# CJC-1295: The GHRH-Analog Research, Drawn as a Whiteboard > CJC-1295 is a long-acting synthetic GHRH analog. Single subcutaneous doses raised growth hormone 2- to 10-fold for six days or more in healthy adults. A cited flowchart digest of the literature. One molecule, two forms, one cascade. The published pharmacokinetic data, the DAC-versus-no-DAC fork the forums conflate, and the anti-doping detection record — sketched as flowcharts, every figure cited. ## What the CJC-1295 literature actually measured CJC-1295 is a long-acting synthetic analog of growth-hormone-releasing hormone (GHRH). In healthy adults, single subcutaneous doses of 30 or 60 micrograms per kilogram raised mean plasma growth hormone 2- to 10-fold for six days or more, and IGF-1 1.5- to 3-fold for nine to eleven days, with an estimated peptide half-life of 5.8 to 8.1 days [1]. That single result — days of elevation from one injection — is the finding that defines the compound, and it is the reason this site exists: to draw out what the studies established and where the record stops. The molecule is built on hGRF(1-29), the first 29 amino acids of human GH-releasing factor, the shortest sequence that keeps 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 protease DPP-IV that clears native GHRH within minutes [7]. In the DAC variant, a maleimidopropionyl linker bonds the peptide covalently to circulating serum albumin, extending its plasma residence toward that of albumin itself [7]. The no-DAC form — [Modified GRF (1-29)](/cjc-1295-no-dac) — keeps the four substitutions but drops the albumin handle, so it is short-acting. CJC-1295 is not approved for human use by the FDA or any major regulator. It is handled as a research chemical, it was not recommended for the 503A compounding bulks list at the 2024 FDA Pharmacy Compounding Advisory Committee, and it is prohibited at all times in sport under Section S2 of the WADA Prohibited List [11][14]. The analytical side of that prohibition — [CJC-1295 detection](/detection-anti-doping) by high-resolution mass spectrometry — is one of the best-documented parts of the record. This page summarizes the published science; it is not medical guidance and it does not endorse use. ## CJC-1295 as a peptide: structure and substitutions As a peptide, CJC-1295 is a tetrasubstituted hGRF(1-29) backbone — 29 residues carrying four engineered changes whose only job is to outlast the enzymes that destroy native GHRH. Native GH-releasing factor is cleaved at its N-terminus by dipeptidylpeptidase-IV within minutes [6]; the D-Ala2 substitution blocks that cut, and the Gln8, Ala15 and Leu27 substitutions guard against deamidation and oxidation while reinforcing the alpha-helix [7]. Those four substitutions are shared by both forms of the molecule. What separates them is one C-terminal addition. The DAC variant carries a maleimidopropionyl group on a terminal lysine that undergoes Michael addition with the free thiol on Cys34 of serum albumin, forming a covalent peptide-albumin conjugate that circulates as a roughly 66-kilodalton complex [7]. Strip that handle away and you have the no-DAC peptide. Same sequence, very different pharmacokinetics — a distinction we draw out in full on the [DAC vs no-DAC half-life](/cjc-1295-no-dac) page. ## What does CJC-1295 do? ### 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 serum-albumin conjugation for a multi-day half-life [7]. The no-DAC form, Modified GRF (1-29), keeps the substitutions but is short-acting [7]. ### What does CJC-1295 do? In studies, CJC-1295 binds the GHRH receptor on anterior-pituitary somatotrophs and stimulates the synthesis and pulsatile release of growth hormone, which in turn raises hepatic IGF-1 [7]. Human pharmacokinetic studies showed sustained, dose-dependent elevation of both GH and IGF-1; in healthy men, a single 60 or 90 µg/kg dose raised basal GH roughly 7.5-fold and mean IGF-1 about 45% one week later, while the natural pulsatile pattern of GH secretion was preserved [8]. The cascade itself is a flowchart: GHRH-receptor binding activates Gs and adenylate cyclase, raising cAMP, which drives PKA and CREB-driven GH gene transcription; pituitary GH then acts on the hepatic GH receptor through JAK2/STAT5 to produce IGF-1 [7]. The whole point of the DAC modification is to keep the first arrow firing for days instead of minutes. The [GH and IGF-1 research](/research) page draws each step and cites the human numbers. ## The two forms, and the honest caveat Most online confusion about this compound collapses into one fork. CJC-1295 with DAC is the multi-day, albumin-conjugated form measured by Teichman and colleagues [1]. CJC-1295 without DAC — Modified GRF (1-29) — is short-acting, clearing on the timescale of native GHRH with protease resistance added [7]. Marketing copy routinely treats them as interchangeable; pharmacokinetically they are not, and the [DAC vs no-DAC half-life](/cjc-1295-no-dac) page exists to keep them apart. The honest part of the record is short and matters most. CJC-1295 is unapproved for human use anywhere. Human evidence is limited to early Phase 1 pharmacokinetic studies in healthy volunteers [1][8]; a ConjuChem Phase 2 trial in HIV-associated visceral obesity (NCT00267527) was discontinued, and the long-acting DAC program did not advance. There are no large efficacy or long-term safety trials. Sustained elevation of GH and IGF-1 raises theoretical safety questions, and the compound is banned in tested sport. Those are the borders of what is known — read them alongside the findings, not after them. --- The CJC-1295 record drawn out on a teaching whiteboard — each finding wired to its study by an arrow, the DAC-versus-no-DAC fork kept apart, and the unapproved status posted in plain marker; no clinic behind the board and nothing here dispensed or sold.