rip2

RIP2 Kinase Inhibitor 3 is a potent and selective inhibitor of RIP2, demonstrating an IC50 of 1 nM.

RIP2 kinase inhibitor 1 is a potent and selective receptor interacting inhibitor of protein 2 (RIP2) kinase(RIP2 FP with an IC50 of 0.03 μM ),and is used for autoinflammatory disorders.

GSK2983559 free acid is an effective and selective inhibitor of receptor-interacting protein 2 (RIP2). GSK2983559 free acid shows excellent activity in blocking many proinflammatory cytokine responses in human inflammatory bowel disease explant samples an

GSK2983559 active metabolite (RIPK2-IN-1) is a potent, selective receptor-interacting protein-2 (RIP2) kinase inhibitor.

RIP2 kinase inhibitor 2 is a compound that inhibits receptor-interacting protein-2 kinase (RIP2).

RIP2 Kinase Inhibitor 4 is a highly potent and selective RIPK2 PROTAC compound that efficiently degrades RIPK2 (pIC50 value of 8) and effectively inhibits the release of TNF-α.

GSK583 is a highly effective and specific RIP2 kinase inhibitor (IC50: 5 nM).

PROTAC RIPK degrader-6 (example 1) is a PROTAC engineered for RIP Kinase degradation, comprising a RIP2 kinase inhibitor linked to a cereblon binder[1].

1. Schisandrol B (Besigomsin) may exert neuroprotective effects by attenuating the microglia-mediated neuroinflammatory response via inhibiting the TLR4-mediated NF-κB and MAPKs signaling pathways. 2. Schisandrol B has anti-inflammatory property, potentially result from the inhibition of COX-2, iNOS, IL-6, TNF-α and NO through the down-regulation of RIP2 and NF-κB activation. 3. Schisandrol B induces marked protective effects against hepatic and renal injury induced by CCl(4) exposure through differential regulation of the MAPK signal transduction pathway. 4. Schisandrol B significantly inhibits cell proliferation in a dose-dependent manner, due to cell cycle arrest in the G1 phase with the downregulation of cyclin D1 expression and Retinoblastoma (RB) phosphorylation.

RIPK2-IN-2 (example 25) is a RIP2 kinase PROTAC inhibitor that effectively blocks RIP2-dependent pro-inflammatory signaling and regulates RIP2 kinase activity in autoinflammatory diseases [1].