the half-life that splits the molecule in two
CJC-1295 DAC vs No-DAC (Modified GRF 1-29): The Pharmacokinetic Difference
One name, two molecules. The DAC variant binds albumin and acts for days; the no-DAC form is short-acting. The marketplace blurs this; the pharmacology does not.
What CJC-1295 DAC is
CJC-1295 DAC is the variant whose C-terminal lysine carries a maleimidopropionyl linker that undergoes a Michael addition with the free thiol on Cys34 of circulating serum albumin, forming a covalent peptide-albumin conjugate [1]. That bond — the Drug Affinity Complex — extends the plasma half-life toward that of albumin itself. The effective circulating species is no longer a small 3.4-kilodalton peptide but a roughly 66-kilodalton peptide-albumin complex that the body clears slowly [1].
The payoff is duration. The albumin conjugate was detectable in rat plasma beyond 72 hours and produced a 4-fold increase in growth-hormone AUC over the unconjugated peptide [1]. In humans, that translated into the multi-day kinetics that gave CJC-1295 its reputation [2].
CJC-1295 half life (DAC vs no-DAC)
The DAC variant's estimated half-life in healthy adults is 5.8-8.1 days, and after multiple doses IGF-1 elevation persisted up to 28 days [2]. That is the number people mean when they call CJC-1295 "long-acting."
The no-DAC form is a different story entirely. Modified GRF (1-29) keeps the four protease-resistant substitutions but lacks the albumin-binding moiety, so it is short-acting — its clearance reflects native GHRH(1-29) kinetics, in the minutes-to-hours range, slowed only by the DPP-IV-resistant substitutions, not by albumin binding [1][9]. Same backbone, radically different residence time. A single number captures the gap: days versus minutes-to-hours.
How much CJC-1295 DAC should I take?
DAC's multi-day half-life (5.8-8.1 days) means it accumulates differently from the short-acting no-DAC form, so dose and frequency are not interchangeable between the two [1][2]. The only human dosing data come from early pharmacokinetic studies (30-90 micrograms per kilogram subcutaneously), not from efficacy trials [2][3]; CJC-1295 is not approved for human use [9].
What Modified GRF (1-29) / no-DAC is
CJC-1295 no DAC
Modified GRF (1-29) — the no-DAC form, also written "Mod GRF 1-29" — is the tetrasubstituted GHRH(1-29) sequence without the DAC albumin handle [1]. It carries the same four substitutions (D-Ala2, Gln8, Ala15, Leu27) that make CJC-1295 protease-resistant, but because it does not bind albumin, it does not accumulate the multi-day half-life [1].
The practical consequence is that no-DAC behaves like a short-pulse GHRH signal rather than a sustained one. This is exactly the form most often conflated with the long-acting DAC variant in marketing and on forums — the single most common factual error about CJC-1295. They share a backbone and a name fragment; they do not share a pharmacokinetic profile [1][9].
CJC-1295 weight loss, body composition and the GH/IGF-1 axis
Because CJC-1295 raises growth hormone and IGF-1, it is frequently framed around weight loss and body composition. The honest mechanism is indirect: CJC-1295 acts on the GH/IGF-1 axis, and growth hormone influences lipolysis and lean-mass metabolism [2][3]. But the molecule itself has no body-composition trial in healthy adults — the discontinued ConjuChem Phase 2 program targeted HIV-associated visceral obesity and did not advance [9].
The closest approved-drug evidence comes from a different molecule in the same class: tesamorelin, a GHRH analog approved for HIV-associated visceral fat reduction [10]. That comparator shows the GHRH-analog mechanism can move visceral fat in a specific clinical population — but it is tesamorelin's evidence, not CJC-1295's, and it does not transfer to weight-loss claims for CJC-1295 in healthy adults [9][10]. Where the data stops, this page stops.
Why the distinction matters
Getting DAC versus no-DAC right is not pedantry — it changes everything downstream. A multi-day half-life means a dose accumulates and acts continuously; a short half-life means it clears between signals [1][2]. Any discussion of dosing frequency, of how long an effect lasts, or of how the molecule fits a research question is meaningless without first naming which variant is on the table.
The published human pharmacokinetics — Teichman 2006 and Ionescu/Frohman 2006 — characterized the DAC-bearing long-acting analog [2][3]. When a source cites "CJC-1295" half-life data and then describes a short-acting molecule, it has merged two different drugs. Keeping them apart is the single most useful thing a reader of this literature can do.