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B9935

Sigma-Aldrich

BMS-345541

≥98% (HPLC), powder

Szinonimák:

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

Bejelentkezésa Szervezeti és Szerződéses árazás megtekintéséhez
Összes fotó(1)

About This Item

Tapasztalati képlet (Hill-képlet):
C14H17N5 · HCl
CAS-szám:
547757-23-3
Molekulatömeg:
291.78
MDL-szám:
MFCD07784499
UNSPSC kód:
12352200
PubChem Substance ID:
24724429
NACRES:
NA.77

Minőségi szint

100

Teszt

≥98% (HPLC)

form

powder

tárolási körülmény

desiccated

oldhatóság

DMSO: 18 mg/mL
H2O: insoluble

kezdeményező

Bristol-Myers Squibb

tárolási hőmérséklet

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

Nemzetközi kémiai azonosító kulcs

MIDKPVLYXNLFGZ-UHFFFAOYSA-N

Alkalmazás

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

Biokémiai/fiziológiai hatások

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.

Tulajdonságok és előnyök

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.

Tárolási osztály kódja

11 - Combustible Solids

WGK

WGK 3

Lobbanási pont (F)

Not applicable

Lobbanási pont (C)

Not applicable

Egyéni védőeszköz

Eyeshields, Gloves, type N95 (US)

Analitikai tanúsítványok (COA)

Analitikai tanúsítványok (COA) keresése a termék sarzs-/tételszámának megadásával. A sarzs- és tételszámok a termék címkéjén találhatók, a „Lot” vagy „Batch” szavak után.

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Az Ön által nemrégiben megvásárolt termékekre vonatkozó dokumentumokat a Dokumentumtárban találja.

Dokumentumtár megtekintése

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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Cikkek

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We offer a variety of small molecule research tools, such as transcription factor modulators, inhibitors of chromatin modifying enzymes, and agonists/antagonists for target identification and validation in gene regulation research; a selection of these research tools is shown below.

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