SML3529
GB83
≥98% (HPLC)
别名:
GB 83, GB-83, N-[(1S)-1-(Cyclohexylmethyl)-2-[[(1S,2S)-1-[(2,3-dihydrospiro[1H-indene-1,4′-piperidin]-1′-yl)carbonyl]-2-methylbutyl]amino]-2-oxoethyl]-5-isoxazolecarboxamide
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关于此项目
经验公式（希尔记法）:
C32H44N4O4
化学文摘社编号:
分子量:
548.72
UNSPSC Code:
51111800
NACRES:
NA.77
MDL number:
产品名称
GB83, ≥98% (HPLC)
InChI
1S/C32H44N4O4/c1-3-22(2)28(31(39)36-19-16-32(17-20-36)15-13-24-11-7-8-12-25(24)32)35-29(37)26(21-23-9-5-4-6-10-23)34-30(38)27-14-18-33-40-27/h7-8,11-12,14,18,22-23,26,28H,3-6,9-10,13,15-17,19-21H2,1-2H3,(H,34,38)(H,35,37)/t22?,26-,28-/m0/s1
SMILES string
CC[C@@H]([C@H](NC([C@@H](NC(C1=CC=NO1)=O)CC2CCCCC2)=O)C(N3CCC4(CC3)CCC5=C4C=CC=C5)=O)C
InChI key
ZXMXAOYWSLZLQM-NZNGGYBSSA-N
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear
storage temp.
2-8°C
Quality Level
Biochem/physiol Actions
GB83 is a serum stable, potent and selective antagonist of human protease activated receptor 2 (PAR2)(IC50 = 2 µM) that reversibly inhibit PAR2 activation by both proteases and PAR2 agonists. GB83 prevented upregulation of PARs, ICAM-1, LOX-1, IL-8, and activation of MAP kinases by coagulation factor X (FXa) in atrial tissue slices
Serum stable, potent and selective antagonist of human protease activated receptor 2 (PAR2)
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
Grant D Barry et al.
Journal of medicinal chemistry, 53(20), 7428-7440 (2010-09-30)
Human protease activated receptor 2 (PAR2) is a G protein-coupled receptor that is associated with inflammatory diseases and cancers. PAR2 is activated by serine proteases that cleave its N-terminus and by synthetic peptides corresponding to the new N-terminus. Peptide agonists
Prophylactic inhibition of neutrophil elastase prevents the development of chronic neuropathic pain in osteoarthritic mice
Muley MM, Krustev E, Reid AR, McDougall JJ
Journal of Neuroinflammation, 14, 168-168 (2017)
Alicja Bukowska et al.
European journal of pharmacology, 869, 172875-172875 (2019-12-27)
There is growing evidence for the contribution of the activated coagulation factor X (FXa) in the development of chronic inflammatory lung diseases. Therefore, we aimed to investigate effects of exogenous FXa on mitochondrial and metabolic function as well as the
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