Vasohibin-2 Inhibitors

Chemical inhibitors of Vasohibin-2 function by obstructing various signaling pathways associated with angiogenesis, in which Vasohibin-2 is implicated. Sunitinib, for instance, acts as a tyrosine kinase inhibitor, directly targeting the vascular endothelial growth factor receptors (VEGFRs), thereby inhibiting the signaling required for new blood vessel formation. Similarly, Sorafenib targets multiple kinases involved in the angiogenic process, effectively obstructing the activity of Vasohibin-2. Pazopanib also shares this multi-targeted approach, aiming at VEGFRs to disrupt the normal functioning of Vasohibin-2. Vandetanib extends its inhibitory action by targeting VEGFR as well, contributing to the collective interference with the angiogenesis pathways involving Vasohibin-2.

Further expanding the list of inhibitors, Lenvatinib inhibits receptor tyrosine kinases (RTKs) that participate in angiogenic signaling, affecting the activity of Vasohibin-2. Axitinib, showing a potent affinity for VEGFRs 1, 2, and 3, suppresses Vasohibin-2's role in the angiogenesis pathway. Cabozantinib's mechanism involves the inhibition of multiple tyrosine kinases, including VEGFRs, curtailing the angiogenic function of Vasohibin-2. Tivozanib, as an oral VEGF receptor tyrosine kinase inhibitor, disrupts VEGF signaling, which is crucial for Vasohibin-2's involvement in angiogenesis. Regorafenib, by targeting a spectrum of angiogenesis-related kinases, inhibits the functional role of Vasohibin-2 in new blood vessel formation. Nintedanib's approach includes targeting VEGFR, PDGFR, and FGFR; all are key players in angiogenesis, thereby inhibiting the associated activity of Vasohibin-2. Lastly, Apatinib and Telatinib exert their effects by selectively inhibiting VEGFR-2 and VEGFR2/3, PDGFRβ, respectively, leading to the inhibition of Vasohibin-2 activity in the angiogenesis process.