CJC-1295 raised growth hormone and IGF-1 for days in early human studies — here is what the literature logged.

What the CJC-1295 record logs

CJC-1295 is a synthetic long-acting analog of growth-hormone-releasing hormone (GHRH). In healthy 20- to 40-year-old men, a single subcutaneous dose raised basal growth hormone roughly 7.5-fold, mean GH about 46%, and IGF-1 about 45% one week later — and the natural pulse-by-pulse rhythm of GH secretion was preserved ^[3]. In a separate healthy-adult study, single 30 or 60 µg/kg doses 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 nine to eleven days; the estimated half-life ran 5.8 to 8.1 days ^[1].

Those are the headline readouts, and they are the reason CJC-1295 reads like a training log rather than a textbook entry. The compound binds the GHRH receptor on pituitary somatotrophs, stimulates the body's own growth-hormone release, and that GH in turn drives hepatic IGF-1 ^[1][2]. Four protease-resistant substitutions, plus — in the DAC variant — a covalent tether to circulating serum albumin, stretch a single dose across days instead of minutes. The albumin tether is the engineering that separates this analog from native GHRH: where the natural hormone is cleared in minutes, a single dose of the DAC form keeps the GH/IGF-1 axis elevated for the better part of a week ^[1].

This site logs that record straight. It is an editorial digest of the peer-reviewed literature on CJC-1295, not a clinic and not a store. Each figure on these pages is tagged to the study that measured it, the long-acting CJC-1295 DAC vs no-DAC distinction is kept apart from the marketing conflation, and the places where human data simply stop are marked rather than papered over. The whole human record amounts to a handful of early-phase studies, and reading it like a recovery tracker is a way to keep both the size of the effect and the smallness of the evidence base in view at once.

CJC-1295 peptide: structure and classification

CJC-1295 peptide is built on hGRF(1-29), the first 29 residues of human growth-hormone-releasing factor — the minimal sequence that keeps full GH-releasing activity. Onto that backbone it carries four amino-acid substitutions (D-Ala at position 2, Gln at 8, Ala at 15, Leu at 27) that stabilize the alpha-helix and block the protease dipeptidylpeptidase-IV from cleaving it, while also resisting deamidation and oxidation ^[2]. The molecule is a peptide GHRH-receptor agonist, not a steroid and not a growth hormone itself; CAS 863288-34-0 is the registry identifier attached to the DAC variant, and PubChem lists CID 91971820, with a molar mass around 3,368 Da for the peptide before albumin conjugation.

The four substitutions are the protease-resistance package; the DAC chemistry, where present, is a separate addition — a C-terminal handle that lets the peptide bind serum albumin and ride it through circulation ^[2]. That two-part design is why one name, CJC-1295, can describe two very differently behaving molecules, and why this site keeps the CJC-1295 DAC vs no-DAC split front and center.

The "shop" in this site's name is a research register, not a checkout. What is shelved here is the documentary record — the structure, the pharmacokinetics, the GH/IGF-1 outcomes — organized so a reader can find the figure and the study behind it quickly.

CJC-1295 as a GHRH analog

As a GHRH analog, CJC-1295 occupies the same drug class as sermorelin and the approved compound tesamorelin: all three are synthetic versions of the body's own growth-hormone-releasing hormone, acting on the GHRH receptor (a class B G-protein-coupled receptor) to stimulate pulsatile GH release ^[2]. What distinguishes CJC-1295 within that class is duration. Native GHRH is cleared in minutes; the four substitutions confer protease resistance, and the DAC modification adds a covalent albumin handle that extends plasma residence toward that of albumin itself, on the order of days rather than minutes ^[1][2]. A 2025 Nature Reviews Endocrinology review situates this long-acting-analog design within the broader pharmacology of GHRH and its analogues ^[10].

For a side-by-side with the unmodified generic analog, see CJC-1295 vs sermorelin. For how the long and short forms differ, see CJC-1295 DAC vs no-DAC.

What this tracker covers

The pages here are organized like a logged compound profile. The CJC-1295 research findings page walks the GH/IGF-1 outcomes, the CJC-1295 half-life data, the GHRH-plus-GHRP rationale behind the CJC-1295 and ipamorelin pairing, and the sleep-and-recovery angle on the GH axis. The CJC-1295 dosage in the literature page logs which doses were administered to which species by which route — strictly as research context, never as a protocol to follow. The two comparison pages keep the DAC-versus-no-DAC and the CJC-versus-sermorelin distinctions clean, and the CJC-1295 references page lists every source behind the figures.

The sleep-and-recovery framing is deliberate, and it is honest only at the level of the axis. Growth-hormone secretion is gated by sleep, and the GHRH axis sits at that gate: GHRH administration enhanced slow-wave sleep and nocturnal GH in normal men ^[6]. CJC-1295 acts on that same axis, but it has not been tested directly against sleep endpoints — so the recovery readout describes the system the compound touches, not a proven outcome for the molecule.

Where the evidence is strong, this tracker says so plainly. Where it is thin — and in healthy adults the human record is genuinely thin and short-term — the gap is logged as openly as the wins. For the safety caveats and the CJC-1295 regulatory status, the FAQ carries the full set; for the source documents, the references page carries every PMID and DOI.