Myosin H Chain Fragment (614-631), mouse

Product Name: Myosin H Chain Fragment (614-631), mouse

Sequence One Letter Code: Ac-RSLKLMATLFSTYASADR

Sequence Three Letter Code: Ac-Arg-Ser-Leu-Lys-Leu-Met-Ala-Thr-Leu-Phe-Ser-Thr-Tyr-Ala-Ser-Ala-Asp-Arg-OH

Chemical Formula:C91H149N25O28S

Molecular Weight: 2073.5

Purity: 95%

Form: Lyophilized

Storage Conditions: - 20 °C

Research Area: Autoimmune Diseases

pecies: mouse, rat

Conjugation: Unconjugated

Code Nacres: NA.26

Application: This peptide corresponds to residues 614–631 of murine α-myosin heavy chain, a cardiac-restricted structural protein. It is widely used to induce experimental autoimmune myocarditis (EAM) in susceptible animal models, recapitulating key immunopathological features of human myocarditis. Administration of this peptide elicits autoreactive CD4⁺ T cell responses, myocardial inflammation, and cardiac dysfunction. As a well-established immunodominant epitope, it enables controlled investigation of T cell–mediated cardiac injury, antigen presentation, and autoimmune disease progression. The peptide is extensively applied in studies exploring inflammatory cardiomyopathy, tolerance induction, and therapeutic immunomodulation strategies targeting autoimmune heart disease.

Current Research: Autoimmune myocarditis is an inflammatory heart disease characterized by immune-mediated damage to cardiac tissue. In humans, the condition can arise following viral infection, immune dysregulation, or exposure to cardiac antigens, and it may progress to dilated cardiomyopathy (DCM) and chronic heart failure. Because direct investigation of autoimmune myocarditis in humans is challenging, experimental models have become essential for understanding disease mechanisms. Among these, the α-myosin heavy chain (α-MyHC) peptide spanning residues 614–631 has emerged as a widely used antigen for inducing experimental autoimmune myocarditis (EAM) in susceptible mouse strains. This peptide corresponds to a cardiac-specific structural protein, making it a highly relevant model antigen for studying immune responses directed against the myocardium. Current research using the α-MyHC (614–631) peptide focuses primarily on the T cell–mediated mechanisms that drive cardiac inflammation. When administered with appropriate adjuvants in susceptible strains such as BALB/c or A/J mice, the peptide stimulates autoreactive CD4⁺ T lymphocytes that recognize the epitope presented by major histocompatibility complex (MHC) class II molecules. These activated T cells infiltrate cardiac tissue and trigger inflammatory cascades involving macrophages, neutrophils, and proinflammatory cytokines. The resulting pathology closely resembles key immunopathological features observed in human autoimmune myocarditis, including myocardial infiltration, cardiomyocyte damage, and impaired cardiac function. One area of active investigation involves understanding the role of specific T helper cell subsets in disease progression. Studies using the α-MyHC peptide model have demonstrated that Th17 cells play a particularly important role in the development and severity of autoimmune myocarditis. Th17-associated cytokines such as interleukin-17 (IL-17) promote recruitment of inflammatory cells and contribute to myocardial tissue injury. In contrast, regulatory T cells (Tregs) can suppress pathogenic immune responses and limit disease severity. Researchers are therefore using this peptide-induced model to study the balance between inflammatory and regulatory immune pathways in autoimmune heart disease. Another important research direction focuses on antigen presentation and immune tolerance. Because the α-MyHC peptide represents a well-defined immunodominant epitope, it provides a controlled system for investigating how cardiac antigens are processed and presented by dendritic cells and other antigen-presenting cells. Studies have shown that defects in peripheral tolerance mechanisms—such as impaired deletion of autoreactive T cells or insufficient regulatory signaling—can contribute to the development of myocarditis. By analyzing how immune cells recognize and respond to the α-MyHC peptide, researchers can better understand how tolerance to cardiac self-antigens is maintained or disrupted. The α-MyHC (614–631) peptide model is also widely used to evaluate novel therapeutic strategies for inflammatory cardiomyopathy. Experimental treatments aimed at reducing autoimmune responses—including cytokine inhibitors, immune checkpoint modulators, and regulatory T cell–enhancing therapies—are frequently tested using peptide-induced EAM models. In addition, antigen-specific tolerance approaches, such as peptide-based tolerization or nanoparticle delivery systems, are being explored to selectively suppress pathogenic immune responses without broadly suppressing the immune system. Recent research has further expanded the use of this model to investigate the transition from acute myocarditis to chronic cardiomyopathy. Long-term studies show that persistent inflammation induced by autoreactive T cells can lead to ventricular remodeling, fibrosis, and reduced cardiac contractility. By monitoring these changes in peptide-induced EAM models, investigators are gaining insights into how early immune-mediated injury evolves into chronic heart disease. Overall, the α-myosin heavy chain (614–631) peptide remains a cornerstone reagent in cardiovascular immunology research. Its ability to reproducibly induce experimental autoimmune myocarditis allows scientists to dissect the immunological pathways underlying cardiac autoimmunity, evaluate therapeutic interventions, and explore mechanisms of immune tolerance. Insights generated from this model continue to inform our understanding of human myocarditis and contribute to the development of targeted treatments for autoimmune heart disease.