Description
L6H21 binds to MD-2 (myeloid differentiation protein-2, Kd=33.3 μM) and blocks its interaction with TLR4 (toll-like receptor 4) in LPS-stimulated cells, inhibiting TNFα and IL-6 production.1 Attenuates disease progression in a high-fat diet (HFD) induced NASH mouse model.2 Inhibits obesity-induced cardiomyopathy and fibrosis.3 Reduces ethanol plus LPS-induced liver injury via inhibition of NLRP3 inflammasome activation.4 Provides cardioprotective effects5 and protects against cognitive impairment and brain pathologies in HFD prediabetic rats6. Cell permeable. Active in vivo.
References
Wang et al. (2015), MD-2 as the target of a novel small molecule, L6H21, in the attenuation of LPS-induced inflammatory response and sepsis; J. Pharmacol., 172 4391
Zhang et al. (2018), Inhibition of MD1-dependent inflammation attenuates the progression of non-alcoholic fatty liver disease; Cell. Mol. Med., 22 936
Fang et al. (2018), Inhibition of myeloid differentiation factor-2 attenuates obesity-induced cardiomyopathy and fibrosis; Biophys. Acta Mol. Basis Dis., 1864 252
Kong et al. (2019), Chalcone Derivative L6H21 Reduces EtOH + LPS-Induced Liver Injury Through Inhibition of NLRP3 Inflammasome Activation; Alcohol Clin. Exp. Res., 43 1662
Sumneang et al. (2022), Inhibition of myeloid differentiation factor-2 attenuates cardiometabolic impairments via reducing cardiac mitochondrial dysfunction, inflammation, apoptosis and ferroptosis in prediabetic rats; Biophys. Acta Mol. Basis Dis., 1868 166301
Oo et al. (2021), L6H21 protects against cognitive impairment and brain pathologies via toll-like receptor 4-myeloid differentiation factor 2 signalling in prediabetic rats; J. Pharmacol., doi:10.1111/bph.15741 Epub ahead of print
