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2i-10 is a novel **anti-inflammatory small molecule** that directly inhibits **myeloid differentiation factor 2 (MD2)**, a critical component of the Toll-like receptor 4 (TLR4)-MD2 signaling complex. By inhibiting MD2, 2i-10 suppresses downstream inflammatory signaling, brain inflammation, and oxidative stress induced by ischemia/reperfusion (I/R) injury. In rat studies of acute cardiac I/R injury, intravenous administration of 2i-10 at the onset of reperfusion reduced cardiac dysfunction, brain inflammation, tau hyperphosphorylation, mitochondrial dysfunction, and preserved neuronal integrity. The agent represents a new approach for ameliorating inflammation-driven neural and cardiac injury after acute ischemia via targeted disruption of the MD2 signaling axis[1].
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