Merck
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文件

SML2703

Sigma-Aldrich

BAY-293

≥98% (HPLC)

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别名:
6,7-Dimethoxy-2-methyl-N-[(R)-1-(4-{2-[(methylamino)methyl]phenyl}thien-2-yl)ethyl]quinazolin-4-amine, BAY 293, BAY293
Empirical Formula (Hill Notation):
C25H28N4O2S
CAS号:
2244904-70-7
分子量:
448.58

质量水平

100

检测方案

≥98% (HPLC)

形式

powder

旋光性

[α]/D -85.0 to -103.0°, c = 1.0 in DMSO

颜色

white to beige

溶解性

DMSO: 2 mg/mL, clear

储存温度

−20°C

SMILES string

C[C@H](C1=CC(C2=CC=CC=C2CNC)=CS1)NC3=C4C=C(C(OC)=CC4=NC(C)=N3)OC

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此商品
SML2704SML2719SML3202
BAY-293 ≥98% (HPLC)

Sigma-Aldrich

SML2703

BAY-293

BAY-294 ≥98% (HPLC)

Sigma-Aldrich

SML2704

BAY-294

AVE 0991 ≥98% (HPLC)

Sigma-Aldrich

SML2719

AVE 0991

TL02-59 ≥98% (HPLC)

Sigma-Aldrich

SML3202

TL02-59

form

powder

form

powder

form

powder

form

powder

color

white to beige

color

white to beige

color

white to beige

color

white to beige

solubility

DMSO: 2 mg/mL, clear

solubility

DMSO: 2 mg/mL, clear

solubility

DMSO: 2 mg/mL, clear

solubility

DMSO: 2 mg/mL, clear

storage temp.

−20°C

storage temp.

−20°C

storage temp.

−20°C

storage temp.

−20°C

Quality Level

100

Quality Level

100

Quality Level

100

Quality Level

100

生化/生理作用

BAY-293 selectively inhibits SOS1-mediated KRAS activation (IC50 = 52 nM; 50 nM wt or G12C hKRAS & 10 nM SOS1cat) via direct SOS1 binding, blocking SOS1-KRAS interaction (IC50 = 21 nM; 10 nM hSOS1cat & 5 nM hKRAS G12C) without affecting (IC50 >20 μM) CRAF RBD-KRAS interaction, KRAS G12C activation by SOS2, Cdc42 activation by DBS, or EGFR kinase activity. BAY-293 downregulates cellular active RAS (IC50 = 200 nM/Calu-1, 410 nM/HeLa) and downstream ERK phosphorylation (K-562, 150 nM/Calu-1) with good target selectivity as assessed over 358 kinases (<37% inhibition at 1 μM) and a panel of 77 GPCRs, transporters, nuclear receptors and enzymes.

储存分类代码

11 - Combustible Solids

WGK

WGK 3

闪点(F)

Not applicable

闪点(C)

Not applicable

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Roman C Hillig et al.
Proceedings of the National Academy of Sciences of the United States of America, 116(7), 2551-2560 (2019-01-27)
Since the late 1980s, mutations in the RAS genes have been recognized as major oncogenes with a high occurrence rate in human cancers. Such mutations reduce the ability of the small GTPase RAS to hydrolyze GTP, keeping this molecular switch

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