BMS CCR2 22 - CAS 445479-97-0
Catalog number: 445479-97-0
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C28H34F3N5O4S
Molecular Weight:
593.66
COA:
Inquire
Targets:
CCR
Description:
High affinity, potent CCR2 antagonist
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Brife Description:
High affinity, potent CCR2 antagonist
Appearance:
White solid
Synonyms:
N-[2-[[2-[(4-methylsulfanylbenzoyl)amino]cyclohexyl]amino]-2-oxoethyl]-2-(propan-2-ylcarbamoylamino)-5-(trifluoromethyl)benzamide;
Solubility:
Soluble to 100 mM in DMSO and to 10 mM in ethanol.
Storage:
Store at +4°C
MSDS:
Inquire
Quantity:
Grams-Kilos
Boiling Point:
764.9° C at 760 mmHg (Predicted)
InChIKey:
IBPXYDUJQWENPM-UHFFFAOYSA-N
InChI:
1S/C28H34F3N5O4S/c1-16(2)33-27(40)36-21-13-10-18(28(29,30)31)14-20(21)26(39)32-15-24(37)34-22-6-4-5-7-23(22)35-25(38)17-8-11-19(41-3)12-9-17/h8-14,16,22-23H,4-7,15H2,1-3H3,(H,32,39)(H,34,37)(H,35,38)(H2,33,36,40)
Canonical SMILES:
CC(C)NC(=O)NC1=C(C=C(C=C1)C(F)(F)F)C(=O)NCC(=O)NC2CCCCC2NC(=O)C3=CC=C(C=C3)S C For Research Use Only. Not Intended for Diagnostic or Therapeutic Use.
1.Age exacerbates the CCR2/5-mediated neuroinflammatory response to traumatic brain injury.
Morganti JM1,2, Riparip LK1, Chou A1,3, Liu S4, Gupta N4,5, Rosi S6,7,8,9. J Neuroinflammation. 2016 Apr 18;13(1):80. doi: 10.1186/s12974-016-0547-1.
BACKGROUND: Traumatic brain injury (TBI) is a major risk factor for the development of multiple neurodegenerative diseases, including Alzheimer's disease (AD) and numerous recent reports document the development of dementia after TBI. Age is a significant factor in both the risk of and the incidence of acquired brain injury. TBI-induced inflammatory response is associated with activation of brain resident microglia and accumulation of infiltrating monocytes, which plays a pivotal role in chronic neurodegeneration and loss of neurological function after TBI. Despite the extensive clinical evidence implicating neuroinflammation with the TBI-related sequelae, the specific role of these different myeloid cells and the influence of age on TBI-initiated innate immune response remain unknown and poorly studied.
2.A novel antagonist of p75NTR reduces peripheral expansion and CNS trafficking of pro-inflammatory monocytes and spares function after traumatic brain injury.
Lee S1, Mattingly A2, Lin A1, Sacramento J1, Mannent L3, Castel MN3, Canolle B3, Delbary-Gossart S4, Ferzaz B3, Morganti JM1, Rosi S1,2, Ferguson AR1,2, Manley GT1, Bresnahan JC1, Beattie MS5,6. J Neuroinflammation. 2016 Apr 22;13(1):88. doi: 10.1186/s12974-016-0544-4.
BACKGROUND: Traumatic brain injury (TBI) results in long-term neurological deficits, which may be mediated in part by pro-inflammatory responses in both the injured brain and the circulation. Inflammation may be involved in the subsequent development of neurodegenerative diseases and post-injury seizures. The p75 neurotrophin receptor (p75NTR) has multiple biological functions, affecting cell survival, apoptotic cell death, axonal growth, and degeneration in pathological conditions. We recently found that EVT901, a novel piperazine derivative that inhibits p75NTR oligomerization, is neuroprotective, reduces microglial activation, and improves outcomes in two models of TBI in rats. Since TBI elicits both CNS and peripheral inflammation, we used a mouse model of TBI to examine whether EVT901 would affect peripheral immune responses and trafficking to the injured brain.
3.Berberine in combination with yohimbine attenuates sepsis-induced neutrophil tissue infiltration and multiorgan dysfunction partly via IL-10-mediated inhibition of CCR2 expression in neutrophils.
Wang Y1, Wang F1, Yang D1, Tang X1, Li H1, Lv X1, Lu D1, Wang H2. Int Immunopharmacol. 2016 Jun;35:217-25. doi: 10.1016/j.intimp.2016.03.041. Epub 2016 Apr 16.
Infiltration of activated neutrophils into the vital organs contributes to the multiple organ dysfunctions in sepsis. In the present study, we investigated the effects of berberine in combination with yohimbine (BY) on neutrophil tissue infiltration and multiple organ damage during sepsis, and further elucidated the involved mechanisms. Sepsis was induced in mice by cecal ligation and puncture (CLP). BY or CCR2 antagonist was administered 2h after CLP, and anti-IL-10 antibody (IL-10 Ab) or control IgG was injected intraperitoneally just before BY treatment. We found that IL-10 production was enhanced by BY therapy in septic mice. BY significantly attenuated neutrophil tissue infiltration and multiple organ injury in CLP-challenged mice, all of which were completely reversed by IL-10 Ab pretreatment. The levels of KC, MCP-1, MIP-1α and MIP-2 in the lung, liver and kidney were markedly increased 6h after CLP. BY reduced the tissue concentrations of these chemokines in septic mice, but IL-10 Ab pretreatment did not completely eliminate these inhibitory effects of BY.
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CAS 445479-97-0 BMS CCR2 22

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