Hexarelin Powder

Hexarelin Powder highly selectively binds to growth hormone secretagogue receptors (GHS‑R1a) on cardiomyocyte membranes, bypassing the traditional growth hormone axis and directly activating endogenous myocardial protective signaling.
This receptor is expressed on cardiomyocytes, vascular endothelial cells, and smooth muscle cells. Upon activation, it rapidly regulates calcium homeostasis, inhibits oxidative stress, and blocks apoptotic pathways. Compared with other GHRPs, it shows higher affinity for GHS‑R1a and slower desensitization, enabling cardioprotection at lower doses and with longer duration. This is also key to its stable efficacy after reconstitution.

Mitochondrial dysfunction is a common pathway in various types of cardiac injury. The product upregulates key factors including PGC‑1α and Nrf2, improves mitochondrial biogenesis and the balance of fission and fusion, enhances ATP production efficiency, and reduces reactive oxygen species (ROS) accumulation.
It stabilizes mitochondrial membrane potential, reduces cytochrome c release, and blocks the endogenous apoptotic cascade. For mitochondrial collapse induced by ischemia, hypoxia, high glucose, or drug toxicity, the product rapidly repairs respiratory chain function, relieves myocardial energy crisis, and provides metabolic support for damaged myocardium.

Oxidative stress and inflammatory amplification drive the progression of myocardial injury. The product increases the activities of antioxidant enzymes such as SOD and GSH‑Px, reduces levels of oxidative markers including MDA and 8‑OHdG, and alleviates lipid peroxidation and oxidative DNA damage.
Meanwhile, it inhibits the NF‑κB and NLRP3 inflammasome pathways, decreases the release of pro‑inflammatory cytokines such as TNF‑α, IL‑1β, and IL‑6, and reduces myocardial inflammatory infiltration and initiation of fibrosis. This dual antioxidant + anti‑inflammatory mechanism confers broad‑spectrum protection in both acute and chronic cardiac injury.

Myocardial ischemia‑reperfusion is a severe complication commonly seen after acute myocardial infarction, cardiac surgery, or shock. It reduces infarct size, improves ventricular wall motion, and decreases the incidence of arrhythmias when used for pretreatment, post‑treatment, or continuous intervention.
Its core value lies in attenuating oxidative burst and calcium overload at the moment of reperfusion, protecting the endothelial barrier, and improving microcirculatory perfusion. Studies show that in I/R models, it reduces myocardial infarct size by more than 40%, improves left ventricular ejection fraction, reduces troponin and LDH leakage, and significantly improves cardiac survival.

Heart failure is characterized by myocardial hypertrophy, interstitial fibrosis, ventricular dilation, and impaired systolic and diastolic function. Hexarelin Powder inhibits pathological hypertrophy of cardiomyocytes, downregulates hypertrophic markers such as ANP, BNP, and β‑MHC, reduces type I/III collagen deposition and TGF‑β1 pathway activation, and reverses interstitial fibrosis and ventricular remodeling.
It enhances myocardial contractility, lowers ventricular filling pressure, improves ejection fraction and diastolic function, and reduces excessive neurohormonal activation and cardiac overload caused by elevated Ang II and aldosterone. The product shows consistent beneficial effects in post‑infarction heart failure, pressure‑overload heart failure, and metabolic heart failure models.

Chemotherapeutic agents represented by doxorubicin often cause dose‑dependent, irreversible myocardial injury, limiting the efficacy of tumor therapy. The product attenuates doxorubicin‑induced myocardial fiber swelling, vacuolar degeneration, and inflammatory infiltration through multiple pathways including antioxidation, anti‑inflammation, anti‑apoptosis, and mitochondrial protection, reduces myocardial enzyme release, and preserves cardiac structure and function.
Its growth hormone‑independent direct cardioprotective property makes it an ideal candidate protective agent in cardio‑oncology research, reducing cardiac risk without interfering with tumor treatment.

Hexarelin Powder is produced by freeze‑drying, appearing as a white, fine powder with no visible impurities. After reconstitution, it is clear and transparent without precipitation or particles, ensuring uniform administration.
With HPLC purity ≥99%, it eliminates interference from impurities, ensuring that experimental results are attributed to the peptide itself rather than excipients or contaminants. It shows high batch‑to‑batch stability, suitable for long‑term, large‑sample, multi‑center cardiovascular mechanistic studies.

Unlike other GHRPs that undergo rapid desensitization, it retains receptor activation efficacy and continuously drives cardioprotective signaling after repeated administration.
This low‑desensitization profile makes it more advantageous in studies requiring long‑term intervention, such as chronic heart failure and diabetic cardiomyopathy, avoiding the attenuation of protective effects due to receptor downregulation.

The product acts directly on myocardial GHS‑R1a, not fully relying on growth hormone release. It provides indirect protection via the GH/IGF‑1 axis and independently activates endogenous myocardial protective pathways.
This feature allows it to remain effective in cardiac disease models with abnormal growth hormone axes or where GH intervention is unsuitable, broadening its application scenarios.