# CJC-1295 half life and pharmacokinetics in published studies
> CJC-1295 half life: the DAC form's estimated half-life is 5.8-8.1 days in healthy adults (Teichman 2006), with IGF-1 elevated to 28 days after multiple doses. The no-DAC form is short-acting.
The 5.8-8.1 day DAC half-life is the defining number on this peptide. Here is where it comes from, what it implies, and how the short-acting no-DAC form differs.
## The CJC-1295 half life, from the source
The CJC-1295 half life is the single most consequential number in this peptide's record, and it belongs to the DAC form. In healthy adults, the estimated half-life of CJC-1295 (with DAC) was 5.8-8.1 days; single subcutaneous doses of 30 or 60 ug/kg produced 2- to 10-fold increases in mean plasma GH for six days or more and 1.5- to 3-fold increases in IGF-1 for nine to eleven days [1]. The multi-day figure is what separates this molecule from every short-acting secretagogue.
The mechanism behind the number is covalent. The DAC modification binds the peptide to circulating serum albumin, so the effective circulating species carries albumin's long residence time rather than the bare peptide's [2]. In the original rat work the albumin conjugate was still detectable in plasma beyond 72 hours, an early signal of the extended exposure later quantified in humans [2].
## Sustained exposure: IGF-1 elevated for weeks
The long half-life translates into sustained downstream signaling. After multiple doses in healthy adults, IGF-1 remained above baseline up to 28 days [1]. A single dose in healthy men raised IGF-1 by about 45% measured one week later [3]. The kinetics are not a brief spike; they are a plateau that holds for the better part of a month under repeated dosing.
The pulsatility finding is what makes the sustained exposure notable rather than alarming on its own terms. Despite continuous GHRH-receptor stimulation, the frequency and magnitude of pulsatile GH secretion were unaltered, and trough/basal GH rose approximately 7.5-fold [3]. The natural pulse pattern persisted under a sustained stimulus — a specific, measured result, not an assumption.
## How the albumin anchor sets the kinetics
The pharmacokinetics follow directly from the chemistry. The DAC modification places a maleimidopropionyl handle on a C-terminal lysine that undergoes a Michael addition with the free thiol on Cys34 of circulating serum albumin, forming a covalent peptide-albumin conjugate [2]. The bound peptide then inherits albumin's slow clearance rather than the rapid clearance of a free ~3.4 kDa peptide — the effective circulating species is roughly 66 kDa.
Two independent stabilizers stack here. The four substitutions (D-Ala2, Gln8, Ala15, Leu27) block dipeptidylpeptidase-IV cleavage, deamidation, and oxidation, so the peptide survives long enough to find albumin; the albumin conjugation then extends its residence into the multi-day range [2]. The rat data captured the first signal of this — the conjugate was detectable in plasma beyond 72 hours and showed a 4-fold increase in GH area-under-the-curve over two hours versus unconjugated hGRF(1-29) [2]. The human 5.8-8.1 day half-life is the quantified endpoint of that same mechanism [1].
## Why the no-DAC form is short-acting
The no-DAC Modified GRF (1-29) form has a completely different kinetic profile. It is short-acting, clearing on the minutes-to-hours timescale of native GHRH(1-29) with the protease-resistant substitutions slowing — but not eliminating — that clearance [16]. Without the albumin handle, there is nothing to extend the plasma residence, so the multi-day half-life simply does not apply [16][2].
This is why the [CJC-1295 DAC vs no-DAC](/dac-vs-no-dac) distinction is not a footnote. A half-life reported for 'CJC-1295' is meaningless until the variant is named: 5.8-8.1 days for DAC, minutes to hours for no-DAC [1][16]. The GHRH-knockout mouse data reinforce that frequency matters even for the long-acting form — once-daily 2 ug normalized growth while every-48-to-72-hour dosing was progressively less effective [4].
## Route and the limits of the pharmacokinetic record
The pharmacokinetic studies used subcutaneous injection as the primary route, with intravenous administration in the early GRF(1-29) work [1]. Oral bioavailability is negligible because CJC-1295 is a peptide, so injection is the only route with a characterized kinetic profile [2].
The limits of the record are worth stating plainly. The half-life estimates come from early-phase studies in modest numbers of healthy volunteers (Teichman 2006; Ionescu/Frohman 2006), not from large pharmacokinetic programs [1][3]. There is no published long-term human PK data beyond the 28-day IGF-1 window, and CJC-1295 is not approved for human use. The numbers on this page are precise within the studies that produced them — and the studies are few. See the [full reference list](/references).
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A flat enterprise console on the CJC-1295 record — every figure logged to its study, every gap marked, no clinic behind the readout and nothing here dispensed or sold.