Hexarelin 5mg

$42.00

Hexarelin (also known as Examorelin, developmental codes EP-23905 and MF-6003) is a synthetic, peptidic, and potent agonist of the ghrelin/growth hormone secretagogue receptor (GHSR-1a). It is a hexapeptide that was developed by Mediolanum Farmaceutici. While primarily known for its powerful ability to stimulate the release of growth hormone (GH) from the pituitary gland, independently and synergistically with Growth Hormone-Releasing Hormone (GHRH), research has revealed that Hexarelin also exerts direct, growth hormone-independent effects, particularly on cardiovascular function. These GH-independent effects are often mediated through binding to the CD36 receptor, especially in the heart. Hexarelin reached Phase II clinical trials for growth hormone deficiency and congestive heart failure but was not ultimately marketed.

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Quantity

Data Sheet

Molecular Formula	C₄₇H₅₈N₁₂O₆
CAS Number	140703-51-1
Molar Mass	887.04 g/mol
Amino Acid Sequence	His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2
PubChem CID	6918297
Primary Research Area	Growth Hormone Secretagogue Growth Hormone Deficiency Cardioprotection Congestive Heart Failure Myocardial Infarction Cardiac Remodeling Neuroprotection Oxidative Stress Inflammation Muscle Growth Adipose Tissue Reduction GHSR-1a Agonism CD36 Receptor Activation
Purity	>99%

Molecular Formula

C₄₇H₅₈N₁₂O₆

CAS Number

140703-51-1

Molar Mass

887.04 g/mol

Amino Acid Sequence

His-D-2-methyl-Trp-Ala-Trp-D-Phe-Lys-NH2

PubChem CID

6918297

Primary Research Area

Growth Hormone Secretagogue
Growth Hormone Deficiency
Cardioprotection
Congestive Heart Failure
Myocardial Infarction
Cardiac Remodeling
Neuroprotection
Oxidative Stress
Inflammation
Muscle Growth
Adipose Tissue Reduction
GHSR-1a Agonism
CD36 Receptor Activation

Purity

>99%

Research Summary	Description
The cardiovascular action of hexarelin	Summary: This concise review article summarizes the evidence for the direct cardiovascular actions of hexarelin. It highlights that beyond its role as a GHSR-1a agonist, hexarelin exerts significant cardioprotective effects, including the inhibition of cardiomyocyte apoptosis (programmed cell death of heart muscle cells), reduction of cardiac fibrosis, and improvement of cardiac function in models of myocardial infarction and heart failure. The review emphasizes that these effects are partly mediated by GHSR-1a but largely by activation of the CD36 receptor, a multifunctional B-type scavenger receptor identified as a specific cardiac receptor for hexarelin. Citation: Zhang, W., & Chen, J. (2014). The cardiovascular action of hexarelin. Endocrine, 47(2), 346–352.
Protective effects of Hexarelin and JMV2894 in a human neuroblastoma cell line expressing the SOD1-G93A mutated protein	Summary: This in vitro study investigated the neuroprotective potential of hexarelin in human neuroblastoma cells overexpressing the SOD1-G93A mutated protein, a model for Amyotrophic Lateral Sclerosis (ALS). The study found that hexarelin effectively antagonized hydrogen peroxide (H2O2)-induced damage to these cells. It improved cell viability, reduced nitrite release (a marker of oxidative stress), and restored normal cell morphologies. Mechanistically, hexarelin reduced caspase-3 activation (an apoptotic enzyme) and modulated the expression of BCL-2 family proteins, suggesting anti-apoptotic effects. It also influenced MAPK and PI3K/Akt signaling pathways, which are crucial for cell survival. Citation: Vittorelli, D., Giustizieri, M. L., De Stefano, S., Costantini, R., Brizzi, A., Manno, R., ... & Fuso, A. (2023). Protective Effects of Hexarelin and JMV2894 in a Human Neuroblastoma Cell Line Expressing the SOD1-G93A Mutated Protein. International Journal of Molecular Sciences, 24(2), 993.
Hexarelin modulates lung mechanics, inflammation, and fibrosis in acute lung injury	Summary: This study investigated the effects of hexarelin in a murine model of HCl-induced acute lung injury (ALI), a condition that can lead to Acute Respiratory Distress Syndrome (ARDS) and lung fibrosis. Hexarelin treatment induced a significant improvement in lung compliance and reduced the total number of immune cells and neutrophil recruitment in bronchoalveolar lavage fluid within 24 hours of injury. It also demonstrated an ability to blunt lung remodeling processes and fibrotic development. The findings suggest that hexarelin can inhibit the early phase of the inflammatory response, thereby preventing subsequent fibrotic changes. Citation: Toscano, M., Cataldi, M., D'Adamo, E., Vitiello, G., Zaccaria, C., Vetrone, S., ... & Gualillo, O. (2021). Hexarelin modulates lung mechanics, inflammation, and fibrosis in acute lung injury. Drug Target Insights, 15, 26–33.
Growth hormone-independent cardioprotective effects of hexarelin in the rat	Summary: This study explored whether hexarelin's cardioprotective effects were independent of its GH-releasing activity. Using hypophysectomized rats (which lack a pituitary gland and thus cannot produce GH), the researchers found that hexarelin treatment prevented the exacerbation of ischemia-reperfusion damage in the heart. Hexarelin prevented increases in left ventricular end-diastolic pressure, coronary perfusion pressure, and reversed the fall in prostacyclin release. Importantly, a control GH-releasing peptide (EP 51389) that does not bind to the heart, but also stimulates GH, was ineffective in this model. Citation: Luciani, S., De Gennaro Colonna, V., & Deghenghi, R. (1999). Growth hormone-independent cardioprotective effects of hexarelin in the rat. Endocrinology, 140(9), 4024–4029.

Research Summary

Description

The cardiovascular action of hexarelin

Summary: This concise review article summarizes the evidence for the direct cardiovascular actions of hexarelin. It highlights that beyond its role as a GHSR-1a agonist, hexarelin exerts significant cardioprotective effects, including the inhibition of cardiomyocyte apoptosis (programmed cell death of heart muscle cells), reduction of cardiac fibrosis, and improvement of cardiac function in models of myocardial infarction and heart failure. The review emphasizes that these effects are partly mediated by GHSR-1a but largely by activation of the CD36 receptor, a multifunctional B-type scavenger receptor identified as a specific cardiac receptor for hexarelin.

Citation:
Zhang, W., & Chen, J. (2014). The cardiovascular action of hexarelin. Endocrine, 47(2), 346–352.

Protective effects of Hexarelin and JMV2894 in a human neuroblastoma cell line expressing the SOD1-G93A mutated protein

Summary: This in vitro study investigated the neuroprotective potential of hexarelin in human neuroblastoma cells overexpressing the SOD1-G93A mutated protein, a model for Amyotrophic Lateral Sclerosis (ALS). The study found that hexarelin effectively antagonized hydrogen peroxide (H2O2)-induced damage to these cells. It improved cell viability, reduced nitrite release (a marker of oxidative stress), and restored normal cell morphologies. Mechanistically, hexarelin reduced caspase-3 activation (an apoptotic enzyme) and modulated the expression of BCL-2 family proteins, suggesting anti-apoptotic effects. It also influenced MAPK and PI3K/Akt signaling pathways, which are crucial for cell survival.

Citation:
Vittorelli, D., Giustizieri, M. L., De Stefano, S., Costantini, R., Brizzi, A., Manno, R., ... & Fuso, A. (2023). Protective Effects of Hexarelin and JMV2894 in a Human Neuroblastoma Cell Line Expressing the SOD1-G93A Mutated Protein. International Journal of Molecular Sciences, 24(2), 993.

Hexarelin modulates lung mechanics, inflammation, and fibrosis in acute lung injury

Summary: This study investigated the effects of hexarelin in a murine model of HCl-induced acute lung injury (ALI), a condition that can lead to Acute Respiratory Distress Syndrome (ARDS) and lung fibrosis. Hexarelin treatment induced a significant improvement in lung compliance and reduced the total number of immune cells and neutrophil recruitment in bronchoalveolar lavage fluid within 24 hours of injury. It also demonstrated an ability to blunt lung remodeling processes and fibrotic development. The findings suggest that hexarelin can inhibit the early phase of the inflammatory response, thereby preventing subsequent fibrotic changes.

Citation:
Toscano, M., Cataldi, M., D'Adamo, E., Vitiello, G., Zaccaria, C., Vetrone, S., ... & Gualillo, O. (2021). Hexarelin modulates lung mechanics, inflammation, and fibrosis in acute lung injury. Drug Target Insights, 15, 26–33.

Growth hormone-independent cardioprotective effects of hexarelin in the rat

Summary: This study explored whether hexarelin's cardioprotective effects were independent of its GH-releasing activity. Using hypophysectomized rats (which lack a pituitary gland and thus cannot produce GH), the researchers found that hexarelin treatment prevented the exacerbation of ischemia-reperfusion damage in the heart. Hexarelin prevented increases in left ventricular end-diastolic pressure, coronary perfusion pressure, and reversed the fall in prostacyclin release. Importantly, a control GH-releasing peptide (EP 51389) that does not bind to the heart, but also stimulates GH, was ineffective in this model.

Citation:
Luciani, S., De Gennaro Colonna, V., & Deghenghi, R. (1999). Growth hormone-independent cardioprotective effects of hexarelin in the rat. Endocrinology, 140(9), 4024–4029.

Peptide Storage Guidelines

Storing peptides correctly is critical for maintaining their stability and biological activity over time. Proper storage protocols can prevent degradation, ensuring that the peptide remains effective for research, therapeutic, or other applications.

Understanding Peptide Stability

Peptides are chains of amino acids linked by peptide bonds. Their stability is influenced by several factors, including:

Amino Acid Sequence: Certain amino acids, such as cysteine, methionine, tryptophan, and glutamine, are more susceptible to oxidation or degradation.
Contaminants: The presence of proteases, bacteria, or other contaminants can lead to peptide breakdown.
Environmental Conditions: Exposure to high temperatures, moisture, and light can accelerate degradation.

General Storage Guidelines

Initial Handling

Upon receiving a peptide, it's essential to check its form. Most are shipped as a lyophilized (freeze-dried) powder, which is the most stable form for long-term storage.

As a Lyophilized Powder: Store the powder at -20°C or colder (e.g., -80°C). This form is highly stable and can be stored for several years. Keep the vial sealed tightly to prevent moisture absorption.
As a Solution: Once dissolved, peptides are significantly less stable. Store solutions at -20°C or -80°C. Avoid storing peptide solutions at 4°C for extended periods.

Working with Peptide Solutions

When preparing a peptide solution, use a high-purity solvent, such as sterile, deionized water or an appropriate buffer.

Single-Use Aliquots

Procedure: Dissolve the entire peptide vial in the appropriate solvent to create a concentrated stock solution. Then, aliquot this stock solution into smaller, labeled microcentrifuge tubes.
Benefits: This method ensures that each time you need to use the peptide, you only thaw a small portion, preserving the integrity of the remaining stock.

Freezing and Thawing

Freezing: Freeze the aliquots quickly by placing them in an ethanol/dry ice bath or a specialized freezer rack to avoid degradation.
Thawing: Thaw the aliquots on ice or in a cold room. Avoid rapid thawing at high temperatures.

Specific Considerations

Peptides Containing Cysteine, Methionine, or Tryptophan

Peptides with these amino acids are prone to oxidation.

Storage: Store under an inert atmosphere (nitrogen or argon) if possible.
Solvent: Use deoxygenated solvents for reconstitution.
Additives: Antioxidants or reducing agents (e.g., DTT) may help, but use cautiously as they can interfere with some assays.

Peptides Containing Glutamine or Asparagine

These amino acids are susceptible to deamidation.

Storage: Store at the coldest possible temperature (-80°C) as a lyophilized powder.
Solvent: For reconstitution, use a slightly acidic buffer (pH ~4-5) to slow deamidation.

Preventing Microbial Contamination

Always use sterile techniques and solvents.
Use sterile, single-use aliquots.
Avoid sodium azide when it may interfere with downstream applications, especially cell-based assays.

Summary of Storage Conditions

Storage Type	Temperature	Duration	Notes
Long-term	-80°C	2-3 years	Optimal for long-term storage
Standard	-20°C	1-2 years	Most common storage condition
Short-term	4°C	1-2 weeks	For immediate use only
Working solution	4°C	1-7 days	Reconstituted peptides