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Arbec Forest Products Inc decynium22
Decynium22, supplied by Arbec Forest Products Inc, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/decynium22/decynium22/pm17689566-150-7-16
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decynium22 - by Bioz Stars, 2026-09
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Article Title: Interaction between nicotine and MPTP/MPP+ in rat brain endothelial cells.
Article Snippet: To examine the interaction between nicotine and MPTP/MPP in the blood–brain barrier, cellular uptake of MPTP and MPP was studied in the presence of nicotine and several compounds, including MPTP/MPP analogs and a specific inhibitor of organic cation transporter (OCT) in an adult rat brain microvascular endothelial cell line (ARBEC).. The kinetic properties of the uptake of MPTP, MPP, and nicotine were also examined.. In addition, a microdialysis study was performed to evaluate the in vivo effect of nicotine (i.p.) on extracellular levels of MPTP and MPP in the brain after intravenous administration of MPTP.



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Inhibition of organic cation transporters by TKIs. (A) The protein sequence of hOCT1, hOCT2, and hOCT3 was aligned by a multiple sequence alignment program (MAFFT). (B) OCT1 protein sequence from indicated organisms was aligned by a multiple sequence alignment program (MAFFT). (C) HEK293 cells were transiently transfected with wild-type (WT), Y240F, Y361F, and Y376F mutant plasmids, uptake assays were performed using [ 14 C] TEA (2 µM) for 15 min. Cellular accumulation of [ 14 C] TEA was determined by liquid scintillation counter, and the graph represents relative uptake values compared to wild-type after normalization of protein levels. (D) Relative transporter function in HEK293 cells stably transfected with hOCT1 was evaluated by a substrate drug TEA in the presence of FDA-approved TKIs (10 µM) previously found to inhibit OCT2. Lapatinib was included as a negative-control TKI, and <t>decynium22</t> as a non-TKI positive control inhibitor. The graph represents relative transport activity of indicated substrate drug compared to DMSO. * p < 0.05 vs. wild-type control. All values represent mean ± SEM.
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Inhibition of organic cation transporters by TKIs. (A) The protein sequence of hOCT1, hOCT2, and hOCT3 was aligned by a multiple sequence alignment program (MAFFT). (B) OCT1 protein sequence from indicated organisms was aligned by a multiple sequence alignment program (MAFFT). (C) HEK293 cells were transiently transfected with wild-type (WT), Y240F, Y361F, and Y376F mutant plasmids, uptake assays were performed using [ 14 C] TEA (2 µM) for 15 min. Cellular accumulation of [ 14 C] TEA was determined by liquid scintillation counter, and the graph represents relative uptake values compared to wild-type after normalization of protein levels. (D) Relative transporter function in HEK293 cells stably transfected with hOCT1 was evaluated by a substrate drug TEA in the presence of FDA-approved TKIs (10 µM) previously found to inhibit OCT2. Lapatinib was included as a negative-control TKI, and <t>decynium22</t> as a non-TKI positive control inhibitor. The graph represents relative transport activity of indicated substrate drug compared to DMSO. * p < 0.05 vs. wild-type control. All values represent mean ± SEM.
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Inhibition of organic cation transporters by TKIs. (A) The protein sequence of hOCT1, hOCT2, and hOCT3 was aligned by a multiple sequence alignment program (MAFFT). (B) OCT1 protein sequence from indicated organisms was aligned by a multiple sequence alignment program (MAFFT). (C) HEK293 cells were transiently transfected with wild-type (WT), Y240F, Y361F, and Y376F mutant plasmids, uptake assays were performed using [ 14 C] TEA (2 µM) for 15 min. Cellular accumulation of [ 14 C] TEA was determined by liquid scintillation counter, and the graph represents relative uptake values compared to wild-type after normalization of protein levels. (D) Relative transporter function in HEK293 cells stably transfected with hOCT1 was evaluated by a substrate drug TEA in the presence of FDA-approved TKIs (10 µM) previously found to inhibit OCT2. Lapatinib was included as a negative-control TKI, and <t>decynium22</t> as a non-TKI positive control inhibitor. The graph represents relative transport activity of indicated substrate drug compared to DMSO. * p < 0.05 vs. wild-type control. All values represent mean ± SEM.
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Inhibition of organic cation transporters by TKIs. (A) The protein sequence of hOCT1, hOCT2, and hOCT3 was aligned by a multiple sequence alignment program (MAFFT). (B) OCT1 protein sequence from indicated organisms was aligned by a multiple sequence alignment program (MAFFT). (C) HEK293 cells were transiently transfected with wild-type (WT), Y240F, Y361F, and Y376F mutant plasmids, uptake assays were performed using [ 14 C] TEA (2 µM) for 15 min. Cellular accumulation of [ 14 C] TEA was determined by liquid scintillation counter, and the graph represents relative uptake values compared to wild-type after normalization of protein levels. (D) Relative transporter function in HEK293 cells stably transfected with hOCT1 was evaluated by a substrate drug TEA in the presence of FDA-approved TKIs (10 µM) previously found to inhibit OCT2. Lapatinib was included as a negative-control TKI, and <t>decynium22</t> as a non-TKI positive control inhibitor. The graph represents relative transport activity of indicated substrate drug compared to DMSO. * p < 0.05 vs. wild-type control. All values represent mean ± SEM.
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Inhibition of organic cation transporters by TKIs. (A) The protein sequence of hOCT1, hOCT2, and hOCT3 was aligned by a multiple sequence alignment program (MAFFT). (B) OCT1 protein sequence from indicated organisms was aligned by a multiple sequence alignment program (MAFFT). (C) HEK293 cells were transiently transfected with wild-type (WT), Y240F, Y361F, and Y376F mutant plasmids, uptake assays were performed using [ 14 C] TEA (2 µM) for 15 min. Cellular accumulation of [ 14 C] TEA was determined by liquid scintillation counter, and the graph represents relative uptake values compared to wild-type after normalization of protein levels. (D) Relative transporter function in HEK293 cells stably transfected with hOCT1 was evaluated by a substrate drug TEA in the presence of FDA-approved TKIs (10 µM) previously found to inhibit OCT2. Lapatinib was included as a negative-control TKI, and <t>decynium22</t> as a non-TKI positive control inhibitor. The graph represents relative transport activity of indicated substrate drug compared to DMSO. * p < 0.05 vs. wild-type control. All values represent mean ± SEM.
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Inhibition of organic cation transporters by TKIs. (A) The protein sequence of hOCT1, hOCT2, and hOCT3 was aligned by a multiple sequence alignment program (MAFFT). (B) OCT1 protein sequence from indicated organisms was aligned by a multiple sequence alignment program (MAFFT). (C) HEK293 cells were transiently transfected with wild-type (WT), Y240F, Y361F, and Y376F mutant plasmids, uptake assays were performed using [ 14 C] TEA (2 µM) for 15 min. Cellular accumulation of [ 14 C] TEA was determined by liquid scintillation counter, and the graph represents relative uptake values compared to wild-type after normalization of protein levels. (D) Relative transporter function in HEK293 cells stably transfected with hOCT1 was evaluated by a substrate drug TEA in the presence of FDA-approved TKIs (10 µM) previously found to inhibit OCT2. Lapatinib was included as a negative-control TKI, and decynium22 as a non-TKI positive control inhibitor. The graph represents relative transport activity of indicated substrate drug compared to DMSO. * p < 0.05 vs. wild-type control. All values represent mean ± SEM.

Journal: Frontiers in Pharmacology

Article Title: Influence of YES1 Kinase and Tyrosine Phosphorylation on the Activity of OCT1

doi: 10.3389/fphar.2021.644342

Figure Lengend Snippet: Inhibition of organic cation transporters by TKIs. (A) The protein sequence of hOCT1, hOCT2, and hOCT3 was aligned by a multiple sequence alignment program (MAFFT). (B) OCT1 protein sequence from indicated organisms was aligned by a multiple sequence alignment program (MAFFT). (C) HEK293 cells were transiently transfected with wild-type (WT), Y240F, Y361F, and Y376F mutant plasmids, uptake assays were performed using [ 14 C] TEA (2 µM) for 15 min. Cellular accumulation of [ 14 C] TEA was determined by liquid scintillation counter, and the graph represents relative uptake values compared to wild-type after normalization of protein levels. (D) Relative transporter function in HEK293 cells stably transfected with hOCT1 was evaluated by a substrate drug TEA in the presence of FDA-approved TKIs (10 µM) previously found to inhibit OCT2. Lapatinib was included as a negative-control TKI, and decynium22 as a non-TKI positive control inhibitor. The graph represents relative transport activity of indicated substrate drug compared to DMSO. * p < 0.05 vs. wild-type control. All values represent mean ± SEM.

Article Snippet: Reference standards of decynium22, a positive control inhibitor, as well as the TKIs bosutinib, dasatinib, gilteritinib, ibrutinib, lapatinib, sunitinib, vandetanib, and CH6953755 were obtained from MedChemExpress (Monmouth Junction, NJ).

Techniques: Inhibition, Sequencing, Transfection, Mutagenesis, Stable Transfection, Negative Control, Positive Control, Activity Assay, Control