READOUT · 04 / FORM COMPARISON · TWO CHANNELS

CJC-1295 DAC vs No-DAC (Modified GRF 1-29)

Two channels, two half-lives. The DAC variant bonds covalently to serum albumin for a multi-day half-life; the no-DAC Modified GRF (1-29) form keeps the four substitutions but clears in minutes to hours. The distinction the whole CJC-1295 literature confuses.

What is CJC-1295 DAC?

CJC-1295 DAC vs no-DAC is the central confusion in this compound, so start with the DAC channel. CJC-1295 DAC is the variant whose C-terminal lysine is functionalized with a maleimidopropionyl (MPA) linker that undergoes a Michael addition with the free thiol on Cys34 of circulating serum albumin, forming a covalent peptide-albumin conjugate [2]. That covalent bond is the whole point: it drags the molecule's plasma residence toward that of albumin itself, extending the estimated half-life to 5.8 to 8.1 days in healthy adults [1].

The effective circulating species after conjugation is therefore not the small ~3,367.9-Da peptide but the far larger peptide-albumin complex, near 66 kDa [2]. CAS 863288-34-0 is the registry number consistently attributed to the DAC variant. This is the form that the human pharmacokinetic studies characterized, and the form responsible for a single dose moving GH and IGF-1 for over a week.

What is CJC-1295 with DAC?

"With DAC" denotes the Drug Affinity Complex modification — a maleimide handle that bonds the peptide to circulating albumin, turning a short-acting GHRH analog into a multi-day one [2]. "DAC" and "with DAC" name the same albumin-conjugating chemistry; the term distinguishes this form from the no-DAC sequence that lacks it.

No-DAC: Short-Acting Modified GRF (1-29)

The CJC-1295 no DAC form is a different pharmacokinetic animal. It keeps the four protease-resistant substitutions — D-Ala2, Gln8, Ala15, Leu27 — but lacks the albumin-binding DAC moiety, so it is short-acting, clearing in a minutes-to-hours window rather than days [11]. Without the covalent albumin bond, there is nothing to anchor it in circulation; the substitutions slow proteolytic clearance relative to native GHRH but do not extend it into the multi-day range.

This is the form most often sold and discussed as "Modified GRF 1-29," and conflating it with CJC-1295 DAC is the single most common error in the marketing and the forums. They share a backbone and four edits; they differ by one chemistry — the DAC handle — and that one difference is the entire half-life story.

Modified GRF (1-29) and the No-DAC Distinction

Modified GRF (1-29) is the encyclopedic name for the tetrasubstituted GHRH(1-29) sequence without the DAC moiety [11]. Reference material describes it as a synthetic GHRH analog carrying the four stabilizing substitutions but lacking the albumin-binding chemistry, and therefore a much shorter duration of action than CJC-1295 DAC [9][11]. The D-Ala2 substitution is what extends GHRH(1-29) half-life and potency against dipeptidylpeptidase-IV in both forms [9]; only the DAC variant adds the albumin bond on top.

The conflation persists for a practical reason: the marketing shorthand collapsed two distinct molecules into one familiar name. "CJC-1295" became a catch-all label, so a buyer or reader encountering the term cannot tell from the name alone whether it refers to the multi-day DAC conjugate that the human pharmacokinetic studies actually characterized [1] or the short-acting no-DAC sequence that those studies did not. The peer-reviewed record keeps them separate; the casual record does not. Reading the literature correctly means treating "CJC-1295 DAC" and "Modified GRF (1-29)" as two entries, not two names for one thing — which is the distinction this entire page exists to hold.

Half-Life: 5.8-8.1 Days (DAC) vs Minutes-to-Hours (No-DAC)

The half-life is the cleanest way to tell the two forms apart, and the numbers are not close. CJC-1295 DAC: an estimated 5.8 to 8.1 days in healthy adults, with IGF-1 elevation persisting up to 28 days after multiple doses [1]. No-DAC Modified GRF (1-29): short-acting, in the minutes-to-hours range, reflecting native GHRH(1-29) clearance modified only by the protease-resistant substitutions [11]. One form is dosed in the literature as a single injection that lasts a week; the other clears before the day is out.

That gap traces entirely to the albumin conjugation. In rats, the albumin-conjugated CJC-1295 produced a four-fold GH AUC over the unconjugated peptide and remained detectable in plasma beyond 72 hours — a direct readout of how much longer the covalent-albumin form persists [2]. The DAC bond converts a short-acting GHRH analog into a multi-day one; remove it and you are left with the short-acting sequence.

The duration difference cascades into how each form behaves in the body. The DAC variant's days-long residence is what let a single dose drive a dose-dependent 2- to 10-fold rise in mean GH for six days or more and a 1.5- to 3-fold rise in IGF-1 for nine to eleven days in healthy adults [1] — a sustained, low-level GHRH stimulus the pituitary answers continuously while still pulsing on its own schedule [3]. The short-acting no-DAC form produces a brief GHRH pulse instead: a sharp, transient signal that clears before it can hold the axis elevated for days. Same backbone, same four substitutions, same receptor — but the presence or absence of one covalent albumin bond is the difference between a multi-day pharmacology and a minutes-to-hours one.

When a source quotes a CJC-1295 half-life, the first question is always which form it means. A figure of "days" describes the DAC conjugate; a figure of "minutes to hours" describes no-DAC Mod GRF (1-29). Numbers quoted without that qualifier are the most common way the two forms get blurred together. For the doses attached to each form, see doses used in research, and for how CJC-1295 compares with shorter GHRH analogs like sermorelin, see CJC-1295 vs sermorelin.