| 包装 | 价格(元) |
| 10mM (in 1mL DMSO) | 电议 |
| 10mg | 电议 |
| 50mg | 电议 |
| 100mg | 电议 |
| 500mg | 电议 |
| 1g | 电议 |
Cell lines | Human microvascular endothelial cells of the lung-blood (HMVEC-LBl) |
Preparation Method | Cells were plated into 24-well plates and grown to confluence in EGM-2MV medium containing 2.5% FBS plus supplements. Only cells in passage 5 were used, with n = 12 wells per experimental condition. |
Reaction Conditions | HMVEC-LBl was exposed to human VEGF-121 (40 ng/mL) in-vitro in serum-free medium for 7 h, in the absence or presence of the VEGF receptor antagonist, SU5416 (3 and 10 μM). |
Applications | SU5416 can block the effects of VEGF and completely prevent VEGFR2 phosphorylation as well. There was no evidence of background VEGFR2 phosphorylation in the HMVEC-LBl and in serum-free medium. Adding SU5416 did not affect the background phosphorylation. In the absence of VEGF, SU5416 increased ET-1 production, by 16% at 10 μM, and SU5416 can completely abolish the VEGF effect on ET-1 production. |
Animal models | Wild-type C57BL/6 mice (male, 8–10 weeks, 20–24 g) and genetically engineered TLR4-deficient mice (male, 8–10 weeks, 20–22 g) |
Preparation Method | Mice were stimulated by intratracheal administration of LPS after anesthetization with an intraperitoneal (i.p.) injection of tribromoethanol. Isopyknic saline-treated mice served as blank control group. After LPS stimulation, the experimental mice were treated with SU5416, DXM or DXM + SU5416 by oral administration for 12 hours. DXM-treated mice were served as positive control group. |
Dosage form | 20 mg/kg, BW solution in DMSO |
Applications | SU5416 could be implemented to suppress immune response in mice with ALI. Normally, excessive activation and penetration of neutrophils is the common pathological process in LPS-induced ALI. Which subsequently enhanced the release of proinflammatory cytokines, which can further aggravate lung injury. SU5416 exhibited inhibitory effect on the population of neutrophil cell (P |
| 产品描述 | SU5416 is a potent small molecule vascular endothelial growth factor receptor (VEGFR) inhibitor. SU5416 is a 3-substituted indolin-2-one compound with relatively high specificity for VEGFR-2 and VEGFR-1, used extensively in animal models of PH, primarily due to effects on pulmonary vascular endothelial cell apoptosis and proliferation.[1] SU416 has been developed for the treatment of solid human tumors as well.[3] In vitro study was performed to examine the inhibitory effect of SU5416 on KDR phosphorylation. Which indicated that pretreatment of BCECs with SU5416 resulted in a dose-dependent inhibition of KDR phosphorylation with an IC50 of 0.29 ± 0.071 μM (n=6) SU5416 almost completely inhibited KDR phosphorylation at the concentration of 3 μM. Few BCECs were stained with trypan blue after the treatment of SU5416, at least up to the concentration of 3 μM for 24 h. This suggested that the inhibitory effect of SU5416 on KDR phosphorylation was not due to the cell toxicity.[2] In vivo study demonstrated that SU5416 could significantly reverse LPS-induced ALI in mice, and exert better protective effect in TLR4 knockout mice. SU5416 could also act as a protective agent against LPS-induced ALI in mice. Moreover, SU5416 dramatically restored the reduction of CD31 expression mediated by LPS, suggesting SU5416 could rescue LPS-induced dysfunction of pulmonary endothelial barrier. In addition, both p-VEGFR2 and VEGFR2 expressions were inhibited by SU5416 in WT and TLR4–/- mice. SU5416 could attenuate LPS-induced ALI through modulating the VEGF/VEGFR and NF-κB pathways, which suggested SU5416 might be used for the treatment of patients with inflammation-mediated ALI.[3] References: |
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