canertinib  (Selleck Chemicals)

 
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  • 93
    Name:
    Canertinib CI 1033
    Description:
    Canertinib CI 1033 is a pan ErbB inhibitor for EGFR and ErbB2 with IC50 of 1 5 nM and 9 0 nM no activity to PDGFR FGFR InsR PKC or CDK1 2 4 Phase 3
    Catalog Number:
    s1019
    Product Aliases:
    PD183805
    Molecular Weight:
    485.94
    Price:
    None
    Category:
    EGFR inhibitor HER2 inhibitor Protein Tyrosine Kinase
    Formula:
    C24H25ClFN5O3
    Buy from Supplier


    Structured Review

    Selleck Chemicals canertinib
    Growth control graphs showing effect of selected HER-family TKIs in doubling concentrations on growth of breast cancer cell lines. ( a ) EGFR reversible inhibitor erlotinib. ( b ) Dual EGFR/HER2 reversible inhibitor lapatinib. ( c ) Pan-HER reversible inhibitor sapitinib. ( d ) Pan-HER irreversible inhibitor <t>canertinib.</t> ( e ) Pan-HER irreversible inhibitor afatinib. Sulforhodamine B colorimetric assay was used to determine the effect of treatment of breast cancer cell lines with doubling dilutions of HER-family inhibiting TKIs. The irreversible pan-inhibitors (e.g. afatinib, canertinib, neratinib) were consistently more effective than the reversible dual and pan inhibitors (e.g. lapatinib, sapitinib), which were in turn more effective than the reversible EGFR inhibitors (e.g. erlotinib, gefitinib). Each point is a representative of the mean ± SD of triplicate samples.
    Canertinib CI 1033 is a pan ErbB inhibitor for EGFR and ErbB2 with IC50 of 1 5 nM and 9 0 nM no activity to PDGFR FGFR InsR PKC or CDK1 2 4 Phase 3
    https://www.bioz.com/result/canertinib/product/Selleck Chemicals
    Average 93 stars, based on 13 article reviews
    Price from $9.99 to $1999.99
    canertinib - by Bioz Stars, 2020-09
    93/100 stars

    Images

    1) Product Images from "Synergistic effects of various Her inhibitors in combination with IGF-1R, C-MET and Src targeting agents in breast cancer cell lines"

    Article Title: Synergistic effects of various Her inhibitors in combination with IGF-1R, C-MET and Src targeting agents in breast cancer cell lines

    Journal: Scientific Reports

    doi: 10.1038/s41598-017-04301-8

    Growth control graphs showing effect of selected HER-family TKIs in doubling concentrations on growth of breast cancer cell lines. ( a ) EGFR reversible inhibitor erlotinib. ( b ) Dual EGFR/HER2 reversible inhibitor lapatinib. ( c ) Pan-HER reversible inhibitor sapitinib. ( d ) Pan-HER irreversible inhibitor canertinib. ( e ) Pan-HER irreversible inhibitor afatinib. Sulforhodamine B colorimetric assay was used to determine the effect of treatment of breast cancer cell lines with doubling dilutions of HER-family inhibiting TKIs. The irreversible pan-inhibitors (e.g. afatinib, canertinib, neratinib) were consistently more effective than the reversible dual and pan inhibitors (e.g. lapatinib, sapitinib), which were in turn more effective than the reversible EGFR inhibitors (e.g. erlotinib, gefitinib). Each point is a representative of the mean ± SD of triplicate samples.
    Figure Legend Snippet: Growth control graphs showing effect of selected HER-family TKIs in doubling concentrations on growth of breast cancer cell lines. ( a ) EGFR reversible inhibitor erlotinib. ( b ) Dual EGFR/HER2 reversible inhibitor lapatinib. ( c ) Pan-HER reversible inhibitor sapitinib. ( d ) Pan-HER irreversible inhibitor canertinib. ( e ) Pan-HER irreversible inhibitor afatinib. Sulforhodamine B colorimetric assay was used to determine the effect of treatment of breast cancer cell lines with doubling dilutions of HER-family inhibiting TKIs. The irreversible pan-inhibitors (e.g. afatinib, canertinib, neratinib) were consistently more effective than the reversible dual and pan inhibitors (e.g. lapatinib, sapitinib), which were in turn more effective than the reversible EGFR inhibitors (e.g. erlotinib, gefitinib). Each point is a representative of the mean ± SD of triplicate samples.

    Techniques Used: Colorimetric Assay

    2) Product Images from "The ectodomain of cadherin-11 binds to erbB2 and stimulates Akt phosphorylation to promote cranial neural crest cell migration"

    Article Title: The ectodomain of cadherin-11 binds to erbB2 and stimulates Akt phosphorylation to promote cranial neural crest cell migration

    Journal: PLoS ONE

    doi: 10.1371/journal.pone.0188963

    Mubritinib and canertinib perturb CNC migration ex vivo . (A-C) Lateral views of tailbud stage X . laevis embryos after in situ hybridization with Sox10 and Twist to visualize CNC positioning. Anterior is to the left, dorsal is up. Embryos treated with 40 μM of the ErbB2 inhibitor, mubritinib (N = 4, n = 72), or 25 μM of the pan-ErbB inhibitor, canertinib (N = 4, n = 68), show no difference in CNC migration compared to DMSO controls (N = 6, n = 100; N = 4, n = 69, respectively). (D-E) The distance of migration within each branchial arch was measured and normalized to the head size. CNC migration as observed in the mandibular (M), hyoid (H), 3 rd and 4 th branchial arches. (F-U) Time-lapse images of CNC explants migrating on fibronectin substrate and treated with 0.5% DMSO (N = 8, n = 24), 6 μM mubritinib (N = 4, n = 12), 10 μM canertinib (N = 4, n = 12), and 20 μM LY294002 (N = 3, n = 9) for indicated lengths of time. (V) Fold change in explant surface area over time. Areas were normalized to measurements calculated at initial time points (t = 0). All inhibitors significantly decreased CNC migration ex vivo . Error bars represent the 95% confidence interval. One-tailed, Student’s t-tests were performed to determine statistical significance. ** p
    Figure Legend Snippet: Mubritinib and canertinib perturb CNC migration ex vivo . (A-C) Lateral views of tailbud stage X . laevis embryos after in situ hybridization with Sox10 and Twist to visualize CNC positioning. Anterior is to the left, dorsal is up. Embryos treated with 40 μM of the ErbB2 inhibitor, mubritinib (N = 4, n = 72), or 25 μM of the pan-ErbB inhibitor, canertinib (N = 4, n = 68), show no difference in CNC migration compared to DMSO controls (N = 6, n = 100; N = 4, n = 69, respectively). (D-E) The distance of migration within each branchial arch was measured and normalized to the head size. CNC migration as observed in the mandibular (M), hyoid (H), 3 rd and 4 th branchial arches. (F-U) Time-lapse images of CNC explants migrating on fibronectin substrate and treated with 0.5% DMSO (N = 8, n = 24), 6 μM mubritinib (N = 4, n = 12), 10 μM canertinib (N = 4, n = 12), and 20 μM LY294002 (N = 3, n = 9) for indicated lengths of time. (V) Fold change in explant surface area over time. Areas were normalized to measurements calculated at initial time points (t = 0). All inhibitors significantly decreased CNC migration ex vivo . Error bars represent the 95% confidence interval. One-tailed, Student’s t-tests were performed to determine statistical significance. ** p

    Techniques Used: Migration, Ex Vivo, In Situ Hybridization, One-tailed Test

    3) Product Images from "Induction of Tyrosine Phosphorylation of UV-Activated EGFR by the Beta-Human Papillomavirus Type 8 E6 Leads to Papillomatosis"

    Article Title: Induction of Tyrosine Phosphorylation of UV-Activated EGFR by the Beta-Human Papillomavirus Type 8 E6 Leads to Papillomatosis

    Journal: Frontiers in Microbiology

    doi: 10.3389/fmicb.2017.02197

    HPV8E6 directly binds to the ubiquitinated EGFR in an UV-dependent manner. (A) RTS3b cells were transiently transfected with a vector directing the expression of FLAG-tagged HPV8E6 under control of the CMV-promoter or the empty vector. Where indicated the cells have been irradiated with UV-light 30 min prior harvesting. 400 μg of extracts were incubated with the anti-EGFR-antibody (lanes 1–4) or with the FLAG-antibody (lanes 5–8), both coupled to sepharose, washed four times in 0.3 M KCl-buffer prior analysis by WB and 40 μg of the extracts were used in the input blots. (B) IP with anti-EGFR sepharose and 800 μg of extracts derived from the stable RTS3b-pLXSN and RTS3b-HPV8E6 lines, either left untreated or UV-irradiated 30 min prior harvesting. FLAG-HPV8E6 and EGFR present in the precipitate as well as in the input were detected by WB. (C) Extracts from UV-irradiated RTS3b cells that have been transiently transfected with the FLAG-HPV8E6 or the FLAG-vector were incubated either with DMSO (lanes 1, 2, 5), 3 μM (lane 3) or 7 μM (lane 4) Canertinib for 30 min. The IP was performed with the FLAG-antibody. All WB were developed with the indicated antibodies. In lanes 6–10, C33A cells were transiently transfected with expression vectors for EGFR-GFP and FLAG-HPV8E6, and UV-irradiated, where indicated, prior harvesting 30 min later. EGFR-GFP was precipitated from 400 μg of extract by the EGFR antibody and bound HPV8E6 was detected by the FLAG-antibody. The input blots were developed with the antibodies against pEGFR-Y1068, GFP, and FLAG. The positions of the molecular weight markers are provided (in kDa).
    Figure Legend Snippet: HPV8E6 directly binds to the ubiquitinated EGFR in an UV-dependent manner. (A) RTS3b cells were transiently transfected with a vector directing the expression of FLAG-tagged HPV8E6 under control of the CMV-promoter or the empty vector. Where indicated the cells have been irradiated with UV-light 30 min prior harvesting. 400 μg of extracts were incubated with the anti-EGFR-antibody (lanes 1–4) or with the FLAG-antibody (lanes 5–8), both coupled to sepharose, washed four times in 0.3 M KCl-buffer prior analysis by WB and 40 μg of the extracts were used in the input blots. (B) IP with anti-EGFR sepharose and 800 μg of extracts derived from the stable RTS3b-pLXSN and RTS3b-HPV8E6 lines, either left untreated or UV-irradiated 30 min prior harvesting. FLAG-HPV8E6 and EGFR present in the precipitate as well as in the input were detected by WB. (C) Extracts from UV-irradiated RTS3b cells that have been transiently transfected with the FLAG-HPV8E6 or the FLAG-vector were incubated either with DMSO (lanes 1, 2, 5), 3 μM (lane 3) or 7 μM (lane 4) Canertinib for 30 min. The IP was performed with the FLAG-antibody. All WB were developed with the indicated antibodies. In lanes 6–10, C33A cells were transiently transfected with expression vectors for EGFR-GFP and FLAG-HPV8E6, and UV-irradiated, where indicated, prior harvesting 30 min later. EGFR-GFP was precipitated from 400 μg of extract by the EGFR antibody and bound HPV8E6 was detected by the FLAG-antibody. The input blots were developed with the antibodies against pEGFR-Y1068, GFP, and FLAG. The positions of the molecular weight markers are provided (in kDa).

    Techniques Used: Transfection, Plasmid Preparation, Expressing, Irradiation, Incubation, Western Blot, Derivative Assay, Molecular Weight

    Inhibition of the RTK-activity of the EGFR by the pan-ErbB-inhibitor Canertinib (CI-1033) suppresses UV-induced papillomatosis in K14-HPV8E6 transgenic mice. (A) Immunohistochemical staining of paraffin embedded sections obtained from skin of K14-HPV8E6 transgenic mice 13 days after UV-exposure with the anti-pEGFR-Y1068 or rabbit IgG isotype control (magnification 1:400). (B) Transgenic mice obtained either Canertinib (CI-1033) (20 mg/kg weight) or the same volume of PBS 4 h prior UV-irradiation followed by applications of Canertinib once daily at a dose of 10 mg/kg weight or 150 μl PBS for 24 days, as given in the time line. The pictures represent examples of the lesions from four mice treated with CI-1033 (M19, 20, 23, and M26) and from one control mouse which obtained PBS (M22). The graph beneath shows the quantification of RT-PCR results with RNA isolated from two PBS and three Canertinib-treated animals to demonstrate the expression of HPV8E6. (C) Histology with H/E staining of skin section obtained from two PBS-control (M21 and M22) and four Canertinib (CI-1033)-treated animals (M19, M20, M23, and M26) 24 days after UV-irradiation.
    Figure Legend Snippet: Inhibition of the RTK-activity of the EGFR by the pan-ErbB-inhibitor Canertinib (CI-1033) suppresses UV-induced papillomatosis in K14-HPV8E6 transgenic mice. (A) Immunohistochemical staining of paraffin embedded sections obtained from skin of K14-HPV8E6 transgenic mice 13 days after UV-exposure with the anti-pEGFR-Y1068 or rabbit IgG isotype control (magnification 1:400). (B) Transgenic mice obtained either Canertinib (CI-1033) (20 mg/kg weight) or the same volume of PBS 4 h prior UV-irradiation followed by applications of Canertinib once daily at a dose of 10 mg/kg weight or 150 μl PBS for 24 days, as given in the time line. The pictures represent examples of the lesions from four mice treated with CI-1033 (M19, 20, 23, and M26) and from one control mouse which obtained PBS (M22). The graph beneath shows the quantification of RT-PCR results with RNA isolated from two PBS and three Canertinib-treated animals to demonstrate the expression of HPV8E6. (C) Histology with H/E staining of skin section obtained from two PBS-control (M21 and M22) and four Canertinib (CI-1033)-treated animals (M19, M20, M23, and M26) 24 days after UV-irradiation.

    Techniques Used: Inhibition, Activity Assay, Transgenic Assay, Mouse Assay, Immunohistochemistry, Staining, Irradiation, Reverse Transcription Polymerase Chain Reaction, Isolation, Expressing

    4) Product Images from "Porcine Esophageal Submucosal Gland Culture Model Shows Capacity for Proliferation and Differentiation"

    Article Title: Porcine Esophageal Submucosal Gland Culture Model Shows Capacity for Proliferation and Differentiation

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    doi: 10.1016/j.jcmgh.2017.07.005

    ESMG-derived spheroids are EGF-dependent. Spheroid formation from passaged cells was evaluated at day 5 after the following treatments: no EGF; 2.5 ng/mL recombinant EGF (rEGF); 25 ng/mL rEGF; 50 ng/mL rEGF; 50 ng/mL rEGF + canertinib (CI-1033), an irreversible pan-EGFR blocker; or 50 ng/mL rEGF with DMSO vehicle without the canertinib. The number of spheroids per well for the treatment groups was 0.5% ± 0.4%, 46% ± 10%, 37% ± 4%, 41% ± 6%, and 1.2% ± 1.2%, and 33% ± 3% for vehicle alone, means ± SEM respectively. Groups labeled under a are statistically significant from groups under b ( P
    Figure Legend Snippet: ESMG-derived spheroids are EGF-dependent. Spheroid formation from passaged cells was evaluated at day 5 after the following treatments: no EGF; 2.5 ng/mL recombinant EGF (rEGF); 25 ng/mL rEGF; 50 ng/mL rEGF; 50 ng/mL rEGF + canertinib (CI-1033), an irreversible pan-EGFR blocker; or 50 ng/mL rEGF with DMSO vehicle without the canertinib. The number of spheroids per well for the treatment groups was 0.5% ± 0.4%, 46% ± 10%, 37% ± 4%, 41% ± 6%, and 1.2% ± 1.2%, and 33% ± 3% for vehicle alone, means ± SEM respectively. Groups labeled under a are statistically significant from groups under b ( P

    Techniques Used: Derivative Assay, Recombinant, Labeling

    5) Product Images from "Porcine Esophageal Submucosal Gland Culture Model Shows Capacity for Proliferation and Differentiation"

    Article Title: Porcine Esophageal Submucosal Gland Culture Model Shows Capacity for Proliferation and Differentiation

    Journal: Cellular and Molecular Gastroenterology and Hepatology

    doi: 10.1016/j.jcmgh.2017.07.005

    ESMG-derived spheroids are EGF-dependent. Spheroid formation from passaged cells was evaluated at day 5 after the following treatments: no EGF; 2.5 ng/mL recombinant EGF (rEGF); 25 ng/mL rEGF; 50 ng/mL rEGF; 50 ng/mL rEGF + canertinib (CI-1033), an irreversible pan-EGFR blocker; or 50 ng/mL rEGF with DMSO vehicle without the canertinib. The number of spheroids per well for the treatment groups was 0.5% ± 0.4%, 46% ± 10%, 37% ± 4%, 41% ± 6%, and 1.2% ± 1.2%, and 33% ± 3% for vehicle alone, means ± SEM respectively. Groups labeled under a are statistically significant from groups under b ( P
    Figure Legend Snippet: ESMG-derived spheroids are EGF-dependent. Spheroid formation from passaged cells was evaluated at day 5 after the following treatments: no EGF; 2.5 ng/mL recombinant EGF (rEGF); 25 ng/mL rEGF; 50 ng/mL rEGF; 50 ng/mL rEGF + canertinib (CI-1033), an irreversible pan-EGFR blocker; or 50 ng/mL rEGF with DMSO vehicle without the canertinib. The number of spheroids per well for the treatment groups was 0.5% ± 0.4%, 46% ± 10%, 37% ± 4%, 41% ± 6%, and 1.2% ± 1.2%, and 33% ± 3% for vehicle alone, means ± SEM respectively. Groups labeled under a are statistically significant from groups under b ( P

    Techniques Used: Derivative Assay, Recombinant, Labeling

    6) Product Images from "Induction of Tyrosine Phosphorylation of UV-Activated EGFR by the Beta-Human Papillomavirus Type 8 E6 Leads to Papillomatosis"

    Article Title: Induction of Tyrosine Phosphorylation of UV-Activated EGFR by the Beta-Human Papillomavirus Type 8 E6 Leads to Papillomatosis

    Journal: Frontiers in Microbiology

    doi: 10.3389/fmicb.2017.02197

    HPV8E6 directly binds to the ubiquitinated EGFR in an UV-dependent manner. (A) RTS3b cells were transiently transfected with a vector directing the expression of FLAG-tagged HPV8E6 under control of the CMV-promoter or the empty vector. Where indicated the cells have been irradiated with UV-light 30 min prior harvesting. 400 μg of extracts were incubated with the anti-EGFR-antibody (lanes 1–4) or with the FLAG-antibody (lanes 5–8), both coupled to sepharose, washed four times in 0.3 M KCl-buffer prior analysis by WB and 40 μg of the extracts were used in the input blots. (B) IP with anti-EGFR sepharose and 800 μg of extracts derived from the stable RTS3b-pLXSN and RTS3b-HPV8E6 lines, either left untreated or UV-irradiated 30 min prior harvesting. FLAG-HPV8E6 and EGFR present in the precipitate as well as in the input were detected by WB. (C) Extracts from UV-irradiated RTS3b cells that have been transiently transfected with the FLAG-HPV8E6 or the FLAG-vector were incubated either with DMSO (lanes 1, 2, 5), 3 μM (lane 3) or 7 μM (lane 4) Canertinib for 30 min. The IP was performed with the FLAG-antibody. All WB were developed with the indicated antibodies. In lanes 6–10, C33A cells were transiently transfected with expression vectors for EGFR-GFP and FLAG-HPV8E6, and UV-irradiated, where indicated, prior harvesting 30 min later. EGFR-GFP was precipitated from 400 μg of extract by the EGFR antibody and bound HPV8E6 was detected by the FLAG-antibody. The input blots were developed with the antibodies against pEGFR-Y1068, GFP, and FLAG. The positions of the molecular weight markers are provided (in kDa).
    Figure Legend Snippet: HPV8E6 directly binds to the ubiquitinated EGFR in an UV-dependent manner. (A) RTS3b cells were transiently transfected with a vector directing the expression of FLAG-tagged HPV8E6 under control of the CMV-promoter or the empty vector. Where indicated the cells have been irradiated with UV-light 30 min prior harvesting. 400 μg of extracts were incubated with the anti-EGFR-antibody (lanes 1–4) or with the FLAG-antibody (lanes 5–8), both coupled to sepharose, washed four times in 0.3 M KCl-buffer prior analysis by WB and 40 μg of the extracts were used in the input blots. (B) IP with anti-EGFR sepharose and 800 μg of extracts derived from the stable RTS3b-pLXSN and RTS3b-HPV8E6 lines, either left untreated or UV-irradiated 30 min prior harvesting. FLAG-HPV8E6 and EGFR present in the precipitate as well as in the input were detected by WB. (C) Extracts from UV-irradiated RTS3b cells that have been transiently transfected with the FLAG-HPV8E6 or the FLAG-vector were incubated either with DMSO (lanes 1, 2, 5), 3 μM (lane 3) or 7 μM (lane 4) Canertinib for 30 min. The IP was performed with the FLAG-antibody. All WB were developed with the indicated antibodies. In lanes 6–10, C33A cells were transiently transfected with expression vectors for EGFR-GFP and FLAG-HPV8E6, and UV-irradiated, where indicated, prior harvesting 30 min later. EGFR-GFP was precipitated from 400 μg of extract by the EGFR antibody and bound HPV8E6 was detected by the FLAG-antibody. The input blots were developed with the antibodies against pEGFR-Y1068, GFP, and FLAG. The positions of the molecular weight markers are provided (in kDa).

    Techniques Used: Transfection, Plasmid Preparation, Expressing, Irradiation, Incubation, Western Blot, Derivative Assay, Molecular Weight

    Inhibition of the RTK-activity of the EGFR by the pan-ErbB-inhibitor Canertinib (CI-1033) suppresses UV-induced papillomatosis in K14-HPV8E6 transgenic mice. (A) Immunohistochemical staining of paraffin embedded sections obtained from skin of K14-HPV8E6 transgenic mice 13 days after UV-exposure with the anti-pEGFR-Y1068 or rabbit IgG isotype control (magnification 1:400). (B) Transgenic mice obtained either Canertinib (CI-1033) (20 mg/kg weight) or the same volume of PBS 4 h prior UV-irradiation followed by applications of Canertinib once daily at a dose of 10 mg/kg weight or 150 μl PBS for 24 days, as given in the time line. The pictures represent examples of the lesions from four mice treated with CI-1033 (M19, 20, 23, and M26) and from one control mouse which obtained PBS (M22). The graph beneath shows the quantification of RT-PCR results with RNA isolated from two PBS and three Canertinib-treated animals to demonstrate the expression of HPV8E6. (C) Histology with H/E staining of skin section obtained from two PBS-control (M21 and M22) and four Canertinib (CI-1033)-treated animals (M19, M20, M23, and M26) 24 days after UV-irradiation.
    Figure Legend Snippet: Inhibition of the RTK-activity of the EGFR by the pan-ErbB-inhibitor Canertinib (CI-1033) suppresses UV-induced papillomatosis in K14-HPV8E6 transgenic mice. (A) Immunohistochemical staining of paraffin embedded sections obtained from skin of K14-HPV8E6 transgenic mice 13 days after UV-exposure with the anti-pEGFR-Y1068 or rabbit IgG isotype control (magnification 1:400). (B) Transgenic mice obtained either Canertinib (CI-1033) (20 mg/kg weight) or the same volume of PBS 4 h prior UV-irradiation followed by applications of Canertinib once daily at a dose of 10 mg/kg weight or 150 μl PBS for 24 days, as given in the time line. The pictures represent examples of the lesions from four mice treated with CI-1033 (M19, 20, 23, and M26) and from one control mouse which obtained PBS (M22). The graph beneath shows the quantification of RT-PCR results with RNA isolated from two PBS and three Canertinib-treated animals to demonstrate the expression of HPV8E6. (C) Histology with H/E staining of skin section obtained from two PBS-control (M21 and M22) and four Canertinib (CI-1033)-treated animals (M19, M20, M23, and M26) 24 days after UV-irradiation.

    Techniques Used: Inhibition, Activity Assay, Transgenic Assay, Mouse Assay, Immunohistochemistry, Staining, Irradiation, Reverse Transcription Polymerase Chain Reaction, Isolation, Expressing

    7) Product Images from "Tumour cell invasiveness and response to chemotherapeutics in adipocyte invested 3D engineered anisotropic collagen scaffolds"

    Article Title: Tumour cell invasiveness and response to chemotherapeutics in adipocyte invested 3D engineered anisotropic collagen scaffolds

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-30107-3

    Analysis of tumour cell migration and response to pathway inhibitors (72 hours). Comparison of Wnt1 tumour cell migratory distance, from the anisotropic collagen scaffold nucleation point to within the scaffold, after 72 hours culture in the absence ( a ) or presence ( b ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without pathway inhibitors ROCKi, GM6001 and Canertinib, all statistically compared to DMSO (vehicle control). The total number of migratory Wnt1 tumour cells within the scaffolds, in the absence ( c ) or presence ( d ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without the pathway inhibitors ROCKi, GM6001 and Canertinib compared to DMSO (vehicle control). The following statistical analyses were applied: non-parametric unpaired/matching Kruskal-Wallis ANOVA with a Geisser-greenhouse correction combined with a Dunn’s multiple comparison test, *p
    Figure Legend Snippet: Analysis of tumour cell migration and response to pathway inhibitors (72 hours). Comparison of Wnt1 tumour cell migratory distance, from the anisotropic collagen scaffold nucleation point to within the scaffold, after 72 hours culture in the absence ( a ) or presence ( b ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without pathway inhibitors ROCKi, GM6001 and Canertinib, all statistically compared to DMSO (vehicle control). The total number of migratory Wnt1 tumour cells within the scaffolds, in the absence ( c ) or presence ( d ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without the pathway inhibitors ROCKi, GM6001 and Canertinib compared to DMSO (vehicle control). The following statistical analyses were applied: non-parametric unpaired/matching Kruskal-Wallis ANOVA with a Geisser-greenhouse correction combined with a Dunn’s multiple comparison test, *p

    Techniques Used: Migration

    Optical clearing of TUBO tumours in anisotropic collagen scaffolds and cancer therapeutic testing. ( a ) Transmission stereoscopic images of uncleared and optically cleared (CUBIC) anisotropic collagen scaffold and TUBO (Her2-neu overexpressing) tumour from a top down view. ( b ) Fluorescent stereoscopic images of TUBO tumour fragments in scaffolds, cultured for 10 days with/without adipocytes (3T3-L1), treated with DMSO (control), ROCKi (Y-27632), GM6001 or Canertinib, CUBIC cleared and immunostained for E-cadherin (green) and Her2 (not shown). Cell nuclei are stained with DAPI (blue). Clusters of cancer cells that have migrated away from the central tumour fragment are marked with arrowheads. ( c , d ) Large tile scan z-stack (1 mm depth) confocal microscopy images of ROCKi treated TUBO tumour fragments in anisotropic collagen scaffolds without/with adipocytes (3T3-L1), cleared and stained as described in ( b ) with DAPI (blue), E-cadherin (green) and Her2 (red). (i) and (ii) show magnified images of migratory clusters of Her2 and E-cadherin positive cells. ( e ) Quantification of the number of tumour/scaffolds that contain one or more visible migratory cell clusters. ( f , g ) Large tile scan z-stack (1 mm depth) confocal microscopy images of Canertinib treated TUBO tumour fragments in anisotropic collagen scaffolds without/with adipocytes (3T3-L1), cleared and stained as described in ( b ) with DAPI (blue), E-cadherin (green) and Her2 (red). (i) and (ii) show few non-migratory E-cadherin and Her2 cells seen in the seeded tumour fragment. No migratory cells were observed in the scaffold with Canertinib treatment at this magnification.
    Figure Legend Snippet: Optical clearing of TUBO tumours in anisotropic collagen scaffolds and cancer therapeutic testing. ( a ) Transmission stereoscopic images of uncleared and optically cleared (CUBIC) anisotropic collagen scaffold and TUBO (Her2-neu overexpressing) tumour from a top down view. ( b ) Fluorescent stereoscopic images of TUBO tumour fragments in scaffolds, cultured for 10 days with/without adipocytes (3T3-L1), treated with DMSO (control), ROCKi (Y-27632), GM6001 or Canertinib, CUBIC cleared and immunostained for E-cadherin (green) and Her2 (not shown). Cell nuclei are stained with DAPI (blue). Clusters of cancer cells that have migrated away from the central tumour fragment are marked with arrowheads. ( c , d ) Large tile scan z-stack (1 mm depth) confocal microscopy images of ROCKi treated TUBO tumour fragments in anisotropic collagen scaffolds without/with adipocytes (3T3-L1), cleared and stained as described in ( b ) with DAPI (blue), E-cadherin (green) and Her2 (red). (i) and (ii) show magnified images of migratory clusters of Her2 and E-cadherin positive cells. ( e ) Quantification of the number of tumour/scaffolds that contain one or more visible migratory cell clusters. ( f , g ) Large tile scan z-stack (1 mm depth) confocal microscopy images of Canertinib treated TUBO tumour fragments in anisotropic collagen scaffolds without/with adipocytes (3T3-L1), cleared and stained as described in ( b ) with DAPI (blue), E-cadherin (green) and Her2 (red). (i) and (ii) show few non-migratory E-cadherin and Her2 cells seen in the seeded tumour fragment. No migratory cells were observed in the scaffold with Canertinib treatment at this magnification.

    Techniques Used: Transmission Assay, Cell Culture, Staining, Confocal Microscopy

    Analysis of tumour cell migration and response to pathway inhibitors (10 days). Comparison of Wnt1 tumour cell migratory distance, from the anisotropic collagen scaffold nucleation point to within the scaffold, after 72 hours culture in the absence ( a ) or presence ( b ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without pathway inhibitors ROCKi, GM6001 and Canertinib, all statistically compared to DMSO (vehicle control). The total number of migratory Wnt1 tumour cells within the scaffolds, in the absence ( c ) or presence ( d ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without the pathway inhibitors ROCKi, GM6001 and Canertinib compared to DMSO (vehicle control). The following statistical analyses were applied: non-parametric unpaired/matching Kruskal-Wallis ANOVA with a Geisser-greenhouse correction combined with a Dunn’s multiple comparison test, *p
    Figure Legend Snippet: Analysis of tumour cell migration and response to pathway inhibitors (10 days). Comparison of Wnt1 tumour cell migratory distance, from the anisotropic collagen scaffold nucleation point to within the scaffold, after 72 hours culture in the absence ( a ) or presence ( b ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without pathway inhibitors ROCKi, GM6001 and Canertinib, all statistically compared to DMSO (vehicle control). The total number of migratory Wnt1 tumour cells within the scaffolds, in the absence ( c ) or presence ( d ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without the pathway inhibitors ROCKi, GM6001 and Canertinib compared to DMSO (vehicle control). The following statistical analyses were applied: non-parametric unpaired/matching Kruskal-Wallis ANOVA with a Geisser-greenhouse correction combined with a Dunn’s multiple comparison test, *p

    Techniques Used: Migration

    8) Product Images from "Tumour cell invasiveness and response to chemotherapeutics in adipocyte invested 3D engineered anisotropic collagen scaffolds"

    Article Title: Tumour cell invasiveness and response to chemotherapeutics in adipocyte invested 3D engineered anisotropic collagen scaffolds

    Journal: Scientific Reports

    doi: 10.1038/s41598-018-30107-3

    Analysis of tumour cell migration and response to pathway inhibitors (72 hours). Comparison of Wnt1 tumour cell migratory distance, from the anisotropic collagen scaffold nucleation point to within the scaffold, after 72 hours culture in the absence ( a ) or presence ( b ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without pathway inhibitors ROCKi, GM6001 and Canertinib, all statistically compared to DMSO (vehicle control). The total number of migratory Wnt1 tumour cells within the scaffolds, in the absence ( c ) or presence ( d ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without the pathway inhibitors ROCKi, GM6001 and Canertinib compared to DMSO (vehicle control). The following statistical analyses were applied: non-parametric unpaired/matching Kruskal-Wallis ANOVA with a Geisser-greenhouse correction combined with a Dunn’s multiple comparison test, *p
    Figure Legend Snippet: Analysis of tumour cell migration and response to pathway inhibitors (72 hours). Comparison of Wnt1 tumour cell migratory distance, from the anisotropic collagen scaffold nucleation point to within the scaffold, after 72 hours culture in the absence ( a ) or presence ( b ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without pathway inhibitors ROCKi, GM6001 and Canertinib, all statistically compared to DMSO (vehicle control). The total number of migratory Wnt1 tumour cells within the scaffolds, in the absence ( c ) or presence ( d ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without the pathway inhibitors ROCKi, GM6001 and Canertinib compared to DMSO (vehicle control). The following statistical analyses were applied: non-parametric unpaired/matching Kruskal-Wallis ANOVA with a Geisser-greenhouse correction combined with a Dunn’s multiple comparison test, *p

    Techniques Used: Migration

    Optical clearing of TUBO tumours in anisotropic collagen scaffolds and cancer therapeutic testing. ( a ) Transmission stereoscopic images of uncleared and optically cleared (CUBIC) anisotropic collagen scaffold and TUBO (Her2-neu overexpressing) tumour from a top down view. ( b ) Fluorescent stereoscopic images of TUBO tumour fragments in scaffolds, cultured for 10 days with/without adipocytes (3T3-L1), treated with DMSO (control), ROCKi (Y-27632), GM6001 or Canertinib, CUBIC cleared and immunostained for E-cadherin (green) and Her2 (not shown). Cell nuclei are stained with DAPI (blue). Clusters of cancer cells that have migrated away from the central tumour fragment are marked with arrowheads. ( c , d ) Large tile scan z-stack (1 mm depth) confocal microscopy images of ROCKi treated TUBO tumour fragments in anisotropic collagen scaffolds without/with adipocytes (3T3-L1), cleared and stained as described in ( b ) with DAPI (blue), E-cadherin (green) and Her2 (red). (i) and (ii) show magnified images of migratory clusters of Her2 and E-cadherin positive cells. ( e ) Quantification of the number of tumour/scaffolds that contain one or more visible migratory cell clusters. ( f , g ) Large tile scan z-stack (1 mm depth) confocal microscopy images of Canertinib treated TUBO tumour fragments in anisotropic collagen scaffolds without/with adipocytes (3T3-L1), cleared and stained as described in ( b ) with DAPI (blue), E-cadherin (green) and Her2 (red). (i) and (ii) show few non-migratory E-cadherin and Her2 cells seen in the seeded tumour fragment. No migratory cells were observed in the scaffold with Canertinib treatment at this magnification.
    Figure Legend Snippet: Optical clearing of TUBO tumours in anisotropic collagen scaffolds and cancer therapeutic testing. ( a ) Transmission stereoscopic images of uncleared and optically cleared (CUBIC) anisotropic collagen scaffold and TUBO (Her2-neu overexpressing) tumour from a top down view. ( b ) Fluorescent stereoscopic images of TUBO tumour fragments in scaffolds, cultured for 10 days with/without adipocytes (3T3-L1), treated with DMSO (control), ROCKi (Y-27632), GM6001 or Canertinib, CUBIC cleared and immunostained for E-cadherin (green) and Her2 (not shown). Cell nuclei are stained with DAPI (blue). Clusters of cancer cells that have migrated away from the central tumour fragment are marked with arrowheads. ( c , d ) Large tile scan z-stack (1 mm depth) confocal microscopy images of ROCKi treated TUBO tumour fragments in anisotropic collagen scaffolds without/with adipocytes (3T3-L1), cleared and stained as described in ( b ) with DAPI (blue), E-cadherin (green) and Her2 (red). (i) and (ii) show magnified images of migratory clusters of Her2 and E-cadherin positive cells. ( e ) Quantification of the number of tumour/scaffolds that contain one or more visible migratory cell clusters. ( f , g ) Large tile scan z-stack (1 mm depth) confocal microscopy images of Canertinib treated TUBO tumour fragments in anisotropic collagen scaffolds without/with adipocytes (3T3-L1), cleared and stained as described in ( b ) with DAPI (blue), E-cadherin (green) and Her2 (red). (i) and (ii) show few non-migratory E-cadherin and Her2 cells seen in the seeded tumour fragment. No migratory cells were observed in the scaffold with Canertinib treatment at this magnification.

    Techniques Used: Transmission Assay, Cell Culture, Staining, Confocal Microscopy

    Analysis of tumour cell migration and response to pathway inhibitors (10 days). Comparison of Wnt1 tumour cell migratory distance, from the anisotropic collagen scaffold nucleation point to within the scaffold, after 72 hours culture in the absence ( a ) or presence ( b ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without pathway inhibitors ROCKi, GM6001 and Canertinib, all statistically compared to DMSO (vehicle control). The total number of migratory Wnt1 tumour cells within the scaffolds, in the absence ( c ) or presence ( d ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without the pathway inhibitors ROCKi, GM6001 and Canertinib compared to DMSO (vehicle control). The following statistical analyses were applied: non-parametric unpaired/matching Kruskal-Wallis ANOVA with a Geisser-greenhouse correction combined with a Dunn’s multiple comparison test, *p
    Figure Legend Snippet: Analysis of tumour cell migration and response to pathway inhibitors (10 days). Comparison of Wnt1 tumour cell migratory distance, from the anisotropic collagen scaffold nucleation point to within the scaffold, after 72 hours culture in the absence ( a ) or presence ( b ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without pathway inhibitors ROCKi, GM6001 and Canertinib, all statistically compared to DMSO (vehicle control). The total number of migratory Wnt1 tumour cells within the scaffolds, in the absence ( c ) or presence ( d ) of differentiated 3T3-L1 cells (known as ET-SIM), with/without the pathway inhibitors ROCKi, GM6001 and Canertinib compared to DMSO (vehicle control). The following statistical analyses were applied: non-parametric unpaired/matching Kruskal-Wallis ANOVA with a Geisser-greenhouse correction combined with a Dunn’s multiple comparison test, *p

    Techniques Used: Migration

    Related Articles

    In Vivo:

    Article Title: The ectodomain of cadherin-11 binds to erbB2 and stimulates Akt phosphorylation to promote cranial neural crest cell migration
    Article Snippet: .. Migration assays Inhibitors were used at the following concentrations to disrupt CNC migration in vivo : 30 μM of LY294002 (IC50 = 1.4μM; Millipore-Calbiochem, #440202), 40 μM of rapamycin (IC50 = 0.1nM; Millipore-Calbiochem, #553211), 40 μM mubritinib (IC50 = 6nM; Selleckchem; #S2216), and 25 μM canertinib (EGFR IC50 = 1.5nM; ErbB2 IC50 = 9nM; Selleckchem; #S1019). .. DMSO was added as a control to a final concentration of 0.15–1.25% (v/v).

    Blocking Assay:

    Article Title: Porcine Esophageal Submucosal Gland Culture Model Shows Capacity for Proliferation and Differentiation
    Article Snippet: .. To experimentally block the EGF receptor, canertinib (CI-1033; Selleckchem), was dissolved in dimethyl sulfoxide (DMSO) to 1 mmol/L and added at 1000× to spheroid media (with 50 ng/mL EGF) for a final concentration of 1 μmol/L. ..

    Concentration Assay:

    Article Title: Porcine Esophageal Submucosal Gland Culture Model Shows Capacity for Proliferation and Differentiation
    Article Snippet: .. Canertinib (CI-1033; Selleckchem, Houston, TX) is an irreversible tyrosine-kinase inhibitor with activity against EGF receptor (median inhibitory concentration, 0.8 nmol/L), HER-2 (median inhibitory concentration, 19 nmol/L), and erb-b2 receptor tyrosine kinase 4 (median inhibitory concentration, 7 nmol/L). .. To experimentally block the EGF receptor, canertinib (CI-1033; Selleckchem), was dissolved in dimethyl sulfoxide (DMSO) to 1 mmol/L and added at 1000× to spheroid media (with 50 ng/mL EGF) for a final concentration of 1 μmol/L.

    Article Title: Porcine Esophageal Submucosal Gland Culture Model Shows Capacity for Proliferation and Differentiation
    Article Snippet: .. To experimentally block the EGF receptor, canertinib (CI-1033; Selleckchem), was dissolved in dimethyl sulfoxide (DMSO) to 1 mmol/L and added at 1000× to spheroid media (with 50 ng/mL EGF) for a final concentration of 1 μmol/L. ..

    other:

    Article Title: Cancer cells harboring MET gene amplification activate alternative signaling pathways to escape MET inhibition but remain sensitive to Hsp90 inhibitors
    Article Snippet: CI-1033 was purchased from Selleck Chemicals Co., Ltd. (Riverside, CA).

    Activity Assay:

    Article Title: Porcine Esophageal Submucosal Gland Culture Model Shows Capacity for Proliferation and Differentiation
    Article Snippet: .. Canertinib (CI-1033; Selleckchem, Houston, TX) is an irreversible tyrosine-kinase inhibitor with activity against EGF receptor (median inhibitory concentration, 0.8 nmol/L), HER-2 (median inhibitory concentration, 19 nmol/L), and erb-b2 receptor tyrosine kinase 4 (median inhibitory concentration, 7 nmol/L). .. To experimentally block the EGF receptor, canertinib (CI-1033; Selleckchem), was dissolved in dimethyl sulfoxide (DMSO) to 1 mmol/L and added at 1000× to spheroid media (with 50 ng/mL EGF) for a final concentration of 1 μmol/L.

    Migration:

    Article Title: The ectodomain of cadherin-11 binds to erbB2 and stimulates Akt phosphorylation to promote cranial neural crest cell migration
    Article Snippet: .. Migration assays Inhibitors were used at the following concentrations to disrupt CNC migration in vivo : 30 μM of LY294002 (IC50 = 1.4μM; Millipore-Calbiochem, #440202), 40 μM of rapamycin (IC50 = 0.1nM; Millipore-Calbiochem, #553211), 40 μM mubritinib (IC50 = 6nM; Selleckchem; #S2216), and 25 μM canertinib (EGFR IC50 = 1.5nM; ErbB2 IC50 = 9nM; Selleckchem; #S1019). .. DMSO was added as a control to a final concentration of 0.15–1.25% (v/v).

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    Selleck Chemicals canertinib
    Growth control graphs showing effect of selected HER-family TKIs in doubling concentrations on growth of breast cancer cell lines. ( a ) EGFR reversible inhibitor erlotinib. ( b ) Dual EGFR/HER2 reversible inhibitor lapatinib. ( c ) Pan-HER reversible inhibitor sapitinib. ( d ) Pan-HER irreversible inhibitor <t>canertinib.</t> ( e ) Pan-HER irreversible inhibitor afatinib. Sulforhodamine B colorimetric assay was used to determine the effect of treatment of breast cancer cell lines with doubling dilutions of HER-family inhibiting TKIs. The irreversible pan-inhibitors (e.g. afatinib, canertinib, neratinib) were consistently more effective than the reversible dual and pan inhibitors (e.g. lapatinib, sapitinib), which were in turn more effective than the reversible EGFR inhibitors (e.g. erlotinib, gefitinib). Each point is a representative of the mean ± SD of triplicate samples.
    Canertinib, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 93/100, based on 15 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Growth control graphs showing effect of selected HER-family TKIs in doubling concentrations on growth of breast cancer cell lines. ( a ) EGFR reversible inhibitor erlotinib. ( b ) Dual EGFR/HER2 reversible inhibitor lapatinib. ( c ) Pan-HER reversible inhibitor sapitinib. ( d ) Pan-HER irreversible inhibitor canertinib. ( e ) Pan-HER irreversible inhibitor afatinib. Sulforhodamine B colorimetric assay was used to determine the effect of treatment of breast cancer cell lines with doubling dilutions of HER-family inhibiting TKIs. The irreversible pan-inhibitors (e.g. afatinib, canertinib, neratinib) were consistently more effective than the reversible dual and pan inhibitors (e.g. lapatinib, sapitinib), which were in turn more effective than the reversible EGFR inhibitors (e.g. erlotinib, gefitinib). Each point is a representative of the mean ± SD of triplicate samples.

    Journal: Scientific Reports

    Article Title: Synergistic effects of various Her inhibitors in combination with IGF-1R, C-MET and Src targeting agents in breast cancer cell lines

    doi: 10.1038/s41598-017-04301-8

    Figure Lengend Snippet: Growth control graphs showing effect of selected HER-family TKIs in doubling concentrations on growth of breast cancer cell lines. ( a ) EGFR reversible inhibitor erlotinib. ( b ) Dual EGFR/HER2 reversible inhibitor lapatinib. ( c ) Pan-HER reversible inhibitor sapitinib. ( d ) Pan-HER irreversible inhibitor canertinib. ( e ) Pan-HER irreversible inhibitor afatinib. Sulforhodamine B colorimetric assay was used to determine the effect of treatment of breast cancer cell lines with doubling dilutions of HER-family inhibiting TKIs. The irreversible pan-inhibitors (e.g. afatinib, canertinib, neratinib) were consistently more effective than the reversible dual and pan inhibitors (e.g. lapatinib, sapitinib), which were in turn more effective than the reversible EGFR inhibitors (e.g. erlotinib, gefitinib). Each point is a representative of the mean ± SD of triplicate samples.

    Article Snippet: Lapatinib, sapitinib, canertinib, neratinib, imatinib and dasatinib were all acquired from Selleckchem (USA).

    Techniques: Colorimetric Assay

    Differential sensitivity of EGFR mutant glioma and lung cancer cell lines to the irreversible EGFR inhibitors HKI-272 and CI-1033

    Journal: Cancer Discovery

    Article Title: Differential Sensitivity of Glioma- versus Lung Cancer-specific EGFR mutations to EGFR Kinase Inhibitors

    doi: 10.1158/2159-8290.CD-11-0284

    Figure Lengend Snippet: Differential sensitivity of EGFR mutant glioma and lung cancer cell lines to the irreversible EGFR inhibitors HKI-272 and CI-1033

    Article Snippet: CI-1033 and HKI-272 were purchased from Selleck Chemicals.

    Techniques: Mutagenesis

    Mubritinib and canertinib perturb CNC migration ex vivo . (A-C) Lateral views of tailbud stage X . laevis embryos after in situ hybridization with Sox10 and Twist to visualize CNC positioning. Anterior is to the left, dorsal is up. Embryos treated with 40 μM of the ErbB2 inhibitor, mubritinib (N = 4, n = 72), or 25 μM of the pan-ErbB inhibitor, canertinib (N = 4, n = 68), show no difference in CNC migration compared to DMSO controls (N = 6, n = 100; N = 4, n = 69, respectively). (D-E) The distance of migration within each branchial arch was measured and normalized to the head size. CNC migration as observed in the mandibular (M), hyoid (H), 3 rd and 4 th branchial arches. (F-U) Time-lapse images of CNC explants migrating on fibronectin substrate and treated with 0.5% DMSO (N = 8, n = 24), 6 μM mubritinib (N = 4, n = 12), 10 μM canertinib (N = 4, n = 12), and 20 μM LY294002 (N = 3, n = 9) for indicated lengths of time. (V) Fold change in explant surface area over time. Areas were normalized to measurements calculated at initial time points (t = 0). All inhibitors significantly decreased CNC migration ex vivo . Error bars represent the 95% confidence interval. One-tailed, Student’s t-tests were performed to determine statistical significance. ** p

    Journal: PLoS ONE

    Article Title: The ectodomain of cadherin-11 binds to erbB2 and stimulates Akt phosphorylation to promote cranial neural crest cell migration

    doi: 10.1371/journal.pone.0188963

    Figure Lengend Snippet: Mubritinib and canertinib perturb CNC migration ex vivo . (A-C) Lateral views of tailbud stage X . laevis embryos after in situ hybridization with Sox10 and Twist to visualize CNC positioning. Anterior is to the left, dorsal is up. Embryos treated with 40 μM of the ErbB2 inhibitor, mubritinib (N = 4, n = 72), or 25 μM of the pan-ErbB inhibitor, canertinib (N = 4, n = 68), show no difference in CNC migration compared to DMSO controls (N = 6, n = 100; N = 4, n = 69, respectively). (D-E) The distance of migration within each branchial arch was measured and normalized to the head size. CNC migration as observed in the mandibular (M), hyoid (H), 3 rd and 4 th branchial arches. (F-U) Time-lapse images of CNC explants migrating on fibronectin substrate and treated with 0.5% DMSO (N = 8, n = 24), 6 μM mubritinib (N = 4, n = 12), 10 μM canertinib (N = 4, n = 12), and 20 μM LY294002 (N = 3, n = 9) for indicated lengths of time. (V) Fold change in explant surface area over time. Areas were normalized to measurements calculated at initial time points (t = 0). All inhibitors significantly decreased CNC migration ex vivo . Error bars represent the 95% confidence interval. One-tailed, Student’s t-tests were performed to determine statistical significance. ** p

    Article Snippet: Migration assays Inhibitors were used at the following concentrations to disrupt CNC migration in vivo : 30 μM of LY294002 (IC50 = 1.4μM; Millipore-Calbiochem, #440202), 40 μM of rapamycin (IC50 = 0.1nM; Millipore-Calbiochem, #553211), 40 μM mubritinib (IC50 = 6nM; Selleckchem; #S2216), and 25 μM canertinib (EGFR IC50 = 1.5nM; ErbB2 IC50 = 9nM; Selleckchem; #S1019).

    Techniques: Migration, Ex Vivo, In Situ Hybridization, One-tailed Test

    Selection of canertinib resistant cells. Tu-2449 cells were treated with canertinib for 10 days. The drug was replenished in the growth medium in 24 hour intervals by half-medium change. After 10 days, drug treatment was discontinued for three days. Cell growth was microscopically monitored after 1, 3, 5, 7, 9 and 13 days. The upper panel shows different fields while the lower panel shows the same field. Magnification, 40×. Drug treatment selects for small cell colonies with higher cell density.

    Journal: MedChemComm

    Article Title: Tumor cell resistance against targeted therapeutics: the density of cultured glioma tumor cells enhances Stat3 activity and offers protection against the tyrosine kinase inhibitor canertinib cell resistance against targeted therapeutics: the density of cultured glioma tumor cells enhances Stat3 activity and offers protection against the tyrosine kinase inhibitor canertinib †The authors declare no conflict of interest.

    doi: 10.1039/c6md00463f

    Figure Lengend Snippet: Selection of canertinib resistant cells. Tu-2449 cells were treated with canertinib for 10 days. The drug was replenished in the growth medium in 24 hour intervals by half-medium change. After 10 days, drug treatment was discontinued for three days. Cell growth was microscopically monitored after 1, 3, 5, 7, 9 and 13 days. The upper panel shows different fields while the lower panel shows the same field. Magnification, 40×. Drug treatment selects for small cell colonies with higher cell density.

    Article Snippet: Chemicals The tyrosine kinase inhibitor canertinib (CI-1033) was purchased from SelleckChem, Munich, Germany, dissolved in sterile dimethyl sulfoxide (DMSO) and stored at –80 °C.

    Techniques: Selection

    Selected canertinib resistant colonies become sensitive again to drug treatment when cultured at low cell densities. Parental and 5 selected colonies of Tu-2449 glioma cells were plated at low densities (comparable to Fig. 2 panel one) and treated with 5 μM canertinib or only the growth medium. The drug was replenished in the growth medium in 24 hour intervals. Cell viability was monitored after 24, 48 and 72 h using the AlamarBlue® assay. Repeated addition of 5 μM canertinib significantly reduced the cell viability in all analyzed cell clones after 72 h. Results are presented as mean ± SD, with respect to 72 h untreated cells; **** p

    Journal: MedChemComm

    Article Title: Tumor cell resistance against targeted therapeutics: the density of cultured glioma tumor cells enhances Stat3 activity and offers protection against the tyrosine kinase inhibitor canertinib cell resistance against targeted therapeutics: the density of cultured glioma tumor cells enhances Stat3 activity and offers protection against the tyrosine kinase inhibitor canertinib †The authors declare no conflict of interest.

    doi: 10.1039/c6md00463f

    Figure Lengend Snippet: Selected canertinib resistant colonies become sensitive again to drug treatment when cultured at low cell densities. Parental and 5 selected colonies of Tu-2449 glioma cells were plated at low densities (comparable to Fig. 2 panel one) and treated with 5 μM canertinib or only the growth medium. The drug was replenished in the growth medium in 24 hour intervals. Cell viability was monitored after 24, 48 and 72 h using the AlamarBlue® assay. Repeated addition of 5 μM canertinib significantly reduced the cell viability in all analyzed cell clones after 72 h. Results are presented as mean ± SD, with respect to 72 h untreated cells; **** p

    Article Snippet: Chemicals The tyrosine kinase inhibitor canertinib (CI-1033) was purchased from SelleckChem, Munich, Germany, dissolved in sterile dimethyl sulfoxide (DMSO) and stored at –80 °C.

    Techniques: Cell Culture, Alamar Blue Assay, Clone Assay

    Canertinib treatment of Tu-2449 glioma cells induces the arrest of cell growth after 24 h and prolonged inhibition causes cell death dependent upon exposure time and drug dose. (A) Tu-2449 cells were treated with a single dose of 5 or 10 μM canertinib or DMSO and cultured for 24 h. Microscopic monitoring after 24 h reveals growth arrest in canertinib treated cells; scale bar: 100 μm. (B) Tu-2449 cells were treated with canertinib or DMSO and the drug was replenished in the growth medium in 24 hour intervals. Cell viability was monitored after 24, 48 and 72 h using the AlamarBlue® assay. Repeated addition of canertinib arrests the cells and causes cell death after 24 h (10 μM canertinib) or 48 h (5 μM canertinib). Results are presented as mean ± SD, expressed as a percentage with respect to 72 h DMSO. ns = not significant, **** p

    Journal: MedChemComm

    Article Title: Tumor cell resistance against targeted therapeutics: the density of cultured glioma tumor cells enhances Stat3 activity and offers protection against the tyrosine kinase inhibitor canertinib cell resistance against targeted therapeutics: the density of cultured glioma tumor cells enhances Stat3 activity and offers protection against the tyrosine kinase inhibitor canertinib †The authors declare no conflict of interest.

    doi: 10.1039/c6md00463f

    Figure Lengend Snippet: Canertinib treatment of Tu-2449 glioma cells induces the arrest of cell growth after 24 h and prolonged inhibition causes cell death dependent upon exposure time and drug dose. (A) Tu-2449 cells were treated with a single dose of 5 or 10 μM canertinib or DMSO and cultured for 24 h. Microscopic monitoring after 24 h reveals growth arrest in canertinib treated cells; scale bar: 100 μm. (B) Tu-2449 cells were treated with canertinib or DMSO and the drug was replenished in the growth medium in 24 hour intervals. Cell viability was monitored after 24, 48 and 72 h using the AlamarBlue® assay. Repeated addition of canertinib arrests the cells and causes cell death after 24 h (10 μM canertinib) or 48 h (5 μM canertinib). Results are presented as mean ± SD, expressed as a percentage with respect to 72 h DMSO. ns = not significant, **** p

    Article Snippet: Chemicals The tyrosine kinase inhibitor canertinib (CI-1033) was purchased from SelleckChem, Munich, Germany, dissolved in sterile dimethyl sulfoxide (DMSO) and stored at –80 °C.

    Techniques: Inhibition, Cell Culture, Alamar Blue Assay