mg blend€50
IpamorelinSelective ghrelin-receptor agonist, 10 mg€35
TesamorelinStabilised GHRH(1-44), 10 mg€55

Cryopept supplies CJC-1295 only in its no-DAC form. Every vial is ≥99 % pure by HPLC, and LC-MS confirms identity, which also clearly separates the no-DAC peptide (3367.9 g/mol) from the heavier DAC version. Each batch comes with Cryopept's internal test protocol (COA). All of these compounds are on the WADA Prohibited List under growth hormone-releasing factors.

For laboratory research use only. Not for human or veterinary use; this article is not medical advice.

Korduma kippuvad küsimused

What is the difference between CJC-1295 with DAC and without DAC?

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Both have the same tetrasubstituted GRF(1-29) sequence. The DAC version adds a lysine-maleimide group that binds blood albumin, giving a half-life of 5.8-8.1 days in healthy adults (Teichman 2006). The no-DAC version, also called Modified GRF(1-29), lacks this group and acts for a short time, producing pulse-like GH release.

What is the half-life of CJC-1295 without DAC?

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It is short, measured in minutes rather than days, and is often quoted at around 30 minutes. No peer-reviewed human pharmacokinetic study of the no-DAC form has been published, so that figure is an estimate. The DAC form's 5.8-8.1 day half-life comes from its albumin binding.

Is Mod GRF 1-29 the same as CJC-1295?

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Modified GRF(1-29) is the same peptide as CJC-1295 without DAC. The name CJC-1295 originally referred to the DAC version developed by ConjuChem, which is why the no-DAC form is usually labelled explicitly to avoid confusion.

Why is CJC-1295 combined with ipamorelin in research?

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CJC-1295 activates the GHRH receptor and ipamorelin activates the ghrelin receptor, two independent pathways that release GH synergistically when stimulated together (Bowers 1990, in healthy men). Ipamorelin is also selective: in 1998 animal studies it did not raise ACTH or cortisol like older GH-releasing peptides.

Is CJC-1295 an approved drug?

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No. CJC-1295 with DAC reached phase 2 trials, but development stopped in 2006 after a trial participant died of a heart attack. Neither form is approved in the EU or US, and both are on the WADA Prohibited List. Tesamorelin, a different GHRH analogue, is FDA-approved for HIV-associated lipodystrophy.

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