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MAZ51 is originally synthesized inhibitor of VEGFR-3 (Flt-4) tyrosine kinase, inhibits VEGF-C-induced activation of VEGFR-3 without blocking VEGF-C-mediated stimulation of VEGFR2. MAZ51 also inhibited cellular proliferation by inducing G2/M phase cell cycle arrest without triggering significant cell death in dose- and time-dependent patterns. MAZ51 blocks proliferation and induces apoptosis in a wide variety of tumor cells. Treatment of glioma cells with MAZ51 increased phosphorylated GSK3β levels by activating Akt and increasing levels of active RhoA.
In vivo, in the rats subcutaneously injected with MT450 rat mammary carcinoma cells, treatment daily with MAZ51 (8 mg/kg, i.p.) significantly suppressed the growth of MT450 tumors when compared with the solvent-treated animals. In the mammary fat pad of BALB/c mice injected with the metastatic mammary tumor cell line Cl66, MAZ51 treatment (i.p.) significantly inhibited tumor growth in a dose-dependent manner.
| Molecular Weight | 314.38 |
| Formula | C21H18N2O |
| CAS Number | 163655-37-6 |
| Solubility (25°C) | DMSO ≥ 7 mg/mL |
| Storage |
Powder -20°C 3 years ; 4°C 2 years In solvent -80°C 6 months ; -20°C 1 month |
| Related VEGFR/PDGFR Products |
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| SU5208
SU5208 inhibits vascular endothelial growth factor receptor-2 (VEGFR2). |
| VEGFR-IN-1
VEGFR-IN-1 is a potent angiogenesis inhibitor with IC50s of 0.02, 0.18, 0.24 7.3, and 7 µM for KDR, Flt-1, c-Kit, EGF-R, and c-Src, respectively. |
| (Z)-Orantinib
(Z)-Orantinib ((Z)-SU6668) is a potent, selective, orally active and ATP competitive inhibitor of Flk‐1/KDR, PDGFRβ, and FGFR1, with IC50s of 2.1, 0.008, and 1.2 µM, respectively. |
| (Rac)-SAR131675
(Rac)-SAR131675 is the racemate of SAR131675. |
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