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You are here:Home-Inhibitors & Agonists-Immunology/Inflammation-MyD88

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MyD88 (Myeloid differentiation primary response gene 88) is a protein that, in humans, is encoded by the MYD88 gene. Available evidence suggests that MYD88 is dispensable for human resistance to common viral infections and to all but a few pyogenic bacterial infections, demonstrating a major difference between mouse and human immune responses. MyD88 is an essential adaptor protein in the IL-1R1 signaling pathway. MyD88 may define a family of signal transduction molecules with an ancestral function in the activation of the immune system. MyD88 functions as a pure adaptor linking the IL-1R1 to downstream IRAK kinases. Mutation in MYD88 at position 265 leading to a change from leucine to proline have been identified in many human lymphomas including ABC subtype of Diffuse Large B-cell Lymphoma and Waldenstrom's Macroglobulinemia.

Cat. No. Product Name CAS No. Information
H4014

T6167923

 		2437475-16-4

T6167923 (T-6167923) is a small molecule inhibitor of MyD88-dependent signaling pathways, disrupts MyD88 homodimeric formation; inhibits SEB-induced inhibition of cytokine production in PBMCs with IC50 of 2-10 uM, also inhibits SEA-induced pro-inflammatory cytokine production, shows no toxicity in primary cells up to 100 uM; specifically inhibits TIR domain-mediated dimerization of full-length MyD88 as well as the recombinant TIR domain protein; dose-dependent in vivo therapeutic efficacy against SEB intoxication.
H4013

T5910047

 		950003-29-9

T5910047 (T-5910047) is a small molecule inhibitor of MyD88-dependent signaling pathways, disrupts MyD88 homodimeric formation; inhibits SEB-induced inhibition of cytokine production in PBMCs with IC50 of 2-10 uM, also inhibits SEA-induced pro-inflammatory cytokine production, shows no toxicity in primary cells up to 100 uM.
H4012

ST-2825

 		894787-30-5

A synthetic peptido-mimetic compound that inhibits MyD88 dimerization in a TIR-dependent manner; interferes with recruitment of IRAK1 and IRAK4 by MyD88, causing inhibition of IL-1beta-mediated activation of NF-kappaB transcriptional activity; inhibits IL-1beta-induced production of IL-6 in treated mice, suppresses B cell proliferation and differentiation into plasma cells in response to CpG-induced activation of TLR9; orally active.

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