Quin-C7 is an orally active FPR2/ALX antagonist. Quin-C7 binds to the orthosteric ligand-binding pocket of FPR2/ALX, modulates receptor activation, and inhibits pro-inflammatory ERK signaling mediated by serum amyloid A (SAA). Quin-C7 reduces pro-inflammatory mediators TNF-α levels, increases anti-inflammatory IL-10, decreases inflammatory neutrophils and pro-inflammatory M1 macrophages, downregulates ERK1/2 phosphorylation, and upregulates JNK1/2/3 phosphorylation. Quin-C7 blocks FPR2/mFpr2 signaling, reduces brain lesion volume. Quin-C7 can be used for the research of inflammatory bowel disease and neuromyelitis optica spectrum disorder [1] [2].
In Vivo, Quin-C7 (0.512-320 mg/kg; I.g.; daily; 7 days) ameliorates DSS -induced acute colitis in male C57BL/6N mice with an ED50 of 2.2110 mg/kg for symptomatic DAI improvement, via modulation of myeloid cell activity and ERK/JNK signaling pathways[1]. Quin-C7 (16-32 mg/kg; i.g.; daily; 4 days) significantly reduces pathology in NMOSD mice[2].
In Vitro, Quin-C7 binds with high affinity to human FPR2/ALX, forming a network of polar and stacking interactions with receptor residues, including a unique hydrogen bond with Q2586.52[1].
References:
[1]. Yang WS, et al. Oral FPR2/ALX modulators tune myeloid cell activity to ameliorate mucosal inflammation in inflammatory bowel disease. Acta Pharmacol Sin. 2025;46(7):1958-1973.
[2]. Qi C, et al. Targeting formyl peptide receptor 2 to suppress neuroinflammation in neuromyelitis optica spectrum disorder. Theranostics. 2025;15(10):4495-4506. Published 2025 Mar 19.
In Vivo, Quin-C7 (0.512-320 mg/kg; I.g.; daily; 7 days) ameliorates DSS -induced acute colitis in male C57BL/6N mice with an ED50 of 2.2110 mg/kg for symptomatic DAI improvement, via modulation of myeloid cell activity and ERK/JNK signaling pathways[1]. Quin-C7 (16-32 mg/kg; i.g.; daily; 4 days) significantly reduces pathology in NMOSD mice[2].
In Vitro, Quin-C7 binds with high affinity to human FPR2/ALX, forming a network of polar and stacking interactions with receptor residues, including a unique hydrogen bond with Q2586.52[1].
References:
[1]. Yang WS, et al. Oral FPR2/ALX modulators tune myeloid cell activity to ameliorate mucosal inflammation in inflammatory bowel disease. Acta Pharmacol Sin. 2025;46(7):1958-1973.
[2]. Qi C, et al. Targeting formyl peptide receptor 2 to suppress neuroinflammation in neuromyelitis optica spectrum disorder. Theranostics. 2025;15(10):4495-4506. Published 2025 Mar 19.