Name | Combretastatin A4 disodium phosphate | CAS# | 168555-66-6 | |
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Price | ¥Inquiry/1g ¥Inquiry/5g ¥Inquiry/10g ¥Inquiry/50g | Purity | 99.0% | |
Stocking Period |
Inquiry | Stock | In Stock |
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Product Information
Product Name: Combretastatin A4 disodium phosphate(CA4P); Fosbretabulin disodium; Combretastatin A-4 phosphate, disodium salt CAS No.: 168555-66-6 Chemical Name: 2-Methoxy-5-[(1Z)-2-(3,4,5-trimethoxyphenyl)ethenyl]phenol dihydrogen phosphate disodium salt Molecular Formula:C18H19Na2O8P Molecular Weight: 440.30 Appearance:White or off-white solid Purity(HPLC):>99% Biological Activity: Combretastatin A4 Phosphate Disodium Salt is the salt form of Combretastatin A4, a phosphorylated microtubule depolymerizing molecule which induces tumor necrosis by regression of unstable nascent tumor neo-vessels. Studies suggest that Combretastatin A4 Phosphate Disodium Salt selectively inhibits endothelial tumor cells via disrupting VE-cadherin (vascular endothelial-cadherin). In addition, Combretastatin A4 Phosphate Disodium Salt can increase the permeability of endothelial cells while inhibiting their migration and suppress capillary tube formation via disruption of VE-cadherin. Furthermore, Combretastatin A4 Phosphate Disodium Salt can change the morphology of endothelial cells by altering their tubulin cytoskeleton. Combretastatin A-4 phosphate (fosbretabulin) is a microtubule destabilizing drug, a type of vascular-targeting agent, a drug designed to damage the vasculature (blood vessels) of cancer tumors causing central necrosis. Fosbretabulin disodium is the disodium salt of a water-soluble phosphate derivative of a natural stilbenoid phenol derived from the African bush willow (Combretum caffrum) with potential vascular disrupting and antineoplastic activities. Upon administration, the prodrug fosbretabulin is dephosphorylated to its active metabolite, the microtubule-depolymerizing agent combretastatin A4, which binds to tubulin dimers and prevents microtubule polymerization, resulting in mitotic arrest and apoptosis in endothelial cells. In addition, this agent disrupts the engagement of the endothelial cell–specific junctional molecule vascular endothelial-cadherin (VE-cadherin) and so the activity of the VE-cadherin/β-catenin/Akt signaling pathway, which may result in the inhibition of endothelial cell migration and capillary tube formation. As a result of fosbretabulin's dual mechanism of action, the tumor vasculature collapses, resulting in reduced tumor blood flow and ischemic necrosis of tumor tissue. |