# CJC-1295: Research Overview — Ascent Peptides > A literature summary of CJC-1295, a tetrasubstituted GHRH analog. Covers the DAC vs. no-DAC distinction, human pharmacokinetic data, GH/IGF-1 findings and regulatory status. A tetrasubstituted hGRF(1-29) analog whose DAC variant covalently binds serum albumin — trading the natural hormone's two-minute half-life for something measured in days. ## The short version CJC-1295 is a synthetic version of the first 29 residues of growth hormone-releasing hormone, carrying four amino-acid changes that stabilize its shape and protect it from the enzyme (DPP-IV) that rapidly degrades natural GHRH. In its DAC form, a chemical linker on the C-terminus attaches covalently to circulating serum albumin — the most abundant protein in blood — and rides along with it for as long as albumin circulates, giving CJC-1295 DAC a measured half-life of roughly five to eight days [4]. In human studies, a single subcutaneous dose produced dose-dependent two- to ten-fold increases in mean GH for six days or more, and a 1.5- to three-fold rise in IGF-1 for nine to eleven days [4]. Pulsatile GH secretion — the natural rhythm the body uses to regulate the axis — was preserved even during this prolonged stimulation [5]. CJC-1295 is not approved for human use anywhere, it is banned in competitive sport, and this page lists no human dose. ## What it is CJC-1295 is a synthetic peptide built on hGRF(1-29) — the 29-amino-acid N-terminal fragment of human growth-hormone-releasing factor. Four substitutions distinguish it from the parent sequence: D-Ala at position 2, Gln at 8, Ala at 15, and Leu at 27. Together these lock the alpha-helix into a conformation that binds the GHRH receptor more effectively and resists enzymatic cleavage, deamidation and oxidation. The DAC ('Drug Affinity Complex') variant adds a maleimidopropionyl (MPA) linker on a C-terminal lysine. That linker undergoes a Michael addition reaction with the free thiol on Cys34 of circulating serum albumin, forming a stable covalent conjugate that extends the peptide's plasma residence time toward that of albumin itself. The no-DAC form ('Modified GRF 1-29') keeps the four stabilizing substitutions but lacks the albumin-binding handle, making it a short-acting compound — pharmacokinetically very different, though the two are routinely conflated [7]. ## How it works CJC-1295 binds the growth-hormone-releasing hormone receptor (GHRHR) on somatotroph cells in the anterior pituitary, activating the Gs/adenylyl cyclase/cAMP/PKA signaling cascade that stimulates both the synthesis and pulsatile release of growth hormone. The resulting rise in GH drives the liver to produce IGF-1, completing the somatotropic axis. The DAC linker strategy was validated in a screen of hGRF(1-29) analogs bearing the maleimidopropionyl-lysine handle [7]. In rats, the lead compound — CJC-1295 — showed a four-fold increase in GH area-under-the-curve over two hours versus unconjugated hGRF(1-29), remained detectable in plasma beyond 72 hours, and was stable against DPP-IV cleavage in vitro [7]. A GHRH-knockout mouse study confirmed that once-daily dosing with CJC-1295 was sufficient to fully normalize body weight and length, while less frequent dosing was progressively less effective — a practical illustration of the receptor dynamics [6]. ## What the research shows *Human pharmacokinetics.* The pivotal human PK study gave single subcutaneous doses of 30 or 60 micrograms per kilogram to healthy adults aged 21 to 61. Mean plasma GH rose two- to ten-fold and remained elevated for six or more days; IGF-1 rose 1.5- to three-fold and stayed above baseline for nine to eleven days. After multiple doses, IGF-1 remained elevated for up to 28 days. Estimated half-life: 5.8 to 8.1 days [4]. *Preserved pulsatility.* In healthy men aged 20 to 40, a single dose raised trough and basal GH approximately 7.5-fold and mean GH by about 46%, with IGF-1 rising about 45% one week later — but the frequency and magnitude of pulsatile GH bursts were statistically unchanged, indicating the natural GH rhythm persists under prolonged GHRH-analog stimulation [5]. *Serum proteome shifts.* In eleven healthy young men, CJC-1295 measurably altered the serum protein profile: apolipoprotein A1 and a transthyretin isoform decreased; an albumin fragment and immunoglobulin species increased; and the immunoglobulin/albumin-fragment signal correlated linearly with IGF-1, identifying candidate biomarkers of GH/IGF-1 axis activation [3]. *Identification in anti-doping context.* High-resolution LC-MS/MS definitively identified CJC-1295 as the active ingredient in an unmarked pharmaceutical preparation seized during anti-doping work — confirming both the detection methodology and the real-world supply [2]. *Pharmacological class review.* A 2025 Nature Reviews Endocrinology synthesis frames CJC-1295 within the broader GHRH-analog class, covering receptor signaling, analog design rationale, and the therapeutic and investigational landscapes for the entire compound family [1]. ## Reported effects, cautions and safety The controversies surrounding CJC-1295 are well documented in the literature and deserve careful reading: - *Not approved; research-chemical status.* CJC-1295 has no approved human indication anywhere. The original ConjuChem DAC program was discontinued; a patient death during that development era is frequently cited in connection with the halted Phase 2 trial, though no causal link to CJC-1295 was established in the public record [1]. - *DAC vs. no-DAC conflation.* CJC-1295 DAC (multi-day half-life) and Modified GRF 1-29 (the no-DAC, short-acting form) are pharmacokinetically very different compounds. Most online protocols treat them as interchangeable; the published literature does not [7]. - *Sustained IGF-1 and theoretical cancer risk.* Epidemiological work links higher IGF-1 to modestly increased risk of certain cancers (notably breast and prostate). GH-axis stimulation can also cause fluid retention, peripheral edema, and effects on insulin sensitivity [1]. - *Regulatory and sport.* FDA briefing materials for the 2024 Pharmacy Compounding Advisory Committee raised immunogenicity and safety concerns for GH secretagogues including CJC-1295; it is also prohibited at all times in sport under WADA Section S2, and detection assays are well established [2]. - *Thin human evidence base.* Published human data are limited to early pharmacokinetic studies; long-term efficacy and safety in humans are unestablished. Most community dosing protocols have no basis in controlled trial data [4][5]. ![CJC-1295 receptor binding and albumin conjugation illustrated in cold glacier tones](/images/cjc-1295.webp) ## Where it fits in GH-axis research Among the three GHRH analogs on this desk, CJC-1295 occupies the extreme long-acting end of the durability spectrum — its albumin-tethering strategy is the most engineered, its half-life the longest, and its evidence base the most focused on pharmacokinetics rather than clinical outcomes [4]. Where [Sermorelin](/sermorelin) is the natural-fragment story and [Tesamorelin](/tesamorelin) has approved human efficacy data, CJC-1295's record in humans is shorter and more recent. It is the compound that makes the GH-axis pulsatility question most interesting: can you stimulate the axis continuously without flattening the natural GH rhythm? The data suggest you can [5]. See how it lines up against the others on the [comparison page](/compare). --- A literature digest tracing three GHRH analogs through the peer-reviewed record — mechanism, evidence, and caution, but never a dose or a product.