Novel small molecule inhibits pro-inflammatory response

Promising compound targeting MyD88 limits inflammatory cytokine production in human primary cells and increases therapeutic efficacy in mice with exposure to toxins

Medical & Biotechnology

MyD88-dependent TLR signaling pathway

Myeloid differentiation primary response protein 88 (MyD88) plays a critical role in the activation of the host pattern recognition receptors, Toll-like receptors (TLRs), and induction of host pro-inflammatory response. There exists, however, a fine line between beneficial and harmful effects of inflammation, and certain infections and diseases may be facilitated or exacerbated by a pro-inflammatory environment.

Researchers at the U.S. Army Medical Research Institute for Infectious Diseases (USAMRIID) and Scripps Research Institute have developed a novel small molecule compound (known as 4210) that effectively blocks MyD88 signaling. In studies, the compound reduced 3 to 4 log the Eastern Equine Encephalitis Virus (EEEV) and Venezuelan Equine Encephalitis Virus (VEEV) replication in infected U87 cells. In addition, 4210 blocked MyD88-mediated pro-inflammatory signaling and protected mice from toxic shock induced death upon lethal exposure to staphylococcal enterotoxin B (SEB). Although initial research has focused on mitigation and treatment of viral and bacterial infections, 4210 has potential application for other disease states dependent on MyD88-dependent pro-inflammatory signaling.

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