CJC-1295 is the long-acting GHRH analog studied for sustained pulsatile growth-hormone release.

What CJC-1295 is

What is CJC-1295?

The specification, in one paragraph.

CJC-1295 is a 30-amino-acid synthetic analog of growth hormone-releasing hormone, derived from the bioactive GHRH (1-29) fragment with four amino-acid substitutions and, in the long-acting form, a drug-affinity-complex (DAC) linker at the C-terminus that covalently binds serum albumin ^[1]. The albumin tether is what does the work: native GHRH clears the plasma in roughly seven to twenty minutes; CJC-1295 without DAC clears in roughly thirty; CJC-1295 with DAC remains measurable in plasma for days ^[2][10]. Across the published phase-1 record, single subcutaneous doses produced dose-dependent two-to-tenfold elevations of mean plasma growth hormone sustained for at least six days and 1.5- to 3-fold elevations of insulin-like growth factor 1 for nine to eleven days ^[1]. The molecule is not FDA-approved ^[13]. It is the subject of an indexed and citable research literature, summarized here as a feature-by-feature platform overview.

What CJC-1295 does in the body

What does CJC-1295 do in the body?

A GHRH-receptor agonist, applied across days rather than minutes.

CJC-1295 binds the growth hormone-releasing hormone receptor on anterior pituitary somatotrophs, activating Gs-coupled cyclic-AMP signaling and triggering endogenous growth-hormone release ^[1]. The downstream cascade — cyclic-AMP, protein kinase A, GH exocytosis, hepatic IGF-1 induction — is the same one native GHRH drives, only stretched across a much longer pharmacokinetic window when the DAC linker is present ^[1]. Pulsatility is preserved: trial data show pulse frequency unchanged and both pulse amplitude and inter-pulse baseline elevated under continuous receptor stimulation, indicating the pulse generator does not desensitize over the studied dosing windows ^[2]. The downstream marker of interest is serum IGF-1, which rises in proportion to sustained GH exposure and falls back toward baseline over the compound's elimination window. See CJC-1295 mechanism of action on the research page for the full cascade.

What CJC-1295 is studied for

What is CJC-1295 used for in research?

Endpoints measured in the published literature.

Research on CJC-1295 has measured a small set of endpoints reproducibly. The Teichman 2006 phase-1 single-ascending-dose trial measured plasma GH and IGF-1 across days following 30, 60, 125, or 250 µg/kg single subcutaneous doses ^[1]. The Teichman 2006 multi-dose arm measured cumulative IGF-1 elevation across 49 days at 60 µg/kg weekly or every other week ^[16]. The Ionescu 2006 companion paper measured pulse frequency, pulse amplitude, and inter-pulse GH baseline under continuous DAC-extended receptor stimulation ^[2]. The Alba 2006 murine work measured restoration of body weight, lean mass, and subcutaneous fat distribution in GHRH-knockout mice receiving daily CJC-1295 ^[3]. The Sackmann-Sala 2009 proteomic study measured downstream serum protein-profile shifts following a single 90 µg/kg dose ^[4]. Together these are pharmacokinetic and pharmacodynamic studies of a long-acting GHRH analog — not clinical-efficacy trials in any indicated population.

The two variants, side by side

Same backbone. Different linker. Different time courses.

The specification ships in two variants. CJC-1295 with DAC carries a maleimidopropionic-acid lysine derivative at the C-terminus that covalently bonds the free Cys34 thiol on circulating serum albumin ^[5]. The albumin tether shields the peptide from proteolytic clearance and extends plasma half-life to approximately 5.8 to 8.1 days in healthy adults ^[1]. CJC-1295 without DAC — the same 30-residue backbone with the same four substitutions — is also known as modified GRF (1-29) and reverts to a plasma half-life of approximately 30 minutes. The four substitutions (D-Ala-2, Gln-8, Ala-15, Leu-27) confer protease resistance to both variants by blocking dipeptidyl-peptidase-IV cleavage between residues 2 and 3 ^[6]. Only the DAC linker produces the multi-day dosing interval. Full variant comparison: CJC-1295 with DAC vs no DAC.

Why CJC-1295 is often studied with ipamorelin

Why is CJC-1295 often paired with ipamorelin?

Two receptors, one somatotroph, additive output.

CJC-1295 is a GHRH-receptor agonist; ipamorelin is a ghrelin / GHS-R1a-receptor agonist ^[7]. They activate distinct receptors on the same anterior-pituitary somatotroph: the GHRH receptor raises intracellular cyclic AMP through Gs; the ghrelin receptor raises intracellular calcium through phospholipase C and IP3 ^[8]. Because the two pathways converge on the same GH-release machinery without competing for the same receptor, co-administration in published research has produced additive — and in some preclinical models synergistic — growth-hormone pulse amplitude versus either compound alone ^[8]. Ipamorelin's selectivity profile (GH release without elevation of ACTH, cortisol, or other pituitary hormones in human and animal studies) is what makes it the conventional GHRP partner alongside a GHRH analog like CJC-1295 ^[15]. Detailed pairing pharmacology: CJC-1295 and ipamorelin pairing.

Regulatory specification

A spec sheet is not a permission.

CJC-1295 is not FDA-approved for any indication ^[13]. The compound was placed on FDA's interim 503A bulk drug substances list at Category 2 — significant safety risks for compounding — in September 2023, and removed from Category 2 in September 2024 only after the nominator withdrew the nomination ^[13]. Removal from Category 2 in that posture is an administrative consequence of withdrawal, not a safety clearance. The compound remains outside any active U.S. approval or pharmacy-compounding pathway. The World Anti-Doping Agency lists CJC-1295 explicitly under Section S2.2 (Growth Hormone Releasing Factors) of the Prohibited List, prohibited at all times in and out of competition ^[12]. This site documents that record — including the CJC-1295 side effects reported in published phase-1 trials and the frequently asked questions drawn from the indexed literature.