necrosome

Necrosulfonamide ((E)-Necrosulfonamide) is a necroptosis inhibitor that targets MLKL and is selective. Necrosulfonamide prevents the MLKL-RIP1-RIP3 necrosomal complex from interacting with its downstream effectors.

RIP1-IN-1 is an orally bioavailable RIP1 inhibitor with a high binding affinity (Kd: 110 nM). This compound exhibits significant activity against necroptosis and effectively suppresses necrosome formation by inhibiting the phosphorylation of RIP1, RIP3, and MLKL pathways. RIP1-IN-1 can inhibit necroptosis and is applicable in research on acute liver injury.

WJH-C19 is an orally active RIPK1 inhibitor with an IC50 of 5.7 nM. It suppresses the RIPK1/RIPK3/MLKL signaling pathway by blocking RIPK1 phosphorylation and inhibiting downstream phosphorylation of RIPK3 and MLKL, thereby disrupting necrosome formation and demonstrating protective effects against necroptosis (Apoptosis) across various cell lines. In a mouse model of colitis, WJH-C19 alleviates inflammatory bowel disease symptoms by modulating the necroptosis pathway. It also reduces inflammation and bone destruction in a rheumatoid arthritis mouse model. WJH-C19 is relevant for research on inflammatory bowel disease and rheumatoid arthritis.

Necrosulfonamide-D4 is the deuterated form of Necrosulfonamide. Necrosulfonamide (T6904) acts as a necroptosis inhibitor by selectively targeting (MLKL). It hinders the interaction between the MLKL-RIP1-RIP3 necrosome complex and its downstream effectors. MLKL serves as a crucial substrate of RIP3 in the necrosis induction process.