Resiquimod

SKU: orb1300307

Description

Resiquimod

Research Area

Immunology & Inflammation, Infectious Disease & Virology, Protein Biochemistry

Key Properties

• CAS Number: 144875-48-9
• MW: 314.38
• Purity: 99.67%
• Formula: C₁₇H₂₂N₄O₂
• SMILES: CCOCc1nc2c(N)nc3ccccc3c2n1CC(C)(C)O
• Target: TLR,HCV Protease
• Solubility: Ethanol:20 mg/mL (63.62 mM);DMSO:247.5 mg/mL (787.26 mM);10% DMSO+90% Saline:0.1 mg/mL (0.32 mM);H2O:< 1 mg/mL (insoluble or slightly soluble)

Bioactivity

• Target IC50:
  TLR8:4.5 ± 3.2 μM (EC50)|TLR7:1.5 ± 0.3 μM (EC50)
• In Vivo:
  METHODS: To detect anti-tumor activity in vivo, Resiquimod (2 mg/kg) and 4D5 anti-HER2 antibody (20 mg/kg) were injected intraperitoneally three times per week for 13 days into Balb/cJ mice bearing CT26-HER2/neu tumors. RESULTS: After 13 days, the tumor growth rate of mice receiving Resiquimod plus antibody was significantly reduced. Statistical tests showed a synergistic effect of 4D5 and Resiquimod in reducing tumor growth rate.
• In Vitro:
  METHODS: Golden pompholyte kidney lymphocytes HKL were treated with Resiquimod (0.175-32 µg/mL) for 12 h. Cell viability was measured by CCK8 assay. RESULTS: CCK8 assay showed that 0.25-32 µg/mL Resiquimod significantly promoted HKL proliferation. METHODS: Peripheral blood mononuclear cells PBM were treated with Resiquimod (0.01-100 µM) for 1-14 h, and the expression levels of target proteins were detected by Western Blot. RESULTS: A dose of 1 µM was sufficient to alter the expression of FcγR, and higher doses did not result in greater changes. the increase in FcγRIIa occurred at a late stage, while a small increase in the γ chain was seen at 3 h, but was higher at 14 h. However, the FcγRIIb protein decreases at 1 h, while the FcγRIIb transcript is maintained until 4 h.
• Cell Research:
  Resiquimod is dissolved in DMSO. For inhibition of lysosomal acidification, cells are incubated with 10 μM CQ for 1 h before Resiquimod (R848) treatment. After treatment, 20 μL of 5 mg/mL MTT is added to the plate. The plate is incubated at 22°C for 4 h, and 200 μL dimethyl sulfoxide is added to the plate to dissolve the reduced formazan. The plate is then read at 490 nm with a microplate reader. To determine the effect of Myd88 inhibition on R848-induced cell proliferation, the Myd88 inhibitor Pepinh-MYD and the control peptide Pepinh-Control are added to PBL at the concentration of 50 μM, and the plate is incubated at 22°C for 6 h. After incubation, the cells are treated with R848 and subjected to MTT assay as above. To determine the effect of NF-κB inactivation on R848-induced cell proliferation, BAY-11-7082, an irreversible inhibitor of IκB-α phosphorylation, is added to the cells at the concentration of 1 μM, and the plate is incubated at 22°C for 1 h. After incubation, the cells are treated with R848 and subjected to MTT assay as earlier. All experiments are performed three times.
• Animal Research:
  Animal Models: Wild-type mice,TLR7-deficient mice,and MyD88-deficient mice. Formulation: saline. Dosages: 50 nmol. Administration: i.p.

Storage & Handling

• Storage: store at low temperature | Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

inhibit, HCVProtease, HCV, HCV Protease, Hepatitis C virus, Inhibitor, Resiquimod, S 28463, S28463, S-28463, TLR, R 848, R848, R-848, Toll-like Receptor (TLR), TLR7, TLR8

Compound Identifiers

PubChem CID

159603