§ FAQ·CJC-1295
Questions that come up.
Direct answers, each one sourced.
What is CJC-1295 and how was it developed?
CJC-1295 is a synthetic 30-amino-acid analog of human growth hormone-releasing hormone, built on the first 29 residues of native GHRH with four protective amino acid substitutions and a C-terminal maleimidopropionic acid linker. It was developed by ConjuChem Biotechnologies — a Montreal-based company — using their Drug Affinity Complex platform, which couples synthetic peptides to circulating serum albumin to extend half-life. The discovery paper appeared in Endocrinology in 2005 [1]. The molecule entered Phase 1 human studies that same year and a Phase 2 trial in HIV-associated visceral obesity (NCT00267527) the year after [7]. The Phase 2 was terminated in late 2006 and the program has not restarted under any sponsor since.
How does CJC-1295 work mechanistically?
CJC-1295 binds the GHRH receptor (GHRHR), a class-B G-protein-coupled receptor on anterior pituitary somatotrophs. Receptor binding activates a Gs/adenylyl cyclase/cAMP/PKA cascade that drives growth hormone gene transcription and pulsatile GH release. Hepatic IGF-1 production follows downstream of GH receptor activation. The four amino acid substitutions in the GRF(1-29) backbone — D-Ala at position 2, Gln at 8, Ala at 15, Leu at 27 — block enzymatic degradation routes that take native GHRH out of circulation in roughly seven minutes. The maleimide linker enables a covalent Michael-addition bond with cysteine 34 of serum albumin after injection, which tethers the peptide to a slow-clearance carrier protein [1][8].
What is the difference between CJC-1295 with DAC and CJC-1295 without DAC?
The two variants share the same modified GRF(1-29) backbone (the four protective substitutions). They differ in whether the C-terminal maleimidopropionic acid linker is present.
CJC-1295 with DAC carries the linker. After subcutaneous injection, the linker forms a covalent bond with the thiol on cysteine 34 of serum albumin, creating a long-lived peptide-albumin bioconjugate. Mean plasma half-life: 5.8 to 8.1 days [3].
CJC-1295 without DAC — properly called modified GRF(1-29) or Mod GRF 1-29 — lacks the linker and therefore lacks the albumin tether. Mean plasma half-life: approximately 30 minutes [8].
The two variants are not pharmacologically interchangeable. The DAC variant produces multi-day GH and IGF-1 elevation from a single dose. The non-DAC variant produces a short pulse of GH release and clears quickly. They are widely conflated in non-peer-reviewed sources.
What is the half-life of CJC-1295 in human studies?
The mean plasma half-life of CJC-1295 (DAC variant) in healthy adult humans is 5.8 to 8.1 days, as reported across dose cohorts in the Teichman Phase 1 [3]. The wide range reflects between-cohort variability and the practical limits of multi-day pharmacokinetic measurement.
The extended half-life is a direct consequence of the covalent bioconjugation to serum albumin. Albumin itself has a turnover measured in days, and the bound peptide is cleared at a comparable rate. Without the albumin tether, the half-life collapses to approximately thirty minutes [8].
What does the published human research literature actually show?
The published human evidence for CJC-1295 is narrow. The Teichman 2006 Phase 1 study in JCEM characterized PK and PD across four single-dose cohorts (30, 60, 125, 250 µg/kg subcutaneous) and several multi-dose cohorts in approximately eleven healthy adults per arm. Results: dose-dependent two- to tenfold elevation in mean plasma GH sustained for at least six days; 1.5- to 3-fold elevation in mean IGF-1 sustained for nine to eleven days after a single dose; sustained IGF-1 elevation up to twenty-eight days in multi-dose cohorts [2][3]. The Ionescu companion paper established that pulsatile GH secretion is preserved during CJC-1295 stimulation [4]. The Sackmann-Sala 2009 proteomic substudy identified five differentially expressed serum proteins one week after a single injection [6]. The Phase 2 trial in HIV-associated visceral obesity (NCT00267527, n=192) was terminated in 2006 and never published its primary endpoints [7]. No further sponsor-funded clinical development has occurred.
What happened to the CJC-1295 Phase 2 clinical trial?
The Phase 2 study NCT00267527 enrolled 192 participants with HIV-associated visceral obesity on a weekly subcutaneous dosing regimen. In October 2006, a participant died from an acute coronary event approximately two hours after receiving the eleventh weekly dose. An independent review attributed the event to pre-existing undiagnosed coronary artery disease and judged it unrelated to study drug [7].
The trial was halted. ConjuChem did not restart the program, and no subsequent sponsor has carried CJC-1295 forward into further clinical development. The primary efficacy endpoints from NCT00267527 were never published in a peer-reviewed journal. That absence is the central gap in the CJC-1295 clinical record.
Why is CJC-1295 commonly paired with ipamorelin in the research literature?
The pairing rationale is grounded in receptor pharmacology, not in a CJC-1295 trial.
CJC-1295 binds the GHRH receptor. Ipamorelin is a selective agonist of the growth hormone secretagogue receptor (GHS-R1a), the ghrelin receptor. Both receptors sit on the same pituitary somatotrophs and both drive GH release, but they do so through different signaling pathways. The two receptors can be activated together, and the combined signal is greater than either alone.
The mechanistic basis for this is foundational work by Bowers and colleagues, published in JCEM in 1990, which showed that combined IV administration of GHRH (1 µg/kg) and GHRP-6 (1 µg/kg) in healthy humans produced a GH secretory response several-fold larger than either agent given alone [9]. Ipamorelin replaces GHRP-6 in the contemporary pairing because it is more selective for the ghrelin receptor and has fewer off-target effects (less cortisol and prolactin elevation) than GHRP-6 or GHRP-2.
The specific CJC-1295 plus ipamorelin combination has not been characterized in a published peer-reviewed clinical trial. The pairing is widely used in research-peptide channels [10] on the strength of the underlying receptor-pharmacology rationale.
Is CJC-1295 FDA approved or available by prescription?
No. CJC-1295 is not approved by the FDA for any human indication. It is not legally prescribable to patients in the United States.
The FDA reviewed CJC-1295 (both DAC and non-DAC variants) at the October 29, 2024 Pharmacy Compounding Advisory Committee meeting for potential inclusion on the Section 503A bulk drug substances list. The committee did not recommend inclusion. CJC-1295 remains in 503A Category 2 — substances reviewed but not approved for routine pharmacy compounding [14]. A December 4, 2024 follow-up PCAC meeting consolidated public comment and adverse-event signal review for the growth-hormone-secretagogue peptide class and reiterated insufficient evidence to support routine 503A compounding access [15].
The word “prescribed” in this site’s domain name refers to the broader regulatory context — the FDA-review status of CJC-1295 — and not to any claim that the compound is currently legally prescribable.
What is CJC-1295’s status under WADA anti-doping rules?
CJC-1295 is on the World Anti-Doping Agency’s 2025 Prohibited List under Section S2 — Peptide Hormones, Growth Factors, Related Substances, and Mimetics. It is prohibited at all times — both in-competition and out-of-competition — for any athlete subject to WADA testing [16].
Routine WADA-compliant urine detection methods have been validated. Thomas and colleagues published nano-LC quadrupole/orbitrap mass spectrometry methods in 2024 capable of detecting CJC-1295 and related GHRH analogs at sub-nanogram-per-milliliter sensitivity in athlete urine, addressing the analytical challenges of peptide instability and very low urinary concentrations [12]. Identification of seized illicit preparations as CJC-1295 has been documented since 2010 [11].
Can CJC-1295 be obtained through a U.S. compounding pharmacy?
Not as part of routine compounding practice. CJC-1295 is in FDA 503A Category 2 — substances reviewed but not approved for inclusion on the Section 503A bulk drug substances list. The 2024 PCAC meetings reviewed but did not recommend the substance for that list [14][15]. Compounding pharmacies operating under 503A authority may not routinely use CJC-1295 as a bulk drug substance for patient prescriptions in the United States.
What doses were used in the published CJC-1295 studies?
The Phase 1 program by Teichman and colleagues used single subcutaneous doses at 30, 60, 125, and 250 µg/kg in cohorts of approximately eleven healthy adults each, plus multi-dose cohorts at weekly or biweekly intervals over 28 to 49 days [2]. The preclinical rescue study by Alba and colleagues in GHRH-knockout mice used 2 µg per injection (≈ 80 µg/kg) at intervals of 24, 48, or 72 hours over five weeks [5]. The Jetté discovery paper in rats used subcutaneous bolus dose-ranging at low µg/kg levels [1]. The Phase 2 trial (NCT00267527) used a weekly subcutaneous regimen, though the full µg/kg specification was not published before termination [7]. These are research-context doses. The site does not recommend any dose for any human use.
What side effects were reported in CJC-1295 clinical trials?
In the published Phase 1 program, the most common adverse events were transient injection-site reactions — pain, swelling, and induration at the subcutaneous injection site. Systemic adverse events were uncommon at the 30 and 60 µg/kg dose levels. The published data did not establish a dose-limiting toxicity in the cohorts studied [18].
Long-term safety has not been characterized in the published CJC-1295 literature. Theoretical concerns associated with sustained, supraphysiological GH and IGF-1 elevation — insulin resistance, edema, joint pain, and theoretical neoplasia risk — are documented in the broader endocrinology literature but have not been specifically characterized in CJC-1295 studies because the Phase 2 program did not complete.
Does CJC-1295 abolish the natural pulsatility of GH release?
No. The Ionescu and Frohman 2006 pharmacodynamic substudy found that a single subcutaneous dose of CJC-1295 raised the basal trough GH approximately 7.5-fold and elevated mean GH approximately 46 percent above baseline while preserving normal pulsatile GH architecture [4]. The pituitary continued to release GH in discrete bursts; the bursts simply sat on a higher baseline. This finding distinguishes CJC-1295’s GHRH-analog mechanism from exogenous recombinant GH, which delivers a flat continuous load and does not preserve pulsatility.
