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Multiple cytokine and growth factor receptors refer to a diverse set of cell surface proteins that initiate intracellular signaling in response to external stimuli, including growth factors like VEGF and PDGF, and cytokines such as IL-6 and interferons (Frontiers in Immunology, 2018; Dove Medical Press, 2012). These receptors are central to regulating cell proliferation, differentiation, and immune responses through pathways like JAK-STAT and MAPK (Frontiers in Immunology, 2018; Sigma-Aldrich). In diseases such as cancer and chronic fibrosis, the simultaneous activation of multiple receptors often drives disease progression and contributes to therapeutic resistance (PLOS One, 2012; Clinical Cancer Research, 2011). Drugs like suramin and multi-kinase inhibitors (e.g., nintedanib) are designed to target this broad array of receptors to disrupt redundant signaling networks (PLOS One, 2012; Blood, 2025). While this multi-targeting approach can enhance efficacy, it also increases the risk of off-target effects and systemic toxicities due to the widespread biological roles of these receptors (Blood, 2025).
Drugs targeting this group typically act by either competitively inhibiting the binding of various ligands to their respective extracellular receptor domains or by blocking the intracellular kinase activity and downstream signaling molecules, such as JAKs or STATs, that are common to multiple receptor families (PLOS One, 2012; Frontiers in Immunology, 2018; Blood, 2025).
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