SB 265610 - CAS 211096-49-0
Catalog number: 211096-49-0
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
C14H9BrN6O
Molecular Weight:
357.16
COA:
Inquire
Targets:
CXCR
Description:
Potent CXCR2 antagonist
Brife Description:
Potent CXCR2 antagonist
Appearance:
Beige solid
Synonyms:
SB-265610; SB 265610; SB265610. 1-(2-bromophenyl)-3-(7-cyano-2H-benzotriazol-4-yl)urea; N-(2-Bromophenyl)-N'-(7-cyano-1H-benzotriazol-4-yl)urea
Solubility:
Soluble to 100 mM in DMSO and to 10 mM in ethanol
Storage:
Store at RT
MSDS:
Inquire
Quality Standard:
In-house
Quantity:
Grams-Kilos
Boiling Point:
527° C at 760 mmHg (Predicted)
Melting Point:
246.53° C (Predicted)
InChIKey:
SEDUMQWZEOMXSO-UHFFFAOYSA-N
InChI:
1S/C14H9BrN6O/c15-9-3-1-2-4-10(9)17-14(22)18-11-6-5-8(7-16)12-13(11)20-21-19-12/h1-6H,(H2,17,18,22)(H,19,20,21)
Canonical SMILES:
C1=CC=C(C(=C1)NC(=O)NC2=CC=C(C3=NNN=C23)C#N)Br
1.Neutrophil elastase-induced elastin degradation mediates macrophage influx and lung injury in 60% O2-exposed neonatal rats.
Masood A;Yi M;Belcastro R;Li J;Lopez L;Kantores C;Jankov RP;Tanswell AK Am J Physiol Lung Cell Mol Physiol. 2015 Jul 1;309(1):L53-62. doi: 10.1152/ajplung.00298.2014. Epub 2015 May 1.
Neutrophil (PMNL) influx precedes lung macrophage (LM) influx into the lung following exposure of newborn pups to 60% O2. We hypothesized that PMNL were responsible for the signals leading to LM influx. This was confirmed when inhibition of PMNL influx with a CXC chemokine receptor-2 antagonist, SB-265610, also prevented the 60% O2-dependent LM influx, LM-derived nitrotyrosine formation, and pruning of small arterioles. Exposure to 60% O2 was associated with increased lung contents of neutrophil elastase and α-elastin, a marker of denatured elastin, and a decrease in elastin fiber density. This led us to speculate that neutrophil elastase-induced elastin fragments were the chemokines that led to a LM influx into the 60% O2-exposed lung. Inhibition of neutrophil elastase with sivelestat or elafin attenuated the LM influx. Sivelestat also attenuated the 60% O2-induced decrease in elastin fiber density. Daily injections of pups with an antibody to α-elastin prevented the 60% O2-dependent LM influx, impaired alveologenesis, and impaired small vessel formation. This suggests that neutrophil elastase inhibitors may protect against neonatal lung injury not only by preventing structural elastin degradation, but also by blocking elastin fragment-induced LM influx, thus preventing tissue injury from LM-derived peroxynitrite formation.
2.Identification and profiling of novel α1A-adrenoceptor-CXC chemokine receptor 2 heteromer.
Mustafa S;See HB;Seeber RM;Armstrong SP;White CW;Ventura S;Ayoub MA;Pfleger KD J Biol Chem. 2012 Apr 13;287(16):12952-65. doi: 10.1074/jbc.M111.322834. Epub 2012 Feb 27.
We have provided the first evidence for specific heteromerization between the α(1A)-adrenoceptor (α(1A)AR) and CXC chemokine receptor 2 (CXCR2) in live cells. α(1A)AR and CXCR2 are both expressed in areas such as the stromal smooth muscle layer of the prostate. By utilizing the G protein-coupled receptor (GPCR) heteromer identification technology on the live cell-based bioluminescence resonance energy transfer (BRET) assay platform, our studies in human embryonic kidney 293 cells have identified norepinephrine-dependent β-arrestin recruitment that was in turn dependent upon co-expression of α(1A)AR with CXCR2. These findings have been supported by co-localization observed using confocal microscopy. This norepinephrine-dependent β-arrestin recruitment was inhibited not only by the α(1)AR antagonist Terazosin but also by the CXCR2-specific allosteric inverse agonist SB265610. Furthermore, Labetalol, which is marketed for hypertension as a nonselective β-adrenoceptor antagonist with α(1)AR antagonist properties, was identified as a heteromer-specific-biased agonist exhibiting partial agonism for inositol phosphate production but essentially full agonism for β-arrestin recruitment at the α(1A)AR-CXCR2 heteromer.
3.CXCL1-CXCR2 axis mediates angiotensin II-induced cardiac hypertrophy and remodelling through regulation of monocyte infiltration.
Wang L;Zhang YL;Lin QY;Liu Y;Guan XM;Ma XL;Cao HJ;Liu Y;Bai J;Xia YL;Du J;Li HH Eur Heart J. 2018 May 21;39(20):1818-1831. doi: 10.1093/eurheartj/ehy085.
Aims: ;Chemokine-mediated monocyte infiltration into the damaged heart represents an initial step in inflammation during cardiac remodelling. Our recent study demonstrates a central role for chemokine receptor CXCR2 in monocyte recruitment and hypertension; however, the role of chemokine CXCL1 and its receptor CXCR2 in angiotensin II (Ang II)-induced cardiac remodelling remain unknown.;Methods and results: ;Angiotensin II (1000 ng kg-1 min-1) was administrated to wild-type (WT) mice treated with CXCL1 neutralizing antibody or CXCR2 inhibitor SB265610, knockout (CXCR2 KO) or bone marrow (BM) reconstituted chimeric mice for 14 days. Microarray revealed that CXCL1 was the most highly upregulated chemokine in the WT heart at Day 1 after Ang II infusion. The CXCR2 expression and the CXCR2+ immune cells were time-dependently increased in Ang II-infused hearts. Moreover, administration of CXCL1 neutralizing antibody markedly prevented Ang II-induced hypertension, cardiac dysfunction, hypertrophy, fibrosis, and macrophage accumulation compared with Immunoglobulin G (IgG) control. Furthermore, Ang II-induced cardiac remodelling and inflammatory response were also significantly attenuated in CXCR2 KO mice and in WT mice treated with SB265610 or transplanted with CXCR2-deficienct BM cells.
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CAS 211096-49-0 SB 265610

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