CJC-1295: A 30-amino-acid GHRH analog with one published Phase 1 study and one halted Phase 2.

The short version

CJC-1295 is a synthetic analog of the peptide that tells your pituitary to release growth hormone (GH). It was engineered in two forms: one that clears in about 30 minutes (no-DAC) and one that stays active for up to eight days by binding to a protein in your blood (DAC). One published Phase 1 study in healthy adults showed it raises GH and IGF-1 — a growth-related hormone — for days. A Phase 2 trial was stopped in 2006 before it could read out results. The compound is not approved by the FDA for any use, is prohibited in sport under WADA rules, and is sold only as a research chemical. See the effects page for what people report in research-use communities.

What CJC-1295 is

CJC-1295 is a synthetic 30-amino-acid analog of growth hormone-releasing hormone (GHRH). The first 29 residues correspond to human GHRH(1-29) with four protective amino-acid substitutions — D-alanine at position 2, glutamine at position 8, alanine at position 15, and leucine at position 27 — that confer resistance to dipeptidyl peptidase-4 (DPP-4) and to deamidation ^[1]. The 30th modification is a C-terminal maleimidopropionic acid group. After subcutaneous injection, that maleimide reacts with the free thiol on cysteine 34 of circulating serum albumin and forms a covalent peptide-albumin bioconjugate ^[1].

This bioconjugation is what makes CJC-1295 'long-acting.' Native human GHRH has a plasma half-life of roughly seven minutes; the modified GRF(1-29) backbone alone extends that to about thirty minutes; the DAC variant — once tethered to albumin — has a measured plasma half-life of 5.8 to 8.1 days in healthy adults ^[2].

The compound is sometimes sold and discussed in two forms. 'CJC-1295 with DAC' carries the maleimide and binds albumin. 'CJC-1295 without DAC' (more accurately called modified GRF(1-29) or 'mod GRF 1-29') is the 29-residue substituted backbone without the maleimide. The two have substantially different pharmacokinetic profiles. They are routinely conflated in non-peer-reviewed sources.

What the human research record actually contains

The published human evidence on CJC-1295 is unusually narrow and well-bounded.

The primary citation is Teichman and colleagues, 2006, in the Journal of Clinical Endocrinology and Metabolism ^[2]. The paper reports two randomized, placebo-controlled, double-blind ascending-dose Phase 1 trials over 28 and 49 days in healthy adults aged 21 to 61. Single subcutaneous injections produced dose-dependent rises in mean plasma growth hormone of two- to ten-fold for six days or more, and rises in mean plasma IGF-1 of 1.5- to three-fold for nine to eleven days. Multiple-dose cohorts maintained IGF-1 above baseline for up to 28 days. No serious adverse reactions were reported.

A second clinical program — a Phase 2 randomized, double-blind, placebo-controlled trial in HIV-associated visceral adiposity, NCT00267527, enrolled 192 participants beginning December 2005 ^[3]. The trial was terminated in October 2006 after a participant died of an acute coronary event approximately two hours after the eleventh weekly dose. An independent review attributed the death to undiagnosed pre-existing coronary artery disease and judged the event unrelated to study drug. Primary outcome data were never published. The sponsor's commercial development of CJC-1295 effectively ended at that point.

That is the entirety of the prospective human clinical record.

What survives, mechanistically

Several pieces of preclinical and mechanistic work continue to anchor the compound's biological plausibility.

Alba and colleagues, 2006, demonstrated that once-daily subcutaneous CJC-1295 normalized linear growth and body weight in GHRH-knockout mice over five weeks at 2 micrograms per injection, and increased somatotroph proliferation in the pituitary ^[4]. Ionescu and Frohman, 2006, demonstrated in human pharmacodynamic substudies that a single CJC-1295 dose preserved pulsatile growth hormone secretion while raising trough GH approximately 7.5-fold — a profile distinct from the tonic flooding produced by exogenous recombinant GH ^[5]. Sackmann-Sala and colleagues, 2009, identified candidate serum protein biomarkers of GH/IGF-1 axis activation one week after a single CJC-1295 injection ^[6].

The combined picture is consistent: CJC-1295 binds the GHRH receptor on anterior pituitary somatotrophs, activates the Gs/adenylyl-cyclase/cAMP/PKA cascade, drives GH gene transcription and pulsatile release, and — because of the albumin tether — does so over days rather than minutes. The downstream IGF-1 elevation is the dominant biochemical signature.

Regulatory and anti-doping status

CJC-1295 is not approved by the U.S. Food and Drug Administration, the European Medicines Agency, or any other major regulator for any human indication. Development ended after the 2006 Phase 2 termination.

In 2023 the FDA classified CJC-1295 under Section 503A bulk drug substances list Category 2, effectively prohibiting routine compounding pharmacy use. The Pharmacy Compounding Advisory Committee reviewed CJC-1295 alongside several related peptides at meetings in October and December 2024 ^[7][8]. The committee did not recommend its inclusion on the 503A bulks list.

The World Anti-Doping Agency lists CJC-1295 under Section S2 — Peptide Hormones, Growth Factors, Related Substances, and Mimetics — and prohibits it at all times, in- and out-of-competition, for any athlete subject to the WADA Code ^[9]. Detection methods using nano-LC orbitrap mass spectrometry are validated for routine doping-control urine analysis ^[10].

How this site is organized

This is a research-summary site, not a clinic, a vendor, or a treatment provider. The pages are organized for a reader who wants to start from the published record and work outward:

• Research — mechanism, the Teichman 2006 paper in detail, the Alba 2006 mouse study, and the terminated Phase 2 program.
• Dosage — what doses were used in the published studies, route, half-life, and pharmacokinetic comparisons with related GHRH analogs. This page describes what was studied; it does not recommend doses for humans.
• FAQ — the questions a careful reader brings to this compound: DAC vs without DAC, why pulsatile secretion matters, what happened to the Phase 2 trial, and where the regulatory line is.
• References — every citation used on the site, with DOI and PubMed link.
• About — editorial standards, what this site is and is not.
• Contact — how to send corrections.

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