产品
编 号：F162752
分子式：C28H27N3O4
分子量：469.53
分子式：C28H27N3O4
分子量：469.53
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
1mg
询价
询价
5mg
询价
询价
10mg
询价
询价
50mg
询价
询价
结构图
CAS No: 1435265-06-7
产品详情
生物活性：
HCH6-1 is a potent and competitive dipeptide antagonist of Formyl peptide receptor 1 (FPR1). HCH6-1 inhibits chemotaxis, superoxide anion generation, and elastase release in human neutrophils specifically activated by fMLF (an FPR1 agonist). HCH6-1 has protective effects against acute lung injury (ALI) in vivo and can be used for the research of FPR1-involved inflammatory lung diseases.
体内研究：
HCH6-1 (intraperitoneal injection; 50 mg/kg; 1 h before LPS spray or 30 min after LPS spray) alone does not induce airspace inflammation. HCH6-1 pretreatment reduces inflammatory cell infiltration and distortion of pulmonary architecture in the presence of LPS. HCH6-1 posttreatment shows inhibitory effects on neutrophil accumulation and lung damage in LPS-induced ALI mice.Animal Model:C57BL/6 mice (20-25 g, 7-8 weeks old)
Dosage:50 mg/kg
Administration:Intraperitoneal injection; 50 mg/kg; 1 h before LPS spray or 30 min after LPS spray
Result:Ameliorated ALI in LPS-induced mice.HCH6-1-mediated decreasing of neutrophil recruitment serves as a protective mechanism in ALI mice.
体外研究：
In a cell-impermeable cytochrome c reduction assay, HCH6-1 significantly inhibits superoxide anion generation in fMLF (FPR1 agonist)-activated neutrophils with anIC50 of 0.32 μM. HCH6-1 has fewer inhibitory effects in WKYMVm (dual FPR1/FPR2 agonist)- and MMK1 (FPR2 agonist)-activated neutrophils, with IC50s of 4.98±0.27 μM and 17.68±2.77 μM, respectively.HCH6-1 does not induce LDH release even at 30 μM, so it does not have cytotoxic effects in human neutrophils. HCH6-1 does not alter the level of xanthine/xanthine oxidase superoxide anion and DPPH radical in cell-free systems.HCH6-1 significantly inhibits elastase release in fMLF-activated neutrophils, with an IC50 of 0.57 μM. However, in neutrophils triggered by WKYMVm or MMK1, HCH6-1 inhibits elastase release at higher concentrations, with IC50s of 5.22±0.69 μM and 10.00±0.65 μM, respectively.
HCH6-1 is a potent and competitive dipeptide antagonist of Formyl peptide receptor 1 (FPR1). HCH6-1 inhibits chemotaxis, superoxide anion generation, and elastase release in human neutrophils specifically activated by fMLF (an FPR1 agonist). HCH6-1 has protective effects against acute lung injury (ALI) in vivo and can be used for the research of FPR1-involved inflammatory lung diseases.
体内研究：
HCH6-1 (intraperitoneal injection; 50 mg/kg; 1 h before LPS spray or 30 min after LPS spray) alone does not induce airspace inflammation. HCH6-1 pretreatment reduces inflammatory cell infiltration and distortion of pulmonary architecture in the presence of LPS. HCH6-1 posttreatment shows inhibitory effects on neutrophil accumulation and lung damage in LPS-induced ALI mice.Animal Model:C57BL/6 mice (20-25 g, 7-8 weeks old)
Dosage:50 mg/kg
Administration:Intraperitoneal injection; 50 mg/kg; 1 h before LPS spray or 30 min after LPS spray
Result:Ameliorated ALI in LPS-induced mice.HCH6-1-mediated decreasing of neutrophil recruitment serves as a protective mechanism in ALI mice.
体外研究：
In a cell-impermeable cytochrome c reduction assay, HCH6-1 significantly inhibits superoxide anion generation in fMLF (FPR1 agonist)-activated neutrophils with anIC50 of 0.32 μM. HCH6-1 has fewer inhibitory effects in WKYMVm (dual FPR1/FPR2 agonist)- and MMK1 (FPR2 agonist)-activated neutrophils, with IC50s of 4.98±0.27 μM and 17.68±2.77 μM, respectively.HCH6-1 does not induce LDH release even at 30 μM, so it does not have cytotoxic effects in human neutrophils. HCH6-1 does not alter the level of xanthine/xanthine oxidase superoxide anion and DPPH radical in cell-free systems.HCH6-1 significantly inhibits elastase release in fMLF-activated neutrophils, with an IC50 of 0.57 μM. However, in neutrophils triggered by WKYMVm or MMK1, HCH6-1 inhibits elastase release at higher concentrations, with IC50s of 5.22±0.69 μM and 10.00±0.65 μM, respectively.
产品资料
Copyright©2015-2024 沪ICP备2022026524号-1
沪公网安备