VHB

HBV-IN-31: strong cccDNA inhibitor, anti-HBV, IC50=0.13 µM HBsAg, hampers cell growth.

HBV-IN-11 is a potent inhibitor of HBsAg secretion (EC50: 0.46 μM).

HBV-IN19 TFA suppresses HBsAg, hampers HBV infection, and aids in HBV research.

HBV-IN-12: strong HBsAg & HBV DNA inhibitor; EC50 0.001-0.05 μM & 0.001-0.02 μM respectively. (WO2021204252A1)

TLR8 agonist 4 inhibits wild-type and lamivudine/entecavir-resistant HBV; IC50: 0.15 μM and 0.10 μM.

FNC-TP trisodium, active intracellular FNC form, inhibits NRTI, fights HIV, HBV, and HCV.

ALG-000184, a prodrug of the potent HBV capsid assembly modulator ALG-001075, shows potential for use in HBV infection research.

HBV-IN-24 inhibits HBV DNA, HBsAg, HBeAg (EC50: 0.6, 0.6, 4.6 nM), and has antiviral properties with neurotoxicity mitigation.

HBV-IN-20 is a potent, orally active HBV inhibitor (EC50: 0.46 μM). HBV-IN-20 is a classical type II CpAM (core protein assembly regulator).

TLR7/8 agonist 13 is an orally active dual agonist of TLR7 (with a lowest effective concentration (LEC) [hTLR7] of 1.6 μM) and TLR8 (LEC [hTLR8] of 1.6 μM). It acts on human peripheral blood mononuclear cells (hPBMC) with agonistic activity (LEC [hPBMC] = 0.5 μM). In mice and cynomolgus monkeys, TLR7/8 agonist 13 induces endogenous IFNα, activates myeloid dendritic cells and monocytes, promoting their differentiation towards a TH1 phenotype. In chronic AAV-HBV mouse models, it reduces viral load and HBV surface antigen levels. TLR7/8 agonist 13 has the potential to indirectly induce IFNγ, facilitating the response of HBV antigen-specific CD8 T cells. This compound is useful for hepatitis B virus research.