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eidd 1931  (MedChemExpress)


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    MedChemExpress eidd 1931
    (A–E) Dose-response curves are shown for various small-molecule inhibitors against rGhV M-GS* (purple) and rNiV (orange). CHO-B2 cells were infected at an MOI of 0.05 and treated with (A) EIDD-2749, (B) GHP-88309, (C) remdesivir, <t>(D)</t> <t>EIDD-1931</t> (molnupiravir active form), or (E) favipiravir (T-705). (F and G) Additional dose-response curves were measured in primary human astrocytes for (F) EIDD-2749 and (G) GHP-88309 under the same MOI and assay conditions. (H) Summary of half-maximal inhibitory concentrations (IC 50 ) derived from the dose-response curves in (A–G). Each row indicates the respective compound, virus, calculated IC 50 , corresponding 95% confidence interval, and the cell type in which the assay was performed. IC 50 values were determined in GraphPad Prism by nonlinear regression of (inhibitor) vs. normalized response. All experiments were conducted in biological triplicate. Error bars depict standard deviation.
    Eidd 1931, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 50 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Images

    1) Product Images from "De novo recovery of Ghana virus, an African bat Henipavirus, reveals differential tropism and attenuated pathogenicity compared to Nipah virus"

    Article Title: De novo recovery of Ghana virus, an African bat Henipavirus, reveals differential tropism and attenuated pathogenicity compared to Nipah virus

    Journal: Cell reports

    doi: 10.1016/j.celrep.2026.117074

    (A–E) Dose-response curves are shown for various small-molecule inhibitors against rGhV M-GS* (purple) and rNiV (orange). CHO-B2 cells were infected at an MOI of 0.05 and treated with (A) EIDD-2749, (B) GHP-88309, (C) remdesivir, (D) EIDD-1931 (molnupiravir active form), or (E) favipiravir (T-705). (F and G) Additional dose-response curves were measured in primary human astrocytes for (F) EIDD-2749 and (G) GHP-88309 under the same MOI and assay conditions. (H) Summary of half-maximal inhibitory concentrations (IC 50 ) derived from the dose-response curves in (A–G). Each row indicates the respective compound, virus, calculated IC 50 , corresponding 95% confidence interval, and the cell type in which the assay was performed. IC 50 values were determined in GraphPad Prism by nonlinear regression of (inhibitor) vs. normalized response. All experiments were conducted in biological triplicate. Error bars depict standard deviation.
    Figure Legend Snippet: (A–E) Dose-response curves are shown for various small-molecule inhibitors against rGhV M-GS* (purple) and rNiV (orange). CHO-B2 cells were infected at an MOI of 0.05 and treated with (A) EIDD-2749, (B) GHP-88309, (C) remdesivir, (D) EIDD-1931 (molnupiravir active form), or (E) favipiravir (T-705). (F and G) Additional dose-response curves were measured in primary human astrocytes for (F) EIDD-2749 and (G) GHP-88309 under the same MOI and assay conditions. (H) Summary of half-maximal inhibitory concentrations (IC 50 ) derived from the dose-response curves in (A–G). Each row indicates the respective compound, virus, calculated IC 50 , corresponding 95% confidence interval, and the cell type in which the assay was performed. IC 50 values were determined in GraphPad Prism by nonlinear regression of (inhibitor) vs. normalized response. All experiments were conducted in biological triplicate. Error bars depict standard deviation.

    Techniques Used: Infection, Derivative Assay, Virus, Standard Deviation



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    (A–E) Dose-response curves are shown for various small-molecule inhibitors against rGhV M-GS* (purple) and rNiV (orange). CHO-B2 cells were infected at an MOI of 0.05 and treated with (A) EIDD-2749, (B) GHP-88309, (C) remdesivir, <t>(D)</t> <t>EIDD-1931</t> (molnupiravir active form), or (E) favipiravir (T-705). (F and G) Additional dose-response curves were measured in primary human astrocytes for (F) EIDD-2749 and (G) GHP-88309 under the same MOI and assay conditions. (H) Summary of half-maximal inhibitory concentrations (IC 50 ) derived from the dose-response curves in (A–G). Each row indicates the respective compound, virus, calculated IC 50 , corresponding 95% confidence interval, and the cell type in which the assay was performed. IC 50 values were determined in GraphPad Prism by nonlinear regression of (inhibitor) vs. normalized response. All experiments were conducted in biological triplicate. Error bars depict standard deviation.
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    Image Search Results


    (A–E) Dose-response curves are shown for various small-molecule inhibitors against rGhV M-GS* (purple) and rNiV (orange). CHO-B2 cells were infected at an MOI of 0.05 and treated with (A) EIDD-2749, (B) GHP-88309, (C) remdesivir, (D) EIDD-1931 (molnupiravir active form), or (E) favipiravir (T-705). (F and G) Additional dose-response curves were measured in primary human astrocytes for (F) EIDD-2749 and (G) GHP-88309 under the same MOI and assay conditions. (H) Summary of half-maximal inhibitory concentrations (IC 50 ) derived from the dose-response curves in (A–G). Each row indicates the respective compound, virus, calculated IC 50 , corresponding 95% confidence interval, and the cell type in which the assay was performed. IC 50 values were determined in GraphPad Prism by nonlinear regression of (inhibitor) vs. normalized response. All experiments were conducted in biological triplicate. Error bars depict standard deviation.

    Journal: Cell reports

    Article Title: De novo recovery of Ghana virus, an African bat Henipavirus, reveals differential tropism and attenuated pathogenicity compared to Nipah virus

    doi: 10.1016/j.celrep.2026.117074

    Figure Lengend Snippet: (A–E) Dose-response curves are shown for various small-molecule inhibitors against rGhV M-GS* (purple) and rNiV (orange). CHO-B2 cells were infected at an MOI of 0.05 and treated with (A) EIDD-2749, (B) GHP-88309, (C) remdesivir, (D) EIDD-1931 (molnupiravir active form), or (E) favipiravir (T-705). (F and G) Additional dose-response curves were measured in primary human astrocytes for (F) EIDD-2749 and (G) GHP-88309 under the same MOI and assay conditions. (H) Summary of half-maximal inhibitory concentrations (IC 50 ) derived from the dose-response curves in (A–G). Each row indicates the respective compound, virus, calculated IC 50 , corresponding 95% confidence interval, and the cell type in which the assay was performed. IC 50 values were determined in GraphPad Prism by nonlinear regression of (inhibitor) vs. normalized response. All experiments were conducted in biological triplicate. Error bars depict standard deviation.

    Article Snippet: Compounds employed in this study include EIDD-2749 (MedChemExpress, HY-146246), GHP-88309 (Sigma Aldrich, SML2997), EIDD-1931 (MedChemExpress, HY-125033), Remdesivir (MedChemExpress HY-104077), and Favipiravir (Cellagen Technology, C8705–5).

    Techniques: Infection, Derivative Assay, Virus, Standard Deviation

    VTA cells were infected with nanoluciferase-expressing SARS-CoV-2 WT or AA at 37°C at an MOI of 0.1 for 1hr after which input was removed, monolayers were washed and then exposed to a dose response of 5-fluorouracil (5-FU), β-d-N4-Hydroxycytidine (NHC, EIDD-1931) or GS-441524 in Infection Media. Concurrently, non-infected cells were treated similarly to determine cytotoxicity. After 24hr, viral replication was assessed by NanoGlo Luciferase Assay System (Promega) and cytotoxicity was determined by CellTiterGlo Assay (Promega). Each condition was evaluated in triplicate in two independent studies. Values were normalized to the uninfected and infected vehicle DMSO controls (0 and 100% infection, respectively). Data were fit using a four-parameter nonlinear regression analysis using GraphPad Prism. EC50 and CC50 (cytotoxic concentration at which 50% of cells are viable) values were then determined as the concentration reducing the signal by 50%.

    Journal: bioRxiv

    Article Title: Loss of nsp14-exonuclease activity impairs the replication, proofreading, fitness and pathogenesis of SARS-CoV-2

    doi: 10.64898/2026.01.12.698941

    Figure Lengend Snippet: VTA cells were infected with nanoluciferase-expressing SARS-CoV-2 WT or AA at 37°C at an MOI of 0.1 for 1hr after which input was removed, monolayers were washed and then exposed to a dose response of 5-fluorouracil (5-FU), β-d-N4-Hydroxycytidine (NHC, EIDD-1931) or GS-441524 in Infection Media. Concurrently, non-infected cells were treated similarly to determine cytotoxicity. After 24hr, viral replication was assessed by NanoGlo Luciferase Assay System (Promega) and cytotoxicity was determined by CellTiterGlo Assay (Promega). Each condition was evaluated in triplicate in two independent studies. Values were normalized to the uninfected and infected vehicle DMSO controls (0 and 100% infection, respectively). Data were fit using a four-parameter nonlinear regression analysis using GraphPad Prism. EC50 and CC50 (cytotoxic concentration at which 50% of cells are viable) values were then determined as the concentration reducing the signal by 50%.

    Article Snippet: After incubation, the virus was removed, the monolayers were washed with 100μL of Infection Media, and the cells were treated with three-fold serial dilution series of 5-fluorouracil (5-FU, Sigma), β-d-N4-Hydroxycytidine (NHC, EIDD-1931, MedChemExpress) or GS-441524 (MedChemExpress) in Infection Media, starting at concentrations of 400μM, 20μM, and 20μM respectively.

    Techniques: Infection, Expressing, Luciferase, Concentration Assay