The distinction / two phrases of one melody
CJC-1295 DAC vs No-DAC in the Research Literature
One molecule, two pharmacokinetic lives. The DAC form binds albumin and acts for days; the no-DAC form, Modified GRF 1-29, is short-acting. The studies separate them; the marketing does not.
CJC-1295 DAC: the albumin-bound, long-acting form
CJC-1295 DAC vs no-DAC is the single distinction worth getting right before anything else about this compound, and the DAC form is where the multi-day behavior comes from. DAC stands for Drug Affinity Complex: a maleimidopropionyl linker on a C-terminal lysine that undergoes Michael addition with the free thiol on cysteine-34 of circulating serum albumin, forming a covalent peptide-albumin conjugate [6]. The peptide stops being a small, fast-cleared molecule and starts traveling with albumin, whose plasma residence is measured in weeks. The effective circulating species is the large peptide-albumin complex, roughly 66 kilodaltons.
That chemistry is what produced the headline pharmacokinetics. In rats, the albumin-conjugated lead delivered a 4-fold larger GH area-under-the-curve than the unconjugated peptide and remained detectable in plasma beyond 72 hours [6]. In healthy adults, the DAC form's half-life was estimated at 5.8 to 8.1 days, with IGF-1 elevated for nine to eleven days after a single dose and above baseline up to 28 days after multiple doses [1]. In GHRH-knockout mice, once-daily dosing fully normalized growth — direct evidence that the long half-life supports an infrequent schedule [7].
What is CJC-1295 DAC?
CJC-1295 DAC is the albumin-conjugating, long-acting form of the tetrasubstituted GHRH(1-29) analog. In rats it gave a 4-fold GH AUC over the unconjugated peptide and was detectable beyond 72 hours [6]. Its multi-day half-life in humans is 5.8 to 8.1 days [1].
What is CJC-1295 with DAC?
The Drug Affinity Complex variant carries a maleimide linker that covalently binds circulating serum albumin via Cys34, extending the plasma half-life toward that of albumin and giving a multi-day duration of action [6].
The No-DAC Form (Modified GRF 1-29)
The no-DAC form is the same tetrasubstituted GHRH(1-29) sequence with the albumin-binding moiety removed — and that single omission changes everything about how long it acts. Without the DAC linker, the peptide keeps its four protease-resistant substitutions but cannot latch onto albumin, so it clears in the minutes-to-hours range, reflecting native GHRH(1-29) kinetics with added protease resistance [6]. This is the short-acting form, and it is the version most often discussed under the name Modified GRF 1-29.
Modified GRF (1-29)
Modified GRF 1-29 is the no-DAC synonym: the four-substitution GHRH(1-29) analog without the Drug Affinity Complex. It is short-acting by design. Because it lacks albumin conjugation, its signal is brief — closer to a sharp pulse than the DAC form's sustained envelope — which is precisely why the two are not interchangeable despite sharing a core sequence [6]. Community protocols that pair a short-acting GHRH analog with a secretagogue lean on this form for its rapid, pulse-like action, but those protocols are not derived from controlled human trials [1].
The reason this section exists at all is that forums and product listings constantly conflate the two. CJC-1295 DAC and Modified GRF 1-29 are pharmacokinetically very different molecules [1]. Reading one study's DAC half-life and applying it to a no-DAC product, or vice versa, is the most common error around this compound — and the easiest to avoid once the albumin distinction is clear.
Half-Life: DAC (5.8-8.1 days) vs No-DAC (short-acting)
The half-life is where CJC-1295 DAC vs no-DAC stops being academic. The DAC form's estimated half-life in healthy adults is 5.8 to 8.1 days [1] — a held note. The no-DAC Modified GRF 1-29 is short-acting, clearing in minutes to hours [6] — a staccato burst. The same core peptide, two completely different durations of action, and the gap between them is entirely the albumin linker.
That difference cascades into everything downstream. The DAC form's multi-day residence is why a single dose kept IGF-1 above baseline for up to 28 days after repeated administration [1], and why once-daily dosing normalized growth in knockout mice [7]. The no-DAC form's brief action is why its signal looks more like the natural GHRH pulse the pituitary already responds to. Neither profile is inherently better; they are different tools, and conflating their durations is how dosing confusion starts.
How much CJC-1295 DAC should I take?
No validated human dose exists for the DAC variant. Its multi-day half-life — 5.8 to 8.1 days — means it was studied with infrequent dosing in pharmacokinetic work [1], and once-daily dosing fully normalized growth in GHRH-knockout mice [7]. These describe research administration in studies, not a human protocol.
For the exact amounts used across the literature, see the doses used in the research page; for how this signal reaches IGF-1, see the GH / IGF-1 axis page.
Modified GRF (1-29) and the conflation problem
A short glossary stop, because the names do real damage. The CAS registry number 863288-34-0 is consistently attributed to CJC-1295 with DAC across chemical-supplier listings, though some listings apply it loosely to the no-DAC sequence as well — a small example of how blurred the labeling is even at the registry level. The molecular formula and weight are likewise reported inconsistently across registries for the DAC peptide before conjugation, which is worth flagging for anyone trying to verify a product against a spec sheet.
What is not ambiguous is the pharmacology. The DAC form binds albumin and acts for days [6]; the no-DAC Modified GRF 1-29 does not and acts for minutes to hours [6]. Every reliable distinction between the two traces back to that one structural feature. When a source discusses CJC-1295 without specifying DAC or no-DAC, it is usually impossible to know which half-life applies — and that ambiguity, not any property of the molecule, is the root of most online confusion.
This page exists to hold the two forms apart cleanly. The rest of the site keeps the distinction: the research page cites the DAC half-life to its source, and the doses used in the research page separates the human DAC pharmacokinetic doses from the community no-DAC protocols that lack trial support.