SU1498 | AG 1498 | VEGFR Inhibitor | AmBeed-信号通路专用抑制剂

SU1498 {[allProObj[0].p_purity_real_show]}

货号：A657558 同义名： AG 1498; Tyrphostin SU 1498

SU1498是一种选择性VEGFR2抑制剂，IC50为700 nM。

SU1498 化学结构
CAS号：168835-82-3

SU1498 3D分子结构
CAS号：168835-82-3

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VEGFR 亚型比较

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-Fms/CSF1R,c-Kit	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	c-Kit,BTK	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	+++ hVEGFR2, IC50: 9 nM mVEGF2, IC50: 165 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。

SU1498 生物活性

描述

SU1498 (AG 1498) is a selective VEGFR2 inhibitor, inhibiting Flk-1 with an IC50 value of 700 nM^[1].

体外研究

In human umbilical vein endothelial cells and human aortic endothelial cells, SU1498 induces the accumulation of phosphorylated ERKs, contingent on the operational status of B-Raf and MEK kinases within the MAPK pathway. This increase in phospho-ERKs is only seen in cells activated by sphingosine 1-phosphate or protein growth factors; without such stimuli, SU1498 has no effect^[2].

SU1498 interferes with VEGFR2 signaling in MS1 VEGF cells. The presence of SU1498 results in reduced Ets-1 levels, indicating that VEGF-VEGFR-2 interactions are integral to the basal expression of Ets-1, and disruption of this autocrine loop by SU1498 diminishes Ets-1 expression^[3].

The application of SU1498 notably influences the proliferation and apoptosis of U87 cells. It triggers a significant increase in lipids and a reduction in glycerophosphocholine. Consequently, the presence of lipid droplets in the cytoplasm of SU1498-treated U87 cells is observed^[4].

SU1498 细胞实验

Cell Line Astrocytes Hippocampal neurons Mouse embryonic cortical neurons Endothelial colony forming cells (ECFCs) Human cardiac endothelial cells (HCECs) Endothelial cells Mouse brain endothelial cells (MBECs)	Concentration	Treated Time	Description	References
Astrocytes	20 µM	20 minutes	SU1498 blocked VEGF-induced increase in PKCα phosphorylation	Glia. 2019 Jul;67(7):1344-1358.
Hippocampal neurons	10 µM	2 to 24 hours	To investigate the effects of VEGFR-2 inhibition on neuronal survival, results showed that SU1498 treatment led to decreased cell viability, oxidative stress, and mitochondrial dysfunction.	Free Radic Biol Med. 2013 Oct;63:421-31.
Mouse embryonic cortical neurons	1–100 µM	24 hours	SU1498 inhibited VEGF's ability to stimulate BrdUrd labeling via VEGFR2/Flk-1 receptors	Proc Natl Acad Sci U S A. 2002 Sep 3;99(18):11946-50.
Endothelial colony forming cells (ECFCs)	1 µM	24 hours	Inhibited P2Y1 receptor agonist (10 μM 2MS-ATP)-induced angiogenesis, reducing stimulation from ~2.6-fold to 1.9-fold control; inhibited VEGF (262 pM)-induced angiogenesis, reducing stimulation from ~2.4-fold to 1.5-fold control	Br J Cancer. 2009 May 5;100(9):1465-70.
Human cardiac endothelial cells (HCECs)	1 µM	24 hours	Inhibited P2Y1/2 receptor agonist (100 μM ATP or 10 μM 2MS-ATP)-induced angiogenesis, reducing stimulation to ~1.3-fold control levels	Br J Cancer. 2009 May 5;100(9):1465-70.
Endothelial cells	5–20 µM	3 days	Inhibition of VEGF signaling, blocking the protective effects of NSPC conditioned medium on endothelial cells under conditions of serum starvation and OGD	J Cereb Blood Flow Metab. 2008 Sep;28(9):1530-42.
Mouse brain endothelial cells (MBECs)	5 µM	5 hours	SU1498, a specific VEGFR2 antagonist, abolished the angiogenesis enhanced by the supernatant from rhEPO-treated neural progenitor cells.	J Cereb Blood Flow Metab. 2008 Jul;28(7):1361-8.

Cell Line

Astrocytes Hippocampal neurons Mouse embryonic cortical neurons Endothelial colony forming cells (ECFCs) Human cardiac endothelial cells (HCECs) Endothelial cells Mouse brain endothelial cells (MBECs)

Concentration

Treated Time

Description

References

Astrocytes

20 µM

20 minutes

SU1498 blocked VEGF-induced increase in PKCα phosphorylation

Glia. 2019 Jul;67(7):1344-1358.

Hippocampal neurons

10 µM

2 to 24 hours

To investigate the effects of VEGFR-2 inhibition on neuronal survival, results showed that SU1498 treatment led to decreased cell viability, oxidative stress, and mitochondrial dysfunction.

Free Radic Biol Med. 2013 Oct;63:421-31.

Mouse embryonic cortical neurons

1–100 µM

24 hours

SU1498 inhibited VEGF's ability to stimulate BrdUrd labeling via VEGFR2/Flk-1 receptors

Proc Natl Acad Sci U S A. 2002 Sep 3;99(18):11946-50.

Endothelial colony forming cells (ECFCs)

1 µM

24 hours

Inhibited P2Y1 receptor agonist (10 μM 2MS-ATP)-induced angiogenesis, reducing stimulation from ~2.6-fold to 1.9-fold control; inhibited VEGF (262 pM)-induced angiogenesis, reducing stimulation from ~2.4-fold to 1.5-fold control

Br J Cancer. 2009 May 5;100(9):1465-70.

Human cardiac endothelial cells (HCECs)

1 µM

24 hours

Inhibited P2Y1/2 receptor agonist (100 μM ATP or 10 μM 2MS-ATP)-induced angiogenesis, reducing stimulation to ~1.3-fold control levels

Br J Cancer. 2009 May 5;100(9):1465-70.

Endothelial cells

5–20 µM

3 days

Inhibition of VEGF signaling, blocking the protective effects of NSPC conditioned medium on endothelial cells under conditions of serum starvation and OGD

J Cereb Blood Flow Metab. 2008 Sep;28(9):1530-42.

Mouse brain endothelial cells (MBECs)

5 µM

5 hours

SU1498, a specific VEGFR2 antagonist, abolished the angiogenesis enhanced by the supernatant from rhEPO-treated neural progenitor cells.

J Cereb Blood Flow Metab. 2008 Jul;28(7):1361-8.

SU1498 动物实验

Species Mice C57BL/6J mice Mice Sprague-Dawley rats	Animal Model VEGFR-1 deficient mice Wild-type and HDC-KO mice Newborn Mice model Chronic unpredictable stress model	Administration	Dosage	Frequency	Description	References
Mice	VEGFR-1 deficient mice	Intraperitoneal injection	100 µl (100 mM in DMSO)	Daily injections from P7 to P20	Inhibition of VEGFR-2 kinase activity reduced angiogenesis in VEGFR-1 deficient mice	Circulation. 2012 Aug 7;126(6):741-52
C57BL/6J mice	Wild-type and HDC-KO mice	Intracerebroventricular injection	250 ng/2 mL	Every 12 hours for a total of 3 injections	SU1498 prevented the protective effect of hypoxic preconditioning in infarct volume and reversed the increased peripheral CBF in WT mice	J Cereb Blood Flow Metab. 2011 Jan;31(1):305-14
Mice	Newborn Mice model	Subcutaneous injection	30 mg/kg	Single dose	To study the inhibitory effect of SU1498 on alveolar development, results showed SU1498-treated mice had attenuated alveolar development with enlarged alveolar volume and sparse, dysmorphic capillaries.	Am J Respir Cell Mol Biol. 2005 Dec;33(6):622-8.
Sprague-Dawley rats	Chronic unpredictable stress model	Intracerebroventricular injection	4 mM	Administered on days 14, 16, 18, and 20	SU1498 completely blocked the antidepressant effects of fluoxetine in the sucrose preference test, novelty suppressed feeding test, and forced swim test	Neuropsychopharmacology. 2009 Oct;34(11):2459-68

Species

Mice C57BL/6J mice Mice Sprague-Dawley rats

Animal Model

VEGFR-1 deficient mice Wild-type and HDC-KO mice Newborn Mice model Chronic unpredictable stress model

Administration

Dosage

Frequency

Description

References

Mice

VEGFR-1 deficient mice

Intraperitoneal injection

100 µl (100 mM in DMSO)

Daily injections from P7 to P20

Inhibition of VEGFR-2 kinase activity reduced angiogenesis in VEGFR-1 deficient mice

Circulation. 2012 Aug 7;126(6):741-52

C57BL/6J mice

Wild-type and HDC-KO mice

Intracerebroventricular injection

250 ng/2 mL

Every 12 hours for a total of 3 injections

SU1498 prevented the protective effect of hypoxic preconditioning in infarct volume and reversed the increased peripheral CBF in WT mice

J Cereb Blood Flow Metab. 2011 Jan;31(1):305-14

Mice

Newborn Mice model

Subcutaneous injection

30 mg/kg

Single dose

To study the inhibitory effect of SU1498 on alveolar development, results showed SU1498-treated mice had attenuated alveolar development with enlarged alveolar volume and sparse, dysmorphic capillaries.

Am J Respir Cell Mol Biol. 2005 Dec;33(6):622-8.

Sprague-Dawley rats

Chronic unpredictable stress model

Intracerebroventricular injection

4 mM

Administered on days 14, 16, 18, and 20

SU1498 completely blocked the antidepressant effects of fluoxetine in the sucrose preference test, novelty suppressed feeding test, and forced swim test

Neuropsychopharmacology. 2009 Oct;34(11):2459-68

SU1498 参考文献

SU1498 实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

2.56mL

0.51mL

0.26mL

12.80mL

2.56mL

1.28mL

25.61mL

5.12mL

2.56mL

SU1498 技术信息

CAS号	168835-82-3
分子式	C₂₅H₃₀N₂O₂
分子量	390.52
SMILES Code	O=C(NCCCC1=CC=CC=C1)/C(C#N)=C/C2=CC(C(C)C)=C(O)C(C(C)C)=C2
MDL No.	MFCD03453026

别名	AG 1498; Tyrphostin SU 1498
运输	蓝冰
InChI Key	JANPYFTYAGTSIN-FYJGNVAPSA-N
Pubchem ID	5941539

存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Sealed in dry, store in freezer, under -20°C

溶解方案

细胞实验：

DMSO: 105 mg/mL(268.87 mM)，配合低频超声助溶，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

动物实验：请根据您的动物给药指南选择适当的溶解方案。
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

方案一

方案二

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