Гексарелин, также называемый Эксаморелин, является синтетическим аналогом грелина и тесно связан с GHRP-6. Фактически, гексарелин и GHRP-6 отличаются друг от друга лишь незначительно благодаря добавлению к GHRP-6 двух метильных групп. Гексарелин, как и многие аналоги грелина, активен и высокоселективен при пероральном и сублингвальном приеме. Гексарелин тщательно исследовался на предмет его влияния на выживаемость клеток сердца после ишемии и дефицита питательных веществ.

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Источник:PubChem

Последовательность:His-D-Trp(2-Me)-Ala-Trp-D-Phe-Lys
Молекулярная формула:С₄₇ЧАС₅₈Н₁₂О₆
Молекулярный вес:887,059 г/моль
Идентификатор клиента PubChem:6918297
Номер КАС:140703-51-1

1. Защищает сердце

Гексарелин напрямую влияет на сердце, связываясь с рецептором CD36 и рецептором, стимулирующим секрецию гормона роста (GHSR). Исследования на мышах показывают, что гексарелин защищает клетки сердца от повреждений при сердечном приступе, связываясь с этими рецепторами и предотвращая апоптоз клеток (запрограммированную гибель клеток). У мышей, получавших гексарелин в этом исследовании, наблюдалось улучшение функции сердца, увеличение количества выживших клеток сердца и снижение выработки малонового диальдегида (маркера гибели клеток сердца). Интересно, что в этом исследовании было обнаружено, что GHRP-6 немного превосходит грелин.^{[1], [2]}.

A study in rats investigating the ability of GHRP-6 to offset problems associated with heart failure found that the peptide reduces oxidative stress in heart failure and prevents myocardial remodeling from taking place. Remodeling is a pathological process associated with a decline in heart function and serious morbidity. Rats treated with GHRP-6 in this study had significant improvements in the function of their heart. These processes are thought to be mediated by GHRP-6 up-regulation of phosphatase and tensin homologue (PTEN) activity as well as down regulation of protein kinase B expression^[3]. PTEN plays a role in cell regeneration while protein kinase B regulates cell survival.

GHRP-6 is so effective in reducing cardiac remodeling that it shifts the balance of nervous system activity away from sympathetic stimulation (higher heart rate, higher blood pressure, etc.) toward parasympathetic dominance. This not only improves short-term health and outcomes, but reduces the need for medication over the long term and likely helps to prevent cardiac remodeling that is secondary to increased stress on the heart. Rats treated with GHRP-6 following a heart attack show substantial reductions in the size of the scar left behind^{[4], [5]}.

Size of damage following heart attack at 24 hours and 14 days in rats treated with standard care or standard care plus hexarelin.
Source: PubMed

Because the mechanism by which hexarelin protects heart cells is not specific to the mechanism of damage in heart attack, researchers speculated that the peptide could be used to protect the heart from other insults as well. Research, again in rats, found that hexarelin improved cardiac function in a model of diabetes by changing the way calcium and potassium are processed by heart muscle cells^[6]–[8].

Diagram showing progression to serious long-term disease following heart attack. Blue ovals indicate how hexarelin interferes with this pathway.
Source: PubMed

2. Improves Fat Measures

Dyslipidemia refers to an abnormal amount of fat in the blood. Interestingly, dyslipidemia is an independent risk factor for the development of diabetes, even in thin and outwardly healthy individuals. In fact, dyslipidemia may help to explain the current diabetes crisis in first-world nations and understanding its effects on human physiology is paramount to combating the growing health concerns associated with modern diets. Research in rats indicates that GHRP-6 can correct dyslipidemia in the setting of insulin resistance (the first step in the pathway to diabetes) while simultaneously lowering blood sugar and insulin resistance^[9]. The peptide may offer an alternative to current lipid medications for the treatment of severe dyslipidemia.

3. Protects Muscle

It isn’t just heart muscle that hexarelin protects. Studies in rat models of cachexia (extreme weight loss due to illness or chemotherapy) indicate that GHRP-6 protects muscle cells by regulating calcium flow as well as mitochondrial dysfunction^[10]. Mitochondria are the power plants of cells. Without them, cells cannot produce the energy they need to carry out normal function and will eventually die.

Calcium regulation is often disrupted by chemotherapy. Calcium dysregulation is one of the primary reasons that muscle mass and lean body mass are affected during cancer treatment. Research in rats indicates GHRP-6 offsets the alterations in calcium regulation caused by chemotherapy^[11].

A. Mitochondrial DNA content relative to control
B. Content of MCH1 and MHC2A mRNA
C. Protein content of of muscle cells relative to controlled
Source: PubMed

Heart disease is the leading cause of death in most developed nations. Understanding the complex process that leads to heart disease, heart failure, and eventually death is not easy, but scientists are beginning to unravel the mystery with help from peptides like hexarelin. Research utilizing hexarelin has revealed a number of new pathways for understanding the function of the heart in health and disease. It has also opened the door to develop new treatments for problems, like cardiac remodeling, that have proved difficult to treat in the past.

Hexarelin exhibits moderate side effects, low oral and excellent subcutaneous bioavailability in mice. Per kg dosage in mice does not scale to humans. Hexarelin for sale at

The above literature was researched, edited and organized by Dr. Logan, M.D. Dr. Logan holds a doctorate degree from Case Western Reserve University School of Medicine and a B.S. in molecular biology.

Aline Moulin’s research while affiliated with French National Centre for Scientific Research and other places are extensive. She is well versed in pharmaceutical development, management, external manufacturing operations, quality control, regulatory control, drug delivery, and drug discovery research. She has used Hexarelin in multiple studies to monitor if certain pharmaceuticals were capable of inhibiting many of its effects.

Aline Moulin’s is being referenced as one of the leading scientists involved in the research and development of Hexarelin. In no way is this doctor/scientist endorsing or advocating the purchase, sale, or use of this product for any reason. There is no affiliation or relationship, implied or otherwise, between

1. J. Huang, Y. Li, J. Zhang, Y. Liu, and Q. 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. [PubMed]
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. [PubMed]
3. E. Agbo 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. [PubMed]
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. [PubMed]
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. [PubMed]
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. [PubMed]
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. [PubMed]
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. [PloS One]
9. R. Mosa et al., “Hexarelin, a Growth Hormone Secretagogue, Improves Lipid Metabolic Aberrations in Nonobese Insulin-Resistant Male MKR Mice,” Endocrinology, vol. 158, no. 10, pp. 3174–3187, 01 2017. [PubMed]
10. G. Sirago 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, Oct. 2017. [nature.com]
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. [PubMed]
12. Torsello, Antonio & Bresciani, Elena & Tamiazzo, Laura & Bulgarelli, Ilaria & Caporali, Simona & Moulin, Aline & Fehrentz, jean-alain & Martinez, Jean & Perissoud, Daniel & Locatelli, Vittorio. (2008). Novel potent and selective non-peptide ligands of ghrelin receptor : characterization of endocrine and extraendocrine actions. [Research Gate]

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