CJC-1295 is a long-acting GHRH analog built on four substitutions and a DAC albumin handle.

What the CJC-1295 record establishes

CJC-1295 is a synthetic, long-acting analog of growth-hormone-releasing hormone (GHRH). It is built on the first 29 residues of human GH-releasing factor, hGRF(1-29), carrying four amino-acid substitutions — D-Ala at position 2, Gln at 8, Ala at 15, Leu at 27 — that stabilize the helix and block the protease dipeptidylpeptidase-IV from clipping it apart ^[9]. In the DAC ("Drug Affinity Complex") variant, a C-terminal lysine carries a maleimidopropionyl linker that bonds covalently to serum albumin, dragging the molecule's clearance toward that of albumin itself ^[2].

The headline number sits in the human pharmacokinetics. In healthy adults, a single subcutaneous dose of 30 or 60 micrograms per kilogram produced a dose-dependent 2- to 10-fold rise in mean plasma growth hormone lasting six days or more, and a 1.5- to 3-fold rise in IGF-1 lasting nine to eleven days; after repeated doses, IGF-1 stayed above baseline as long as 28 days, with the analog's estimated half-life landing at 5.8 to 8.1 days ^[1]. That multi-day window — a single injection moving a hormone axis for over a week — is the property the four substitutions and the albumin handle were engineered to produce.

A second human study sharpened the picture. In healthy men aged 20 to 40, a single 60 or 90 micrograms-per-kilogram dose raised basal GH roughly 7.5-fold and IGF-1 about 45% one week later, while the natural pulsatile pattern of GH secretion stayed intact — the analog raised the floor the pituitary pulsed from without overriding its rhythm ^[3]. The preclinical work established the same duration mechanism from the other direction: in rats, the albumin-conjugated peptide produced a four-fold GH area-under-the-curve over the unconjugated form and was still detectable in plasma beyond 72 hours ^[2].

This site reads that record straight. It is an editorial digest of the peer-reviewed CJC-1295 literature, organized like a console: each finding logged to its study, each form (DAC versus short-acting no-DAC) tagged, and each gap in the human evidence marked rather than glossed. The aim is a reference a careful reader can check line by line, not a pitch.

CJC-1295 as a research peptide

As a research peptide, CJC-1295 has a sharp, queryable identity. The DAC peptide carries CAS number 863288-34-0 and a molar mass of roughly 3,367.9 Da before albumin conjugation; the effective circulating species after the DAC bond forms is the far larger peptide-albumin complex, near 66 kDa ^[2]. PubChem catalogs it under CID 91971820. It is administered subcutaneously in the published work, has negligible oral bioavailability as a peptide, and is handled in the lab as a lyophilized powder reconstituted in bacteriostatic water ^[1].

What it is not is equally important. CJC-1295 is not an anabolic steroid; it acts on the GHRH receptor to stimulate the body's own growth hormone, an entirely different axis. It is not FDA-approved for any human indication anywhere, and the 2024 FDA Pharmacy Compounding Advisory Committee did not recommend it for the 503A compounding bulks list. It is prohibited at all times in sport under Section S2 of the WADA Prohibited List ^[6]; the full regulatory and WADA status is laid out on the FAQ. The doses used in research are study doses, not protocols, and nothing on this site is dispensed or sold.

How CJC-1295 works at the molecular level

CJC-1295 binds the growth-hormone-releasing hormone receptor (GHRHR), a class B G-protein-coupled receptor sitting on the somatotroph cells of the anterior pituitary ^[7]. Receptor occupancy couples through Gs to adenylate cyclase, raising cyclic AMP, activating PKA, and driving CREB-mediated transcription of the growth-hormone gene — the proximal cascade that GHRH-sensitive adenylate cyclase studies first characterized in pituitary cells ^[8]. The released GH then acts on hepatic GH receptors through JAK2/STAT5 to raise IGF-1, the downstream hormone that carries much of GH's anabolic signal.

The engineering sits upstream of that biology. The four substitutions defeat the proteases that clear native GHRH in minutes; the D-Ala2 swap alone markedly extends the half-life and potency of GHRH(1-29) by blocking dipeptidylpeptidase-IV cleavage ^[9]. The DAC albumin conjugation then stretches plasma residence from minutes to days ^[2]. Cryo-EM structures published in 2020 resolved exactly how peptide agonists engage and activate GHRHR, clarifying the receptor conformation that analogs such as CJC-1295 stabilize ^[7]. The result is a molecule that reads like a system spec — a sequence, four named edits, a linker chemistry, a receptor, and a multi-day readout — which is why this digest renders it as one.

Where CJC-1295 sits among GHRH analogs

CJC-1295 belongs to a small family of GHRH-analog molecules that all stimulate the same receptor but differ in how long they last. Sermorelin is GHRH(1-29) itself, short-acting and cleared quickly. Tesamorelin is a stabilized GHRH analog that is FDA-approved for one narrow indication and serves as the closest approved-drug benchmark. CJC-1295's distinguishing feature within that ladder is duration: the DAC variant's covalent albumin bond gives it a half-life measured in days rather than minutes ^[1].

A 2024/2025 Nature Reviews Endocrinology review synthesized the pharmacology of GHRH and its synthetic analogs — the class that spans sermorelin, tesamorelin and CJC-1295 — describing the receptor signaling, the rationale for long-acting design, and the therapeutic and investigational landscape ^[12]. The short-acting Modified GRF (1-29) sits at the other end of the same family, and the two-receptor logic behind pairing CJC-1295 and ipamorelin is a separate thread covered in the research. For the side-by-side, see CJC-1295 vs sermorelin; for the form distinction that defines CJC-1295 itself, see CJC-1295 DAC vs no-DAC. The full reference list carries every study cited across this site.