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The antiviral effect of TRAM-34 is independent of its cellular target KCa3.1. (A) Structures of TRAM-34, clotrimazole, senicapoc, and <t>NS6180.</t> (B) Dose-response characteristics of candidate drugs against VSV pseudotypes displaying MACV GP or VSV G. Monolayers of A549 cells were pretreated with increasing drug concentrations for 30 min, followed by infection with the indicated pseudotypes and detection of infection as in Fig. 2B. (C) Apparent IC50 of the tested drugs against MACV pseudotypes calculated from panel B compared to the reported IC50 against the pharmacological drug target KCa3.1. Please note that the antiviral activity of drugs does not correlate with their published target-specific efficacy. (D) Deletion of KCa3.1 does not affect infection with MACV pseudotypes. Wild-type (WT) and KCa3.1 null HeLa cells were pretreated with TRAM-34 (20 μM) or solvent control (DMSO) and infected with the indicated VSV pseudotypes as in Fig. 2B. Infection was detected by direct fluorescence detection of the EGFP and the control (DMSO) set at 100%. The data are means + the SD (n = 3).
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The antiviral effect of TRAM-34 is independent of its cellular target KCa3.1. (A) Structures of TRAM-34, clotrimazole, senicapoc, and <t>NS6180.</t> (B) Dose-response characteristics of candidate drugs against VSV pseudotypes displaying MACV GP or VSV G. Monolayers of A549 cells were pretreated with increasing drug concentrations for 30 min, followed by infection with the indicated pseudotypes and detection of infection as in Fig. 2B. (C) Apparent IC50 of the tested drugs against MACV pseudotypes calculated from panel B compared to the reported IC50 against the pharmacological drug target KCa3.1. Please note that the antiviral activity of drugs does not correlate with their published target-specific efficacy. (D) Deletion of KCa3.1 does not affect infection with MACV pseudotypes. Wild-type (WT) and KCa3.1 null HeLa cells were pretreated with TRAM-34 (20 μM) or solvent control (DMSO) and infected with the indicated VSV pseudotypes as in Fig. 2B. Infection was detected by direct fluorescence detection of the EGFP and the control (DMSO) set at 100%. The data are means + the SD (n = 3).
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The antiviral effect of TRAM-34 is independent of its cellular target KCa3.1. (A) Structures of TRAM-34, clotrimazole, senicapoc, and <t>NS6180.</t> (B) Dose-response characteristics of candidate drugs against VSV pseudotypes displaying MACV GP or VSV G. Monolayers of A549 cells were pretreated with increasing drug concentrations for 30 min, followed by infection with the indicated pseudotypes and detection of infection as in Fig. 2B. (C) Apparent IC50 of the tested drugs against MACV pseudotypes calculated from panel B compared to the reported IC50 against the pharmacological drug target KCa3.1. Please note that the antiviral activity of drugs does not correlate with their published target-specific efficacy. (D) Deletion of KCa3.1 does not affect infection with MACV pseudotypes. Wild-type (WT) and KCa3.1 null HeLa cells were pretreated with TRAM-34 (20 μM) or solvent control (DMSO) and infected with the indicated VSV pseudotypes as in Fig. 2B. Infection was detected by direct fluorescence detection of the EGFP and the control (DMSO) set at 100%. The data are means + the SD (n = 3).
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The antiviral effect of TRAM-34 is independent of its cellular target KCa3.1. (A) Structures of TRAM-34, clotrimazole, senicapoc, and <t>NS6180.</t> (B) Dose-response characteristics of candidate drugs against VSV pseudotypes displaying MACV GP or VSV G. Monolayers of A549 cells were pretreated with increasing drug concentrations for 30 min, followed by infection with the indicated pseudotypes and detection of infection as in Fig. 2B. (C) Apparent IC50 of the tested drugs against MACV pseudotypes calculated from panel B compared to the reported IC50 against the pharmacological drug target KCa3.1. Please note that the antiviral activity of drugs does not correlate with their published target-specific efficacy. (D) Deletion of KCa3.1 does not affect infection with MACV pseudotypes. Wild-type (WT) and KCa3.1 null HeLa cells were pretreated with TRAM-34 (20 μM) or solvent control (DMSO) and infected with the indicated VSV pseudotypes as in Fig. 2B. Infection was detected by direct fluorescence detection of the EGFP and the control (DMSO) set at 100%. The data are means + the SD (n = 3).
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The antiviral effect of TRAM-34 is independent of its cellular target KCa3.1. (A) Structures of TRAM-34, clotrimazole, senicapoc, and <t>NS6180.</t> (B) Dose-response characteristics of candidate drugs against VSV pseudotypes displaying MACV GP or VSV G. Monolayers of A549 cells were pretreated with increasing drug concentrations for 30 min, followed by infection with the indicated pseudotypes and detection of infection as in Fig. 2B. (C) Apparent IC50 of the tested drugs against MACV pseudotypes calculated from panel B compared to the reported IC50 against the pharmacological drug target KCa3.1. Please note that the antiviral activity of drugs does not correlate with their published target-specific efficacy. (D) Deletion of KCa3.1 does not affect infection with MACV pseudotypes. Wild-type (WT) and KCa3.1 null HeLa cells were pretreated with TRAM-34 (20 μM) or solvent control (DMSO) and infected with the indicated VSV pseudotypes as in Fig. 2B. Infection was detected by direct fluorescence detection of the EGFP and the control (DMSO) set at 100%. The data are means + the SD (n = 3).
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The antiviral effect of TRAM-34 is independent of its cellular target KCa3.1. (A) Structures of TRAM-34, clotrimazole, senicapoc, and <t>NS6180.</t> (B) Dose-response characteristics of candidate drugs against VSV pseudotypes displaying MACV GP or VSV G. Monolayers of A549 cells were pretreated with increasing drug concentrations for 30 min, followed by infection with the indicated pseudotypes and detection of infection as in Fig. 2B. (C) Apparent IC50 of the tested drugs against MACV pseudotypes calculated from panel B compared to the reported IC50 against the pharmacological drug target KCa3.1. Please note that the antiviral activity of drugs does not correlate with their published target-specific efficacy. (D) Deletion of KCa3.1 does not affect infection with MACV pseudotypes. Wild-type (WT) and KCa3.1 null HeLa cells were pretreated with TRAM-34 (20 μM) or solvent control (DMSO) and infected with the indicated VSV pseudotypes as in Fig. 2B. Infection was detected by direct fluorescence detection of the EGFP and the control (DMSO) set at 100%. The data are means + the SD (n = 3).
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Nanoshel LLC lfp nanopowder 80-100 99.9% purity
The antiviral effect of TRAM-34 is independent of its cellular target KCa3.1. (A) Structures of TRAM-34, clotrimazole, senicapoc, and <t>NS6180.</t> (B) Dose-response characteristics of candidate drugs against VSV pseudotypes displaying MACV GP or VSV G. Monolayers of A549 cells were pretreated with increasing drug concentrations for 30 min, followed by infection with the indicated pseudotypes and detection of infection as in Fig. 2B. (C) Apparent IC50 of the tested drugs against MACV pseudotypes calculated from panel B compared to the reported IC50 against the pharmacological drug target KCa3.1. Please note that the antiviral activity of drugs does not correlate with their published target-specific efficacy. (D) Deletion of KCa3.1 does not affect infection with MACV pseudotypes. Wild-type (WT) and KCa3.1 null HeLa cells were pretreated with TRAM-34 (20 μM) or solvent control (DMSO) and infected with the indicated VSV pseudotypes as in Fig. 2B. Infection was detected by direct fluorescence detection of the EGFP and the control (DMSO) set at 100%. The data are means + the SD (n = 3).
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The antiviral effect of TRAM-34 is independent of its cellular target KCa3.1. (A) Structures of TRAM-34, clotrimazole, senicapoc, and <t>NS6180.</t> (B) Dose-response characteristics of candidate drugs against VSV pseudotypes displaying MACV GP or VSV G. Monolayers of A549 cells were pretreated with increasing drug concentrations for 30 min, followed by infection with the indicated pseudotypes and detection of infection as in Fig. 2B. (C) Apparent IC50 of the tested drugs against MACV pseudotypes calculated from panel B compared to the reported IC50 against the pharmacological drug target KCa3.1. Please note that the antiviral activity of drugs does not correlate with their published target-specific efficacy. (D) Deletion of KCa3.1 does not affect infection with MACV pseudotypes. Wild-type (WT) and KCa3.1 null HeLa cells were pretreated with TRAM-34 (20 μM) or solvent control (DMSO) and infected with the indicated VSV pseudotypes as in Fig. 2B. Infection was detected by direct fluorescence detection of the EGFP and the control (DMSO) set at 100%. The data are means + the SD (n = 3).
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Potent KCa3 1 channel blocker
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The antiviral effect of TRAM-34 is independent of its cellular target KCa3.1. (A) Structures of TRAM-34, clotrimazole, senicapoc, and NS6180. (B) Dose-response characteristics of candidate drugs against VSV pseudotypes displaying MACV GP or VSV G. Monolayers of A549 cells were pretreated with increasing drug concentrations for 30 min, followed by infection with the indicated pseudotypes and detection of infection as in Fig. 2B. (C) Apparent IC50 of the tested drugs against MACV pseudotypes calculated from panel B compared to the reported IC50 against the pharmacological drug target KCa3.1. Please note that the antiviral activity of drugs does not correlate with their published target-specific efficacy. (D) Deletion of KCa3.1 does not affect infection with MACV pseudotypes. Wild-type (WT) and KCa3.1 null HeLa cells were pretreated with TRAM-34 (20 μM) or solvent control (DMSO) and infected with the indicated VSV pseudotypes as in Fig. 2B. Infection was detected by direct fluorescence detection of the EGFP and the control (DMSO) set at 100%. The data are means + the SD (n = 3).

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Figure Lengend Snippet: The antiviral effect of TRAM-34 is independent of its cellular target KCa3.1. (A) Structures of TRAM-34, clotrimazole, senicapoc, and NS6180. (B) Dose-response characteristics of candidate drugs against VSV pseudotypes displaying MACV GP or VSV G. Monolayers of A549 cells were pretreated with increasing drug concentrations for 30 min, followed by infection with the indicated pseudotypes and detection of infection as in Fig. 2B. (C) Apparent IC50 of the tested drugs against MACV pseudotypes calculated from panel B compared to the reported IC50 against the pharmacological drug target KCa3.1. Please note that the antiviral activity of drugs does not correlate with their published target-specific efficacy. (D) Deletion of KCa3.1 does not affect infection with MACV pseudotypes. Wild-type (WT) and KCa3.1 null HeLa cells were pretreated with TRAM-34 (20 μM) or solvent control (DMSO) and infected with the indicated VSV pseudotypes as in Fig. 2B. Infection was detected by direct fluorescence detection of the EGFP and the control (DMSO) set at 100%. The data are means + the SD (n = 3).

Article Snippet: Clotrimazole and senicapoc were obtained from MedChem Express, TRAM-34 was obtained from Sigma, and NS6180 was obtained from Alomone.

Techniques: Infection, Activity Assay, Fluorescence