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Vatalanib dihydrochloride (PTK787) Chemical Structure
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Biological Activity
Vatalanib dihydrochloride (PTK787) is a novel VEGFR and c-Kit tyrosine kinases and angiogenesis inhibitor with IC50 of 0.037, 0.077, 0.27 and 0.73 μM for KDR, Flt-1, Flk and c-Kit, respectively. Measurement of VEGF-induced autophosphorylation of KDR in a double antibody chemiluminescence assay, using either HUVECs or CHO cells transfected with the KDR receptor, showed that vatalanib dihydrochloride (PTK787) inhibits the VEGF-induced phosphorylation with an IC50 of 17 and 34 nM for the HUVECs and CHO cells , respectively. Selective inhibition of VEGFRs by vatalanib dihydrochloride (PTK787)leads to inhibition of primary tumor growth and development of metastases in murine renal cell carcinoma. Vatalanib dihydrochloride (PTK787) caused no obvious side effects in the RENCA model . Vatalanib dihydrochloride (PTK787) causes significant anti-arthritic effects in models of rheumatoid arthritis. [1][2][3]
References on Vatalanib dihydrochloride (PTK787)
- [1] Cancer Res 2000;60:2178-2189
- [2] Cancer Res 2000;60:4819-4824
- [3] Inflamm. res 2004;53:133–142
Chemical Information
| Molecular Weight (WM): | 419.73 |
|---|---|
| Formula: | C20H15ClN4•2HCl |
| CAS No.: | 212141-51-0 |
| Synonyms: |
ZK222584
|
| Dissolve in (25°C): | DMSO ≥28mg/mL |
| Water ≥10mg/mL | |
| Ethanol ≥6mg/mL | |
| Storage: | 2 years-20°CPowder |
| 1 week-4°Cin DMSO | |
| 1 month-80°in DMSO |
Quality Control & MSDS
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Selleck's high quality products have been used in several published research findings, including the following:
Combinatory action of VEGFR2 and MAP kinase pathways maintains endothelial-cell integrity.
Orai1 and CRAC Channel Dependence of VEGF-Activated Ca2+ Entry and Endothelial Tube Formation
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Combinational treatment of kinase inhibitors induces the similar phenotype produced by PP1. All images are lateral view with dorsal to the top and anterior to the left. The combinational treatment of Dasatinib (D) or U0126 (U) with Sunitinib (SU),PTK787 (PTK), or ZM323881 (Z) resulted in the shrinkage of dorsal aorta. - Combinational treatment of kinase inhibitors induces the similar phenotype produced by PP1. All images are lateral view with dorsal to the top and anterior to the left. The combinational treatment of Dasatinib (D) or U0126 (U) with Sunitinib (SU),PTK787 (PTK), or ZM323881 (Z) resulted in the shrinkage of dorsal aorta.
Data from [Cell Res 2011 Jul;21:1080-7] Vatalanib dihydrochloride (PTK787) purchased from Selleck
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Mechanisms of VEGF-activated Ca2 entry. All data were from HUVECs. a, Mean 100 ng/mL VEGF-evoked Ca2 entry in the presence of 100 nmol/L sorafenib (n/N3/40), 10 nmol/L vatalanib (n/N=3/24), or 10 mol/L U73122 (n/N=3/24) normalized to their matched controls. b and c, eYFP-STIM1 (green) before (control) (b) and after exposure to 100 ng/mL VEGF (c). d, Summary data for 100 ng/mL VEGF-evoked transient and sustained Ca2 signals after transfection with STIM1.si or sc.si (n/N3/64). e, Example merged image of a cell labeled with anti-VEGFR2 antibody (green), anti-Orai1 antibody (red), and the nuclear counter stain, DAPI (blue). - Mechanisms of VEGF-activated Ca2 entry. All data were from HUVECs. a, Mean 100 ng/mL VEGF-evoked Ca2 entry in the presence of 100 nmol/L sorafenib (n/N3/40), 10 nmol/L vatalanib (n/N=3/24), or 10 mol/L U73122 (n/N=3/24) normalized to their matched controls. b and c, eYFP-STIM1 (green) before (control) (b) and after exposure to 100 ng/mL VEGF (c). d, Summary data for 100 ng/mL VEGF-evoked transient and sustained Ca2 signals after transfection with STIM1.si or sc.si (n/N3/64). e, Example merged image of a cell labeled with anti-VEGFR2 antibody (green), anti-Orai1 antibody (red), and the nuclear counter stain, DAPI (blue).
Data from [Circ Res 2011 May;108:1190-1198] Vatalanib dihydrochloride (PTK787) purchased from Selleck
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| Combinational treatment of kinase inhibitors induces the similar phenotype produced by PP1. All images are lateral view with dorsal to the top and anterior to the left. The combinational treatment of Dasatinib (D) or U0126 (U) with Sunitinib (SU),PTK787 (PTK), or ZM323881 (Z) resulted in the shrinkage of dorsal aorta. |
Data from [Cell Res 2011 Jul;21:1080-7]
| Mechanisms of VEGF-activated Ca2 entry. All data were from HUVECs. a, Mean 100 ng/mL VEGF-evoked Ca2 entry in the presence of 100 nmol/L sorafenib (n/N3/40), 10 nmol/L vatalanib (n/N=3/24), or 10 mol/L U73122 (n/N=3/24) normalized to their matched controls. b and c, eYFP-STIM1 (green) before (control) (b) and after exposure to 100 ng/mL VEGF (c). d, Summary data for 100 ng/mL VEGF-evoked transient and sustained Ca2 signals after transfection with STIM1.si or sc.si (n/N3/64). e, Example merged image of a cell labeled with anti-VEGFR2 antibody (green), anti-Orai1 antibody (red), and the nuclear counter stain, DAPI (blue). |
Data from [Circ Res 2011 May;108:1190-1198]
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