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MedChemExpress - Model HCH6-1 -1435265-06-7
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[1].MCE products for research use only. We do not sell to patients.
HCH6-1
MCE China：HCH6-1
Brand：MedChemExpress (MCE)
Cat. No.HY-101283
CAS：1435265-06-7
Purity：99.16%
Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Shipping：Room temperature in continental US; may vary elsewhere.
Description：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.
In Vitro：In a cell-impermeable cytochrome c reduction assay, HCH6-1 significantly inhibits superoxide anion generation in fMLF (FPR1 agonist)-activated neutrophils with an IC50 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[1].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[1].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[1].
In Vivo：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[1].
IC50 & Target：IC50: Formyl peptide receptor 1 (FPR1)[1] Cellular Effect Cell Line Type Value Description References
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References：
[1]. Yang SC, et al. Dipeptide HCH6-1 inhibits neutrophil activation and protects against acute lung injury by blocking FPR1. Free Radic Biol Med. 2017 May;106:254-269 [Content Brief]
Brand introduction:
• MCE (MedChemExpress) has a global exclusive compound library of more than 200 kinds, and we are committed to providing the most comprehensive range of high-quality small molecule active compounds for scientific research customers around the world；
• More than 50,000 highly selective inhibitors and agonists are involved in various popular signaling pathways and disease areas；
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