CJC-1295 (with and without DAC) is supplied strictly as a laboratory research material. It is not approved, intended or authorised for human consumption or any therapeutic use in this context. This article is written for qualified researchers and is not medical advice.
One peptide, two release profiles
CJC-1295 is a single molecule with two identities. Both versions are the same 29-amino-acid synthetic analogue of growth hormone-releasing hormone (GHRH), modified at four positions to resist enzymatic breakdown and bind the same target. What separates them is not the peptide — it is the addition of a Drug Affinity Complex (DAC), a linker that latches onto circulating albumin and rewrites the compound's kinetics entirely. The version without DAC, commonly called Mod GRF 1-29, acts and clears within minutes. The DAC version lingers for days. Everything else in the comparison flows from that one distinction. For the full mechanistic background, our CJC-1295 knowledgebase page covers the receptor pharmacology in detail; here we put the two variants directly side by side.
| CJC-1295 (no DAC) | CJC-1295 DAC | |
|---|---|---|
| Class / peptide type | GHRH analogue (Mod GRF 1-29) | GHRH analogue + Drug Affinity Complex |
| Primary target | GHRH receptor (anterior pituitary) | GHRH receptor (anterior pituitary) |
| Structure note | 29 aa · ~3647 g/mol · substituted at 2, 8, 15, 27 | Same base + maleimidyl linker binding albumin Cys-34 |
| Half-life / duration | ~30 minutes (short pulse) | ~5.8–8.1 days (sustained) |
| Release pattern | Sharp, pulsatile GH burst | Prolonged GH/IGF-1 elevation |
| Typical pairing | Ipamorelin (GHS-R1a agonist) | Studied standalone or with a GHS |
| Regulatory status | Not FDA-approved · research reagent | Not FDA-approved · research reagent |
CJC-1295 (no DAC): the short, pulsatile version
Strip away the DAC and you are left with the tetrasubstituted GHRH analogue often labelled Mod GRF 1-29. It binds selectively to the GHRH receptor on somatotroph cells in the anterior pituitary, activates the Gs/cAMP/PKA cascade, and triggers a sharp pulse of growth hormone secretion — which in turn drives hepatic IGF-1 production. The defining feature is speed: with a half-life of roughly 30 minutes, it rises and clears quickly, producing a burst that mimics the body's own pulsatile GH rhythm rather than a flat, continuous signal.
That short window is exactly why the non-DAC version is the natural partner for a growth hormone secretagogue. Because it works through a different receptor and G-protein pathway than ghrelin-mimetic secretagogues, co-administration can produce a GH response substantially greater than either compound alone — the pharmacological rationale behind the classic dual-pathway pairing with ipamorelin. Researchers reaching for a tightly timed, pulse-like probe of the GH axis tend to buy CJC-1295 UK in the no-DAC form for precisely this reason.
CJC-1295 DAC: the long-acting depot
The DAC version is the same peptide with one addition that changes everything: a maleimidyl linker that binds covalently to cysteine-34 on circulating albumin. By hitching to a carrier protein that itself has a long circulating life, the peptide is protected from rapid clearance and effectively becomes a slow-release depot. Half-life stretches from minutes to an estimated 5.8–8.1 days, and the pharmacology shifts from a pulse to a plateau.
In the principal human pharmacokinetic work on the DAC variant, single injections raised mean GH concentrations several-fold for at least six days and IGF-1 for well over a week, with repeated dosing keeping IGF-1 above baseline for up to roughly four weeks. Researchers also noted apparent increases in total pituitary GH mRNA, hinting that sustained GHRH-receptor stimulation may support synthetic capacity beyond acute secretion. The trade-off is that the DAC version does not reproduce the natural pulsatile rhythm — it holds the axis elevated continuously. For a long-duration model of GHRH-receptor signalling, laboratories tend to source CJC-1295 DAC research material where a days-long, stable exposure is the whole point.
What the differences mean in a research context
The comparison table has one column that actually matters, and it is duration. Target, structure and downstream signalling are identical; both variants converge on the same GHRH receptor and drive the same GH/IGF-1 axis. The DAC is not a different drug — it is a kinetic switch. That reframes the choice as a question about the experimental question itself.
If a model calls for discrete, time-resolved GH pulses — the kind that let you watch onset, peak and clearance, or that pair cleanly with a secretagogue on a second pathway — the short half-life of the non-DAC version is a feature, not a limitation. If instead the aim is to study the effects of chronic, sustained GHRH-receptor tone and prolonged IGF-1 elevation, the DAC depot delivers a stable exposure that a minutes-long pulse never could. One favours temporal precision; the other favours duration and steadiness.
Both carry the same regulatory footing: neither is FDA-approved, and GHRH analogues in general have drawn regulatory attention over immunogenicity and cardiovascular signals such as flushing and transient hypotension. Both are supplied purely as research reagents. The practical point for a lab is that switching between the two changes the shape of the exposure curve, not the biology of the target — which is what makes them such a clean pair for isolating the effect of release kinetics on a shared pathway.
The bottom line
CJC-1295 and CJC-1295 DAC are the same GHRH analogue separated by a single design decision: whether to bind albumin and trade a minutes-long pulse for a days-long plateau. Choose the non-DAC version for pulsatile, tightly timed work and secretagogue pairings; choose the DAC version for sustained, continuous GHRH-receptor stimulation. Both are stocked as research-grade material — see our page to buy CJC-1295 UK for both variants, each ≥99% purity with a COA, and read the full receptor pharmacology on the CJC-1295 knowledgebase profile.