NVP-BAW2881是一种血管内皮生长因子(VEGF)抑制剂,IC50值在1.0 nM至4.3 nM之间,针对VEGFR1、VEGFR2、VEGFR3。它还能够抑制PDGFRβ、c-Kit和RET的活性。


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| 产品名称 | VEGFR1 ↓ ↑ | VEGFR2 ↓ ↑ | VEGFR3 ↓ ↑ | 其他靶点 | 纯度 | ||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| Motesanib Diphosphate |
++++
VEGFR1, IC50: 2 nM |
++++
VEGFR2/Flk1, IC50: 3 nM VEGFR2, IC50: 3 nM |
+++
VEGFR3, IC50: 6 nM |
RET,PDGFR | 97% | ||||||||||||||
| Tivozanib |
++
VEGFR1, IC50: 30 nM |
+++
VEGFR2, IC50: 6.5 nM |
++
VEGFR3, IC50: 15 nM |
99%+ | |||||||||||||||
| Brivanib |
+
VEGFR1, IC50: 380 nM |
++
Flk1, IC50: 25 nM VEGFR2, IC50: 25 nM |
99%+ | ||||||||||||||||
| Regorafenib |
+++
VEGFR1, IC50: 13 nM |
+++
VEGFR2, IC50: 4.2 nM |
+
VEGFR3, IC50: 46 nM |
RET | 98% | ||||||||||||||
| Pazopanib |
+++
VEGFR1, IC50: 10 nM |
++
VEGFR2, IC50: 30 nM |
+
VEGFR3, IC50: 47 nM |
c-Kit,PDGFR,FGFR | 99% | ||||||||||||||
| Sitravatinib |
+++
VEGFR1 (FLT1), IC50: 6 nM |
+++
VEGFR2 (KDR), IC50: 5 nM |
++++
VEGFR3 (FLT4), IC50: 2 nM |
99%+ | |||||||||||||||
| Foretinib |
+++
VEGFR1/FLT1, IC50: 6.8 nM |
++++
KDR, IC50: 0.86 nM |
++++
VEGFR3/FLT4, IC50: 2.8 nM |
Tie-2 | 99%+ | ||||||||||||||
| MGCD-265 analog |
++++
VEGFR1, IC50: 3 nM |
++++
VEGFR2, IC50: 3 nM |
++++
VEGFR3, IC50: 4 nM |
Tie-2 | 99%+ | ||||||||||||||
| Lactate |
+++
VEGFR1/FLT1, IC50: 10 nM |
+++
VEGFR2/Flk1, IC50: 13 nM |
+++
VEGFR3/FLT4, IC50: 8 nM |
FLT3,c-Kit | 85% | ||||||||||||||
| AEE788 |
+
FLT1, IC50: 59 nM |
+
KDR, IC50: 77 nM |
EGFR | 98+% | |||||||||||||||
| Linifanib |
++++
VEGFR1/FLT1, IC50: 3 nM |
++++
VEGFR2/KDR, IC50: 4 nM |
+
VEGFR3/FLT4, IC50: 190 nM |
FLT3 | 99%+ | ||||||||||||||
| Vatalanib 2HCl |
+
VEGFR1/FLT1, IC50: 77 nM |
++
VEGFR2/Flk1, IC50: 270 nM VEGFR2/KDR, IC50: 37 nM |
+
VEGFR3/FLT4, IC50: 660 nM |
c-Kit,c-Fms/CSF1R | 99%+ | ||||||||||||||
| Axitinib |
++++
VEGFR1/FLT1, IC50: 0.1 nM |
++++
VEGFR2/Flk1, IC50: 0.18 nM VEGFR2/KDR, IC50: 0.2 nM |
98% | ||||||||||||||||
| Dovitinib |
+++
VEGFR1/FLT1, IC50: 10 nM |
+++
VEGFR2/Flk1, IC50: 13 nM |
+++
VEGFR3/FLT4, IC50: 8 nM |
FLT3,c-Kit | 99%+ | ||||||||||||||
| ZM 306416 |
+
VEGFR1, IC50: 0.33 μM |
Src | 99%+ | ||||||||||||||||
| KRN-633 |
+
VEGFR1, IC50: 170 nM |
+
VEGFR2, IC50: 160 nM |
+
VEGFR3, IC50: 125 nM |
BTK,c-Kit | 98% | ||||||||||||||
| OSI-930 |
+++
FLT1, IC50: 8 nM |
+++
KDR, IC50: 9 nM |
99%+ | ||||||||||||||||
| Lenvatinib |
++
VEGFR1/FLT1, IC50: 22 nM |
++++
VEGFR2/KDR, IC50: 4.0 nM |
+++
VEGFR3/FLT4, IC50: 5.2 nM |
98% | |||||||||||||||
| NVP-BAW2881 |
+
hVEGFR1, IC50: 820 nM |
+++
mVEGF2, IC50: 165 nM hVEGFR2, IC50: 9 nM |
+
hVEGFR3, IC50: 420 nM |
99% | |||||||||||||||
| Cediranib |
+++
VEGFR1/FLT1, IC50: 5 nM |
++++
VEGFR2/KDR, IC50: 0.5 nM |
c-Kit | 99%+ | |||||||||||||||
| Nintedanib |
++
VEGFR1, IC50: 34 nM |
+++
VEGFR2, IC50: 13 nM |
+++
VEGFR3, IC50: 13 nM |
FLT3 | 99+% | ||||||||||||||
| BMS-794833 |
++
VEGFR2, IC50: 15 nM |
99%+ | |||||||||||||||||
| SKLB1002 |
++
VEGFR2, IC50: 32 nM |
99% | |||||||||||||||||
| Cabozantinib S-malate |
++++
VEGFR2/KDR, IC50: 0.035 nM |
99+% | |||||||||||||||||
| Ki8751 |
++++
VEGFR2, IC50: 0.9 nM |
c-Kit | 99% | ||||||||||||||||
| SU 5402 |
++
VEGFR2, IC50: 20 nM |
98% | |||||||||||||||||
| Apatinib mesylate |
++++
VEGFR2, IC50: 1 nM |
RET | 98+% | ||||||||||||||||
| Ponatinib |
++++
VEGFR2, IC50: 1.5 nM |
98% | |||||||||||||||||
| LY2874455 |
+++
VEGFR2, IC50: 7 nM |
99%+ | |||||||||||||||||
| ZM323881 HCl |
++++
VEGFR2, IC50: <2 nM |
98% | |||||||||||||||||
| AZD2932 |
+++
VEGFR-2, IC50: 8 nM |
c-Kit | 99% | ||||||||||||||||
| Cabozantinib |
++++
VEGFR2/KDR, IC50: 0.035 nM |
98% | |||||||||||||||||
| Sorafenib |
++
VEGFR2/Flk1, IC50: 90 nM VEGFR2, IC50: 90 nM |
99% | |||||||||||||||||
| CYC-116 |
++
VEGFR2, Ki: 44 nM |
FLT3 | 99%+ | ||||||||||||||||
| Golvatinib |
++
VEGFR2, IC50: 16 nM |
99%+ | |||||||||||||||||
| Sunitinib |
+
VEGFR2 , IC50: 80 nM |
FLT3 | 98% | ||||||||||||||||
| RAF265 |
++
VEGFR2, EC50: 30 nM |
99%+ | |||||||||||||||||
| PD173074 | 99%+ | ||||||||||||||||||
| BFH772 |
++++
VEGFR2, IC50: 3 nM |
98% | |||||||||||||||||
| Semaxinib |
+
VEGFR2/Flk1, IC50: 1.23 μM |
98% | |||||||||||||||||
| Vandetanib |
++
VEGFR2, IC50: 40 nM |
+
VEGFR3, IC50: 110 nM |
EGFR | 99% | |||||||||||||||
| SAR131675 |
++
VEGFR3, IC50: 23 nM |
99%+ | |||||||||||||||||
| ENMD-2076 |
+
VEGFR2/KDR, IC50: 58.2 nM |
++
VEGFR3/FLT4, IC50: 15.9 nM |
FLT3,RET | 98% | |||||||||||||||
| Telatinib |
+++
VEGFR2, IC50: 6 nM |
++++
VEGFR3, IC50: 4 nM |
c-Kit | 99%+ | |||||||||||||||
| 1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。 | |||||||||||||||||||
| 靶点 |
|
| 描述 | BAW2881 is a vascular endothelial growth factor (VEGF) receptor tyrosine-kinase inhibitor that potently inhibits VEGFR1-3 at 1.0-4.3 nanomolar (nM) concentrations and inhibits PDGFRβ, c-Kit, and RET at 45-72 nM concentrations. |
| Concentration | Treated Time | Description | References | |
| Lymphatic Endothelial Cells (LECs) | 1 nM to 1 μM | 72 h | NVP-BAW2881 significantly inhibited VEGF-A and VEGF-C-induced proliferation, migration, and tube formation in LECs. | Am J Pathol. 2008 Jul;173(1):265-77. |
| Human Umbilical Vein Endothelial Cells (HUVECs) | 1 nM to 1 μM | 72 h | NVP-BAW2881 significantly inhibited VEGF-A-induced proliferation, migration, and tube formation in HUVECs. | Am J Pathol. 2008 Jul;173(1):265-77. |
| Lymphatic endothelial cells (LECs) | 1 nM - 1 μM | 72 h | NVP-BAW2881 significantly inhibited VEGF-A and VEGF-C-induced proliferation of LECs. | Am J Pathol. 2008 Jul;173(1):265-77. |
| Human umbilical vein endothelial cells (HUVECs) | 1 nM - 1 μM | 72 h | NVP-BAW2881 significantly inhibited VEGF-A-induced proliferation of HUVECs. | Am J Pathol. 2008 Jul;173(1):265-77. |
| Administration | Dosage | Frequency | Description | References | ||
| Mice | Transgenic mouse model of psoriasis | Oral | 25 mg/kg | Once daily for 14 days | NVP-BAW2881 significantly reduced psoriasis-like skin inflammation, decreased the number of blood and lymphatic vessels, and normalized the epidermal architecture. | Am J Pathol. 2008 Jul;173(1):265-77. |
| Mice and domestic pigs | K14/VEGF-A transgenic mouse model and UVB-induced skin inflammation model | Oral and topical administration | Oral 25 mg/kg/day, topical 0.1% to 0.5% | Oral once daily, topical twice daily for 14 days | NVP-BAW2881 significantly reduced skin inflammation symptoms, including decreased numbers of blood and lymphatic vessels, reduced leukocyte infiltration, and normalized epidermal architecture. | Am J Pathol. 2008 Jul;173(1):265-77. |
| 计算器 | ||||
| 存储液制备 | ![]() |
1mg | 5mg | 10mg |
|
1 mM 5 mM 10 mM |
2.36mL 0.47mL 0.24mL |
11.78mL 2.36mL 1.18mL |
23.56mL 4.71mL 2.36mL |
|
| CAS号 | 861875-60-7 |
| 分子式 | C22H15F3N4O2 |
| 分子量 | 424.38 |
| SMILES Code | O=C(NC1=CC=CC(C(F)(F)F)=C1)C2=C3C=CC(OC4=NC(N)=NC=C4)=CC3=CC=C2 |
| MDL No. | MFCD30343850 |
| 别名 | BAW2881 |
| 运输 | 蓝冰 |
| InChI Key | MLLQJNIKDWEEFT-UHFFFAOYSA-N |
| Pubchem ID | 16004702 |
| 存储条件 |
In solvent -20°C: 3-6个月 -80°C: 12个月 Pure form Keep in dark place, inert atmosphere, 2-8°C |
| 溶解方案 |
DMSO: 35 mg/mL(82.47 mM),注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO 以下溶解方案都请先按照体外实验的方式配制澄清的储备液,再依次添加助溶剂: ——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议现用现配,当天使用; 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶
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