afatinib Search Results


afatinib  (MedChemExpress)
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MedChemExpress afatinib
Afatinib, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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s1011  (Selleck Chemicals)
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Selleck Chemicals s1011
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afatinib  (Toronto Research Chemicals)
90
Toronto Research Chemicals afatinib
Afatinib, supplied by Toronto Research Chemicals, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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tysosine kinase inhibitors  (Santa Cruz Biotechnology)
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Santa Cruz Biotechnology tysosine kinase inhibitors
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afatinib  (Tocris)
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Tocris afatinib
Afatinib, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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afatinib dimaleate  (Tocris)
93
Tocris afatinib dimaleate
Fig. 7. Inhibition of EGFR and growth factor pathway components prevented TRPV3 mRNA upregulation after injury. (A) HBEC3-KT cells were treated with 5 mM solutions of inhibitors of multiple ErbB receptor tyrosine kinase isoforms: ErbB1 (EGFR)-specific inhibitor AG-1478, ErbB pan-inhibitors AZD8931 and <t>Afatinib,</t> and a selective <t>ErbB2</t> (HER2) inhibitor CP-724 for 2 hours in the cell passaging injury model, fol- lowed by analysis of TRPV3 mRNA. (B) Downstream targets of EGFR activation were also inhibited, and TRPV3 expression was subsequently measured 2 hours after cell passaging injury. Inhibitors included 5 mM TWS119 (GSK3b), 20 mM CCT036477 (b-catenin), 10 mM PD169316 (p38 MAPK), and 10 mM SP600125 (JNK). (C) Inhibition of NF-jB (20 mM BMS-345541) and effects on TRPV3 mRNA 2 hours after cell passaging injury. (D) Inhibitors of Wnt7a and Fzd signaling were also used: 10 ng/ml secreted Frizzled-related protein (sFRP) and IWP 2 (Porcupine inhibitor) reduced TRPV3 upregulation after injury. Furthermore, SB 431542 (TGFbRI inhibitor) and 150 mM ITD-1 (TGFbRII inhibitor) were also tested, and SB 431542 treatment prevented TRPV3 expression as well. Values were normalized to vehicle controls and are presented as mean ± S.D. from n $ 3 replicates. Statistical significance was determined using one-way ANOVA with the Dunnett post-test. ***P < 0.001, ****P < 0.0001. For Fig. 4C, an unpaired t test was used. ****P < 0.0001.
Afatinib Dimaleate, supplied by Tocris, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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afatinib  (Selleck Chemicals)
93
Selleck Chemicals afatinib
Fig. 7. Inhibition of EGFR and growth factor pathway components prevented TRPV3 mRNA upregulation after injury. (A) HBEC3-KT cells were treated with 5 mM solutions of inhibitors of multiple ErbB receptor tyrosine kinase isoforms: ErbB1 (EGFR)-specific inhibitor AG-1478, ErbB pan-inhibitors AZD8931 and <t>Afatinib,</t> and a selective <t>ErbB2</t> (HER2) inhibitor CP-724 for 2 hours in the cell passaging injury model, fol- lowed by analysis of TRPV3 mRNA. (B) Downstream targets of EGFR activation were also inhibited, and TRPV3 expression was subsequently measured 2 hours after cell passaging injury. Inhibitors included 5 mM TWS119 (GSK3b), 20 mM CCT036477 (b-catenin), 10 mM PD169316 (p38 MAPK), and 10 mM SP600125 (JNK). (C) Inhibition of NF-jB (20 mM BMS-345541) and effects on TRPV3 mRNA 2 hours after cell passaging injury. (D) Inhibitors of Wnt7a and Fzd signaling were also used: 10 ng/ml secreted Frizzled-related protein (sFRP) and IWP 2 (Porcupine inhibitor) reduced TRPV3 upregulation after injury. Furthermore, SB 431542 (TGFbRI inhibitor) and 150 mM ITD-1 (TGFbRII inhibitor) were also tested, and SB 431542 treatment prevented TRPV3 expression as well. Values were normalized to vehicle controls and are presented as mean ± S.D. from n $ 3 replicates. Statistical significance was determined using one-way ANOVA with the Dunnett post-test. ***P < 0.001, ****P < 0.0001. For Fig. 4C, an unpaired t test was used. ****P < 0.0001.
Afatinib, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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afatinib d6  (Toronto Research Chemicals)
91
Toronto Research Chemicals afatinib d6
Fig. 7. Inhibition of EGFR and growth factor pathway components prevented TRPV3 mRNA upregulation after injury. (A) HBEC3-KT cells were treated with 5 mM solutions of inhibitors of multiple ErbB receptor tyrosine kinase isoforms: ErbB1 (EGFR)-specific inhibitor AG-1478, ErbB pan-inhibitors AZD8931 and <t>Afatinib,</t> and a selective <t>ErbB2</t> (HER2) inhibitor CP-724 for 2 hours in the cell passaging injury model, fol- lowed by analysis of TRPV3 mRNA. (B) Downstream targets of EGFR activation were also inhibited, and TRPV3 expression was subsequently measured 2 hours after cell passaging injury. Inhibitors included 5 mM TWS119 (GSK3b), 20 mM CCT036477 (b-catenin), 10 mM PD169316 (p38 MAPK), and 10 mM SP600125 (JNK). (C) Inhibition of NF-jB (20 mM BMS-345541) and effects on TRPV3 mRNA 2 hours after cell passaging injury. (D) Inhibitors of Wnt7a and Fzd signaling were also used: 10 ng/ml secreted Frizzled-related protein (sFRP) and IWP 2 (Porcupine inhibitor) reduced TRPV3 upregulation after injury. Furthermore, SB 431542 (TGFbRI inhibitor) and 150 mM ITD-1 (TGFbRII inhibitor) were also tested, and SB 431542 treatment prevented TRPV3 expression as well. Values were normalized to vehicle controls and are presented as mean ± S.D. from n $ 3 replicates. Statistical significance was determined using one-way ANOVA with the Dunnett post-test. ***P < 0.001, ****P < 0.0001. For Fig. 4C, an unpaired t test was used. ****P < 0.0001.
Afatinib D6, supplied by Toronto Research Chemicals, used in various techniques. Bioz Stars score: 91/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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afatinib  (Biosynth Carbosynth)
89
Biosynth Carbosynth afatinib
Fig. 7. Inhibition of EGFR and growth factor pathway components prevented TRPV3 mRNA upregulation after injury. (A) HBEC3-KT cells were treated with 5 mM solutions of inhibitors of multiple ErbB receptor tyrosine kinase isoforms: ErbB1 (EGFR)-specific inhibitor AG-1478, ErbB pan-inhibitors AZD8931 and <t>Afatinib,</t> and a selective <t>ErbB2</t> (HER2) inhibitor CP-724 for 2 hours in the cell passaging injury model, fol- lowed by analysis of TRPV3 mRNA. (B) Downstream targets of EGFR activation were also inhibited, and TRPV3 expression was subsequently measured 2 hours after cell passaging injury. Inhibitors included 5 mM TWS119 (GSK3b), 20 mM CCT036477 (b-catenin), 10 mM PD169316 (p38 MAPK), and 10 mM SP600125 (JNK). (C) Inhibition of NF-jB (20 mM BMS-345541) and effects on TRPV3 mRNA 2 hours after cell passaging injury. (D) Inhibitors of Wnt7a and Fzd signaling were also used: 10 ng/ml secreted Frizzled-related protein (sFRP) and IWP 2 (Porcupine inhibitor) reduced TRPV3 upregulation after injury. Furthermore, SB 431542 (TGFbRI inhibitor) and 150 mM ITD-1 (TGFbRII inhibitor) were also tested, and SB 431542 treatment prevented TRPV3 expression as well. Values were normalized to vehicle controls and are presented as mean ± S.D. from n $ 3 replicates. Statistical significance was determined using one-way ANOVA with the Dunnett post-test. ***P < 0.001, ****P < 0.0001. For Fig. 4C, an unpaired t test was used. ****P < 0.0001.
Afatinib, supplied by Biosynth Carbosynth, used in various techniques. Bioz Stars score: 89/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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Image Search Results


Fig. 7. Inhibition of EGFR and growth factor pathway components prevented TRPV3 mRNA upregulation after injury. (A) HBEC3-KT cells were treated with 5 mM solutions of inhibitors of multiple ErbB receptor tyrosine kinase isoforms: ErbB1 (EGFR)-specific inhibitor AG-1478, ErbB pan-inhibitors AZD8931 and Afatinib, and a selective ErbB2 (HER2) inhibitor CP-724 for 2 hours in the cell passaging injury model, fol- lowed by analysis of TRPV3 mRNA. (B) Downstream targets of EGFR activation were also inhibited, and TRPV3 expression was subsequently measured 2 hours after cell passaging injury. Inhibitors included 5 mM TWS119 (GSK3b), 20 mM CCT036477 (b-catenin), 10 mM PD169316 (p38 MAPK), and 10 mM SP600125 (JNK). (C) Inhibition of NF-jB (20 mM BMS-345541) and effects on TRPV3 mRNA 2 hours after cell passaging injury. (D) Inhibitors of Wnt7a and Fzd signaling were also used: 10 ng/ml secreted Frizzled-related protein (sFRP) and IWP 2 (Porcupine inhibitor) reduced TRPV3 upregulation after injury. Furthermore, SB 431542 (TGFbRI inhibitor) and 150 mM ITD-1 (TGFbRII inhibitor) were also tested, and SB 431542 treatment prevented TRPV3 expression as well. Values were normalized to vehicle controls and are presented as mean ± S.D. from n $ 3 replicates. Statistical significance was determined using one-way ANOVA with the Dunnett post-test. ***P < 0.001, ****P < 0.0001. For Fig. 4C, an unpaired t test was used. ****P < 0.0001.

Journal: Molecular pharmacology

Article Title: Dynamic Expression of Transient Receptor Potential Vanilloid-3 and Integrated Signaling with Growth Factor Pathways during Lung Epithelial Wound Repair following Wood Smoke Particle and Other Forms of Lung Cell Injury.

doi: 10.1124/molpharm.121.000280

Figure Lengend Snippet: Fig. 7. Inhibition of EGFR and growth factor pathway components prevented TRPV3 mRNA upregulation after injury. (A) HBEC3-KT cells were treated with 5 mM solutions of inhibitors of multiple ErbB receptor tyrosine kinase isoforms: ErbB1 (EGFR)-specific inhibitor AG-1478, ErbB pan-inhibitors AZD8931 and Afatinib, and a selective ErbB2 (HER2) inhibitor CP-724 for 2 hours in the cell passaging injury model, fol- lowed by analysis of TRPV3 mRNA. (B) Downstream targets of EGFR activation were also inhibited, and TRPV3 expression was subsequently measured 2 hours after cell passaging injury. Inhibitors included 5 mM TWS119 (GSK3b), 20 mM CCT036477 (b-catenin), 10 mM PD169316 (p38 MAPK), and 10 mM SP600125 (JNK). (C) Inhibition of NF-jB (20 mM BMS-345541) and effects on TRPV3 mRNA 2 hours after cell passaging injury. (D) Inhibitors of Wnt7a and Fzd signaling were also used: 10 ng/ml secreted Frizzled-related protein (sFRP) and IWP 2 (Porcupine inhibitor) reduced TRPV3 upregulation after injury. Furthermore, SB 431542 (TGFbRI inhibitor) and 150 mM ITD-1 (TGFbRII inhibitor) were also tested, and SB 431542 treatment prevented TRPV3 expression as well. Values were normalized to vehicle controls and are presented as mean ± S.D. from n $ 3 replicates. Statistical significance was determined using one-way ANOVA with the Dunnett post-test. ***P < 0.001, ****P < 0.0001. For Fig. 4C, an unpaired t test was used. ****P < 0.0001.

Article Snippet: Afatinib dimaleate (EGFR, ErbB2, HER4/receptor tyrosine kinase 4), IWP 2 (inhibitor of Wnt production 2, targeting porcupine), SB 431542 (TGFbRI), and ITD 1 (1,4-dihydropyridine inducer of TGFbRII degradation-1) were purchased from Tocris (Minneapolis, MN).

Techniques: Inhibition, Passaging, Activation Assay, Expressing