All information below describes the compound's chemical identity, laboratory handling, and the published research literature. It describes molecular targets and results in laboratory and animal models only — not effects in humans — and is not evidence of any human benefit.
What Is CJC-1295 with DAC?
CJC-1295 with DAC (CAS 863288-34-0) is a synthetic peptide analogue of growth hormone-releasing hormone (GHRH). It incorporates a Drug Affinity Complex (DAC) modification, a design feature that has been characterized in the literature in relation to reversible serum-albumin binding and extended plasma persistence relative to unmodified GHRH analogues. It belongs to the class of synthetic GHRH-analogue peptides.
It is supplied as a reference compound for in vitro and animal research use only. The sections below summarize its chemical identity, laboratory handling, the molecular targets and model systems examined in the published literature, and the primary references — without describing outcomes, efficacy, or effects in humans.
Research Targets & Pathways
Published literature has examined CJC-1295 with DAC in relation to several molecular systems. These are pathway associations reported in laboratory, animal, and pharmacokinetic model systems; refer to the cited studies for methods and findings.
- GHRH receptor (GHRHR) — examined in relation to pituitary somatotroph signaling in GH-secretion and receptor-binding assays.
- Serum-albumin binding (DAC mechanism) — examined in relation to the half-life-extension mechanism, characterized as reversible albumin conjugation.
- GH / IGF-1 axis — examined in relation to somatotroph secretory dynamics and downstream IGF-1 signaling.
- Anti-apoptotic signaling pathways — examined in pancreatic beta-cell and cardiac cell-line assay systems.
- HIF-1α signaling — examined in cardiomyocyte model systems.
- Oxidative-stress and ferroptosis markers — examined in diabetic kidney-tissue model systems.
Model Systems Studied
CJC-1295 with DAC and related GHRH analogues have been used as test compounds across a range of published model systems. Refer to the cited literature for study designs, endpoints, and findings.
- Pituitary cell culture — GH-secretion assay systems.
- Receptor-binding assays — GHRH receptor binding and structure-activity assay systems.
- Rodent and primate models — somatotroph responsiveness and GH secretion-dynamics models.
- Cell lines — pancreatic beta-cell, cardiac cell, and cardiomyocyte model systems.
- Diabetic mouse kidney tissue — oxidative-stress and ferroptosis marker model systems.
- Aging model systems — GH-axis and IGF-1 signaling assessments.
- Clinical pharmacokinetics — early-phase (Phase 1/2) pharmacokinetic studies in healthy adult subjects.
Note: several of the 2025–2026 citations are recent preprints or early publications, and independent replication is ongoing.
Molecular & Technical Profile
C165H269N47O46 | MW 3647.28 g/mol | CAS 863288-34-0 | Synthetic GHRH analogue (no explicit residue sequence specified by source)
Storage, Reconstitution & Working Concentrations
Storage, reconstitution, and working-concentration values are general laboratory guidance for in vitro and animal research; always confirm against the lot-specific Certificate of Analysis.
Current Research Status
As of the time of this writing, CJC-1295 with DAC has not been approved by the U.S. Food and Drug Administration (FDA) for any human therapeutic use; the published regulatory literature likewise notes that CJC-1295 is not approved for human therapeutic use. Although CJC-1295 was evaluated in early-phase (Phase 1/2) clinical pharmacokinetic studies in healthy adults, no approved drug product exists. The research-grade material supplied by Explicit Research is a reference compound for laboratory research use only and is not an approved drug product. The available evidence base is primarily preclinical and pharmacokinetic, and several recent citations are preprints or early publications for which independent replication is ongoing.
Research FAQ
Is CJC-1295 with DAC approved for human use?
No. CJC-1295 with DAC has not been approved by the FDA for any human therapeutic use, and the published literature notes that CJC-1295 is not approved for human therapeutic use. Although it was evaluated in early-phase clinical pharmacokinetic studies, no approved drug product exists. It is supplied for laboratory research use only — not for human consumption.
What is CJC-1295 with DAC's molecular formula and sequence?
A synthetic GHRH analogue with molecular formula C165H269N47O46, MW 3647.28 g/mol, CAS 863288-34-0. The source reference material does not publish an explicit amino-acid residue sequence.
How is CJC-1295 with DAC stored and reconstituted?
Store lyophilized at −20°C, protected from light and moisture. Reconstitute in sterile or bacteriostatic water added slowly to the vial wall and swirled gently (do not vortex); store the reconstituted solution at 2–8°C and use within ~28 days, avoiding repeated freeze–thaw.
What targets and model systems has CJC-1295 with DAC been studied for?
Published work has examined the GHRH receptor, the GH/IGF-1 axis, reversible serum-albumin binding (the DAC half-life-extension mechanism), and downstream signaling pathways, across pituitary cell culture, GHRH receptor binding assays, rodent and primate somatotroph models, cardiac and pancreatic cell lines, diabetic kidney-tissue models, and early-phase clinical pharmacokinetic studies. Several 2025–2026 citations are recent preprints; independent replication is ongoing.
Selected References
- Jetté et al. — Characterization of the half-life extension mechanism of CJC-1295 via drug affinity complex (DAC) technology — J Pept Res, 2005.
- Teichman et al. — Prolonged stimulation of GH and IGF-1 secretion measured in healthy adults following single and multiple doses of CJC-1295, a long-acting GHRH analog — J Clin Endocrinol Metab, 2006.
- Ionescu and Frohman — GHRH receptor binding and structure-activity relationships of synthetic GHRH analogs — Endocr Rev, 2006.
- Frohman et al. — Pituitary somatotroph responsiveness to GHRH and GH secretion dynamics measured in rodent and primate models — Endocrinology, 1999.
- Thorner et al. — Somatotroph cell responsiveness and GH pulse amplitude measured following GHRH analog administration in humans — J Clin Endocrinol Metab, 1988.
- Popovic et al. — GH secretory dynamics measured across dosing intervals in healthy subjects administered long-acting GHRH peptide analogs — Eur J Endocrinol, 1998.
- Vance et al. — IGF-1 serum concentrations and pulsatile GH release patterns measured in GH-deficient adults following GHRH analog treatment — J Clin Endocrinol Metab, 1995.
- Alba et al. — Serum protein profile changes measured in normal adult subjects following GH/IGF-1 axis activation by CJC-1295 — Growth Horm IGF Res, 2009.
- Mavrych et al. — GH axis activation and downstream IGF-1 signaling assessed in aging models with GHRH agonist treatment — Front Aging, 2026.
- Yarasheski et al. — Muscle protein fractional synthesis rate measured by stable isotope tracer methods in GH-treated older adults — J Clin Endocrinol Metab, 2001.
- Böger et al. — Lean body mass and nitrogen retention measured in GH-deficient subjects following IGF-1 axis restoration — Metabolism, 1997.
- Salomon et al. — Body composition changes including fat mass reduction and lean mass increase measured in GH-deficient adults receiving GH replacement — N Engl J Med, 1992.
- Mayfield et al. — Lean mass accrual and muscle protein synthesis markers measured in preclinical models following sustained GHRH analog exposure — Am J Sports Med, 2026.
- Coutinho et al. — Skeletal muscle hypertrophy indices and body composition metrics assessed in exercise-model subjects treated with GH-stimulating peptides — J Sports Med Phys Fitness, 2026.
- Nørrelund et al. — Lipolytic flux and free fatty acid mobilization measured by tracer dilution in GH-treated fasting subjects — J Clin Endocrinol Metab, 1999.
- Møller et al. — Visceral adipose tissue reduction and lipid oxidation rates measured in GH-deficient adults following GH axis stimulation — J Clin Endocrinol Metab, 2004.
- Johannsson et al. — Regional body fat distribution and metabolic substrate utilization measured in GH-deficient adults on GH therapy — Int J Obes Relat Metab Disord, 1996.
- Granata et al. — GHRH receptor signaling and anti-apoptotic pathway activation measured in pancreatic beta-cell and cardiac cell lines — PLoS One, 2015.
- Paulino et al. — HIF-1alpha cardiomyocyte expression and cardioprotective signaling pathways measured in GHRH-treated cardiac cell models — bioRxiv, 2025.
- Chen et al. — Oxidative stress markers and ferroptosis indices measured in diabetic mouse kidney tissue following GHRH agonist MR409 treatment — Front Pharmacol, 2025.
