RESEARCH CONSOLE / GHRH ANALOG
CJC-1295 is a long-acting GHRH analog whose DAC and no-DAC forms split sharply on half-life.
A stencilled spec sheet of what the pharmacokinetic literature measured — GH and IGF-1 elevation lasting days, a 5.8-8.1-day DAC half-life, and the point where the human data stop. Every figure is cited.

What CJC-1295 is, and what the data show
CJC-1295 is a synthetic analog of growth-hormone-releasing hormone (GHRH), built on the first 29 residues of human GH-releasing factor — hGRF(1-29) — with four amino-acid substitutions that block enzymatic cleavage. In its long-acting DAC form, a single subcutaneous dose elevates growth hormone (GH) and insulin-like growth factor 1 (IGF-1) for days, with an estimated half-life of 5.8-8.1 days in healthy adults [1].
The numbers are specific. In healthy adults, single subcutaneous doses of 30 or 60 ug/kg 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; after multiple doses, IGF-1 stayed above baseline for up to 28 days [1]. In healthy men, a single 60- or 90-ug/kg dose raised basal GH roughly 7.5-fold and IGF-1 about 45% one week later, while the pulsatile pattern of GH release was unchanged [2].
That last detail matters. CJC-1295 does not flatten GH into a continuous infusion; it raises the baseline while the body keeps its natural pulses [2]. The mechanism is a GHRH analog acting on the pituitary GHRH receptor, traced in detail on the GH and IGF-1 findings page.
This site is an editorial digest, not a clinic and not a vendor. It reads the published record and cites it — the doses used in studies, the DAC vs no-DAC half-life split, the sleep and recovery research, and the side effects and safety picture. CJC-1295 is not approved for human use anywhere; the framing here is research-context only.
CJC-1295 as a GHRH-Analog Peptide
CJC-1295 is a peptide — a 29-residue chain based on hGRF(1-29), molecular weight approximately 3367.9 Da, CAS 863288-34-0. The four substitutions (D-Ala at position 2, Gln at 8, Ala at 15, Leu at 27) stabilize the alpha-helix and block dipeptidylpeptidase-IV (DPP-IV) cleavage, deamidation, and oxidation [3].
It is not a steroid and not a growth hormone. It is a secretagogue: it prompts the pituitary to release the body's own GH rather than supplying GH directly [1]. That distinction shapes everything downstream — the response stays under the body's regulatory feedback, and the pulsatile rhythm of GH secretion is preserved rather than overridden [2]. Oral bioavailability is negligible, so the route studied is subcutaneous injection [1][2].
The DAC ('Drug Affinity Complex') variant adds one further modification — a C-terminal lysine functionalized with a maleimidopropionyl linker that binds covalently to circulating serum albumin, extending the plasma half-life toward that of albumin itself [3]. The no-DAC form, Modified GRF 1-29, keeps the four substitutions but omits the albumin handle and is short-acting. The two are pharmacokinetically very different, which is why marketing that treats them as one molecule is misleading [12]. The full citation set is on the full reference list.
The headline figures, measured
Four figures define the CJC-1295 record. The estimated DAC half-life is 5.8-8.1 days in healthy adults [1]. IGF-1 rose roughly 45% one week after a single 60- or 90-ug/kg dose [2]. Basal GH rose about 7.5-fold after that same single dose [2]. And there is no established human dose — the human data come from early pharmacokinetic (PK) studies, not efficacy or long-term safety trials [1][12].
Those four numbers are not a marketing claim; they are the boundary of what was actually measured, in small studies of healthy volunteers. The IGF-1 figure is a biomarker, not a clinical outcome. The half-life is a property of the DAC form specifically. And the missing dose is the honest gap: a well-characterized pharmacokinetic profile sits next to an absence of the efficacy and safety dose-finding that an approved drug carries [12].
Everything below those headlines is documented on the topic pages: the receptor mechanism and the GH and IGF-1 findings, the doses used in studies, the DAC vs no-DAC pharmacokinetic split, and the side effects and safety summary. The honest gaps are surfaced, not buried: most 'protocols' circulating online are not derived from controlled human trials [12], and the original long-acting DAC development program was discontinued.
Where CJC-1295 sits, and where this site stops
CJC-1295 belongs to the GHRH-analog class, alongside sermorelin and the FDA-approved tesamorelin — the closest approved-drug comparator, approved for a specific clinical indication [7]. A 2024/2025 Nature Reviews Endocrinology review synthesizes the pharmacology of GHRH and its synthetic analogues, describing receptor signaling and the rationale for long-acting analog design [7]. CJC-1295 itself is not approved anywhere; it is handled as a research chemical and is prohibited at all times in sport under WADA Section S2 [6].
This is an instrument of record, not a storefront. It does not list prices, vendors, or order links, and it never will within this project. The 'get' in the domain means get the facts: a stencilled spec sheet of what the literature measured, with the preclinical-only results labeled and the human gaps left visible.
What is solid, and what is contested
Read across the record and three things are solid. The pharmacokinetics are well characterized: a 5.8-8.1-day DAC half-life and IGF-1 elevation lasting days to weeks after a single dose [1]. The mechanism is established: GHRH-receptor agonism that raises GH and IGF-1 while preserving pulsatility [1][2]. And the DAC-vs-no-DAC distinction is chemically real, not a marketing nuance — the two forms clear on completely different timescales [1][3].
Three things are contested or unresolved. There is no established human dose and no efficacy or long-term safety trial in healthy adults [12]. The development history carries unresolved questions — the long-acting DAC program was discontinued, with a development-era patient death frequently cited in connection with the halted trial, though a causal link to CJC-1295 was not established in the public record. And much of the popular framing of CJC-1295 as an anti-aging or muscle-building aid runs well ahead of a peer-reviewed evidence base that, in healthy adults, is thin and short-term [12][13]. Holding both lists at once is the accurate stance, and it is the one this site takes.