SECTION 03 / VARIANT CONTRAST
CJC-1295 DAC vs No-DAC (Modified GRF 1-29) in the Research Literature
Two molecules routinely sold under one name, separated by a single albumin-binding moiety and a pharmacokinetic gulf of days versus minutes.
CJC-1295 DAC vs no-DAC: the one difference that changes everything
CJC-1295 DAC vs no-DAC comes down to one structural feature with an outsized pharmacokinetic consequence. Both forms share the same four protease-resistant substitutions on the hGRF(1-29) backbone [2]. The DAC variant adds a maleimidopropionyl linker on a C-terminal lysine that covalently binds the free thiol on circulating serum albumin, forming a peptide-albumin conjugate and extending the plasma half-life toward that of albumin itself — a multi-day duration, measured at 5.8-8.1 days in healthy adults [1][2]. The no-DAC form lacks that moiety and is short-acting [11].
The difference is not cosmetic. The DAC variant's effective circulating species is a roughly 66-kDa peptide-albumin complex, while the no-DAC peptide clears on a timescale closer to native GHRH(1-29) with protease protection — minutes to hours [11]. Marketing and forums routinely conflate the two; pharmacokinetically they are very different agents [11].
What is CJC-1295 with DAC?
CJC-1295 with DAC is the variant carrying a maleimidopropionyl "Drug Affinity Complex" linker that covalently binds circulating serum albumin, extending plasma half-life toward that of albumin itself — a multi-day duration [2]. The albumin conjugation is what converts a short-acting GHRH analog into one whose single dose elevates GH and IGF-1 for days [1].
What is CJC-1295 DAC?
CJC-1295 DAC is the albumin-conjugated, long-acting form with a multi-day half-life; the no-DAC "Modified GRF 1-29" keeps the four substitutions but lacks the albumin-binding moiety and is short-acting [2][11]. When a source says "CJC-1295" without specifying, the long-acting DAC variant is usually meant — but the term is used loosely, which is exactly the conflation this page exists to separate.
Modified GRF (1-29): The No-DAC Form
Modified GRF 1-29 is the no-DAC, tetrasubstituted GHRH(1-29) sequence — the four stabilizing substitutions without the albumin-binding DAC moiety, and therefore a much shorter duration of action than CJC-1295 DAC [11]. Reference material describes it as a synthetic GHRH analog distinct from the long-acting form precisely on that one feature [11]. Because Modified GRF 1-29 is short-acting, its pharmacokinetics resemble a pulse rather than a plateau: it raises GH briefly and clears, where the DAC form holds the elevation for days [1][11]. The two are routinely sold under overlapping names; they are not interchangeable, and the CJC-1295 half-life and PK data make the gap explicit.
Why the conflation matters
The conflation is not a pedantic point. The published human pharmacokinetics — the 5.8-8.1-day half-life, the 28-day IGF-1 elevation — were measured on the DAC variant [1]. Those numbers do not transfer to the no-DAC Modified GRF 1-29, which has no comparable published human PK and a fundamentally shorter duration [11]. Any claim that imports DAC kinetics onto the no-DAC form, or vice versa, is mixing two pharmacokinetic profiles. The 2024 FDA Pharmacy Compounding Advisory Committee reviewed the GH-secretagogue class and did not recommend CJC-1295 for the 503A compounding bulks list [1] — a class-level regulatory signal that applies regardless of which variant a supplier ships.
How much CJC-1295 DAC should I take?
No validated human dose exists. The DAC variant's multi-day half-life — 5.8-8.1 days in Teichman 2006 — is precisely why its dosing logic differs from the short-acting no-DAC form; research used single subcutaneous microgram-per-kilogram doses (30, 60, or 90 ug/kg) [1][3]. This site reports the studied doses, not human-use guidance, and there is no controlled trial establishing a regimen for the DAC variant.
The chemistry of the DAC linker
The albumin bond is a specific, well-characterized reaction. In the DAC variant, a C-terminal lysine is functionalized with a maleimidopropionyl (MPA) linker that undergoes Michael addition with the free thiol on Cys34 of circulating serum albumin [2]. The product is a covalent peptide-albumin conjugate — not a reversible, transient binding, but a chemical bond that ties the peptide to one of the longest-lived proteins in plasma [2]. That is the mechanistic reason the half-life moves from minutes-to-hours into days: the peptide is cleared on albumin's schedule, not its own [1][2]. The no-DAC Modified GRF 1-29 has no such handle and therefore no such anchor [11].
The defining rat study confirmed the consequence experimentally: the conjugate produced a 4-fold GH area-under-the-curve over two hours versus the unconjugated peptide and remained detectable in plasma beyond 72 hours [2]. The same chemistry that buys the duration is what the GHRH-knockout mouse work then read out as once-daily 2 ug normalizing growth where less frequent dosing fell off [4].
Two molecules, two duration profiles
Treating the two as one agent is the single most common error in the literature around this compound. The DAC form's published human kinetics — the 5.8-8.1-day half-life, GH elevated for six days or more, IGF-1 elevated to 28 days after multiple doses — were all measured on the albumin-conjugated variant [1]. The no-DAC Modified GRF 1-29 has no comparable published human pharmacokinetic dataset and a fundamentally shorter, pulse-like duration [11]. A claim that takes a number from one column and applies it to the other is mixing two pharmacokinetic profiles that happen to share a backbone and a name [11]. The full half-life dataset for the DAC variant is laid out under CJC-1295 half-life and PK.