SU9516 | CDK | AmBeed-信号通路专用抑制剂

SU9516 {[allProObj[0].p_purity_real_show]}

货号：A269439

SU9516是一种选择性且强效的CDK2抑制剂，IC50为22 nM，对CDK1/CDK4的抑制效力较弱（IC50=40/200 nM），并且不抑制PKC、EGFR、p38MAPK等。

SU9516 化学结构
CAS号：377090-84-1

SU9516 3D分子结构
CAS号：377090-84-1

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CDK 亚型比较

产品名称	Cdc ↓ ↑	CDK1 ↓ ↑	CDK19 ↓ ↑	CDK2 ↓ ↑	CDK3 ↓ ↑	CDK4 ↓ ↑	CDK5 ↓ ↑	CDK6 ↓ ↑	CDK7 ↓ ↑	CDK8 ↓ ↑	CDK9 ↓ ↑	CLK ↓ ↑	其他靶点	纯度
XL413 HCl	++++ Cdc7, IC50: 3.4 nM													99%+
SU9516		+++ CDK1, IC50: 40 nM		+++ CDK2, IC50: 22 nM		++ CDK4, IC50: 200 nM								99%+
RO-3306		+++ CDK1, Ki: 20 nM											SGK,ERK	98%
R547		++++ CDK1/CyclinB, Ki: 2 nM		++++ CDK2/CyclinE, Ki: 3 nM		++++ CDK4/CyclinD1, Ki: 1 nM								99%+
BMS-265246		++++ CDK1/CyclinB, IC50: 6 nM		++++ CDK2/CyclinE, IC50: 9 nM		+ CDK4/CyclinD, IC50: 230 nM								99%+
NU6027		+ CDK1, Ki: 2.5 μM		+ CDK2, Ki: 1.3 μM									DNA-PK	98%
Purvalanol A	++++ Cdc2/CyclinB, IC50: 4 nM			+++ CDK2/CyclinE, IC50: 35 nM CDK2/CyclinA, IC50: 70 nM		+ CDK4/CyclinD1, IC50: 850 nM								99%+
SCH900776				++ CDK2, IC50: 0.16 μM										99%+
AUZ 454				++++ CDK2(C118L), Kd: 18.6 nM CDK2(A144C), Kd: 9.7 nM										99%+
A-674563 HCl				++ CDK2, Ki: 46 nM									PKA	99%
JNJ-7706621		++++ CDK1/CyclinB, IC50: 9 nM		++++ CDK2/CyclinE, IC50: 3 nM CDK2/CyclinA, IC50: 4 nM	++ CDK3/CyclinE, IC50: 58 nM	+ CDK4/CyclinD1, IC50: 253 nM		++ CDK6/CyclinD1, IC50: 175 nM						99%+
AT7519		++ CDK1/CyclinB, IC50: 210 nM		++ CDK2/CyclinA, IC50: 47 nM	+ CDK3/CyclinE, IC50: 360 nM	++ CDK4/CyclinD1, IC50: 100 nM	+++ CDK5/p35, IC50: 13 nM	++ CDK6/CyclinD3, IC50: 170 nM			++++ CDK9/CyclinT, IC50: <10 nM			98+%
PHA-793887		++ CDK1/CyclinB, IC50: 60 nM		++++ CDK2/CyclinE, IC50: 8 nM CDK2/CyclinA, IC50: 8 nM		++ CDK4/CyclinD1, IC50: 62 nM	++++ CDK5/p25, IC50: 5 nM		++++ CDK7/CyclinH, IC50: 10 nM		++ CDK9/CyclinT1, IC50: 138 nM			99%+
Milciclib		+ CDK1/CyclinB, IC50: 398 nM		++ CDK2/CyclinE, IC50: 363 nM CDK2/CyclinA, IC50: 45 nM		++ CDK4/CyclinD1, IC50: 160 nM	+ CDK5/p35, IC50: 265 nM		++ CDK7/CyclinH, IC50: 150 nM					99%+
Kenpaullone		+ CDK1/CyclinB, IC50: 0.4μM		+ CDK2/CyclinE, IC50: 7.5μM CDK2/CyclinA, IC50: 0.68μM			+ CDK5/p35, IC50: 0.85μM							98%
SNS-032				+++ CDK2/CyclinE, IC50: 48 nM CDK2/CyclinA, IC50: 38 nM			+ CDK5/p35, IC50: 340 nM		++ CDK7/CyclinH, IC50: 62 nM		++++ CDK9/CyclinT, IC50: 4 nM			99%+
Dinaciclib		++++ CDK1, IC50: 3 nM		++++ CDK2, IC50: 1 nM			++++ CDK5, IC50: 1 nM				++++ CDK9, IC50: 4 nM			99%+
PHA-767491 HCl	++++ Cdc7, IC50: 10 nM	+ CDK1, IC50: 250 nM		+ CDK2, IC50: 240 nM			+ CDK5, IC50: 460 nM				+++ CDK9, IC50: 34 nM		MK2	99%
(R)-Roscovitine	+ Cdc2/CyclinB, IC50: 0.65 μM			+ CDK2/CyclinE, IC50: 0.7 μM CDK2/CyclinA, IC50: 0.7 μM			++ CDK5/p35, IC50: 0.16 μM							99%+
Narazaciclib						++++ CDK4/CyclinD1, IC50: 3.87 nM		++++ CDK6/CyclinD1, IC50: 9.82 nM					RET	99%+
Palbociclib						++++ CDK4/CyclinD3, IC50: 9 nM CDK4/CyclinD1, IC50: 11 nM		+++ CDK6/CyclinD2, IC50: 15 nM						99%
Abemaciclib						++++ CDK4, IC50: 2 nM		++++ CDK6, IC50: 10 nM						99%
Ribociclib						++++ CDK4, IC50: 10 nM		+++ CDK6, IC50: 39 nM						98%
Palbociclib isethionate						++++ CDK4/CyclinD3, IC50: 9 nM CDK4/CyclinD1, IC50: 11 nM		+++ CDK6/CyclinD2, IC50: 15 nM						99%+
BS-181 HCl									+++ CDK7, IC50: 21 nM					99%+
(E/Z)-THZ1 2HCl									++++ CDK7, IC50: 3.2 nM					99%+
LDC4297									++++ CDK7, IC50: 0.13 nM					99%+
Senexin A			+ CDK19, Kd: 0.31 μM							+ CDK8, Kd: 0.83 μM				99%
MSC2530818										++++ CDK8, IC50: 2.6 nM				99%+
Wogonin											✔			99%+
Riviciclib HCl		++ CDK1/CyclinB, IC50: 79 nM		+ CDK2/CyclinE, IC50: 2.54 μM CDK2/CyclinA, IC50: 224 nM		++ CDK4/CyclinD1, IC50: 63 nM		+ CDK6/CyclinD3, IC50: 396 nM	+ CDK7/CyclinH, IC50: 2.87 μM		+++ CDK9/CyclinT1, IC50: 20 nM			98%
LDC000067				+ CDK2, IC50: 2.441 μM							++ CDK9, IC50: 44 nM			98%
Flavopiridol		+++ CDK1, IC50: 40 nM		+++ CDK2, IC50: 40 nM		+++ CDK4, IC50: 40 nM		+++ CDK6, IC50: 40 nM	+ CDK7, IC50: 300 nM		+++ CDK9, IC50: 20 nM			99%+
LY2857785									+ CDK7, IC50: 0.246 μM	+++ CDK8, IC50: 0.016 μM	+++ CDK9, IC50: 0.011 μM			99%+
AZD-5438		+++ CDK1, IC50: 16 nM		++++ CDK2, IC50: 6 nM							+++ CDK9, IC50: 20 nM			99%+
ML167												++ Dyrk1B , IC50: 1648 nM CLK4, IC50: 136 nM		99%+
(E/Z)-TG003												+++ mCLK1, IC50: 200 nM mCLK4, IC50: 15 nM		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。

SU9516 生物活性

靶点

CDK4

CDK4, IC50:200 nM
CDK2

CDK2, IC50:22 nM
CDK1

CDK1, IC50:40 nM

描述

Progression through the cell cycle is determined by sequential and specific phosphorylation events by holoenzymes involving cyclins and their catalytic partners, the CDKs. SU9516, a novel 3-substituted indolinone compound, binds to and selectively inhibits the activity of CDK2 with IC₅₀ of 22 nM. It also inhibits CDK1 and CDK4 with IC₅₀s of 40 nM and 200 nM. Continuous exposure to SU9516 (5 μM) for 24, 48, or 72 h resulted in a 4-52% decrease (P≤ 0.05) in CDK2-specific phosphorylation of pRb (retinoblastoma protein, a known CDK substrate) in RKO cells. The addition of 5 μM SU9516 produced a 27.6% decrease in RKO G₀-G₁ populations by 48 h post-drug addition and a 39.1% decrease by 72 h. A concomitant increase in RKO G₂-M populations results in a G₂-M block with G₂-M populations increasing by 13.1% over controls at 24 h to a 34.1% at 72 h post-drug addition. After continuous exposure to 5 μM SU9516 for 24, 48, and 72 h, both RKO (10-15%) and SW480 (4-22%) cells demonstrated an increase (P ≤ 0.01) in apoptosis. With inhibition of pRb phosphorylation, proliferation in both RKO and SW480 cells decreased in a dose-dependent manner at 20 h after treatment with SU9516^[3].

作用机制

SU9516’s planar structure binds to the catalytic domain of CDK2. The imidazole ring of SU9516 occupies the sugar-binding region. The N3 nitrogen on SU9516 may interact favorably with the side chain amino acid Lys89.

SU9516 细胞实验

Cell Line MV4-11 Human DMD patient myotubes K562 cells CCRF-CEM cells Jurkat cells Jurkat cells Kasumi-1 VMCF-7DNp53 cells Human normal foreskin skin fibroblast primary cells (CRL-2097) SUM149PT cells SUM149PT cells VMCF-7DNp53/Aurora-A cells VMCF-7DNp53 cells CDK2	Concentration	Treated Time	Description	References
MV4-11	500 nM	72 h	Evaluate the apoptotic effect of SU9516 in combination with ABT-737 and AKTi-1/2 on MV4-11 cells, showing significant increase in apoptosis	Int J Mol Sci. 2023 Mar 16;24(6):5717.
Human DMD patient myotubes	0.1 μM		SU9516 increased levels of α7β1 integrin and inhibited the SPAK/OSR1 kinase pathway	J Rare Dis Res Treat. 2017;2(5):1-4.
K562 cells	5 μM	24 hours	SU9516 significantly enhanced the sensitivity of K562 cells to MTX, with significant growth inhibition at 0.05 μM MTX or higher concentrations.	Cancer Sci. 2010 Mar;101(3):728-34.
CCRF-CEM cells	5 μM	24 hours	SU9516 significantly enhanced the sensitivity of CCRF-CEM cells to MTX, with significant growth inhibition at 0.05 μM MTX or higher concentrations.	Cancer Sci. 2010 Mar;101(3):728-34.
Jurkat cells	2 μM	6, 12, 24 hours	SU9516 started to decrease DHFR mRNA expression after 6 hours and DHFR protein levels after 12 hours.	Cancer Sci. 2010 Mar;101(3):728-34.
Jurkat cells	1, 2, 5, 10 μM	24 to 72 hours	SU9516 significantly inhibited the growth of Jurkat cells in a dose-dependent manner. After 72 h, cell growth was inhibited to 56%, 31%, 17%, and 9% of controls by SU9516 at 1, 2, 5, and 10 μM, respectively.	Cancer Sci. 2010 Mar;101(3):728-34.
Kasumi-1	500 nM	72 h	Evaluate the apoptotic effect of SU9516 in combination with ABT-737 and AKTi-1/2 on Kasumi-1 cells, showing significant increase in apoptosis	Int J Mol Sci. 2023 Mar 16;24(6):5717.
VMCF-7DNp53 cells	5 μM		Inhibited cdk2 activity, preventing centriole reduplication and centrosome amplification in vMCF-7DNp53 cells	Oncogene. 2008 Jun 26;27(28):3901-11.
Human normal foreskin skin fibroblast primary cells (CRL-2097)	10 μM	1 day	Convert fibroblasts into induced oligodendrocyte-like cells (iOLCs) expressing oligodendrocyte-specific marker O4.	Cells. 2022 Mar 24;11(7):1091.
SUM149PT cells	1 µM SU9516 combined with 0.5 µM paclitaxel	72 hours	To evaluate the cytotoxic effect of SU9516 combined with paclitaxel, showing that the combination significantly enhanced apoptosis.	Int J Oncol. 2014 Sep;45(3):1193-9.
SUM149PT cells	1 µM	72 hours	To evaluate the cytotoxic effect of SU9516 on CD44+/CD24-/Low CSCs, showing that CD44+/CD24-/Low CSCs were highly sensitive to SU9516.	Int J Oncol. 2014 Sep;45(3):1193-9.
VMCF-7DNp53/Aurora-A cells	1 µM	48 h	Inhibition of Cdk2 activity reduces Aurora-A centrosomal localization and suppresses centrosome amplification	Oncol Rep. 2013 May;29(5):1785-8.
VMCF-7DNp53 cells	1 µM	48 h	Inhibition of Cdk2 activity reduces Aurora-A centrosomal localization and suppresses centrosome amplification	Oncol Rep. 2013 May;29(5):1785-8.
CDK2	0.13 μM		SU9516 is an ATP-competitive inhibitor of CDK2 with an IC50 value of 0.13 μM	ACS Chem Biol. 2011 May 20;6(5):492-501.

Cell Line

Concentration

Treated Time

Description

References

MV4-11

500 nM

72 h

Evaluate the apoptotic effect of SU9516 in combination with ABT-737 and AKTi-1/2 on MV4-11 cells, showing significant increase in apoptosis

Int J Mol Sci. 2023 Mar 16;24(6):5717.

Human DMD patient myotubes

0.1 μM

SU9516 increased levels of α7β1 integrin and inhibited the SPAK/OSR1 kinase pathway

J Rare Dis Res Treat. 2017;2(5):1-4.

K562 cells

5 μM

24 hours

SU9516 significantly enhanced the sensitivity of K562 cells to MTX, with significant growth inhibition at 0.05 μM MTX or higher concentrations.

Cancer Sci. 2010 Mar;101(3):728-34.

CCRF-CEM cells

5 μM

24 hours

SU9516 significantly enhanced the sensitivity of CCRF-CEM cells to MTX, with significant growth inhibition at 0.05 μM MTX or higher concentrations.

Cancer Sci. 2010 Mar;101(3):728-34.

Jurkat cells

2 μM

6, 12, 24 hours

SU9516 started to decrease DHFR mRNA expression after 6 hours and DHFR protein levels after 12 hours.

Cancer Sci. 2010 Mar;101(3):728-34.

Jurkat cells

1, 2, 5, 10 μM

24 to 72 hours

SU9516 significantly inhibited the growth of Jurkat cells in a dose-dependent manner. After 72 h, cell growth was inhibited to 56%, 31%, 17%, and 9% of controls by SU9516 at 1, 2, 5, and 10 μM, respectively.

Cancer Sci. 2010 Mar;101(3):728-34.

Kasumi-1

500 nM

72 h

Evaluate the apoptotic effect of SU9516 in combination with ABT-737 and AKTi-1/2 on Kasumi-1 cells, showing significant increase in apoptosis

Int J Mol Sci. 2023 Mar 16;24(6):5717.

VMCF-7DNp53 cells

5 μM

Inhibited cdk2 activity, preventing centriole reduplication and centrosome amplification in vMCF-7DNp53 cells

Oncogene. 2008 Jun 26;27(28):3901-11.

Human normal foreskin skin fibroblast primary cells (CRL-2097)

10 μM

1 day

Convert fibroblasts into induced oligodendrocyte-like cells (iOLCs) expressing oligodendrocyte-specific marker O4.

Cells. 2022 Mar 24;11(7):1091.

SUM149PT cells

1 µM SU9516 combined with 0.5 µM paclitaxel

72 hours

To evaluate the cytotoxic effect of SU9516 combined with paclitaxel, showing that the combination significantly enhanced apoptosis.

Int J Oncol. 2014 Sep;45(3):1193-9.

SUM149PT cells

1 µM

72 hours

To evaluate the cytotoxic effect of SU9516 on CD44+/CD24-/Low CSCs, showing that CD44+/CD24-/Low CSCs were highly sensitive to SU9516.

Int J Oncol. 2014 Sep;45(3):1193-9.

VMCF-7DNp53/Aurora-A cells

1 µM

48 h

Inhibition of Cdk2 activity reduces Aurora-A centrosomal localization and suppresses centrosome amplification

Oncol Rep. 2013 May;29(5):1785-8.

VMCF-7DNp53 cells

1 µM

48 h

Inhibition of Cdk2 activity reduces Aurora-A centrosomal localization and suppresses centrosome amplification

Oncol Rep. 2013 May;29(5):1785-8.

CDK2

0.13 μM

SU9516 is an ATP-competitive inhibitor of CDK2 with an IC50 value of 0.13 μM

ACS Chem Biol. 2011 May 20;6(5):492-501.

SU9516 动物实验

Species C57/BL6 mice Mdx mice	Animal Model Cuprizone-induced demyelination model Duchenne muscular dystrophy model	Administration	Dosage	Frequency	Description	References
C57/BL6 mice	Cuprizone-induced demyelination model	Direct injection into the corpus callosum	100 μM	Single injection, lasting 2 weeks	Test the ability of the chemical cocktail to promote remyelination in vivo, showing significantly higher remyelination levels in the chemical cocktail injection group compared to the PBS control group.	Cells. 2022 Mar 24;11(7):1091.
Mdx mice	Duchenne muscular dystrophy model	Oral gavage	5mg/kg	Daily from 3 to 10 weeks of age	SU9516 treatment significantly improved weight gain, forelimb grip strength, diaphragm function, and reduced fibrosis	J Rare Dis Res Treat. 2017;2(5):1-4.

Species

C57/BL6 mice Mdx mice

Animal Model

Cuprizone-induced demyelination model Duchenne muscular dystrophy model

Administration

Dosage

Frequency

Description

References

C57/BL6 mice

Cuprizone-induced demyelination model

Direct injection into the corpus callosum

100 μM

Single injection, lasting 2 weeks

Test the ability of the chemical cocktail to promote remyelination in vivo, showing significantly higher remyelination levels in the chemical cocktail injection group compared to the PBS control group.

Cells. 2022 Mar 24;11(7):1091.

Mdx mice

Duchenne muscular dystrophy model

Oral gavage

5mg/kg

Daily from 3 to 10 weeks of age

SU9516 treatment significantly improved weight gain, forelimb grip strength, diaphragm function, and reduced fibrosis

J Rare Dis Res Treat. 2017;2(5):1-4.

SU9516 动物研究

Dose

Nude mice: 2.5 mg/kg/day - 10 mg/kg/day^[3] (p.o.)

Administration

p.o.

SU9516 参考文献

SU9516 实验方案

计算器

存储液制备

1mg

5mg

10mg

1 mM

5 mM

10 mM

4.15mL

0.83mL

0.41mL

20.73mL

4.15mL

2.07mL

41.45mL

8.29mL

4.15mL

SU9516 技术信息

CAS号	377090-84-1
分子式	C₁₃H₁₁N₃O₂
分子量	241.25
SMILES Code	O=C1NC2=C(C=C(OC)C=C2)/C1=C/C3=CNC=N3
MDL No.	MFCD17010284

别名
运输	蓝冰
InChI Key	QNUKRWAIZMBVCU-WCIBSUBMSA-N
Pubchem ID	5289419

存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Sealed in dry, 2-8°C

溶解方案

细胞实验：

DMSO: 105 mg/mL(435.24 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

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

SU9516 {[allProObj[0].p_purity_real_show]}

SU9516 纯度/质量文件产品仅供科研

全球学术期刊中引用的产品

SU9516 质控信息

SU9516 生物活性

SU9516 细胞实验

SU9516 动物实验

SU9516 动物研究

SU9516 参考文献

SU9516 实验方案

SU9516 技术信息

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靶点	CDK4 CDK4, IC50:200 nM CDK2 CDK2, IC50:22 nM CDK1 CDK1, IC50:40 nM
描述	Progression through the cell cycle is determined by sequential and specific phosphorylation events by holoenzymes involving cyclins and their catalytic partners, the CDKs. SU9516, a novel 3-substituted indolinone compound, binds to and selectively inhibits the activity of CDK2 with IC₅₀ of 22 nM. It also inhibits CDK1 and CDK4 with IC₅₀s of 40 nM and 200 nM. Continuous exposure to SU9516 (5 μM) for 24, 48, or 72 h resulted in a 4-52% decrease (P≤ 0.05) in CDK2-specific phosphorylation of pRb (retinoblastoma protein, a known CDK substrate) in RKO cells. The addition of 5 μM SU9516 produced a 27.6% decrease in RKO G₀-G₁ populations by 48 h post-drug addition and a 39.1% decrease by 72 h. A concomitant increase in RKO G₂-M populations results in a G₂-M block with G₂-M populations increasing by 13.1% over controls at 24 h to a 34.1% at 72 h post-drug addition. After continuous exposure to 5 μM SU9516 for 24, 48, and 72 h, both RKO (10-15%) and SW480 (4-22%) cells demonstrated an increase (P ≤ 0.01) in apoptosis. With inhibition of pRb phosphorylation, proliferation in both RKO and SW480 cells decreased in a dose-dependent manner at 20 h after treatment with SU9516^[3].
作用机制	SU9516’s planar structure binds to the catalytic domain of CDK2. The imidazole ring of SU9516 occupies the sugar-binding region. The N3 nitrogen on SU9516 may interact favorably with the side chain amino acid Lys89.

CDK4	CDK4, IC50:200 nM
CDK2	CDK2, IC50:22 nM
CDK1	CDK1, IC50:40 nM

SU9516 {[allProObj[0].p_purity_real_show]}

SU9516 纯度/质量文件 产品仅供科研

全球学术期刊中引用的产品

SU9516 质控信息

SU9516 生物活性

SU9516 细胞实验

SU9516 动物实验

SU9516 动物研究

SU9516 参考文献

SU9516 实验方案

SU9516 技术信息

最近浏览的产品

大规格询价

摩尔计算器

靶点

总药量计算器

工作液计算器

细胞研究

临床研究

确认信息

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SU9516 纯度/质量文件产品仅供科研