anti src family kinases Search Results


ldv  (MedChemExpress)
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Schematics of the anti-HCV drug targets and the experimental system. (A) HCV life cycle and drug targets. After entry into the host cell, HCV genomic RNA is translated into viral precursor polyprotein and processed into functional proteins (C, E1, E2, p7, NS2, NS3, NS4A, NS4B, NS5A, and NS5B). HCV RNA replicates inside the isolated membrane compartments derived from the endoplasmic reticulum (ER), and assembles into viral particles on lipid droplets, which traffic through the Golgi and are released outside of the cell. PIs (TPV, DPV, ASV, <t>and</t> <t>SMV)</t> inhibit the processing step, and drugs such as NI (SOF), NNIs (VX, DAS, NSV, and TGV), NS5AIs (DCV and <t>LDV),</t> and CIs (CsA and SCY) target HCV RNA replication. IFNs (IFN-α and IFN-λ1) supposedly inhibit at least the step(s) of translation and replication. (B) HCV replication activity was evaluated using an HCV subgenomic replicon (genotype 1b, strain NN) carrying a fusion of the firefly luciferase gene (Luc) with the neomycin phosphotransferase (Neor). The replicon autonomously and persistently replicates in Huh-7 cells. Cells treated with drugs were incubated for 72 h and then harvested for luciferase assay. Inhibition of HCV replication was measured by the luciferase activity in drug-treated cells, relative to activity in DMSO-treated cells.
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Schematics of the anti-HCV drug targets and the experimental system. (A) HCV life cycle and drug targets. After entry into the host cell, HCV genomic RNA is translated into viral precursor polyprotein and processed into functional proteins (C, E1, E2, p7, NS2, NS3, NS4A, NS4B, NS5A, and NS5B). HCV RNA replicates inside the isolated membrane compartments derived from the endoplasmic reticulum (ER), and assembles into viral particles on lipid droplets, which traffic through the Golgi and are released outside of the cell. PIs (TPV, DPV, ASV, and SMV) inhibit the processing step, and drugs such as NI (SOF), NNIs (VX, DAS, NSV, and TGV), NS5AIs (DCV and LDV), and CIs (CsA and SCY) target HCV RNA replication. IFNs (IFN-α and IFN-λ1) supposedly inhibit at least the step(s) of translation and replication. (B) HCV replication activity was evaluated using an HCV subgenomic replicon (genotype 1b, strain NN) carrying a fusion of the firefly luciferase gene (Luc) with the neomycin phosphotransferase (Neor). The replicon autonomously and persistently replicates in Huh-7 cells. Cells treated with drugs were incubated for 72 h and then harvested for luciferase assay. Inhibition of HCV replication was measured by the luciferase activity in drug-treated cells, relative to activity in DMSO-treated cells.

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: Quantifying antiviral activity optimizes drug combinations against hepatitis C virus infection

doi: 10.1073/pnas.1610197114

Figure Lengend Snippet: Schematics of the anti-HCV drug targets and the experimental system. (A) HCV life cycle and drug targets. After entry into the host cell, HCV genomic RNA is translated into viral precursor polyprotein and processed into functional proteins (C, E1, E2, p7, NS2, NS3, NS4A, NS4B, NS5A, and NS5B). HCV RNA replicates inside the isolated membrane compartments derived from the endoplasmic reticulum (ER), and assembles into viral particles on lipid droplets, which traffic through the Golgi and are released outside of the cell. PIs (TPV, DPV, ASV, and SMV) inhibit the processing step, and drugs such as NI (SOF), NNIs (VX, DAS, NSV, and TGV), NS5AIs (DCV and LDV), and CIs (CsA and SCY) target HCV RNA replication. IFNs (IFN-α and IFN-λ1) supposedly inhibit at least the step(s) of translation and replication. (B) HCV replication activity was evaluated using an HCV subgenomic replicon (genotype 1b, strain NN) carrying a fusion of the firefly luciferase gene (Luc) with the neomycin phosphotransferase (Neor). The replicon autonomously and persistently replicates in Huh-7 cells. Cells treated with drugs were incubated for 72 h and then harvested for luciferase assay. Inhibition of HCV replication was measured by the luciferase activity in drug-treated cells, relative to activity in DMSO-treated cells.

Article Snippet: SMV, ASV, DAS, NSV, TGV, and LDV were purchased from MedChem Express.

Techniques: Functional Assay, Isolation, Membrane, Derivative Assay, Activity Assay, Luciferase, Incubation, Inhibition

Quantification of the IIP of single-HCV drugs. (A) Log–log plots of dose–response curves normalized by IC50, determined from the replicon assay, of PIs (TPV, DPV, SMV, and ASV; red), the NI (SOF; blue), NNIs (VX, DAS, NSV, and TGV; orange), NS5AIs (DCV and LDV; green), IFNs (IFN-α and IFN-λ1; cyan), and CIs (CsA and CSY; purple). Each point represents the mean of three experiments. (B) IIP of classes or subclasses of antiviral drugs, normalized by IC50, calculated from the experimentally measured fu by Eq. 1. (C) IIP values at drug concentration D = 100 × IC50 (IIP100) determined by extrapolation.

Journal: Proceedings of the National Academy of Sciences of the United States of America

Article Title: Quantifying antiviral activity optimizes drug combinations against hepatitis C virus infection

doi: 10.1073/pnas.1610197114

Figure Lengend Snippet: Quantification of the IIP of single-HCV drugs. (A) Log–log plots of dose–response curves normalized by IC50, determined from the replicon assay, of PIs (TPV, DPV, SMV, and ASV; red), the NI (SOF; blue), NNIs (VX, DAS, NSV, and TGV; orange), NS5AIs (DCV and LDV; green), IFNs (IFN-α and IFN-λ1; cyan), and CIs (CsA and CSY; purple). Each point represents the mean of three experiments. (B) IIP of classes or subclasses of antiviral drugs, normalized by IC50, calculated from the experimentally measured fu by Eq. 1. (C) IIP values at drug concentration D = 100 × IC50 (IIP100) determined by extrapolation.

Article Snippet: SMV, ASV, DAS, NSV, TGV, and LDV were purchased from MedChem Express.

Techniques: Concentration Assay