Inflachromene

Inflachromene, a microglial inhibitor, binds to HMGB1 and HMGB2 and exerts anti-inflammatory effects. Inflachromene effectively downregulates proinflammatory functions of HMGB and reduces neuronal damage. Inflachromene can be used for the research of neuroinflammatory disorders^[1][2]. IC50 & Target:HMGB^[2] In Vitro: Inflachromene (0.01-100 μM; 24 h) efficiently blocks LPS-induced nitrite release in a dose-dependent manner without any toxicity in BV-2 microglial cells^[2].
Inflachromene (1-10 μM) suppresses the increased levels of inflammation-related genes, such as Il6, Il1b, Nos2 and Tnf, after LPS stimulation^[2].
Inflachromene (5 μM) reduces LPS-induced secretion of the proinflammatory cytokine TNF-α^[2].
Inflachromene (5 μM; 30 min) substantially suppresses the nuclear translocation of NF-κB and the degradation of IκB^[2].
Inflachromene (1-10 μM; 30 min) inhibits LPS-induced phosphorylation of ERK, JNK and p38 MAPK in microglia^[2].
Inflachromene (10 μM; 30 min) completely prevents the death of cocultured neuroblastoma and primary neuronal cells by inhibiting microglia-mediated neurotoxicity^[2].
Inflachromene (1-10 μM; 24 h) has no significant effect on the viability of neurons^[2]. In Vivo: Inflachromene (2-10 mg/kg; i.p. once daily for 4 days) effectively blocks LPS-mediated microglial activation^[2].
Inflachromene (10 mg/kg; i.p. once daily for 30 days) significantly reduces the progression of disease, as determined by EAE clinical score^[2].
Inflachromene (1 mg/kg; i.v.) exhibits long half-life (14.1±6.43 h) and moderate V_ss (2.02±1.02 L/kg)^[1].
Inflachromene (1 mg/kg; p.o.) exhibits high oral bioavailability (94%) and C_max (0.59±0.16 g/mL)^[1].