CJC-1295 is a long-acting GHRH analog whose growth-hormone research runs as a multi-day cycle.

What the CJC-1295 literature establishes

CJC-1295 is a synthetic long-acting analog of growth-hormone-releasing hormone (GHRH). In healthy adults, single subcutaneous doses of 30 or 60 micrograms per kilogram produced dose-dependent increases in mean plasma growth hormone of two- to ten-fold for six days or more, and increases in IGF-1 of 1.5- to three-fold lasting nine to eleven days; the estimated half-life was 5.8 to 8.1 days ^[1]. That is the headline the rest of this site unpacks.

The molecule is built on hGRF(1-29), the first 29 amino acids of human growth-hormone-releasing factor — the minimal sequence that retains full GH-releasing activity. Four substitutions (D-Ala at position 2, Gln at 8, Ala at 15, Leu at 27) stabilize the helix and block the proteases that clear native GHRH within minutes ^[2]. In the DAC variant, a maleimide linker covalently binds the peptide to circulating serum albumin, extending plasma residence toward that of albumin itself ^[2].

That chemistry is why a single dose keeps working for days. It is also why two forms are constantly confused: the albumin-conjugated DAC variant is the multi-day species, while the no-DAC form — Modified GRF (1-29) — keeps the four substitutions but lacks the albumin handle and is short-acting. The two are pharmacokinetically very different, and most of this site's care goes into keeping them apart.

CJC-1295 is not approved by the FDA or any major regulator for human use. The published human evidence is limited to early-phase pharmacokinetic studies; there are no controlled efficacy or long-term safety trials in healthy adults. This is an editorial digest of that record — what it measured, and where it stops.

CJC-1295 as a research peptide

CJC-1295 is a peptide, not a steroid. It does not touch the androgen receptor; it acts on the GHRH receptor on pituitary somatotrophs to stimulate the body's own growth-hormone release ^[2]. As a research peptide it is supplied lyophilized, reconstituted with bacteriostatic water in laboratory handling, and has negligible oral bioavailability — the route studied is subcutaneous injection ^[1].

The identity has been confirmed analytically in unexpected places: high-resolution LC-MS/MS identified CJC-1295 as the active ingredient in an unknown "GHRH" preparation seized in an anti-doping context ^[6]. The compound is also well covered by modern doping-control methods for peptides in the 2-10 kilodalton range ^[13]. Those are the assays that make it detectable; they are not endorsements of use.

The quantitative figures across this site — the 5.8-8.1-day half-life, the 30/60/90 microgram-per-kilogram doses, the molecular weight near 3367.9 daltons, CAS 863288-34-0 — each trace to a study or registry on the full reference list.

Where CJC-1295 sits among GHRH analogs

GHRH analogs are a small class. CJC-1295 belongs to it alongside sermorelin (the short native fragment) and tesamorelin, the one member approved by the FDA. A 2025 Nature Reviews Endocrinology review of GHRH and its synthetic analogs maps the receptor signaling and the rationale for long-acting design that defines this family ^[12].

The distinction worth holding onto is evidence weight. Tesamorelin reached Phase 3 randomized trials and approval ^[8]. CJC-1295 reached early human pharmacokinetics and stopped — its long-acting DAC development program was discontinued ^[1]. The comparison page treats the approved GHRH analog tesamorelin as a benchmark, not an equivalent, and the whole site marks each finding with the tier of evidence behind it.

For the mechanism in detail, see the GH and IGF-1 findings. For doses, the doses used in the research. For the variant that causes the most confusion, the DAC-versus-no-DAC split below the fold.

How the GH/IGF-1 cycle actually runs

The reason this site is laid out as a process rather than a list is that CJC-1295's biology is a loop. A dose binds the GHRH receptor on pituitary somatotrophs; the receptor drives cAMP and PKA signaling; that signaling raises growth-hormone transcription and release; the released GH reaches the liver and raises IGF-1; and IGF-1 feeds back on the axis ^[2]. Six stages, one cycle, output feeding input.

What the DAC chemistry changes is how long the cycle keeps turning from a single input. Native GHRH is cleared within minutes by dipeptidylpeptidase-IV; the four substitutions block that cleavage, and the albumin conjugation keeps the peptide circulating for days ^[2]. The pharmacodynamic consequence was measured directly: a single 60- or 90-microgram-per-kilogram dose raised basal growth hormone roughly 7.5-fold and, a week later, mean GH about 46% and IGF-1 about 45%, with the natural pulsatile pattern of GH secretion left intact ^[3].

That preserved pulsatility is the detail most often lost in summaries. A continuously elevated GHRH signal might be expected to flatten the GH rhythm; in the published human data it does not ^[3]. The cycle keeps its shape while running longer — which is the entire pharmacological argument for a long-acting GHRH analog, and the thing the rest of these pages document.