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    Resiquimod (R848)
    Resiquimod (R848)

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V1867
    CAS #: 144875-48-9Purity ≥98%

    Description: Resiquimod (formerly known as R-848; S-28463; VML-600; R848, S27609) is a potent imidazoquinolinamine-based immune response modifier that acts as an agonist of the TLR 7/8 receptors (Toll-like receptor 7/8) with antiviral and antitumour activity. It can induce the levels of cytokines such as TNF-α, IL-6 and IFN-α. Resiquimod is the analogue of imiquimod (also called R-837,S-26308) with potential immunostimulatory activity. Resiquimod has been reported to dose-dependently induce cytokines including IFN, TNF, IL-1β and IL-6 in human peripheral blood mononuclear (PBMCs). In addition, Resiquimod has been revealed to stimulate intracellular IL-1β increased approximately 15%. The results have also been noted that both monocytes and B cells produced IFN in response to Resiquimod. On April 28, 2016, orphan designation (EU/3/16/1653) was granted by the European Commission to resiquimod for the treatment of cutaneous T-cell lymphoma.

    References: Nat Immunol. 2002 Feb;3(2):196-200; J Immunol. 2003 Oct 15;171(8):4320-8.

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    Molecular Weight (MW)314.38 
    FormulaC17H22N4O2 
    CAS No.144875-48-9 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 63 mg/mL (200.4 mM) 
    Water: <1 mg/mL
    Ethanol: 21 mg/mL (66.8 mM) 
    SMILES CodeCC(O)(C)CN1C(COCC)=NC2=C1C3=CC=CC=C3N=C2N
    SynonymsR-848; S-28463; VML600; R848; S 28463; VML 600; R 848; S28463; VML-600.


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    In Vitro

    In vitro activity: Resiquimod activates immune cells and induces proliferation of wild-type splenocytes via the Toll-like receptor 7 (TLR7)-MyD88-dependent signaling pathway. Resiquimod also modulates dendritic cells to augment cytomegalovirus- and HIV-1-specific T cell responses. Resiquimod induces the differentiation of myeloid-derived suppressor cells into macrophages and dendritic cells, and may improve cancer immunotherapy by reducing immunosuppressive MDSCs.


    Kinase Assay: For luciferase assay, FG-9307 cells are transfected with the firefly NF-κB-specific luciferase reporter vector pNFκB-Met-Luc2. Transfection efficiency is monitored by co-transfection with the pSEAP2 control vector, which constitutively expresses the human secreted enhanced alkaline phosphatase (SEAP). Then the cells are treated with Resiquimod (R848, 1 µg/mL), CQ (10 µM), CQ plus R848 or PBS and incubated at 22°C for 24 h. The culture medium of the transfectants is then analyzed for luciferase activity and SEAP activity using Luciferase Assay Kit and the Great EscAPe™ SEAP Chemiluminescence Detection Kit, respectively. The assay is performed three times. 


    Cell Assay: Unlike LPS-induced activation, which was MyD88-independent, Resiquimod-induced activation of NF-κB was completely dependent on MyD88. It was implied that Resiquimod activated macrophages via TLRs.

    In VivoIn wild-type mice, Resiquimod (50 nmol, i.p.) induces increased serum concentrations of IFN-alpha, TNF-alpha and IL-12, while neither TLR7-deficient mice nor MyD88-deficient mice show an increase in these cytokines. In a murine model of allergic asthma, Resiquimod (i.n., 20 μg/mouse) reduces allergen induced airway reactivity and inflammation via reduction in Nrf2 signaling. 
    Animal modelWild-type mice, TLR7-deficient mice, and MyD88-deficient mice
    Formulation & DosageDissolved in saline; 50 nmol; i.p. injection 
    ReferencesNat Immunol. 2002 Feb;3(2):196-200; J Immunol. 2003 Oct 15;171(8):4320-8. 


    These protocols are for reference only. InvivoChem does not independently validate these methods.

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