Angiogenesis

Angiogenesis (also known as neovascularization) is the generation of new blood vessels from pre-existing vasculature. It is a normal process in growth and development and is required for the formation of arteries, veins, and capillaries in an embryo.Angiogenesis has become an important target for cancer research with the recognition that it is one of the critical events necessary for cancer growth and metastasis. As a tumor develops, its size is limited by the diffusion of metabolites from existing blood vessels. Tumor angiogenesis, the growth of the new blood vessels, is essential for cancerous tumors to keep growing and spreading.As a tumor grows, cells at the center become starved of oxygen, inducing the expression of a transcription factor - hypoxia inducible factor-1 (HIF-1) - which upregulates the expression of a range of angiogenic factors. Growth factor signaling also initiates HIF-1 activity, pre-empting the need for growing cells to maintain oxygen homeostasis. As a result, HIF-1 itself has been isolated as a therapeutic target for cancer. More than a dozen different proteins, as well as several smaller molecules, have been identified as angiogenic meaning that they are released by tumors as signals for angiogenesis. Inhibitors of angiogenesis (antiangiogenics) are currently the focus of intense cancer research.As well as its detrimental effects in tumor growth and inflammatory disorders, the generation of new blood vessels is a vital process in the context of stroke, cardiovascular disease and diabetes. Many of the pathologies associated with diabetes, such diabetic neuropathy, reduced wound healing and diabetic ulcers, are caused by a reduced blood supply to the downstream tissue. Therefore, promoting angiogenesis in diabetic patients may represent an important strategy in reducing morbidity. Recent work using adenovirus-mediated transfer of VEGF165 showed that promoting angiogenesis significantly accelerated wound healing.

Angiogenesis Products Targets

Products for Angiogenesis - Page 3

  1. Cat.No. Product Name Information/Activity
  2. BCC2193 AG-490 AG-490 is a tyrosine kinase inhibitor that inhibits EGFR, Stat-3 and JAK2/3. AG-490 chemical structure
  3. BCC6722 AG 494 Potent EGFR-kinase inhibitor AG 494 chemical structure
  4. BCC6721 AG 555 AG 555, a potent antiretroviral drug, is a potent and selective inhibitor of EGFR and blocks Cdk2 activation. AG 555 chemical structure
  5. BCC6720 AG 556 EGFR-kinase inhibitor AG 556 chemical structure
  6. BCC7113 AG 825 AG-825 (Tyrphostin AG-825) is a selective and ATP-competitive ErbB2 inhibitor which suppresses tyrosine phosphorylation, with an IC50 of 0.35 μM. AG-825 displays anti-cancer activity. AG825 significantly accelerates apoptosis of human neutrophils. AG-825 is a potential agent for overcoming Mn-induced neurotoxicity or AD development. AG 825 chemical structure
  7. BCC4514 Tyrphostin AG 879 Tyrphostin AG 879 (AG 879) is a tyrosine kinase inhibitor that inhibits TrKA phosphorylation (IC50 of 10 μM), but not TrKB and TrKC. Tyrphostin AG 879 is also a selective ErbB2 tyrosine kinase inhibitor with an IC50 of 1 μM, and has at least 500-fold higher selectivity to ErbB2 than EGFR. Tyrphostin AG 879 has anticancer activity. Tyrphostin AG 879 chemical structure
  8. BCC6667 AG 99 (E)-AG 99 ((E)-Tyrphostin 46; (E)-Tyrphostin AG 99) is a potent EGFR inhibitor. AG 99 chemical structure
  9. BCC5120 AV-412 free base AV-412 free base (MP-412 free base) is an EGFR inhibitor with IC50s of 0.75, 0.5, 0.79, 2.3, 19 nM for EGFR, EGFRL858R, EGFRT790M, EGFRL858R/T790M and ErbB2, respectively. AV-412 free base chemical structure
  10. BCC7356 BIBU 1361 dihydrochloride Selective inhibitor of EGFR-kinase BIBU 1361 dihydrochloride chemical structure
  11. BCC1449 Canertinib dihydrochloride Canertinib dihydrochloride (CI-1033 dihydrochloride) is a potent and irreversible EGFR inhibitor; inhibits cellular EGFR and ErbB2 autophosphorylation with IC50s of 7.4 and 9 nM. Canertinib dihydrochloride chemical structure

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