Molecular Weight(MW): 362.37
CU-CPT22 shows dose-dependent inhibitory effects blocking Pam3CSK4-induced TLR1/2 activation with an IC50 of 0.58 ± 0.09 µM while no significant inhibition to TLR2/6. It demonstrates minimal non-specific inhibition against a panel of 10 representative kinases (PDGFRB, MET, DDR2, SRC, MAPK1, PAK1, AKT1, PKC-γ, CAMK1, and PLK4).
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Choose Selective TLR Inhibitors
|Description||CU-CPT22 shows dose-dependent inhibitory effects blocking Pam3CSK4-induced TLR1/2 activation with an IC50 of 0.58 ± 0.09 µM while no significant inhibition to TLR2/6. It demonstrates minimal non-specific inhibition against a panel of 10 representative kinases (PDGFRB, MET, DDR2, SRC, MAPK1, PAK1, AKT1, PKC-γ, CAMK1, and PLK4).|
CU-CPT22 can compete with the synthetic triacylated lipoprotein (Pam3CSK4) binding to TLR1/2 with high inhibitory activity and specificity. The inhibition constant (Ki) is 0.41 ± 0.07 µM. CU-CPT22 inhibits TLR1/2 signaling without affecting other TLRs, showing it is highly selective in intact cells. It has no significant cytotoxicity at various concentrations up to 100 µM in RAW 264.7 cells using MTT assay. Kinase profiling shows that CU-CPT22 demonstrates minimal non-specific inhibition against a panel of 10 representative kinases (PDGFRB, MET, DDR2, SRC, MAPK1, PAK1, AKT1, PKC-γ, CAMK1, and PLK4). CU-CPT22 suppresses TLR1/2-mediated inflammation response. It inhibits about 60% of TNF-α and 95% of IL-1β at 8 µM in the RAW 264.7 cells.
|In vivo||Cu-CPT22 administered before myocardial infarction (MI) significantly suppresses MI-induced upregulation of kidney injury molecule-1 (KIM-1), TLR2, TLR4, MyD88, and chemokine (C-C motif) ligand 2 levels and activation of NF-κB, whereas neutrophil gelatinase-associated lipocalin (NGAL) levels and IL-6 and TNF-α expression levels are unchanged.|
|In vitro||DMSO||72 mg/mL (198.69 mM)|
|Ethanol||9 mg/mL (24.83 mM)|
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