Myokines

Myokines belong to the family of cytokines, which mediate intercellular communication in processes such as immune signaling, tissue homeostasis, and inflammation. Myokines are, in contrast to chemokines or interleukins, defined by their cellular source rather than by structural or receptor-based classification. While chemokines and interleukins represent distinct cytokine families characterized by conserved structural motifs and receptor systems, myokines refer to signaling proteins that are produced and secreted by skeletal muscle cells, particularly in response to contraction or metabolic stress. As a result, several classical cytokines—including certain interleukins—can also function as myokines when released from muscle tissue. Upon release into the local environment or systemic circulation, myokines enable skeletal muscle to function not only as a contractile tissue but also as an active signaling hub with endocrine and immunomodulatory functions.

Initially studied in the context of exercise physiology and metabolic regulation, myokines are now recognized as important mediators of inter-organ communication. Through autocrine, paracrine, and endocrine signaling, muscle-derived factors influence processes in adipose tissue, liver, bone, and the central nervous system. In particular, growing evidence highlights a muscle–brain axis, where myokines contribute to neuronal survival, synaptic plasticity, neuroinflammation, and cognitive function, illustrating how peripheral physiology can shape central nervous system activity.

antibodies-online offers a wide range of antibodies, proteins, and kits for myokines. Below you will find an overview of selected myokines. Learn more about the targets down below alongside with corresponding products.

Feimin

Feimin is a recently described muscle-derived signaling protein that has been proposed as a member of the expanding class of myokines—cytokine-like factors secreted by skeletal muscle that mediate communication with distant tissues. Emerging evidence suggests that Feimin participates in pathways linking muscle activity, metabolic regulation, and inflammatory signaling, highlighting a potential role in systemic homeostasis.

Studies indicate that Feimin exerts its function through the receptor tyrosine kinase MERTK, initiating downstream AKT signaling. Through this pathway, Feimin appears to integrate into a broader network of insulin-sensitizing factors. Experimental work in murine models suggests that Feimin enhances glucose uptake in peripheral tissues while simultaneously reducing hepatic glucose production, pointing to a role in maintaining metabolic balance after nutrient intake.

Of particular interest is the potential involvement of Feimin in neuroinflammatory pathways. Myokine-mediated muscle–brain communication has emerged as an important mechanism by which peripheral physiology influences neuronal function and inflammatory signaling in the central nervous system. In this context, Feimin has been reported to modulate inflammatory gene expression in microglial cells through the AKT–mTOR axis. These findings suggest a possible protective role in diet-induced neuroinflammation and position Feimin as a potential contributor to muscle–brain signaling pathways.

Although the molecular mechanisms and receptor interactions of Feimin are still under active investigation, the protein represents a promising target for further research into muscle-derived endocrine signaling. Understanding the biological functions of Feimin may provide new insight into the integration of metabolic, immune, and neurobiological pathways, and could support the development of experimental tools to investigate these emerging signaling networks.

Feimin Antibodies

Feimin Proteins

Interleukin-6

Interleukin-6 (IL-6) is a pleiotropic cytokine that plays a central role in immune regulation, inflammation, and metabolic signaling. As illustrated in the pathway above, increased IL-6 expression is frequently associated with pro-inflammatory signaling cascades, which in certain contexts can contribute to neuroinflammatory responses and neuronal apoptosis.

IL-6 signals through a receptor complex consisting of the IL-6 receptor (IL-6R) and the signal-transducing co-receptor gp130, activating downstream pathways such as JAK/STAT3, MAPK, and PI3K signaling. Through these pathways, IL-6 regulates a wide range of cellular processes including inflammatory gene expression, immune cell recruitment, and stress responses.

Beyond its established role in inflammation, IL-6 also functions as a myokine and can be released by skeletal muscle during physiological stress such as exercise. In this setting, IL-6 contributes to systemic metabolic adaptation and immune modulation, highlighting how the biological effects of this cytokine strongly depend on cellular context and signaling mode.

Because of this dual role, IL-6 sits at the intersection of metabolic regulation, immune signaling, and neuroinflammation. Dysregulated IL-6 signaling has therefore been implicated in a range of pathological conditions, including chronic inflammatory disorders, metabolic disease, and neurodegenerative processes, making it an important molecule for studying how systemic inflammation influences neuronal health.

IL 6 Antibodies

Interleukin-15

Interleukin-15 (IL-15) is a cytokine with well-established roles in immune regulation that has also been recognized as a muscle-derived myokine. It is highly expressed in skeletal muscle and can be released in response to physiological stimuli such as exercise, linking muscle activity to systemic metabolic and immunological processes.

IL-15 signals through a heterotrimeric receptor complex consisting of IL-15Rα, IL-2Rβ, and the common γ-chain, activating intracellular pathways including JAK/STAT signaling. Through these pathways, IL-15 promotes the proliferation and activation of natural killer (NK) cells and CD8⁺ T cells, highlighting its role at the interface between muscle physiology and immune surveillance.

Beyond its immunological functions, IL-15 has been implicated in metabolic regulation and body composition. Experimental studies suggest that IL-15 can influence lipid metabolism, improve insulin sensitivity, and modulate the balance between muscle and adipose tissue. These observations have led to the hypothesis that IL-15 contributes to some of the systemic metabolic benefits associated with physical activity.

Given its combined roles in immune cell activation, metabolic regulation, and muscle signaling, IL-15 represents an important mediator within the broader network of muscle–immune communication and has attracted increasing attention as a potential target in metabolic disease and immunotherapy research.

IL 15 Antibodies

Brain-Derived Neurotrophic Factor

Brain-Derived Neurotrophic Factor (BDNF) is a neurotrophin best known for its role in neuronal survival, synaptic plasticity, and cognitive function. In addition to its classical functions in the nervous system, BDNF can also be produced in peripheral tissues, including skeletal muscle, where it has been proposed to act as a myokine involved in muscle–brain communication.

BDNF exerts its biological effects primarily through binding to the TrkB receptor, triggering downstream signaling pathways such as MAPK/ERK, PI3K–AKT, and PLCγ signaling. These pathways regulate neuronal survival, synaptic remodeling, and cellular stress responses. Through these mechanisms, BDNF plays a central role in processes underlying learning, memory formation, and neuroprotection.

Within skeletal muscle, BDNF appears to function primarily in autocrine or paracrine signaling, influencing metabolic pathways such as fatty acid oxidation and energy metabolism. Exercise-induced changes in BDNF signaling are thought to contribute to the emerging concept of a muscle–brain axis, whereby muscle activity can modulate central nervous system physiology and neuroinflammatory processes.

Because of its dual involvement in metabolic regulation and neuronal function, BDNF has become a key molecule in research exploring the molecular links between physical activity, brain health, and neurodegenerative disease.

BDNF Antibodies

Myostatin

Myostatin, also known as growth differentiation factor 8 (GDF-8), is a member of the transforming growth factor-β (TGF-β) superfamily and functions as a major negative regulator of skeletal muscle growth. Unlike many other myokines that promote metabolic adaptation or immune signaling, myostatin primarily acts to limit muscle mass and regulate muscle homeostasis.

Myostatin signals through binding to activin type II receptors (ActRIIA/ActRIIB), which subsequently activate intracellular SMAD2/3 signaling pathways. These signaling cascades inhibit myoblast proliferation and differentiation, ultimately suppressing muscle fiber growth and protein synthesis.

Genetic and experimental studies have demonstrated that inhibition or loss of myostatin signaling leads to dramatic increases in skeletal muscle mass, a phenotype observed in several animal models and rare human cases. Beyond its role in muscle development, myostatin has also been implicated in metabolic regulation, cachexia, and muscle wasting disorders.

Because of its central role in controlling muscle mass, myostatin has become an important target for therapeutic strategies aimed at treating muscle wasting conditions, including sarcopenia, cancer cachexia, and muscular dystrophies. In this context, myostatin represents a key node in the regulatory network governing muscle growth, metabolism, and systemic physiology.

Myostatin Antibodies