PwPepwise

a.k.a. DAC: CJC-1295 DAC · no-DAC: Mod GRF 1-29

GHRH analog

CJC-1295 is a synthetic analog of growth hormone-releasing hormone (GHRH), the natural signal.

§Dosing at a glance

1 protocol · from the research
What it's forDoseHow oftenHowFor how long
Animal model reference data2 mcgDailySubcutaneousInjected just under the skin, into the fat layer.

Approximate values pulled from the research — double-check before dosing.

§01Summary

CJC-1295 is a synthetic analog of growth hormone-releasing hormone (GHRH), the natural signal that prompts the pituitary gland to release growth hormone (GH). Unlike native GHRH, which breaks down within minutes, CJC-1295 is engineered to bind covalently to albumin — the most abundant protein in blood — giving it a half-life of approximately 5.8 to 8.1 days in humans1,3. This means a single injection can sustain elevated GH levels for nearly a week and raise insulin-like growth factor 1 (IGF-1) levels for up to 11 days1.

In clinical studies involving healthy adults, CJC-1295 has produced dose-dependent increases in GH concentrations of 2- to 10-fold above baseline1, and IGF-1 increases of roughly 45% following a single injection3. Notably, it appears to preserve the body's natural pulsatile pattern of GH release rather than replacing it with a flat, continuous signal3,11. Research interest has spanned healthy aging, body composition, and HIV-associated metabolic changes2, with the evidence base continuing to develop. CJC-1295 is classified as a prohibited performance-enhancing substance under WADA regulations14 and is not approved by the FDA for any therapeutic indication.

This is the layperson summary. Mechanism, dosing, the evidence base, and the published literature are in the sections below — every claim links to its source.

§02In depth

CJC-1295 is a 29-amino-acid synthetic analog of human growth hormone-releasing hormone (hGRF[1-29]) incorporating four amino acid substitutions designed to enhance proteolytic stability and introduce a reactive chemical handle for in vivo albumin conjugation6. The substitutions include replacement of susceptible residues to confer resistance to dipeptidylpeptidase-IV (DPP-IV), the enzyme primarily responsible for rapid N-terminal cleavage of native GHRH6. Critically, CJC-1295 contains a C-terminal N-epsilon-3-maleimidopropionamide lysine residue — a maleimido group that reacts spontaneously and covalently with the free thiol of Cys34 on circulating serum albumin following subcutaneous injection6,11. At least 90% of administered CJC-1295 undergoes this covalent albumin conjugation in vivo, with trace amounts also binding to fibrinogen and IgG11. This Drug Affinity Complex (DAC) technology effectively transforms an otherwise short-lived peptide into a long-circulating albumin-bound species.

The pharmacokinetic consequence of albumin conjugation is a plasma half-life of approximately 5.8–8.1 days in humans1, compared to minutes for unmodified GHRH. Albumin-bound CJC-1295 is detectable from 15 minutes through at least 24 hours post-injection, with Western blot confirming the conjugated form in circulation6. The extended half-life enables sustained receptor engagement at the GHRH receptor (GHRHR) on somatotroph cells of the anterior pituitary.

CJC-1295 activates the GHRHR — a Gs protein-coupled receptor — stimulating intracellular cAMP accumulation and downstream activation of protein kinase A, which drives both GH gene transcription and pulsatile GH secretion6. Notably, despite continuous GHRH receptor stimulation from the long-acting molecule, the normal somatotroph pulsatile secretion pattern is preserved; CJC-1295 primarily elevates trough (interpulse) GH concentrations rather than altering pulse frequency or amplitude3,11. This observation suggests that the hypothalamic somatostatin-regulated gating mechanism for GH pulse generation remains intact during CJC-1295 exposure, and that interpulse trough GH levels — rather than pulsatile parameters — may be a principal driver of downstream IGF-1 production3.

Elevated GH stimulates hepatic IGF-1 synthesis and secretion, producing IGF-1 increases of 45–200% depending on dose and measurement timepoint1,3. IGF-1 in turn mediates anabolic effects on muscle, bone, and adipose tissue via IGF-1 receptor (IGF1R) signaling. Proteomic analyses of serum following CJC-1295 administration have detected downstream changes including decreased apolipoprotein A1 and transthyretin isoforms and increased beta-hemoglobin and C-terminal albumin fragments, suggesting broad systemic metabolic effects of sustained GH/IGF-1 axis activation7. In animal models, CJC-1295 also stimulated somatotroph cell proliferation, as evidenced by increased pituitary GH mRNA and confirmed by immunohistochemistry4, indicating that chronic GHRHR stimulation may have trophic effects on the pituitary gland itself.

§04Evidence & efficacy

Evidence base
28Studies
11Human
5Animal

CJC-1295 has demonstrated consistent, dose-dependent activation of the GH/IGF-1 axis in human pharmacokinetic studies. A single subcutaneous injection produced GH increases of 2- to 10-fold above baseline lasting at least 6 days, and IGF-1 increases of 1.5- to 3-fold lasting 9 to 11 days1. With repeated weekly or biweekly dosing, IGF-1 levels appear to remain elevated above baseline for up to 28 days with a cumulative effect across injections1. These GH and IGF-1 effects have been replicated across independent human studies1,3,11, providing consistent pharmacodynamic evidence.

A mechanistically important finding is that CJC-1295 appears to preserve natural pulsatile GH secretion while elevating trough (interpulse) GH concentrations — a pattern distinct from exogenous GH administration3,11. The 7.5-fold increase in trough GH levels and 46% increase in mean GH levels observed at one week post-injection3 are consistent with this mechanism.

In animal models, once-daily CJC-1295 fully normalized body weight, body length, and bone length in GHRH-deficient mice, with partial normalization observed at less frequent dosing intervals4. Serum proteomic analysis in human subjects has identified downstream changes in apolipoprotein A1, transthyretin, and immunoglobulin/albumin fragment levels following CJC-1295 administration, suggesting broad GH/IGF-1-mediated systemic effects7.

For specific clinical indications — including body composition improvement, HIV-associated visceral adiposity, or anti-aging applications — human efficacy data is actively being developed, with early trials registered but results not yet published2.

§05Safety

In published human studies, CJC-1295 has been described as safe and relatively well tolerated, particularly at doses of 30 or 60 mcg/kg subcutaneously1. No serious adverse reactions were reported across the controlled human pharmacokinetic studies1. These studies were, however, short in duration and limited in sample size, so the characterization of tolerability reflects early-phase, limited-duration observation rather than comprehensive long-term surveillance.

In animal studies, CJC-1295 appeared well tolerated across all tested dosing intervals in mice, with no adverse events reported4. One notable preclinical finding is that daily CJC-1295 administration stimulated somatotroph cell proliferation in GHRH-knockout mice, evidenced by increased pituitary GH mRNA4 — a biological observation that ongoing and future research will help contextualize in long-term human use.

The sustained elevation of GH and IGF-1 levels — particularly the cumulative IGF-1 increases observed with repeated weekly or biweekly dosing1 — is an active area of physiological investigation. A broader review of GHRH analogs and related peptides used in athletic and image-enhancement contexts has identified theoretical concerns including cardiovascular strain, insulin resistance, and dyslipidemia as areas warranting study, though these have not been formally quantified in CJC-1295-specific clinical trials9.

A meaningful real-world safety concern is the widespread availability of CJC-1295 through unregulated black-market channels14,15,16, where product identity, purity, and dosage are unverified. Users in online communities have reported products not performing as expected and concerns about substituted or contaminated preparations10.

No drug interaction data, contraindication profiles, or long-term endocrine safety assessments have been published for CJC-1295 in peer-reviewed human studies.

§06History

CJC-1295 was developed by ConjuChem Biotechnologies, a Canadian biopharmaceutical company, as part of a Drug Affinity Complex (DAC) technology platform designed to extend the half-life of therapeutic peptides through in vivo albumin conjugation. The foundational chemistry was established in the early 2000s, with seminal mechanistic work published in 2005 identifying CJC-1295 — formally designated as a tetrasubstituted hGRF(1-29) analog with a C-terminal maleimidopropionamide lysine — as the lead long-acting GHRH compound6. This work demonstrated that subcutaneous injection leads to spontaneous covalent binding to Cys34 of serum albumin, producing a circulating bioconjugate with GH-stimulating activity persisting beyond 72 hours in rats6.

The first major human clinical pharmacokinetic study was published in December 2005, establishing CJC-1295's half-life of 5.8–8.1 days and its capacity to produce sustained, dose-dependent GH and IGF-1 elevation in healthy adults1. A complementary study published in 2006 confirmed preservation of pulsatile GH secretion during continuous CJC-1295 exposure3. ConjuChem proceeded to register a Phase 2 randomized controlled trial in HIV-associated visceral obesity around 20052, representing the compound's most advanced therapeutic development program; results from this trial have not been published in the peer-reviewed literature.

Despite the absence of regulatory approval or completed Phase 2–3 efficacy trials, CJC-1295 began appearing on illicit drug markets by the late 2000s. Norwegian authorities submitted a seized preparation for forensic identification in 200914, and forensic surveillance studies through the 2010s documented its global distribution in the bodybuilding and performance-enhancement community15,16. WADA classified CJC-1295 as a prohibited substance under Section S2 of its Prohibited List14, prompting development of increasingly sophisticated detection methodologies5,8,12. Research interest in anti-doping detection and real-world use patterns has continued into the 2020s9,10.

§07References