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Merck
CN

B9935

Sigma-Aldrich

BMS-345541

≥98% (HPLC), powder

别名:

N-(1,8-二甲基咪唑并[1,2-a] 喹喔啉-4-基)-1,2-乙二胺 盐酸盐

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About This Item

经验公式(希尔记法):
C14H17N5 · HCl
分子量:
291.78
MDL编号:
UNSPSC代码:
12352200
PubChem化学物质编号:
NACRES:
NA.77

质量水平

检测方案

≥98% (HPLC)

形式

powder

储存条件

desiccated

溶解性

DMSO: 18 mg/mL
H2O: insoluble

创始人

Bristol-Myers Squibb

储存温度

2-8°C

SMILES字符串

Cl[H].Cc1ccc2nc(NCCN)c3ncc(C)n3c2c1

InChI

1S/C14H17N5.ClH/c1-9-3-4-11-12(7-9)19-10(2)8-17-14(19)13(18-11)16-6-5-15;/h3-4,7-8H,5-6,15H2,1-2H3,(H,16,18);1H

InChI key

MIDKPVLYXNLFGZ-UHFFFAOYSA-N

相关类别

应用

BMS-345541已用于:
  • 作为IκB 激酶 (IKK) 复合抑制剂,研究其对由自然杀伤 (NK) 细胞产生的干扰素γ (IFN-γ)的影响
  • 作为 IKK 抑制剂,研究其对牙龈成纤维细胞中嗜酸性粒细胞趋化因子和单核细胞趋化蛋白-1 (MCP-1) mRNA 表达的影响
  • 作为核因子 κB (NF-κB) 通路抑制剂,研究其对在人口腔鳞状细胞癌细胞所产生的肿瘤坏死因子α (TNFα)的影响

生化/生理作用

BMS-345541 具有抗炎特性。它还可以阻断促炎细胞因子的核因子 κB (NF-κB) 依赖性转录。BMS-345541具有抗炎活性,并在某些动物模型中起到阻止骨侵蚀的作用。
BMS-345541是一种 IKB(IKK)变构位点抑制剂。

特点和优势

该化合物由Bristol-Myers Squibb开发。要浏览其他药物开发化合物和批准的药物/候选药物列表,请点击此处
这种化合物是基因调控研究的特色产品。点击此处发现更多特色基因调控产品。在sigma.com/discover-bsm可了解更多关于生物活性小分子的其他研究领域。

WGK

WGK 3

闪点(°F)

Not applicable

闪点(°C)

Not applicable

个人防护装备

Eyeshields, Gloves, type N95 (US)


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Neety Sahu et al.
JCI insight, 7(20) (2022-10-05)
No disease-modifying drug exists for osteoarthritis (OA). Despite success in animal models, candidate drugs continue to fail in clinical trials owing to the unmapped interpatient heterogeneity and disease complexity. We used a single-cell platform based on cytometry by time-of-flight (cyTOF)
James R Burke et al.
The Journal of biological chemistry, 278(3), 1450-1456 (2002-10-31)
The signal-inducible phosphorylation of serines 32 and 36 of I kappa B alpha is critical in regulating the subsequent ubiquitination and proteolysis of I kappa B alpha, which then releases NF-kappa B to promote gene transcription. The multisubunit I kappa
Zhiyang Chen et al.
The Journal of experimental medicine, 216(1), 152-175 (2018-12-12)
Organism aging is characterized by increased inflammation and decreased stem cell function, yet the relationship between these factors remains incompletely understood. This study shows that aged hematopoietic stem and progenitor cells (HSPCs) exhibit increased ground-stage NF-κB activity, which enhances their
Christina Ward et al.
Tissue barriers, 3(1-2), e982424-e982424 (2015-04-04)
NF-κB (p50/p65) is the best characterized transcription factor known to regulate cell responses to inflammation. However, NF-κB is also constitutively expressed. We used inhibitors of the classical NF-κB signaling pathway to determine whether this transcription factor has a role in
Aminah Ikner et al.
The Journal of biological chemistry, 286(24), 21546-21554 (2011-04-29)
The tumor necrosis factor (TNF) superfamily member TNF-like weak inducer of apoptosis (TNFSF12, CD255) (TWEAK) can stimulate apoptosis in certain cancer cells. Previous studies suggest that TWEAK activates cell death indirectly, by inducing TNFα-mediated autocrine signals. However, the underlying death-signaling

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