Colletodiol is a fungal metabolite that has been found inD. grovesiiand has immunosuppressant and antiviral activities.1,2It inhibits concanavalin A- or LPS-induced proliferation of isolated mouse splenocytes (IC50s = 12 and 5 μg ml, respectively).1Colletodiol inhibits influenza A viral replication in HeLa-IAV-Luc cells.2 1.Fujimoto, H., Nagano, J., Yamaguchi, K., et al.Immunosuppressive components from an ascomycete, Diplogelasinospora grovesiChem. Pharm. Bull.46(3)423-429(1998) 2.Lai, W., Wang, S., and Ye, X.Colletodiol inhibits the replication of influenza A virus WSN H1N1 by reducing the activity of viral RNA polymeraseWei Sheng Wu Xue Bao53(12)1334-1339(2013)
Defensin HNP-3 is a peptide secreted by human polymorphonuclear leukocytes (PMNs) that has antimicrobial properties. It induces lysis of mammalian cells when used at a concentration of 25 μg mL. It also inhibits growth of E. faecalis (ED50 = 100 nM) and clinical isolates of P. aeruginosa (MIC90 = 4 μM). HNP-3 binds to recombinant HIV-1 envelope glycoprotein (gp120) and human CD4 (Kds = 52.8 and 34.9 nM, respectively). It also binds to recombinant, immobilized human surfactant protein D (SP-D; Kd = 55.7 nM) and inhibits focus formation in Madin-Darby canine kidney (MDCK) cells infected with influenza A virus (IAV).
Influenza A virus-IN-1, a dihydropyrrolidones derivative, is a highly effective inhibitor of various subtypes of influenza A virus (IAV) with IC 50 values ranging from 3.11 μM to 7.13 μM. It effectively suppresses IAV replication and enhances the expression of key antiviral cytokines, such as IFN-β, and the antiviral protein MxA.
Influenza A virus-IN-5 (Compound 16e) is a highly potent and orally active agent against the influenza A virus (IAV), exhibiting an IC 50 of 1.29 μM. It effectively inhibits the transcription and replication of viral RNA while maintaining acceptable levels of cytotoxicity [1].
CBS1194 is a novel antiviral agent against influenza A virus (IAV), and is more specifically, a group 2 IAV fusion inhibitor. CBS1194 prevents membrane fusion of the virus through the inhibition of the conformational change of hemagglutinin (HA). CBS1194 causes steric hinderance that prevents the rearrangement of the HA that would normally be induced by low-pH, by fitting into the pocket by the fusion peptide.