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B9935

Sigma-Aldrich

BMS-345541

≥98% (HPLC), powder

Synonym(s):

N-(1,8-Dimethylimidazo[1,2-a]quinoxalin-4-yl)-1,2-ethanediamine hydrochloride

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About This Item

Empirical Formula (Hill Notation):
C14H17N5 · HCl
CAS Number:
547757-23-3
Molecular Weight:
291.78
MDL number:
MFCD07784499
UNSPSC Code:
12352200
PubChem Substance ID:
24724429
NACRES:
NA.77

Quality Level

100

assay

≥98% (HPLC)

form

powder

storage condition

desiccated

solubility

DMSO: 18 mg/mL
H2O: insoluble

originator

Bristol-Myers Squibb

storage temp.

2-8°C

SMILES string

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

Application

BMS-345541 has been used:
  • as an IκB kinase (IKK) complex inhibitor to study its effects on the interferon-γ (IFN-γ) production by natural killer (NK) cells
  • as an IKK inhibitor to study its effects on the expression of eotaxin and monocyte chemoattractant protein-1 (MCP-1) mRNA in gingival fibroblasts
  • as nuclear factor κB (NF-κB) pathway inhibitor to study its effects on tumor necrosis factor α (TNFα) production in human oral squamous carcinoma cells

Biochem/physiol Actions

BMS-345541 possesses anti-inflammatory properties. It also blocks the nuclear factor κB (NF-κB)-dependent transcription of pro-inflammatory cytokines. BMS-345541 possesses anti-inflammatory activity and plays a role in arresting bone erosion in certain animal models.
BMS-345541 is an IKB kinase (IKK) allosteric site inhibitor.

Features and Benefits

This compound is a featured product for Gene Regulation research. Click here to discover more featured Gene Regulation products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.
This compound was developed by Bristol-Myers Squibb. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

ppe

Eyeshields, Gloves, type N95 (US)

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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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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