Research digest / Pharmacokinetics

CJC-1295 is a long-acting GHRH analog whose pharmacokinetics set the DAC and no-DAC forms apart.

A clear, browsable digest of the published CJC-1295 research: the multi-day half-life of the DAC variant, the short-acting no-DAC form, and exactly where the human data stand — every quantitative claim cited.

Clean marketplace-style illustration of a coral multi-day pharmacokinetic decay curve over slate day-marks with a small short plum reference curve, on a cool near-white ground

What the CJC-1295 record actually shows

CJC-1295 is a synthetic long-acting analog of growth-hormone-releasing hormone (GHRH), built on the first 29 residues of human GH-releasing factor with four protease-resistant substitutions, and in its DAC variant a covalent tether to circulating serum albumin that stretched its plasma half-life to an estimated 5.8-8.1 days in healthy adults [1]. That single number is the headline of the literature: where native GHRH(1-29) is cleared in minutes, the engineered molecule kept mean growth hormone (GH) and insulin-like growth factor 1 (IGF-1) elevated for days after one subcutaneous dose [1].

This page is a digest, not a clinic and not a vendor. It reads the published record straight, tags each finding to its study, and keeps the two forms of the molecule cleanly apart — because most of the confusion online comes from conflating them.

In the foundational human study, single subcutaneous doses of 30 or 60 micrograms per kilogram produced dose-dependent 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 9 to 11 days; after multiple doses, IGF-1 stayed above baseline up to 28 days [1]. A companion study in healthy young men found basal GH raised roughly 7.5-fold and mean GH up about 46% one week after a single dose, while the natural pulsatile pattern of GH secretion was preserved — the molecule sustained the signal without flattening the pulses [3].

The animal and biochemical work explains why. The lead analog combined four substitutions that block dipeptidylpeptidase-IV cleavage with albumin bioconjugation, producing a roughly 4-fold increase in GH exposure over two hours versus the unconjugated peptide in rats, with the conjugate detectable in plasma beyond 72 hours [2]. None of this carries an approved human indication — the DAC development program was discontinued, and CJC-1295 is handled as an unapproved research chemical [1].

What is CJC-1295?

CJC-1295 is a synthetic long-acting analog of growth-hormone-releasing hormone, built on hGRF(1-29) with four protease-resistant substitutions; the DAC variant adds covalent albumin conjugation for a multi-day half-life [1][2]. The no-DAC form, often called Modified GRF (1-29), keeps the four substitutions but omits the albumin tether and is therefore short-acting [12].

The four substitutions — D-Ala at position 2, Gln at 8, Ala at 15, and Leu at 27 — stabilize the peptide's alpha-helix and block the enzymes that rapidly degrade native GHRH [8]. The D-Ala2 swap alone markedly increases half-life and potency by resisting dipeptidylpeptidase-IV cleavage [7]. That stability is the foundation; the DAC tether is what turns hours into days. For the full mechanism, see how the GHRH receptor is engaged.

What does CJC-1295 do?

It binds the GHRH receptor on anterior-pituitary somatotrophs and stimulates pulsatile growth-hormone release, which in turn raises hepatic IGF-1; in human studies it elevated GH and IGF-1 for days after a single dose [1][3]. The receptor is a class B G-protein-coupled receptor, and engaging it activates the Gs/cAMP/PKA cascade that drives GH gene transcription and release [2].

What makes the molecule notable in the literature is duration without distortion: the sustained stimulation did not erase GH pulsatility [3]. The pulses kept coming; the baseline simply rose. This is the property that distinguishes a long-acting GHRH analog from a continuous infusion, and it is documented in healthy adults [1][3].

CJC-1295 as a research peptide

As a research peptide, CJC-1295 is a lyophilized powder reconstituted with bacteriostatic water and refrigerated in laboratory handling; oral bioavailability is negligible because it is a peptide [1]. It has been studied almost entirely by subcutaneous injection, with intravenous dosing used in the early GRF(1-29) pharmacokinetic work [9].

The peer-reviewed CJC-1295 evidence base in healthy adults is real but thin and short-term — a handful of early-phase pharmacokinetic studies, the rat bioconjugate work, and a GHRH-knockout mouse growth study [1][2][4]. A 2024/2025 Nature Reviews Endocrinology review places the molecule within the broader GHRH-analog class and its investigational landscape [13]. The doses studied are documented under doses used in research; the kinetics under CJC-1295 half-life.

GHRH analogs as a class

GHRH analogs are synthetic versions of the hypothalamic hormone that tells the pituitary to release growth hormone, engineered to resist the proteases that clear the native peptide in minutes [7][8]. The class includes sermorelin, tesamorelin (the one FDA-approved member, for HIV-associated lipodystrophy), and CJC-1295 [13].

What unites them is the target — the GHRH receptor — and the design problem: native GHRH(1-29) is degraded primarily by dipeptidylpeptidase-IV and trypsin-like enzymes, so every useful analog carries protease-resistant chemistry [8]. What separates them is half-life. CJC-1295 DAC pushed that further than any sibling by covalently binding albumin [2]. A 2024/2025 class review describes the receptor signaling and the rationale for long-acting design [13]. See where CJC-1295 and ipamorelin fit, and the DAC vs no-DAC comparison.