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
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)
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
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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