DDR2 inhibitors encompass a variety of compounds that target the kinase activity of DDR2 (Discoidin Domain Receptor 2), significantly impacting its role in cellular signaling related to cancer progression and metastasis. Key inhibitors such as Imatinib, Dasatinib, Nilotinib, Bosutinib, and AP 24534 are multi-targeted tyrosine kinase inhibitors. These drugs effectively inhibit DDR2, thereby disrupting its function in promoting cell adhesion, migration, proliferation, and extracellular matrix remodeling, which are crucial in tumor development and metastatic processes. Their inhibition of DDR2 highlights the kinase's integral role in cellular processes associated with oncogenesis, providing a targeted approach to modulating these pathways.
In addition to these specific DDR2 inhibitors, other compounds such as Sorafenib, D,L-2-Phenylglycine-d5, BIBF1120, Vandetanib, XL-184 free base, Axitinib, and Osimertinib, though having broader targets, also impact DDR2 activity. Sorafenib, for instance, while primarily targeting RAF kinases, affects DDR2 and consequently influences angiogenesis and tumor growth. Linsitinib and Vandetanib, targeting IGF-1R and various tyrosine kinases, respectively, modulate DDR2 signaling pathways, affecting processes like fibrosis and angiogenesis in cancer. XL-184 free base, Axitinib, and Osimertinib exhibit inhibitory effects on DDR2 among other kinases, targeting tumor angiogenesis and progression. These diverse compounds demonstrate the complex regulation of DDR2 and underscore the potential of kinase inhibitors in targeting specific pathological processes driven by aberrant DDR2 signaling. Their actions range from direct kinase inhibition to the modulation of associated signaling pathways, reflecting the multifaceted approaches to influencing DDR2's activity in various biological contexts, particularly in cancer.