Hexarelin

Compound Identification and Classification

Hexarelin, alternatively designated as Examorelin, functions as a laboratory-designed duplicate of the naturally occurring hormone ghrelin. Its chemical blueprint shows remarkable resemblance to GHRP-6, differentiated solely through inclusion of two supplementary methyl groups onto GHRP-6's molecular framework. The substance shows effectiveness when ingested orally or administered by injection, with selective binding to specific cellular targets. Scientific investigation has concentrated substantially on assessing its value in maintaining cardiac cell viability in circumstances of reduced blood supply and cellular nutrient scarcity.

Hexarelin Structure

Pharmacological Effects and Cellular Actions

Myocardial Protection and Adaptation

Hexarelin provides cardioprotective benefits by connecting with receptor proteins designated CD36 and the growth hormone secretagogue receptor system. Multiple animal investigations confirm hexarelin prevents the destructive remodeling of ventricular structure and inhibits cell death mechanisms in heart muscle cells. Experimental subjects treated with hexarelin exhibited strengthened cardiac output, extended lifespan of heart cells, and decreased cardiac cell death indicators. Investigations also observed that GHRP-6 performed either equivalently or better compared to the natural hormone ghrelin.

Related investigation into GHRP-6 addressed its effectiveness against heart failure by establishing diminished oxidative cellular damage and cessation of destructive ventricular remodeling. The therapy functions through modification of PTEN expression and reduction of protein kinase B activation—both essential for cellular restoration and cellular longevity. By encouraging parasympathetic system dominance in place of sympathetic activation, GHRP-6 generates extended cardiac stability. Post-surgical application resulted in 40% less scar formation in examined tissue.

The underlying mechanism provides protection independent of conventional calcium-dependent cardiac disease processes, making it beneficial for numerous cardiac injury categories, including those stemming from ion imbalance pathways.

Plasma Lipid Profile Enhancement

Dyslipidemia—a disorder involving excessive blood lipids—functions as an isolated indicator predicting future diabetes risk. Statistics indicate dyslipidemia occurrence in metabolically standard subjects. This issue potentially clarifies the expanding diabetes epidemic in weight-excess populations of affluent societies. Research with test animals shows GHRP-6 can overturn faulty insulin metabolism and create positive alterations in lipid concentrations alongside decreasing blood glucose and insulin abnormalities. This substance demonstrates potential in treating acute dyslipidemia manifestations.

Skeletal Tissue Preservation and Function

Beyond cardiac tissue defense, hexarelin guards skeletal muscle fibers. Investigational models of wasting syndrome—extreme weight loss from disease or chemotherapy exposure—demonstrate hexarelin maintains muscle fiber cell structures by managing internal calcium stability and resolving mitochondrial malfunction. Faulty mitochondria result in cellular energy reduction, leading eventually to cell death.

Chemotherapy commonly disrupts typical calcium equilibrium, contributing substantially to muscle fiber breakdown. Test outcomes indicate GHRP-6 corrects calcium dysregulation and mitochondrial deterioration accountable for muscle cell loss.

Research Development Status and Constraints

Cardiovascular illness represents the foremost cause of mortality in technologically sophisticated populations. Comprehending complex cardiac disease mechanisms presents obstacles, though hexarelin-type peptides assist scientific experts in unraveling cardiac operation in wellness and pathology. These investigations have enabled creation of novel therapeutic approaches for historically challenging conditions including cardiac chamber enlargement and systolic impairment.

Toxicological evaluation shows moderate side effects, restricted oral delivery capability, and strong parenteral transmission in test animals. Mathematical translation of animal dose measurements to human applications lacks supporting evidence.

Hexarelin access remains confined to scholarly and scientific investigation only. Human consumption applications are prohibited. Only institutional research professionals with proper credentials may obtain hexarelin compound.

Investigator and Contributor Information

Dr. Logan, M.D. performed examination, collation, and arrangement of scientific resources. Dr. Logan maintains a medical doctorate from Case Western Reserve University School of Medicine combined with undergraduate credentials in molecular biology.

Anne Moulin maintains investigation partnerships with France's National Center for Scientific Research (CNRS). Her specializations incorporate synthetic organic compound creation, peptide construction, creation supervision, purity administration, regulatory framework compliance, therapeutic molecule distribution, and discovery of pharmaceutical substances. She maintains extensive authorship of investigative publications examining pharmaceutical suppression characteristics.

Anne Moulin neither endorses nor promotes the procurement, circulation, or consumption of this substance. Neither Peptide Sciences nor Anne Moulin maintain any formal or inferred business connection. The reference objective honors the intensive scientific contributions of hexarelin research investigators. Anne Moulin is referenced in [12].

Referenced Citations

1. J. Huang, Y. Li, J. Zhang, Y. Liu, and G. Lu, "The Growth Hormone Secretagogue Hexarelin Protects Rat Cardiomyocytes From in vivo Ischemia/Reperfusion Injury Through Interleukin-1 Signaling Pathway," Int. Heart J., vol. 58, no. 2, pp. 257–263, Apr. 2017.
2. Y. Mao et al., "Hexarelin treatment in male ghrelin knockout mice after myocardial infarction," Endocrinology, vol. 154, no. 10, pp. 3847–3854, Oct. 2013.
3. E. Aglio et al., "Modulation of PTEN by hexarelin attenuates coronary artery ligation induced heart failure in rats," Turk. J. Med. Sci., vol. 49, no. 3, May 2019.
4. H. McDonald et al., "Hexarelin treatment preserves myocardial function and reduces cardiac fibrosis in a mouse model of acute myocardial infarction," Physiol. Rep., vol. 6, no. 9, p. e13699, 2018.
5. X. Xu et al., "Chronic administration of hexarelin attenuates cardiac fibrosis in the spontaneously hypertensive rat," Am. J. Physiol. Heart Circ. Physiol., vol. 303, no. 6, pp. H703-711, Sep. 2012.
6. X. Zhang, L. Qu, L. Chen, and C. Chen, "Improvement of cardiomyocyte function by in vivo hexarelin treatment in streptozotocin-induced diabetic rats," Physiol. Rep., vol. 6, no. 4, 2018.
7. Y. Mao, T. Tokudome, I. Kishimoto, K. Otani, M. Miyazato, and K. Kangawa, "One dose of oral hexarelin protects chronic cardiac function after myocardial infarction," Peptides, vol. 56, pp. 156–162, Jun. 2014.
8. Y. Ma, L. Zhang, J. N. Edwards, B. S. Launikonis, and C. Chen, "Growth hormone secretagogues protect mouse cardiomyocytes from in vitro ischemia/reperfusion injury through regulation of intracellular calcium," PloS One, vol. 7, no. 4, p. e35265, 2012.
9. R. Muset et al., "Hexarelin, a Growth Hormone Secretagogue, Improves Lipid Metabolic Alterations in Nonobese Insulin Resistant Male MICK Mice," Endocrinology, vol. 159, no. 10, pp. 3174–3187, 01 2017.
10. G. Singer et al., "Growth hormone secretagogues hexarelin and JMV2894 protect skeletal muscle from mitochondrial damages in a rat model of cisplatin-induced cachexia," Sci. Rep., vol. 7, 06 2017.
11. E. Conte et al., "Growth hormone secretagogues prevent dysregulation of skeletal muscle calcium homeostasis in a rat model of cisplatin-induced cachexia," J. Cachexia Sarcopenia Muscle, vol. 8, no. 3, pp. 386–404, Jun. 2017.
12. Torsello, Antonio & Bresciani, Elena & Tarrazzo, Laura & Bulgarelli, Ilaria & Caprioli, Simona & Moulin, Aline & Fehrentz, Jean-alain & Martinez, Jean & Deghenghi, David & Locatelli, Vittorio. (2008). Novel hexarelin analogs stimulate the secretion of peptide ligands of ghrelin receptor - characterization of endocrine and extraendocrine effects.