Gardiquimod diTFA, an imidazoquinoline analog and TLR7/8 agonist, inhibits HIV-1 infection of macrophages and activated peripheral blood mononuclear cells (PBMCs), and specifically activates TLR7 at concentrations below 10 μM. As an immune system modifier and reverse transcriptase inhibitor, it serves as a novel therapeutic agent to block systemic and mucosal transmission of HIV-1.[1][2]

Gardiquimod diTFA (6-60 μM ) significantly inhibits HIV-1 reverse transcriptase to synthesis of cDNA [1].

Gardiquimod, when administered intraperitoneally at a dosage of 1 mg/kg per mouse daily for 7 days, significantly augmented the anti-tumor effects of natural killer (NK) cells in conjunction with dendritic cells (DCs) on human HepG2 liver carcinoma xenografts in male athymic nude mice (Balb-nu/nu, 5 weeks old). This regimen notably suppressed the growth of the carcinoma xenografts, demonstrating the potential of Gardiquimod as a powerful adjunct in cancer immunotherapy strategies.