This blend is strictly for laboratory research and is commonly employed in the following investigational areas:

Synergistic Somatotropic Axis Modulation

The blend is utilized as a chemical probe to study the complex biophysics of pituitary receptor activation. Researchers use it to quantify the massive, synergistic release of GH when the GHRH receptor and the ghrelin receptor are activated simultaneously, effectively overriding endogenous somatostatinergic tone in isolated neuroendocrine models.

Episodic Pulsatility and Endocrine Senescence

Unlike long-acting DAC-conjugated analogues, CJC 1295 no DAC is employed in this blend to observe acute neuroendocrine rhythms. Experimental protocols assess how short-duration, high-amplitude receptor stimulation impacts physiological GH pulsatility and maintains receptor sensitivity over time.

Cardioprotection & Ischemia-Reperfusion (I/R) Injury

Because of Hexarelin’s CD36 receptor affinity, the blend is heavily researched in cardiovascular models. Assays focus on quantifying the reduction of infarct size, the preservation of left ventricular (LV) ejection fraction, and the prevention of cardiomyocyte apoptosis following experimentally induced myocardial ischemia and reperfusion.

Lipid Metabolism & Extracellular Matrix Remodeling

Experimental protocols evaluate the blend for its broad metabolic properties. Studies investigate Hexarelin’s ability to upregulate specific sterol transporters via peroxisome proliferator-activated receptor (PPAR)-γ pathways, while simultaneously measuring the downstream lipolytic effects of the amplified, pulsatile GH release driven by the CJC 1295 no DAC component.

Pathway / Mechanistic Context

The primary mechanism of action for this blend involves the integration of distinct cellular signaling pathways spanning both endocrine and cardiovascular systems:

• GHRHR Activation (CJC 1295 no DAC): Binds to GHRHR, activating adenylate cyclase, which increases intracellular cAMP and stimulates GH synthesis and episodic release.
• GHSR-1a Activation (Hexarelin): Binds to the ghrelin receptor, activating the phospholipase C (PLC) pathway to trigger an influx of intracellular calcium, driving immediate GH vesicle exocytosis. The simultaneous activation of both GHRHR and GHSR-1a results in a highly amplified, synergistic hormonal pulse.
• CD36 Receptor Activation (Hexarelin): Binds to the CD36 scavenger receptor on peripheral tissues (cardiomyocytes, endothelial cells). This initiates downstream transcriptional activation of PPARγ, which upregulates target genes involved in cellular lipid metabolism and directly attenuates cardiac fibrosis by reducing collagen I and III mRNA expression.

Preclinical Research Summary

Published preclinical literature documents investigations of these constituent peptides across multiple experimental models:

• Neuroendocrine Synergy: Studies demonstrate that co-administration of GHRH analogues and GHRPs (like Hexarelin) elicits a GH pulse significantly greater than the sum of their individual effects, due to complementary intracellular signaling cascades and the direct inhibition of endogenous somatostatin.
• Cardiovascular Recovery: In myocardial infarction models, Hexarelin administration significantly preserves left ventricular function, reduces interstitial collagen deposition, and decreases pro-inflammatory cytokine expression (e.g., TNF-α).
• Receptor Sensitivity: In isolated cellular models, the ~30-minute half-life of Modified GRF (1-29) combined with the acute action of Hexarelin maintains optimal somatotroph responsiveness, preventing the receptor downregulation typically seen with continuous exposure to long-acting bioconjugates.
• Metabolic Homeostasis: Data from nonobese insulin-resistant models show that targeted GHSR/CD36 activation improves glucose tolerance, decreases hepatic triglycerides, and corrects abnormal body composition by facilitating localized adipocyte differentiation.

Form & Analytical Testing

This material is produced via robust chemical synthesis and supplied as a lyophilized (freeze-dried) powder.

• Lyophilization: Removes water content under vacuum to maintain compound integrity and extend shelf-life.
• Identity Verification: Each lot undergoes Mass Spectrometry (MS) to confirm molecular weight and identity.
• Purity Verification: High-Performance Liquid Chromatography (HPLC) is performed to ensure the product meets the ≥99% purity standard required for reproducible research data.

Referenced Citations

References are provided for informational purposes only and are not clinical claims.

• Bodart, V., et al. (2002). CD36 Mediates the Cardiovascular Action of Growth Hormone-Releasing Peptides in the Heart. Circulation Research. https://doi.org/10.1161/01.res.0000016164.02525.b4
• Jetté, L., Léger, R., Thibaudeau, K., et al. (2005). Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog. Endocrinology. https://doi.org/10.1210/en.2004-1286
• Zhao, I. G., et al. (2011). Chronic administration of hexarelin attenuates cardiac fibrosis in the spontaneously hypertensive rat. American Journal of Physiology-Heart and Circulatory Physiology.https://pubmed.ncbi.nlm.nih.gov/22842067/
• Soule, S., King, J. A., Millar, R. P. (1994). Incorporation of D-Ala2 in growth hormone-releasing hormone-(1-29)-NH2 increases the half-life and decreases metabolic clearance in normal men. The Journal of Clinical Endocrinology & Metabolism. https://doi.org/10.1210/jcem.79.4.7962295
• McDonald, H., et al. (2020). Hexarelin targets neuroinflammatory pathways to preserve cardiac morphology and function in a mouse model of myocardial ischemia-reperfusion. Biomedicine & Pharmacotherapy. https://doi.org/10.1016/j.biopha.2020.110165
• Berti, F., et al. (1998). Hexarelin exhibits protective activity against cardiac ischaemia in hearts from growth hormone-deficient rats. Growth Hormone & IGF Research.https://pubmed.ncbi.nlm.nih.gov/10990152/
• Mao, Y., et al. (2014). One dose of oral hexarelin protects chronic cardiac function after myocardial infarction. Peptides. https://doi.org/10.1016/j.peptides.2014.04.004
• Huang, J., et al. (2007). Hexarelin suppresses cardiac fibroblast proliferation and collagen synthesis in rat. American Journal of Physiology-Heart and Circulatory Physiology. https://doi.org/10.1152/ajpheart.00004.2007
• Teichman, S. L., Neale, A., Lawrence, B., et al. (2006). Prolonged Stimulation of Growth Hormone (GH) and Insulin-Like Growth Factor I Secretion by CJC-1295, a Long-Acting Analog of GH-Releasing Hormone, in Healthy Adults. The Journal of Clinical Endocrinology & Metabolism. https://doi.org/10.1210/jc.2005-1536
• Mosa, R., et al. (2017). Hexarelin, a Growth Hormone Secretagogue, Improves Lipid Metabolic Aberrations in Nonobese Insulin-Resistant Male MKR Mice. Endocrinology. https://doi.org/10.1210/en.2017-00168
• Maheshwari, H. G., et al. (1999). Selective Lack of Growth Hormone (GH) Response to the GH-Releasing Peptide Hexarelin in Patients with GH-Releasing Hormone Receptor Deficiency. The Journal of Clinical Endocrinology & Metabolism.https://pubmed.ncbi.nlm.nih.gov/10084578/
• Korbonits, M., et al. (1999). The growth hormone secretagogue hexarelin stimulates the hypothalamo-pituitary-adrenal axis via arginine vasopressin. The Journal of Clinical Endocrinology & Metabolism. https://doi.org/10.1210/jcem.84.7.5811
• Torsello, A., et al. (2004). Hexarelin modulates the expression of growth hormone secretagogue receptor type 1a mRNA at hypothalamic and pituitary sites. Neuroendocrinology. https://doi.org/10.1159/000080793
• Dixit, V. D., et al. (2002). Growth Hormone Secretagogue (GHS) Analogue, Hexarelin Stimulates GH From Peripheral Lymphocytes. Hormone and Metabolic Research. https://doi.org/10.1055/s-2002-34991
• Locatelli, V., et al. (1997). Cardiac ischemia and impairment of vascular endothelium function in hearts from growth hormone-deficient rats: protection by hexarelin. European Journal of Pharmacology. https://doi.org/10.1016/s0014-2999(97)01178-3

• Stable at room temperature for up to 90 days. For long-term storage, keep at -20°C (-4°F) or colder.
• Once mixed with a solvent (e.g., bacteriostatic water), the solution must be stored at 4 °C (39°F) and utilized within 30 days. Avoid repeated freeze-thaw cycles, as this degrades the peptide structure.

RESEARCH USE ONLY

This product is intended strictly for laboratory research use only. It is not for human or veterinary use. It is not intended for diagnosis, treatment, cure, or prevention of any disease. All purchases are subject to our Terms of Service and Purity Guarantee.

No COAs available for this product.