# CJC-1295 DAC: The Long-Acting Variant on the GH/IGF-1 Axis > CJC-1295 DAC is the albumin-conjugated, long-acting form (half-life 5.8-8.1 days), distinct from short-acting no-DAC Modified GRF 1-29. The chemistry and kinetics, cited. The albumin-conjugation chemistry that turns a short GHRH fragment into a multi-day molecule — and why it is not the same as Modified GRF 1-29. ## What CJC-1295 DAC is CJC-1295 DAC is the long-acting form of the peptide, and the difference is one piece of chemistry. The DAC — Drug Affinity Complex — variant carries a maleimidopropionyl-lysine handle at the C-terminus that undergoes Michael addition with the free thiol on Cys34 of circulating serum albumin, forming a covalent peptide-albumin conjugate [2]. The resulting species is the much larger (~66 kDa) peptide-albumin complex, which is detectable in plasma beyond 72 hours and clears at a rate closer to albumin than to a free peptide [2]. That single bond is what produced the multi-day half-life of 5.8 to 8.1 days seen in healthy adults [1]. Without it, the same four-substitution backbone is short-acting. CJC-1295 DAC is therefore not a stronger version of the no-DAC form — it is a kinetically different molecule that happens to share a sequence, and treating the two as interchangeable is the central error in most online writing about the compound. ## What is CJC-1295 with DAC? The Drug Affinity Complex variant carries a maleimidopropionyl-lysine handle that covalently binds the Cys34 thiol of serum albumin, forming a roughly 66 kDa peptide-albumin conjugate detectable in plasma beyond 72 hours [2]. This albumin tethering is the entire reason the DAC form lasts days rather than minutes, and it is what the "DAC" in the name refers to — not a higher dose or a different sequence. ## What is CJC-1295 DAC? CJC-1295 DAC is the albumin-conjugated, long-acting form, with a half-life of 5.8 to 8.1 days [1]. It is distinct from no-DAC "Modified GRF 1-29," which keeps the four substitutions but lacks the albumin-binding moiety and is short-acting [2]. The two are routinely conflated in marketing and forums, but pharmacokinetically they sit at opposite ends of the duration scale. ## CJC-1295 No-DAC (Modified GRF 1-29): The Short-Acting Form The no-DAC form keeps the design that resists enzymes but drops the design that extends duration. Modified GRF 1-29 retains the four protease-resistant substitutions (D-Ala2, Gln8, Ala15, Leu27) but has no maleimidopropionyl handle and therefore does not bind albumin [2]. It is short-acting, with a clearance profile in the minutes-to-hours range that reflects native GHRH(1-29) kinetics modified only by the substitutions [2]. This is why the two forms are not interchangeable. The DAC form's days-long elevation comes from albumin tethering; the no-DAC form has none, so its GH-release effect is brief and pulse-like. Any figure — half-life, dose, dosing interval — that applies to one form does not transfer to the other, and a reader who keeps the two apart has already avoided the most common mistake about CJC-1295. ## Is Modified GRF 1-29 the Same as CJC-1295? Not exactly, and the distinction is the most-conflated point about this compound. Modified GRF 1-29 is the no-DAC, short-acting sequence — the tetrasubstituted GHRH(1-29) without the albumin-binding DAC moiety [2]. "CJC-1295" with DAC is the long-acting, albumin-conjugated form with a 5.8-8.1 day half-life [1]. They share a backbone but differ entirely in duration, so treating the names as synonyms produces the central error in most online discussion of the peptide. ## The kinetics the DAC form produces Sustained, dose-dependent elevation. In healthy adults, single subcutaneous 30 or 60 micrograms per kilogram doses of CJC-1295 raised GH 2- to 10-fold for six or more days and IGF-1 1.5- to 3-fold for nine to eleven days, with IGF-1 staying above baseline up to 28 days after multiple doses [1]. In healthy men, a single 60-90 micrograms per kilogram dose raised basal GH about 7.5-fold and mean GH and IGF-1 by roughly 46% and 45% one week later, while GH pulsatility was preserved [3]. The supporting chemistry — a 4-fold GH-AUC increase over unconjugated peptide in rats, with detectable conjugate beyond 72 hours — is what makes those durations possible [2]. ## What the DAC program's history adds The long-acting DAC program has a cautionary arc worth stating plainly. The original ConjuChem development of the DAC form was discontinued; a Phase 2 trial in HIV-associated visceral obesity (NCT00267527) did not advance, and the program ended [1]. A patient death during the development era is frequently cited in connection with the halted trial, though a causal link to CJC-1295 was not established in the public record. The molecule that remains in research use is the same chemistry — multi-day, albumin-tethered — but without the large-trial validation a completed program would have produced, which is part of why its long-term safety profile in humans is unknown. --- A curated night-board of the CJC-1295 record — each study, kinetic figure, and honest gap lit in its own tile and weighed by what the literature can actually carry, with no clinic behind the board and nothing here dispensed or sold.