CJC-1295
A 30-residue GHRH analog conjugated to serum albumin via a maleimide-thiol bond, with an effective half-life of 5.8 to 8.1 days in healthy adults.
The short version
CJC-1295 is a synthetic peptide that tells the pituitary gland to release more growth hormone. It is not a steroid and it is not growth hormone itself — it acts upstream, nudging the body's own hormone system rather than replacing it. A single injection can keep growth hormone elevated for up to a week, and IGF-1 (the main downstream signal) stays above baseline for nine to eleven days. That long duration is produced by a chemical modification called DAC (Drug Affinity Complex), which binds the peptide to a common blood protein and slows its clearance. Research communities use it and often pair it with a second compound called ipamorelin. It is not approved for any medical use and has never completed Phase 3 clinical trials. WADA prohibits it in sport. Read about what people actually report on the effects page.
What CJC-1295 is
CJC-1295 is a synthetic analog of the first 29 residues of human growth hormone-releasing hormone (hGRH 1-29), extended to 30 residues by a lysine bearing the Drug Affinity Complex (DAC) maleimide group at the C-terminus [4]. Its developer, ConjuChem Biotechnologies of Montreal, introduced four amino acid substitutions — at positions 2, 8, 15, and 27 — that block the primary DPP-IV cleavage site and reduce chemical instability relative to the native sequence [7]. The DAC maleimide group reacts with Cys34 of circulating serum albumin after subcutaneous injection, forming a stable thioether bond and producing a conjugate of approximately 67 kDa [8]. That conjugate is too large for renal filtration and rides albumin's 19–21-day endogenous circulatory lifespan, extending CJC-1295's effective half-life to 5.8–8.1 days [2].
The compound's formal name is DAC:GRF. It appears in the literature under several synonyms: Modified GRF 1-29, Mod GRF 1-29, CJC-1295 without DAC (referring specifically to the version lacking the albumin-conjugating group), and hGRF(1-29) analog. These are not interchangeable. The unmodified Modified GRF 1-29 carries the four position substitutions but no maleimide group and therefore has a plasma half-life of approximately 30 minutes — long enough to matter versus native GHRH's under-10-minute window, but fundamentally different from the multi-day profile of CJC-1295 with DAC [7].
CJC-1295 is not approved by the U.S. Food and Drug Administration for any therapeutic indication. Phase 2 clinical development by ConjuChem was discontinued. The compound is listed on the World Anti-Doping Agency's prohibited substances list under Section S2 — Peptide Hormones, Growth Factors, Related Substances and Mimetics — both in-competition and out-of-competition.
What the Phase 1 data shows
The most complete human pharmacokinetic and pharmacodynamic data for CJC-1295 comes from a randomized, placebo-controlled Phase 1/2 trial by Teichman et al. published in 2006 in the Journal of Clinical Endocrinology and Metabolism [1]. In that study, healthy adults aged 21–61 years received single subcutaneous doses of 30, 60, 90, or 120 μg/kg. At 30 and 60 μg/kg, mean plasma GH concentrations rose 2- to 10-fold above baseline and remained elevated for six or more days. IGF-1 — the primary downstream effector of GH — increased 1.5- to 3-fold and remained above baseline for 9–11 days after a single injection [2]. With repeated dosing, IGF-1 stayed elevated for up to 28 days [2].
A second study by Ionescu and Frohman, also published in 2006, characterized what CJC-1295 does to the architecture of GH secretion [3]. GH is released in pulses, not as a continuous level, and the largest pulse of the 24-hour cycle occurs during slow-wave sleep. Exogenous recombinant GH suppresses this pattern via negative feedback. CJC-1295 does not: basal (trough) GH levels rose 7.5-fold (P < 0.0001) and mean GH increased 46% (P < 0.01), but pulse frequency and pulse characteristics remained intact [3]. The same paper noted a 45% rise in IGF-1 (P < 0.001). Pulsatility was preserved because CJC-1295 acts upstream — stimulating pituitary somatotrophs to respond more strongly to endogenous GHRH signals — rather than substituting for GH itself [17].
The rodent mechanistic data is consistent. Jetté et al. (2005) demonstrated that the albumin bioconjugate remained detectable in rat plasma beyond 72 hours after subcutaneous administration and produced a 4-fold increase in GH area under the curve compared to unmodified hGRF(1-29) [4]. In GHRH-knockout mice, once-daily subcutaneous CJC-1295 at 2 μg/dose over 5 weeks fully normalized body weight, body length, femur and tibia development, and body composition — confirming GHRH-R-mediated mechanism exclusively [5]. Dosing every 48 or 72 hours produced only partial restoration in the same model [5].
The receptor and the signal cascade
CJC-1295 binds the growth hormone-releasing hormone receptor (GHRH-R), a G protein-coupled receptor expressed on pituitary somatotroph cells and, at lower levels, on cardiac myocytes, lymphocytes, gonads, skin, and kidney [13]. Binding activates the Gαs subunit, which stimulates adenylyl cyclase, elevates intracellular cyclic AMP (cAMP), and activates protein kinase A (PKA). PKA phosphorylates the transcription factor CREB, which drives Pit-1-mediated GH gene expression and opens voltage-gated calcium channels, triggering direct GH granule exocytosis [13].
Downstream, GH stimulates hepatic IGF-1 production via the JAK2/STAT5 pathway. IGF-1 then drives skeletal muscle protein synthesis through the PI3K/Akt/mTORC1 axis — Akt phosphorylates TSC1/2, activating Rheb-GTP and mTORC1, which in turn phosphorylates p70S6K to enhance ribosomal protein translation [12]. GH also activates lipolysis in visceral adipose tissue via hormone-sensitive lipase, providing a mechanistic basis for the body composition changes studied in related GHRH analog trials [16].
A 2025 study in Cell by Ding et al. provided circuit-level context: during NREM sleep, activity in hypothalamic GHRH neurons rises while somatostatin neuron activity falls, producing the large GH pulse characteristic of slow-wave sleep [14]. By sustaining pituitary GHRH-R engagement across multiple sleep cycles, CJC-1295 continuously primes somatotrophs to respond to these endogenous nocturnal GHRH surges — an explanation for why trough GH (the between-pulse baseline) rises substantially while pulse architecture is preserved [3].
The evidence base: what is and is not established
CJC-1295's human data is narrow but specific. Two Phase 1/2 studies in healthy adults — enrolling 21–61 year-olds at doses of 30–120 μg/kg — established the pharmacokinetic profile and confirmed GH/IGF-1 elevation. No Phase 3 trial exists. Long-term cardiovascular outcomes, glucose regulation, oncogenic risk, and effects in patient populations (as opposed to healthy volunteers) are not characterized. A 2026 gerontology review noted CJC-1295 as the best-characterized long-acting GHRH analog in healthy human adults and simultaneously flagged those gaps as unresolved [18].
Most extrapituitary biology attributed to the GHRH analog class — wound healing, cardioprotection, islet survival, anti-tumor activity in xenograft models — derives from analogs developed by the Schally laboratory (MR-409, MR-502) rather than from CJC-1295 itself [10][16]. Class-level inference requires caution; the specific effects of CJC-1295 on peripheral tissues have not been directly studied in humans.
This site summarizes what the published literature contains. It does not offer advice, estimate appropriate doses for human use, or interpret findings outside the research context in which they were generated.