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cftr inhibitor ppq  (TargetMol)


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    TargetMol cftr inhibitor ppq
    Cftr Inhibitor Ppq, supplied by TargetMol, used in various techniques. Bioz Stars score: 94/100, based on 2 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/cftr inhibitor ppq/product/TargetMol
    Average 94 stars, based on 2 article reviews
    cftr inhibitor ppq - by Bioz Stars, 2026-03
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    Glutamic acid derivatives potentiation on <t>G551D-CFTR.</t> (a) FLIPR channel function studies of WT-CFTR (blue trace) and G551D-CFTR (gray trace) stimulated with 10 μM cAMP agonist, forskolin (FSK), and <t>then</t> <t>inhibited</t> with 10 μM CFTRinh-172. Averaged traces ( n = 3) of response of G551D-CFTR to chronic treatment of 1 μM 1 (black trace), and glutamic acid derivatives of 1 : 2 (orange trace), 3 (green trace), and 4 (red trace). (b) Quantification of the maximum peak of FSK stimulation in the FLIPR assay relative to the baseline shows that acute treatment with 1 μM 1–4 shows significantly potentiated CFTR chloride flux compared to 10 μM FSK alone ( n = 3 for all conditions). Results are presented as mean ± SD and analyzed by one-way ANOVA and Dunnett’s post hoc test (** P < 0.02; *** P < 0.0002; **** P < 0.0001 compared with 10 μM FSK).
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    Glutamic acid derivatives potentiation on G551D-CFTR. (a) FLIPR channel function studies of WT-CFTR (blue trace) and G551D-CFTR (gray trace) stimulated with 10 μM cAMP agonist, forskolin (FSK), and then inhibited with 10 μM CFTRinh-172. Averaged traces ( n = 3) of response of G551D-CFTR to chronic treatment of 1 μM 1 (black trace), and glutamic acid derivatives of 1 : 2 (orange trace), 3 (green trace), and 4 (red trace). (b) Quantification of the maximum peak of FSK stimulation in the FLIPR assay relative to the baseline shows that acute treatment with 1 μM 1–4 shows significantly potentiated CFTR chloride flux compared to 10 μM FSK alone ( n = 3 for all conditions). Results are presented as mean ± SD and analyzed by one-way ANOVA and Dunnett’s post hoc test (** P < 0.02; *** P < 0.0002; **** P < 0.0001 compared with 10 μM FSK).

    Journal: ACS Omega

    Article Title: Synthesis and Evaluation of Ivacaftor Derivatives with Reduced Lipophilicity

    doi: 10.1021/acsomega.3c05839

    Figure Lengend Snippet: Glutamic acid derivatives potentiation on G551D-CFTR. (a) FLIPR channel function studies of WT-CFTR (blue trace) and G551D-CFTR (gray trace) stimulated with 10 μM cAMP agonist, forskolin (FSK), and then inhibited with 10 μM CFTRinh-172. Averaged traces ( n = 3) of response of G551D-CFTR to chronic treatment of 1 μM 1 (black trace), and glutamic acid derivatives of 1 : 2 (orange trace), 3 (green trace), and 4 (red trace). (b) Quantification of the maximum peak of FSK stimulation in the FLIPR assay relative to the baseline shows that acute treatment with 1 μM 1–4 shows significantly potentiated CFTR chloride flux compared to 10 μM FSK alone ( n = 3 for all conditions). Results are presented as mean ± SD and analyzed by one-way ANOVA and Dunnett’s post hoc test (** P < 0.02; *** P < 0.0002; **** P < 0.0001 compared with 10 μM FSK).

    Article Snippet: CFTR activity was then inhibited with the CFTR inhibitor CFTR inh -172 (10 μM, MedChemExpress, Princeton, NJ).

    Techniques: