Inflachromene (ICM) is an inhibitor of HMGB1 and HMGB expression with anti-inflammatory activity.Inflachromene reduces seizure severity in a mouse model of epilepsy by inhibiting HMGB1 translocation, inhibits endothelial proliferation through the HMGB1/2-regulated TLR4-NF-κB pathway, and inhibits autophagy by regulating Beclin 1 activity. Inflachromene can be used to study epilepsy.

In BV-2 microglial cells, Inflachromene efficiently blocks LPS-induced nitrite release in a dose-dependent manner (0.01-100 μM; 24 h) without any toxicity[1].
After LPS stimulation, Inflachromene (1-10 μM) suppresses the increased levels of inflammation-related genes, such as Il6, Il1b, Nos2, and Tnf[1].
At a concentration of 5 μM, Inflachromene reduces LPS-induced secretion of the proinflammatory cytokine TNF-α[1].
In microglia, Inflachromene (5 μM; 30 min) substantially suppresses the nuclear translocation of NF-κB and the degradation of IκB[1].
The phosphorylation of ERK, JNK, and p38 MAPK in microglia induced by LPS is inhibited by Inflachromene (1-10 μM; 30 min)[1].
In the co-culture of neuroblastoma and primary neuronal cells, Inflachromene (10 μM; 30 min) completely prevents the death by inhibiting microglia-mediated neurotoxicity[1].There is no significant effect on the viability of neurons with Inflachromene (1-10 μM; 24 h)[1].

In a dose-dependent manner (2-10 mg/kg; i.p. once daily for 4 days), Inflachromene effectively blocks LPS-mediated microglial activation[1].
For a duration of 30 days (10 mg/kg; i.p. once daily), Inflachromene significantly reduces the progression of disease, as determined by EAE clinical score[1].
When administered intravenously (i.v.) at a dose of 1 mg/kg, Inflachromene exhibits a long half-life (14.1±6.43 h) and moderate Vss (2.02±1.02 L/kg)[2].
Given orally (p.o.) at a dose of 1 mg/kg, Inflachromene shows high oral bioavailability (94%) and Cmax (0.59±0.16 g/mL)[2].