CLEC-14A Inhibitors
Chemical inhibitors of CLEC-14A can affect its function in angiogenesis through various mechanisms. Suramin, a polysulfonated naphthylurea, inhibits interactions between CLEC-14A and extracellular matrix components or growth factors, which are essential for the endothelial cell-cell interactions and vessel formation that CLEC-14A facilitates. By blocking these interactions, Suramin functionally inhibits the angiogenesis process that CLEC-14A supports. Similarly, Fumagillin, by irreversibly binding to methionine aminopeptidase-2, hampers endothelial cell proliferation, indirectly affecting the angiogenic role of CLEC-14A. TNP-470, another angiogenesis inhibitor, targets the proliferative capacity of endothelial cells, thereby inhibiting the CLEC-14A-dependent formation and organization of blood vessels. Combretastatin A4, which binds to tubulin, disrupts the cytoskeletal framework within endothelial cells, impeding processes such as cell migration and capillary tube formation where CLEC-14A is involved.
Other inhibitors like Sunitinib and Axitinib, which are receptor tyrosine kinase inhibitors, reduce angiogenic signaling by targeting VEGFRs, thereby decreasing the function of CLEC-14A in vascular formation and repair. Pazopanib, another multi-targeted receptor tyrosine kinase inhibitor, suppresses the angiogenic signals that CLEC-14A relies upon to mediate new blood vessel formation. Endostatin, known for its anti-angiogenic properties, interferes with endothelial cell migration and proliferation, reducing the angiogenic activity where CLEC-14A plays a significant role. Bevacizumab, by binding VEGF-A, indirectly inhibits CLEC-14A by decreasing VEGF signaling pathways that contribute to angiogenesis. Cilengitide, by targeting integrins, prevents the cell adhesion and signaling that are necessary for the angiogenic activity of CLEC-14A. Additionally, Thalidomide disrupts growth factor signaling, which is essential for the endothelial cell functions that CLEC-14A supports in angiogenesis. Lastly, Erlotinib, an EGFR inhibitor, can functionally reduce CLEC-14A's activity by impeding EGFR-related signaling pathways involved in angiogenesis and vascular remodeling.
SEE ALSO...
| Product Name | CAS # | Catalog # | QUANTITY | Price | Citations | RATING |
|---|---|---|---|---|---|---|
Suramin sodium | 129-46-4 | sc-507209 sc-507209F sc-507209A sc-507209B sc-507209C sc-507209D sc-507209E | 50 mg 100 mg 250 mg 1 g 10 g 25 g 50 g | $152.00 $214.00 $728.00 $2601.00 $10965.00 $21838.00 $41096.00 | 5 | |
Suramin is a polysulfonated naphthylurea that inhibits various growth factors. It can inhibit CLEC-14A by blocking its interaction with extracellular matrix components and growth factors that are essential for angiogenesis, thereby inhibiting endothelial cell-cell interactions and vessel formation. | ||||||
Fumagillin | 23110-15-8 | sc-200377 sc-200377A sc-200377B sc-200377C sc-200377D | 1 mg 5 mg 25 mg 100 mg 500 mg | $104.00 $393.00 $541.00 $1363.00 $5212.00 | 1 | |
Fumagillin is an irreversible inhibitor of methionine aminopeptidase-2, which is necessary for endothelial cell proliferation. By inhibiting this enzyme, Fumagillin indirectly limits the angiogenic processes where CLEC-14A is involved. | ||||||
Sunitinib, Free Base | 557795-19-4 | sc-396319 sc-396319A | 500 mg 5 g | $153.00 $938.00 | 5 | |
Sunitinib is a receptor tyrosine kinase inhibitor that targets VEGFR and PDGFR among others. By inhibiting these receptors, Sunitinib can decrease angiogenic signaling and thereby functionally inhibit CLEC-14A's role in angiogenesis. | ||||||
Pazopanib | 444731-52-6 | sc-396318 sc-396318A | 25 mg 50 mg | $130.00 $182.00 | 2 | |
Pazopanib is a multi-targeted receptor tyrosine kinase inhibitor, with activity against VEGFR, PDGFR, and KIT. By inhibiting these receptors, Pazopanib reduces the angiogenic signals required for CLEC-14A to function in new blood vessel formation. | ||||||
TNP 470 | 129298-91-5 | sc-296547 | 10 mg | $235.00 | ||
TNP-470 is an angiogenesis inhibitor that targets endothelial cell growth. It can functionally inhibit CLEC-14A by preventing the endothelial cell proliferation and organization that CLEC-14A promotes. | ||||||
Combrestatin A4 | 117048-59-6 | sc-204697 sc-204697A | 1 mg 5 mg | $46.00 $81.00 | ||
Combretastatin A4 is a tubulin-binding agent that disrupts cytoskeletal organization. By disrupting endothelial cell microtubule formation, it indirectly inhibits CLEC-14A's role in angiogenesis. | ||||||
Cilengitide | 188968-51-6 | sc-507335 | 5 mg | $215.00 | ||
Cilengitide is an integrin inhibitor that targets cell adhesion molecules. By inhibiting integrins, it prevents the endothelial cell adhesion and signaling required for angiogenesis, where CLEC-14A plays a role. | ||||||
Thalidomide | 50-35-1 | sc-201445 sc-201445A | 100 mg 500 mg | $111.00 $357.00 | 8 | |
Thalidomide exhibits anti-angiogenic properties by inhibiting growth factor signaling, which is crucial for endothelial cell migration and proliferation. This inhibition can functionally reduce CLEC-14A's role in angiogenesis. | ||||||
Erlotinib, Free Base | 183321-74-6 | sc-396113 sc-396113A sc-396113B sc-396113C sc-396113D | 500 mg 1 g 5 g 10 g 100 g | $87.00 $135.00 $293.00 $505.00 $3827.00 | 42 | |
Erlotinib is an EGFR tyrosine kinase inhibitor that can indirectly inhibit CLEC-14A by blocking EGFR signaling pathways that contribute to angiogenesis and vascular remodeling where CLEC-14A is active. | ||||||