PART V — THE QUESTIONS
CJC-1295: Frequently Asked Questions
The questions readers most often ask about CJC-1295 — its mechanism, its half-life, its dose range, its discontinued clinical program — answered from the peer-reviewed record and cited where the answer is quantitative.
What is CJC-1295?
CJC-1295 is a 30-amino-acid synthetic analog of growth hormone-releasing hormone (GHRH 1-29), modified at four positions to resist DPP-IV degradation. Originally developed by ConjuChem in the early 2000s as a long-acting GH secretagogue, the DAC variant carries a C-terminal lysine-maleimide linker that covalently binds serum albumin, extending plasma half-life to several days [01][02].
What does CJC-1295 do to your body?
It binds the GHRH receptor on pituitary somatotrophs and amplifies the body's endogenous pulsatile growth hormone release, raising downstream IGF-1. In Teichman 2006, single subcutaneous doses in healthy adults produced two- to ten-fold GH elevations sustained for six days or more and 1.5- to 3-fold IGF-1 elevations sustained for nine to eleven [01].
What is the difference between CJC-1295 DAC and CJC-1295 no DAC?
DAC (drug affinity complex) is a maleimidopropionyl linker on a C-terminal lysine that covalently binds serum albumin, extending plasma half-life to 5.8-8.1 days [01][02]. Non-DAC, also called modified GRF 1-29, lacks this linker; its half-life is about 30 minutes and research protocols use multiple daily injections [13].
What is CJC-1295 half-life?
For the DAC variant, Teichman 2006 reported an estimated plasma half-life of 5.8 to 8.1 days in healthy human volunteers [01]. For the non-DAC variant (modified GRF 1-29), plasma half-life is approximately 30 minutes — extended from native sermorelin's sub-10-minute clearance by DPP-IV-resistant substitutions but no longer [04][13].
How long does it take to see results from CJC-1295?
Published trials measured GH and IGF-1 elevation within 24-48 hours of single subcutaneous dose; sustained IGF-1 elevation was observed across the 28-day multi-dose Phase 1 trial window [01]. Body-composition endpoints from Phase 2 (NCT00267527) were never published — the trial was terminated before completion [18].
What are the side effects of CJC-1295?
Phase 1 and Phase 2 trials reported injection-site reactions, transient flushing, and headache as the most common adverse events [01][18]. Mild peripheral edema, consistent with the class-level fluid-retention effect of GH-axis stimulation, was noted in a subset of subjects [06]. Long-term safety data is limited; the development program was discontinued before late-stage trials [07].
Is CJC-1295 safe?
The published Phase 1/2 record is limited and the compound is not FDA-approved for any indication [20]. Available short-term human data did not show severe adverse events at the doses studied (Teichman 2006, up to 250 mcg/kg single SC) [01]. Longer-term safety in healthy adults, in clinical populations, and at multi-year exposure is unestablished in the public peer-reviewed record.
Does CJC-1295 affect testosterone?
CJC-1295 acts on the GHRH/GH/IGF-1 axis and is not a direct modulator of the hypothalamic-pituitary-gonadal axis [01]. No published clinical trial of CJC-1295 has demonstrated a clinically meaningful change in serum testosterone in either sex. Mechanistically, the receptor (GHRHR) is expressed on pituitary somatotrophs, not gonadotrophs.
How does CJC-1295 raise growth hormone?
It binds pituitary GHRH receptors (GHRHR), amplifying the endogenous pulsatile release of GH from somatotrophs rather than supplying exogenous GH [05][20]. GHRHR is a Gαs-coupled class B GPCR; agonist binding raises cAMP, activates PKA, induces Pit-1, and triggers Ca2+ influx that drives GH vesicle exocytosis [05]. The DAC variant extends this signal across days through albumin binding.
What is the mechanism of action of CJC-1295?
CJC-1295 is a synthetic GHRH(1-29) analog with four amino-acid substitutions (D-Ala2, Gln8, Ala15, Leu27) for DPP-IV resistance [02]. The DAC variant additionally bears a C-terminal lysine with a maleimidopropionic acid linker that covalently couples to Cys34 of serum albumin in vivo, extending plasma persistence [02][12]. At the target receptor, agonism activates Gαs/cAMP/PKA/CREB/Pit-1 signaling and triggers calcium-mediated GH vesicle exocytosis from somatotrophs [05].
What dose of CJC-1295 was used in clinical trials?
Teichman 2006 used single subcutaneous ascending doses of 30, 60, 125, and 250 mcg/kg in healthy adults, and a multiple-dose arm at 30-60 mcg/kg weekly or biweekly over 28-49 days [01]. The Phase 2 HIV-lipodystrophy trial (NCT00267527) used weekly escalating doses across two arms (60-120 mcg/kg low, 60-240 mcg/kg high) over twelve weeks [18].
Is CJC-1295 FDA-approved?
No. CJC-1295 has never received FDA approval for any indication. ConjuChem suspended its clinical program in 2006 before late-stage trials [07]. In December 2024, the FDA Pharmacy Compounding Advisory Committee reviewed CJC-1295 (free base, acetate, and DAC variants) and the agency's published analysis did not support inclusion on the Section 503A Bulks List [20].
What is modified GRF 1-29?
Modified GRF 1-29 is the scientific name for tetrasubstituted GHRH(1-29) — chemically identical to non-DAC CJC-1295, with the same four amino-acid substitutions (D-Ala2, Gln8, Ala15, Leu27) but no albumin-binding linker [02]. Plasma half-life is approximately 30 minutes; research protocols use multiple daily subcutaneous injections [13].
How is CJC-1295 different from ipamorelin?
CJC-1295 is a GHRH analog that binds GHRH receptors (GHRHR) [02]. Ipamorelin is a growth hormone secretagogue receptor agonist that binds GHS-R1a, the ghrelin receptor [10]. Different receptors, different intracellular signaling pathways (Gαs/cAMP/PKA for GHRHR; Gq/PLC/IP3/Ca2+ for GHS-R1a), complementary effects on somatotroph GH exocytosis — which is why the two pathways are often studied together [10].
What is CJC-1295 made of?
A 30-residue peptide: the GHRH(1-29) backbone with four substitutions (D-Ala2, Gln8, Ala15, Leu27) plus a C-terminal lysine bearing — in the DAC variant — a maleimidopropionic acid group that conjugates to albumin in vivo [02][12]. The non-DAC variant has the same backbone with an amidated C-terminus and no linker.
Who developed CJC-1295?
ConjuChem Inc. of Montreal developed CJC-1295 in the early 2000s using its Drug Affinity Complex (DAC) albumin-binding technology [02][12]. The stated clinical goal was weekly subcutaneous dosing for adult GH deficiency. The original preclinical pharmacology paper (Jetté et al., Endocrinology, 2005) identifies CJC-1295 as the most potent of three maleimido hGRF(1-29) bioconjugates the company synthesized [03].
How long does CJC-1295 stay in your system?
DAC variant: detectable in plasma for roughly 14-21 days due to albumin binding, with effective signaling persisting six to eight days per dose [01][12]. Non-DAC (modified GRF 1-29): cleared in hours; the 30-minute half-life implies functional clearance within several hours of injection [13].
What is CJC-1295 used for in research?
It has been studied as a long-acting GH secretagogue in adult GH-deficiency models, in body-composition endpoints in healthy adults, and in animal models of muscle, bone, and fat metabolism [01][03][18]. The compound is also used in analytical and anti-doping research as a reference peptide for LC-MS detection method development [08][09][19].
Does CJC-1295 cause water retention?
GH elevation is mechanistically associated with sodium and water retention via increased renal tubular sodium reabsorption [22]. Published trials of CJC-1295 noted mild edema in a subset of subjects, consistent with this class-level GH-axis effect [06][22]. Tesamorelin Phase 3 trials reported peripheral edema in about 6% of patients versus 2% on placebo, framing the class-level prevalence [06].
How often is CJC-1295 administered in studies?
DAC variant: weekly subcutaneous injection in human Phase 1/2 trials, supported by the multi-day plasma half-life [01][18]. Non-DAC (modified GRF 1-29): multiple daily injections (typically 1-3 times/day) in research protocols owing to the 30-minute plasma half-life [13].
What endpoints did CJC-1295 trials measure?
Pulsatile GH amplitude and area-under-curve, mean serum GH, serum IGF-1, serum IGFBP-3, safety and adverse events, and pharmacokinetic parameters of the peptide itself (peak plasma concentration, half-life, time to peak) [01]. The Phase 2 lipodystrophy program added visceral adipose tissue by imaging as the primary efficacy endpoint, but that data was never published [18].
Was CJC-1295 ever tested in humans?
Yes. At least four Phase 1 and Phase 1/2 trials are documented in the published literature and trial registry, including the two ascending-dose trials reported in Teichman 2006 and the Phase 2 HIV-lipodystrophy trial NCT00267527 [01][18]. Late-stage development was halted in 2006.
Why was CJC-1295 development discontinued?
ConjuChem suspended its Phase 2 trial in 2006 following a fatality (myocardial infarction) in a Phase 2 participant; the investigator attributed the death to pre-existing coronary artery disease rather than CJC-1295 [07]. The sponsor wound down its broader DAC peptide program. CJC-1295 was never independently linked to the event in published reporting, but the program did not resume [07].
Does CJC-1295 cause cancer?
No published study has demonstrated a direct carcinogenic effect of CJC-1295 itself [21]. Sustained IGF-1 elevation is a class-level theoretical concern across the GH/IGF-1 axis because IGF-1 has mitogenic signaling activity, but this is a class-level monitoring concern noted in the broader GH-axis literature, not a CJC-1295-specific finding [21]. Long-term carcinogenicity of the peptide has not been characterized in the public literature.