MyD88 Inhibitor

TJ-M2010-5 is a MyD88 inhibitor that binds to the TIR domain of MyD88 to interfere with its homodimerization, and the TLR/MyD88 signal pathway. TJ-M2010-5 can be used for the research of myocardial ischemia/reperfusion injury (MIRI).

ST 2825 is a specific MyD88 dimerization inhibitor. ST2825 interferes with recruitment of IRAK1 and IRAK4 by MyD88, causing inhibition of IL-1β-mediated activation of NF-κB transcriptional activity.

Emavusertib is an orally active inhibitor for IRAK4 (IC₅₀=57 nM) and FLT3. Emavusertib inhibits NF-κB and MyD88 signaling pathways, reduces the generation of pro-inflammatory cytokines like IL-6 and IL-10, thereby exhibiting anti-inflammatory and anti-proliferative activities against cancer cells, leading to cell apoptosis. Emavusertib exhibits antitumor activity in mouse model

Schaftoside is a flavonoid found in a variety of Chinese herbal medicines, such as Eleusine indica. Schaftoside inhibits the expression of TLR4 and Myd88. Schaftoside also decreases Drp1 expression and phosphorylation, and reduces mitochondrial fission.

MR-39 is a FPR2 agonist (EC₅₀ = 3.9 μM). MR-39 activates FPR2 to promote neuroinflammation resolution (downregulates IL-1β and TNF-α, modulates NF-κB), upregulates synaptic proteins (synaptic proteins) and improves dendritic spine morphology. MR-39 inhibits MAPK/ERK and AKT phosphorylation in glioblastoma, induces S-phase arrest, and suppresses migration, angiogenesis, and hypoxic adaptation. MR-39 reduces Aβ plaque burden via inhibiting MyD88/NF-κB and NLRP3 inflammasome. MR-39 can be used for research on autism spectrum disorder, Alzheimer's disease, and glioblastoma.

Copper sulfate pentahydrate, for cell culture, 98% is a biochemical reagent. Copper sulfate pentahydrate, for cell culture, 98% reduces the production of ROS and the expression levels of MyD88 as well as c-Rel genes. Copper sulfate pentahydrate, for cell culture, 98% decreases the activities of T-SOD, CAT, and GSH, increases the activities of caspase-3, caspase-8, and caspase-9. Copper sulfate pentahydrate, for cell culture, 98% is cytotoxic to various cells.

T6167923 is a selective inhibitor of MyD88-dependent signaling pathways. T6167923 directly binds to Toll/IL1 receptor (TIR) domain of MyD88 and disrupts MyD88 homodimeric formation. T6167923 inhibits NF-κB driven Staphylococcus enterotoxin AP (SEAP) activity, and improves anti-inflammatory activity with IC₅₀s of 2.7 μM, 2.9 μM, 2.66 μM and 2.66 μM for IFN-γ, IL-1β, IL-6 and TNF-α, respectively.

Copper sulfate pentahydrate, 99% is a biochemical reagent. Copper sulfate pentahydrate, 99% reduces the production of ROS and the expression levels of MyD88 as well as c-Rel genes. Copper sulfate pentahydrate, 99% decreases the activities of T-SOD, CAT, and GSH, increases the activities of caspase-3, caspase-8, and caspase-9. Copper sulfate pentahydrate, 99% is cytotoxic to various cells. Copper sulfate pentahydrate, 99% has antioxidant activity. Copper sulfate pentahydrate, 99% can be used in the research of diabetes, Parkinson's disease and DMBA (HY-W011845)-induced tumors.

MyD88-IN-1 (Compound c17) is an orally active MyD88 inhibitor. MyD88-IN-1 inhibits the interaction of TLR4 and MyD88 and suppressed the NF-κB pathway. MyD88-IN-1 can be used in research of cancer and inflammatory.

Raffinose (Melitose) regulates intestinal flora, inhibits TLR4-MyD88-NF-κB signaling pathway, and activates Nrf2 signaling pathway. Raffinose exhibits anti-inflammatory, antioxidant, and immunomodulatory activities. Raffinose is orally active.

Tomaralimab (OPN-305) is a humanized anti-TLR2 IgG4 monoclonal antibody. Tomaralimab inhibits TLR2, MyD88, NLRP3, and reduces pro-inflammatory cytokine (IL-1β, IL-6, IL-8) production. Tomaralimab reduces tau pathology. Tomaralimab improves cognition, atopic dermatitis. Tomaralimab has anticancer effects on pancreatic ductal adenocarcinoma. Tomaralimab is being studied in myelodysplastic syndrome (MDS), atopic dermatitis, pancreatic ductal adenocarcinoma, Alzheimer's disease, and myocardial ischemia/reperfusion injury.

Atractyloside A is an orally active inhibitor of the TLR4/MyD88/NF-κB signaling pathway and also an opener of the mitochondrial permeability transition pore (MPTP). Atractyloside A interferes with the activation of the TLR4/MyD88/NF-κB pathway, thereby inhibiting intestinal inflammatory responses. Atractyloside A reverses mucin synthesis impairment, improves intestinal barrier integrity, and restores homeostasis by altering the composition of the gut microbiota. Atractyloside A can be used in studies related to spleen deficiency diarrhea and myocardial injury.

Astringin (trans-Astringin) is an orally active natural phenolic stilbene glucoside. Astringin can inhibit the production of oxidative stress, inflammatory factors, etc. Astringin has multiple activities such as anti-oxidation, anti-inflammation, and anti-apoptosis. Astringin is also an inhibitor of ferroptosis. Astringin can be used in the research of diseases such as acute lung injury.

N-(p-Coumaroyl) Serotonin is an orally active polyphenol found in safflower seeds with potent anti-inflammatory, antioxidant, and antitumor activities. N-(p-Coumaroyl) Serotonin suppresses NF‑κB, TLR4/MyD88 and MAPK signaling, activates NQO1/HO‑1 pathways, and inhibits pro‑inflammatory cytokines, iNOS and COX‑2 and ROS production. N-(p-Coumaroyl) Serotonin induces S‑phase arrest and apoptosis in glioblastoma cells, reduces atherosclerotic lesions, and alleviates renal and vascular injuries. N-(p-Coumaroyl) Serotonin acts as a vasodilator, regulates calcium dynamics. N-(p-Coumaroyl) Serotonin can be used for the research of neurodegenerative diseases, atherosclerosis, glioblastoma, and acute renal failure.

Pepinh-MYD is a MyD88 inhibitor that contains a domain sequence from MyD88 TIR and a protein transduction sequence, enabling it to penetrate the cell membrane. Pepinh-MYD interferes with MyD88-mediated TLR signaling pathways, thereby inhibiting related immune responses. It holds potential for studying the role of MyD88 in viral infections.

2,4′-Dihydroxybenzophenone (Ultraviolet absorber UV-0) occupies the hydrophobic pocket of MD2 and blocks the dimerization of TLR4. 2,4′-Dihydroxybenzophenone inhibits the LPS induced mtROS production, and LPS induced inflammatory response by downregulating pro-inflammatory mediators and decreasing the expression of MyD88, p-IRAK4, and NF-κB. 2,4′-Dihydroxybenzophenone is also a UV absorber.

Pepinh-MYD TFA is a MyD88 inhibitor that contains a domain sequence from MyD88 TIR and a protein transduction sequence, enabling it to penetrate the cell membrane. Pepinh-MYD TFA interferes with MyD88-mediated TLR signaling pathways, thereby inhibiting related immune responses. Pepinh-MYD TFA holds potential for studying the role of MyD88 in viral infections.

6-Methoxyflavone is an orally active methoxyflavone. 6-Methoxyflavone suppresses neuroinflammation in microglia through the inhibition of TLR4/MyD88/p38 MAPK/NF-κB dependent pathways and the activation of HO-1/NQO-1 signaling. 6-Methoxyflavone induces S-phase arrest through the CCNA2/CDK2/p21CIP1 signaling pathway in HeLa cells. 6-Methoxyflavone inhibits NFAT Translocation into the nucleus and suppresses T cell activation. 6-Methoxyflavone partially restores chronic ethanol-induced behavioral deficits in mice. 6-Methoxyflavone antagonizes chronic constriction injury and diabetes associated neuropathic nociception expression. 6-Methoxyflavone can be used for the study of cancer, inflammation and neurological diseases.

MyD88-IN-2 (compound A5S) is a Myeloid differentiation primary response 88 (MyD88) inhibitor with the K_d of 15 μM. MyD88-IN-2 shows protective effects on LPS (HY-D1056)-induced and sepsis-induced ALI mouse models.

TLR8 antagonist-1 (Compound 10) is a selective TLR8 antagonist. TLR8 antagonist-1 can inhibit TLR8-mediated inflammation and signaling pathways, reduce the recruitment of MyD88, and inhibit the NF-κB and IRF pathways. TLR8 antagonist-1 has anti-inflammatory activity.