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nesolicaftor  (MedChemExpress)
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Effects of <t>nesolicaftor</t> (NES) on modulator-corrected F508del CFTR function in 16HBEge cells in vitro. ( A ) Confluent monolayers of F508del CFTR 16HBEge cells were treated with DMSO, NES (10 µM), lumacaftor (5 µM)/ivacaftor (1 µM) (LI), LI + NES, tezacaftor (5 µM)/ivacaftor (1 µM) (TI), TI + NES, elexacaftor (1 µM)/tezacaftor (5 µM)/ivacaftor (1 µM) (ETI), or ETI + NES both apically and basolaterally for 24 h. CFTR-dependent short-circuit currents (I SC ) were measured in Ussing chambers as the change in I SC after CFTR inh -172 (10 µM) following forskolin (10 µM) stimulation in the presence of amiloride (10 µM) and ivacaftor (IVA; 1 µM). ( B ) Nesolicaftor alone increases F508del CFTR function. Nesolicaftor further increases F508del CFTR function in 16HBEge cells treated with LI or TI. Nesolicaftor does not improve F508del CFTR function in 16HBEge cells treated with ETI. n = 5. Statistics: * p < 0.05, Student’s t -test between treatment groups after assessing normality with Shapiro-Wilk. ns = not significant.
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Effects of nesolicaftor (NES) on modulator-corrected F508del CFTR function in 16HBEge cells in vitro. ( A ) Confluent monolayers of F508del CFTR 16HBEge cells were treated with DMSO, NES (10 µM), lumacaftor (5 µM)/ivacaftor (1 µM) (LI), LI + NES, tezacaftor (5 µM)/ivacaftor (1 µM) (TI), TI + NES, elexacaftor (1 µM)/tezacaftor (5 µM)/ivacaftor (1 µM) (ETI), or ETI + NES both apically and basolaterally for 24 h. CFTR-dependent short-circuit currents (I SC ) were measured in Ussing chambers as the change in I SC after CFTR inh -172 (10 µM) following forskolin (10 µM) stimulation in the presence of amiloride (10 µM) and ivacaftor (IVA; 1 µM). ( B ) Nesolicaftor alone increases F508del CFTR function. Nesolicaftor further increases F508del CFTR function in 16HBEge cells treated with LI or TI. Nesolicaftor does not improve F508del CFTR function in 16HBEge cells treated with ETI. n = 5. Statistics: * p < 0.05, Student’s t -test between treatment groups after assessing normality with Shapiro-Wilk. ns = not significant.

Journal: International Journal of Molecular Sciences

Article Title: The CFTR Amplifier Nesolicaftor Rescues TGF-β1 Inhibition of Modulator-Corrected F508del CFTR Function

doi: 10.3390/ijms231810956

Figure Lengend Snippet: Effects of nesolicaftor (NES) on modulator-corrected F508del CFTR function in 16HBEge cells in vitro. ( A ) Confluent monolayers of F508del CFTR 16HBEge cells were treated with DMSO, NES (10 µM), lumacaftor (5 µM)/ivacaftor (1 µM) (LI), LI + NES, tezacaftor (5 µM)/ivacaftor (1 µM) (TI), TI + NES, elexacaftor (1 µM)/tezacaftor (5 µM)/ivacaftor (1 µM) (ETI), or ETI + NES both apically and basolaterally for 24 h. CFTR-dependent short-circuit currents (I SC ) were measured in Ussing chambers as the change in I SC after CFTR inh -172 (10 µM) following forskolin (10 µM) stimulation in the presence of amiloride (10 µM) and ivacaftor (IVA; 1 µM). ( B ) Nesolicaftor alone increases F508del CFTR function. Nesolicaftor further increases F508del CFTR function in 16HBEge cells treated with LI or TI. Nesolicaftor does not improve F508del CFTR function in 16HBEge cells treated with ETI. n = 5. Statistics: * p < 0.05, Student’s t -test between treatment groups after assessing normality with Shapiro-Wilk. ns = not significant.

Article Snippet: Nesolicaftor (PTI-428; Cat. No. HY-111680) was acquired from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: In Vitro

Nesolicaftor (NES) improves ETI-corrected F508del CFTR function in primary CFBE cells in vitro. ( A ) Fully differentiated ALI cultures of primary human CFBE cells homozygous for F508del were treated with elexacaftor (1 µM)/tezacaftor (5 µM)/ivacaftor (1 µM) (ETI) or ETI + NES (10 µM) for 24 h and CFTR-dependent I SC was measured in Ussing chambers. ( B ) Nesolicaftor significantly increases F508del CFTR function in ETI-treated CFBE cells after 24 h. n = 6, 3 CF lungs. ( C ) Nesolicaftor significantly increases expression levels of CFTR mRNA compared to ETI alone. n = 6, 3 CF lungs. ( D , E ) Amiloride-sensitive I SC (ENaC function) ( D ) and UTP-stimulated I SC (CaCC function) ( E ) are significantly increased by nesolicaftor in ETI-treated CFBE cells after 24 h. n = 6, 3 CF lungs. ( F , G ) Nesolicaftor significantly increases the expression of SCNN1B , but not SCNN1A , mRNA in ETI-treated CFBE cells after 24 h. n = 5, 3 CF lungs. ( H ) Nesolicaftor also causes a significant increase in the expression of ANO1 mRNA in ETI-treated CFBE cells after 24 h. n = 5, 3 CF lungs. Statistics: * p < 0.05, Student’s t -test after assessing normality with Shapiro-Wilk.

Journal: International Journal of Molecular Sciences

Article Title: The CFTR Amplifier Nesolicaftor Rescues TGF-β1 Inhibition of Modulator-Corrected F508del CFTR Function

doi: 10.3390/ijms231810956

Figure Lengend Snippet: Nesolicaftor (NES) improves ETI-corrected F508del CFTR function in primary CFBE cells in vitro. ( A ) Fully differentiated ALI cultures of primary human CFBE cells homozygous for F508del were treated with elexacaftor (1 µM)/tezacaftor (5 µM)/ivacaftor (1 µM) (ETI) or ETI + NES (10 µM) for 24 h and CFTR-dependent I SC was measured in Ussing chambers. ( B ) Nesolicaftor significantly increases F508del CFTR function in ETI-treated CFBE cells after 24 h. n = 6, 3 CF lungs. ( C ) Nesolicaftor significantly increases expression levels of CFTR mRNA compared to ETI alone. n = 6, 3 CF lungs. ( D , E ) Amiloride-sensitive I SC (ENaC function) ( D ) and UTP-stimulated I SC (CaCC function) ( E ) are significantly increased by nesolicaftor in ETI-treated CFBE cells after 24 h. n = 6, 3 CF lungs. ( F , G ) Nesolicaftor significantly increases the expression of SCNN1B , but not SCNN1A , mRNA in ETI-treated CFBE cells after 24 h. n = 5, 3 CF lungs. ( H ) Nesolicaftor also causes a significant increase in the expression of ANO1 mRNA in ETI-treated CFBE cells after 24 h. n = 5, 3 CF lungs. Statistics: * p < 0.05, Student’s t -test after assessing normality with Shapiro-Wilk.

Article Snippet: Nesolicaftor (PTI-428; Cat. No. HY-111680) was acquired from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: In Vitro, Expressing

Nesolicaftor (NES) rescues TGF-β1-induced reductions in CFTR function and ciliary beating in primary CFBE cells in vitro. ( A ) Fully differentiated ALI cultures of primary human CFBE cells homozygous for F508del were treated with elexacaftor (1 µM)/tezacaftor (5 µM)/ivacaftor (1 µM) (ETI), ETI + TGF-β1 (5 ng/mL), or ETI + TGF-β1 + NES (10 µM) for 24 h and CFTR-dependent I SC was measured in Ussing chambers. ( B ) Nesolicaftor reverses the reduction in ETI-corrected F508del CFTR function caused by TGF-β1. n = 8, 3 CF lungs. ( C ) TGF-β1 significantly reduces levels of CFTR mRNA expression in ETI-treated CFBE cells. CFTR mRNA levels are restored by nesolicaftor. n = 6, 3 CF lungs. ( D ) Amiloride-sensitive I SC (ENaC function) is significantly reduced by TGF-β1. Nesolicaftor increases ENaC function in the presence of TGF-β1. n = 8, 3 CF lungs. ( E ) TGF-β1 does not significantly affect UTP-stimulated I SC (CaCC function). Nesolicaftor significantly increases CaCC function in the presence of TGF-β1. n = 8, 3 CF lungs. ( F ) TGF-β1 causes a significant reduction in ciliary beat frequency (CBF) in ETI-treated F508del CFTR CFBE cells after 24 h. TGF-β1-induced reductions in CBF are reversed by nesolicaftor. n = 5, 3 CF lungs. Statistics: * p < 0.05, one-way ANOVA followed by Holm-Sidak ( B , D , F ) or Friedman test ( C , E ) after assessing normality with Shapiro-Wilk. ns = not significant.

Journal: International Journal of Molecular Sciences

Article Title: The CFTR Amplifier Nesolicaftor Rescues TGF-β1 Inhibition of Modulator-Corrected F508del CFTR Function

doi: 10.3390/ijms231810956

Figure Lengend Snippet: Nesolicaftor (NES) rescues TGF-β1-induced reductions in CFTR function and ciliary beating in primary CFBE cells in vitro. ( A ) Fully differentiated ALI cultures of primary human CFBE cells homozygous for F508del were treated with elexacaftor (1 µM)/tezacaftor (5 µM)/ivacaftor (1 µM) (ETI), ETI + TGF-β1 (5 ng/mL), or ETI + TGF-β1 + NES (10 µM) for 24 h and CFTR-dependent I SC was measured in Ussing chambers. ( B ) Nesolicaftor reverses the reduction in ETI-corrected F508del CFTR function caused by TGF-β1. n = 8, 3 CF lungs. ( C ) TGF-β1 significantly reduces levels of CFTR mRNA expression in ETI-treated CFBE cells. CFTR mRNA levels are restored by nesolicaftor. n = 6, 3 CF lungs. ( D ) Amiloride-sensitive I SC (ENaC function) is significantly reduced by TGF-β1. Nesolicaftor increases ENaC function in the presence of TGF-β1. n = 8, 3 CF lungs. ( E ) TGF-β1 does not significantly affect UTP-stimulated I SC (CaCC function). Nesolicaftor significantly increases CaCC function in the presence of TGF-β1. n = 8, 3 CF lungs. ( F ) TGF-β1 causes a significant reduction in ciliary beat frequency (CBF) in ETI-treated F508del CFTR CFBE cells after 24 h. TGF-β1-induced reductions in CBF are reversed by nesolicaftor. n = 5, 3 CF lungs. Statistics: * p < 0.05, one-way ANOVA followed by Holm-Sidak ( B , D , F ) or Friedman test ( C , E ) after assessing normality with Shapiro-Wilk. ns = not significant.

Article Snippet: Nesolicaftor (PTI-428; Cat. No. HY-111680) was acquired from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: In Vitro, Expressing

Nesolicaftor (NES) reverses TGF-β1-induced increases in IL-6 and IL-8 levels in primary CFBE cells in vitro. ( A ) Nesolicaftor rescues the increase in IL-6 protein levels induced by TGF-β1 in ETI-treated CFBE cells after 24 h. IL-6 expression was measured in the basolateral media. n = 6, 3 CF lungs. ( B ) Nesolicaftor led to a non-significant reduction in IL-8 protein levels induced by TGF-β1 in ETI-treated CFBE cells after 24 h. IL-8 levels were measured in the basolateral media. n = 6, 3 CF lungs. Statistics: * p < 0.05, Friedman test ( A ) or one-way ANOVA followed by Holm-Sidak ( B ) after assessing normality with Shapiro-Wilk. ns = not significant.

Journal: International Journal of Molecular Sciences

Article Title: The CFTR Amplifier Nesolicaftor Rescues TGF-β1 Inhibition of Modulator-Corrected F508del CFTR Function

doi: 10.3390/ijms231810956

Figure Lengend Snippet: Nesolicaftor (NES) reverses TGF-β1-induced increases in IL-6 and IL-8 levels in primary CFBE cells in vitro. ( A ) Nesolicaftor rescues the increase in IL-6 protein levels induced by TGF-β1 in ETI-treated CFBE cells after 24 h. IL-6 expression was measured in the basolateral media. n = 6, 3 CF lungs. ( B ) Nesolicaftor led to a non-significant reduction in IL-8 protein levels induced by TGF-β1 in ETI-treated CFBE cells after 24 h. IL-8 levels were measured in the basolateral media. n = 6, 3 CF lungs. Statistics: * p < 0.05, Friedman test ( A ) or one-way ANOVA followed by Holm-Sidak ( B ) after assessing normality with Shapiro-Wilk. ns = not significant.

Article Snippet: Nesolicaftor (PTI-428; Cat. No. HY-111680) was acquired from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: In Vitro, Expressing

Nesolicaftor (NES) improves miR-145 -induced reductions in CFTR function and mRNA expression in primary CFBE cells in vitro. ( A ) Primary human CFBE cells homozygous for F508del were infected with a miR-145 lentiviral expression vector during differentiation. Fully differentiated ALI cultures overexpressing miR-145 were treated with elexacaftor (1 µM)/tezacaftor (5 µM)/ivacaftor (1 µM) (ETI) or ETI + NES (10 µM) for 24 h and CFTR-dependent I SC was measured in Ussing chambers. ( B ) Nesolicaftor significantly increases ETI-corrected F508del CFTR function in miR-145 -overexpressing CFBE cells after 24 h. n ≥ 9, 3 CF lungs. ( C ) Nesolicaftor significantly increases expression levels of CFTR mRNA compared to ETI + miR-145 alone. n = 7, 3 CF lungs. ( D,E ) Amiloride-sensitive I SC (ENaC function) ( D ) and UTP-stimulated I SC (CaCC function) ( E ) are significantly increased by nesolicaftor in ETI-treated miR-145 -overexpressing CFBE cells after 24 h. n ≥ 7, 3 CF lungs. Statistics: * p < 0.05, unpaired t -test ( B , D ), Wilcoxon test ( C ), or Mann-Whitney test ( E ) after assessing normality with Shapiro-Wilk.

Journal: International Journal of Molecular Sciences

Article Title: The CFTR Amplifier Nesolicaftor Rescues TGF-β1 Inhibition of Modulator-Corrected F508del CFTR Function

doi: 10.3390/ijms231810956

Figure Lengend Snippet: Nesolicaftor (NES) improves miR-145 -induced reductions in CFTR function and mRNA expression in primary CFBE cells in vitro. ( A ) Primary human CFBE cells homozygous for F508del were infected with a miR-145 lentiviral expression vector during differentiation. Fully differentiated ALI cultures overexpressing miR-145 were treated with elexacaftor (1 µM)/tezacaftor (5 µM)/ivacaftor (1 µM) (ETI) or ETI + NES (10 µM) for 24 h and CFTR-dependent I SC was measured in Ussing chambers. ( B ) Nesolicaftor significantly increases ETI-corrected F508del CFTR function in miR-145 -overexpressing CFBE cells after 24 h. n ≥ 9, 3 CF lungs. ( C ) Nesolicaftor significantly increases expression levels of CFTR mRNA compared to ETI + miR-145 alone. n = 7, 3 CF lungs. ( D,E ) Amiloride-sensitive I SC (ENaC function) ( D ) and UTP-stimulated I SC (CaCC function) ( E ) are significantly increased by nesolicaftor in ETI-treated miR-145 -overexpressing CFBE cells after 24 h. n ≥ 7, 3 CF lungs. Statistics: * p < 0.05, unpaired t -test ( B , D ), Wilcoxon test ( C ), or Mann-Whitney test ( E ) after assessing normality with Shapiro-Wilk.

Article Snippet: Nesolicaftor (PTI-428; Cat. No. HY-111680) was acquired from MedChemExpress (Monmouth Junction, NJ, USA).

Techniques: Expressing, In Vitro, Infection, Plasmid Preparation, MANN-WHITNEY