# CJC-1295 DAC vs No-DAC: A Pharmacokinetic Comparison

> CJC-1295 DAC vs no-DAC: the DAC variant is the multi-day-half-life form (5.8-8.1 days); the no-DAC Modified GRF (1-29) is short-acting. A cited, side-by-side pharmacokinetic comparison.

Two molecules, one name. The DAC variant is long-acting via albumin conjugation; the no-DAC Modified GRF (1-29) is short-acting. Here is the distinction the literature draws, laid out to scan.

## The comparison in one card

CJC-1295 DAC and the no-DAC form differ in one decisive spec: duration. The DAC ('Drug Affinity Complex') variant covalently binds serum albumin and held an estimated 5.8-8.1 day half-life in healthy adults, keeping IGF-1 elevated up to 28 days after multiple doses [1][2]. The no-DAC form, Modified GRF (1-29), keeps the same four protease-resistant substitutions but omits the albumin tether and is short-acting, in the minutes-to-hours range [12].

Same sequence core, same receptor target, opposite kinetics. Everything else on this page expands that single distinction — because marketing and forums routinely conflate the two, and the pharmacokinetic difference is large [1][12].

## What is CJC-1295 with DAC?

The DAC ('Drug Affinity Complex') version functionalizes a C-terminal lysine so the peptide covalently binds Cys34 of serum albumin, extending the plasma half-life toward that of albumin itself [2]. That covalent tether is the entire reason the DAC form is long-acting: the circulating species becomes a peptide-albumin complex that clears on albumin's timescale, not the peptide's [2].

## What is CJC-1295 DAC?

CJC-1295 DAC is the long-acting form: the tetrasubstituted hGRF(1-29) sequence plus an albumin-binding moiety, giving a multi-day half-life, distinct from the short-acting no-DAC Modified GRF (1-29) [1][2][12]. It is the variant whose 5.8-8.1 day half-life and multi-day GH/IGF-1 elevation were characterized in healthy adults [1].

## What Is Modified GRF (1-29) / No-DAC?

Modified GRF (1-29) is the no-DAC form of the molecule: the tetrasubstituted GHRH(1-29) sequence with the four stabilizing substitutions but without the albumin-binding DAC moiety, hence a much shorter duration of action than CJC-1295 DAC [12]. It is short-acting, in the minutes-to-hours range, reflecting native GHRH(1-29) clearance modified only by protease resistance [9][12].

The single most consequential substitution is D-Ala at position 2, which on its own markedly increases the half-life and potency of GHRH(1-29) by resisting dipeptidylpeptidase-IV cleavage [7]. That substitution is what makes the no-DAC form more durable than truly native GRF(1-29), but without the DAC tether it remains short-acting [7][12].

## Modified GRF (1-29) Terminology

The terminology around Modified GRF 1-29 is a frequent source of confusion. 'Modified GRF (1-29)', 'Mod GRF 1-29' and 'CJC-1295 no-DAC' all refer to the same short-acting tetrasubstituted GHRH(1-29) peptide [12]. 'CJC-1295', used precisely, refers to the DAC variant with the albumin-binding moiety and the multi-day half-life [1][2].

The practical consequence: a product or protocol labeled 'CJC-1295' without specifying DAC status is ambiguous, because the two forms differ by orders of magnitude in duration [1][12]. Reference sources describe Modified GRF (1-29) as the no-DAC analog precisely to keep this distinction clear [12].

## The shared core, the divergent kinetics

It helps to separate what the two forms share from where they split. Both are built on hGRF(1-29), the first 29 residues of human GH-releasing factor that retain full GH-releasing activity, and both carry the same four substitutions — D-Ala2, Gln8, Ala15, Leu27 — that stabilize the helix and block proteolytic clearance [7][8]. Both bind the same GHRH receptor and drive the same Gs/cAMP/PKA cascade [2]. The receptor pharmacology is identical.

The split is the C-terminus. The DAC variant functionalizes a C-terminal lysine with a maleimidopropionyl linker that covalently bonds to Cys34 of serum albumin; the no-DAC form simply does not [2][12]. That one chemical difference is the entire kinetic story: with the tether, the molecule clears on albumin's multi-day timescale; without it, it clears on the timescale of a protease-resistant small peptide, in minutes to hours [2][12]. Same biology at the receptor, opposite biology in the bloodstream.

## Why the distinction matters historically

The DAC and no-DAC labels are not just chemistry trivia; they map onto two different chapters of the molecule's history. The long-acting DAC form was the one carried into formal development: the human pharmacokinetic studies that produced the 5.8-8.1 day half-life used the DAC variant, and the discontinued ConjuChem program and its Phase 2 trial in HIV-associated visceral obesity (NCT00267527) concerned that long-acting form [1]. The no-DAC Modified GRF (1-29) never had that development arc; it circulates mainly through research-supply and community channels [12].

This is why conflating them distorts the evidence. The human data — the multi-day GH and IGF-1 elevation, the preserved pulsatility — belongs to the DAC form [1][3]. The no-DAC form's short action is inferred from native GRF(1-29) kinetics plus the protease-resistant substitutions, not from an equivalent set of dedicated human pharmacokinetic studies [9][12]. When a claim cites '5.8-8.1 days,' it is, by definition, a claim about CJC-1295 DAC [1]. For the kinetics in depth, see [CJC-1295 half-life](/half-life); for what the studies measured, [the published human research](/research).

## How much CJC-1295 DAC should I take?

Human PK studies of the DAC variant used 30, 60 or 90 micrograms per kilogram subcutaneously; community fixed-dose 'protocols' are not derived from controlled human trials and there is no established human dose [1][3]. Those study doses characterized the kinetics; they are not a regimen, and no regulator has set a human dose for CJC-1295 DAC [1].

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A marketplace-style listing of the published CJC-1295 record — the DAC and no-DAC forms shelved on separate channels, every figure tagged to its study, nothing here dispensed, prescribed, or for sale.
