CJC-1295 DAC vs no DAC: the Modified GRF 1-29 distinction in the research literature

CJC-1295 DAC vs no DAC: one molecule, two durations

CJC-1295 DAC vs no DAC is the distinction that organizes everything else about this peptide. Both forms are the tetrasubstituted hGRF(1-29) sequence — D-Ala2, Gln8, Ala15, Leu27 — that resists the protease dipeptidylpeptidase-IV ^[2]. The difference is a single chemical handle: the DAC ('Drug Affinity Complex') variant adds a maleimidopropionyl linker that covalently binds the peptide to circulating serum albumin, while the no-DAC form omits it ^[2][16].

That one difference reorders the pharmacokinetics by orders of magnitude. The DAC form's estimated half-life in healthy adults is 5.8-8.1 days, and a single dose elevated IGF-1 for 9-11 days ^[1]. The no-DAC form is short-acting, clearing on the timescale of native GHRH(1-29) — minutes to hours — because nothing tethers it to albumin ^[16]. Marketing and forums routinely sell both as 'CJC-1295' without naming which one; pharmacokinetically they are not interchangeable.

What CJC-1295 DAC is

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What CJC-1295 DAC Is

CJC-1295 DAC is the albumin-conjugated, long-acting form (half-life 5.8-8.1 days); the no-DAC 'Modified GRF 1-29' keeps the four substitutions but lacks the albumin-binding moiety and is short-acting ^[1][16]. The maleimide handle undergoes a Michael addition with the free thiol on Cys34 of serum albumin, forming a covalent peptide-albumin conjugate whose effective circulating species is roughly 66 kDa — far larger than the ~3.4 kDa peptide itself ^[2]. That bulk is the whole point: it is what slows clearance to the multi-day range.

The DAC form is the one with the published human pharmacokinetic record ^[1][3], and the one that entered — and exited — Phase 2 development as the ConjuChem long-acting analog ^[7].

Modified GRF (1-29): the no-DAC form

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Modified GRF (1-29): The No-DAC Form

Modified GRF (1-29) is the no-DAC, tetrasubstituted GHRH(1-29) often conflated with CJC-1295. Reference material describes it as a synthetic GHRH analog carrying the four stabilizing substitutions but without the albumin-binding DAC moiety, giving it a much shorter duration of action than CJC-1295 DAC ^[16]. It is also called Mod GRF 1-29 or, loosely and confusingly, 'CJC-1295 without DAC.'

The substitutions still matter — they make Modified GRF (1-29) more stable than native GHRH(1-29) against DPP-IV cleavage — but without the albumin anchor the molecule behaves like a short pulse rather than a multi-day plateau ^[16][2]. The practical upshot in the literature: the long-duration pharmacokinetic findings (the 5.8-8.1 day half-life, the IGF-1-to-28-days data) belong to the DAC form and do not transfer to the no-DAC form ^[1].

Why the two forms are constantly conflated

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The conflation is not accidental — it is structural to how the peptide is marketed. Both forms carry the same name root, the same four substitutions, and the same target, so a label reading 'CJC-1295' tells a reader nothing about which species is in the vial ^[2]. The duration is the only thing that separates them, and duration is invisible on a label.

The scientific literature is careful here even where the market is not. The human pharmacokinetic studies that produced the headline numbers used the DAC analog specifically ^[1][3], and the rat work that established the albumin-conjugation mechanism was explicitly about identifying CJC-1295 as a long-lasting analog ^[2]. When CJC-1295 was identified by LC-MS/MS in a seized black-market preparation, the analytical work resolved the exact molecular species rather than the marketing name ^[6]. The lesson the record teaches is procedural: read the variant before reading the claim.

The DAC form also carries the regulatory history. It was the ConjuChem long-acting analog that entered Phase 2 in HIV-associated visceral obesity (NCT00267527) and was discontinued ^[7]; the no-DAC Modified GRF (1-29) form has no comparable development record. So 'CJC-1295' in a clinical-history sense almost always means the DAC analog — the one with both the published kinetics and the halted program.

Reading the two forms side by side

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The two forms share a target and a sequence and diverge on duration. Both bind the pituitary GHRH receptor and drive pulsatile GH release ^[2]. Both carry the four protease-resistant substitutions that resist DPP-IV cleavage ^[2]. Both are unapproved research chemicals with no large human safety trials ^[7].

Where they part: the DAC form is albumin-conjugated, long-acting (5.8-8.1 day half-life), and the species with the human PK record ^[1]; the no-DAC Modified GRF (1-29) form is unconjugated and short-acting ^[16]. When a source reports a duration, the first question is which variant it measured — because the answer is the difference between days and hours. See the CJC-1295 half-life and pharmacokinetics for the full kinetic picture and the full reference list.