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Characterization of ErlR and AfaR HNSCC cell models. A and B, Dose response curves for ( A ) Fadu and ( B ) Cal27 parental, ErlR, or AfaR cell lines treated with the indicated dose range of afatinib or <t>erlotinib</t> for 72 hours. C, Representative Western blot images for active RTKs EGFR, MET, and HER2. D, Quantification of Western blots shown in C , with values normalized to those in parental cell lines. Graphs display baseline activation relative to total levels of each protein, based on n = 3. Note that for some proteins analyzed (e.g., MET), there was a significant intensity difference between FaDu and Cal27 models. For these cases, multiple exposures were taken for the relevant data, and quantification was performed based on primary Western blot data within a linear signal range. E, GSEA comparing Fadu and Cal27 AfaR or ErlR vs. Fadu and Cal27 parental cells, as indicated. RNA-seq analysis shown is averaged from two biological replicates. F and G, Representative Western blot images ( F ) and quantification ( G ) for indicated biomarkers of epithelial identity or EMT, based on n = 3 biological repeats. Bar graphs display data normalized for each parental cell line. P values are based on one-way ANOVA followed by Tukey multiple comparison test. *, P ≤ 0.05; **, P ≤ 0.001; ****, P ≤ 0.0001. Data are shown as mean ± SEM of three biological replicates. ES, enrichment score.
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Expression of PSA in <t>erlotinib-treated</t> LNCaP cells cultured on a collagen-coated surface RNA was isolated from LNCaP cells cultured either on a plain surface or collagen-coated and treated with±10 nM EGF, ± 5 μM flutamide, or ± 5 μM erlotinib for 48hrs. The extracted RNA was converted into cDNA using reverse transcriptase and used as a template to perform qRT-PCR. The bar represents the relative expression levels of PSA with respect to vehicle ± S.E.M., normalized to RPL35. The experiments were repeated three times and figures represents average of three experiments. A significance of difference was analyzed using 2-way ANOVA test.
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Expression of PSA in <t>erlotinib-treated</t> LNCaP cells cultured on a collagen-coated surface RNA was isolated from LNCaP cells cultured either on a plain surface or collagen-coated and treated with±10 nM EGF, ± 5 μM flutamide, or ± 5 μM erlotinib for 48hrs. The extracted RNA was converted into cDNA using reverse transcriptase and used as a template to perform qRT-PCR. The bar represents the relative expression levels of PSA with respect to vehicle ± S.E.M., normalized to RPL35. The experiments were repeated three times and figures represents average of three experiments. A significance of difference was analyzed using 2-way ANOVA test.
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Image Search Results


Characterization of ErlR and AfaR HNSCC cell models. A and B, Dose response curves for ( A ) Fadu and ( B ) Cal27 parental, ErlR, or AfaR cell lines treated with the indicated dose range of afatinib or erlotinib for 72 hours. C, Representative Western blot images for active RTKs EGFR, MET, and HER2. D, Quantification of Western blots shown in C , with values normalized to those in parental cell lines. Graphs display baseline activation relative to total levels of each protein, based on n = 3. Note that for some proteins analyzed (e.g., MET), there was a significant intensity difference between FaDu and Cal27 models. For these cases, multiple exposures were taken for the relevant data, and quantification was performed based on primary Western blot data within a linear signal range. E, GSEA comparing Fadu and Cal27 AfaR or ErlR vs. Fadu and Cal27 parental cells, as indicated. RNA-seq analysis shown is averaged from two biological replicates. F and G, Representative Western blot images ( F ) and quantification ( G ) for indicated biomarkers of epithelial identity or EMT, based on n = 3 biological repeats. Bar graphs display data normalized for each parental cell line. P values are based on one-way ANOVA followed by Tukey multiple comparison test. *, P ≤ 0.05; **, P ≤ 0.001; ****, P ≤ 0.0001. Data are shown as mean ± SEM of three biological replicates. ES, enrichment score.

Journal: Cancer Research Communications

Article Title: Combination AURKA and WEE1 Inhibition Exhibits Efficacy in EGFR or Pan-ERBB Inhibitor–Resistant Head and Neck Squamous Cell Carcinoma

doi: 10.1158/2767-9764.CRC-26-0368

Figure Lengend Snippet: Characterization of ErlR and AfaR HNSCC cell models. A and B, Dose response curves for ( A ) Fadu and ( B ) Cal27 parental, ErlR, or AfaR cell lines treated with the indicated dose range of afatinib or erlotinib for 72 hours. C, Representative Western blot images for active RTKs EGFR, MET, and HER2. D, Quantification of Western blots shown in C , with values normalized to those in parental cell lines. Graphs display baseline activation relative to total levels of each protein, based on n = 3. Note that for some proteins analyzed (e.g., MET), there was a significant intensity difference between FaDu and Cal27 models. For these cases, multiple exposures were taken for the relevant data, and quantification was performed based on primary Western blot data within a linear signal range. E, GSEA comparing Fadu and Cal27 AfaR or ErlR vs. Fadu and Cal27 parental cells, as indicated. RNA-seq analysis shown is averaged from two biological replicates. F and G, Representative Western blot images ( F ) and quantification ( G ) for indicated biomarkers of epithelial identity or EMT, based on n = 3 biological repeats. Bar graphs display data normalized for each parental cell line. P values are based on one-way ANOVA followed by Tukey multiple comparison test. *, P ≤ 0.05; **, P ≤ 0.001; ****, P ≤ 0.0001. Data are shown as mean ± SEM of three biological replicates. ES, enrichment score.

Article Snippet: For drug treatments, cells were treated with vehicle (0.01% DMSO), VIC-1911 (VITRAC), adavosertib (MedChemExpress, HY-10993), erlotinib (MedChemExpress, E-4997), or afatinib (MedChemExpress, HY-10261).

Techniques: Western Blot, Activation Assay, RNA Sequencing, Comparison

Response of parental, AfaR, and ErlR models to AURKAi combinations with erlotinib or afatinib. A, Loewe synergy plot showing synergistic interaction between VIC-1911 and afatinib or erlotinib in FaDu and Cal27 parental, ErlR, and AfaR cell lines treated for 72 hours, n = 3. B, Quantification of dead cells from the models indicated treated for 72 hours with drugs indicated. FaDu and derived models were treated with vehicle, VIC-1911 (0.6 μmol/L), afatinib (0.2 μmol/L), erlotinib (1 μmol/L), or combination. Cal27 and derived models were treated with vehicle, VIC-1911 (0.6 μmol/L), afatinib (0.8 μmol/L), erlotinib (2 μmol/L), or combination for 24 hours. C and D, Clonogenic survival assay primary data ( C ) and corresponding ( D ) quantification. Cells were treated with the drug concentration indicated in C for 11 days. E, Quantification of annexin-positive cells for Fadu parental and Fadu AfaR treated for 3 days (left) and 5 days (right) with VIC-1911 (600 nmol/L). P values are based on one-way ANOVA followed by the Tukey multiple comparison test. *, P ≤ 0.05; **, P ≤ 0.01; ***, P ≤ 0.001; ****, P ≤ 0.0001. Data are shown as mean ± SEM of three biological replicates.

Journal: Cancer Research Communications

Article Title: Combination AURKA and WEE1 Inhibition Exhibits Efficacy in EGFR or Pan-ERBB Inhibitor–Resistant Head and Neck Squamous Cell Carcinoma

doi: 10.1158/2767-9764.CRC-26-0368

Figure Lengend Snippet: Response of parental, AfaR, and ErlR models to AURKAi combinations with erlotinib or afatinib. A, Loewe synergy plot showing synergistic interaction between VIC-1911 and afatinib or erlotinib in FaDu and Cal27 parental, ErlR, and AfaR cell lines treated for 72 hours, n = 3. B, Quantification of dead cells from the models indicated treated for 72 hours with drugs indicated. FaDu and derived models were treated with vehicle, VIC-1911 (0.6 μmol/L), afatinib (0.2 μmol/L), erlotinib (1 μmol/L), or combination. Cal27 and derived models were treated with vehicle, VIC-1911 (0.6 μmol/L), afatinib (0.8 μmol/L), erlotinib (2 μmol/L), or combination for 24 hours. C and D, Clonogenic survival assay primary data ( C ) and corresponding ( D ) quantification. Cells were treated with the drug concentration indicated in C for 11 days. E, Quantification of annexin-positive cells for Fadu parental and Fadu AfaR treated for 3 days (left) and 5 days (right) with VIC-1911 (600 nmol/L). P values are based on one-way ANOVA followed by the Tukey multiple comparison test. *, P ≤ 0.05; **, P ≤ 0.01; ***, P ≤ 0.001; ****, P ≤ 0.0001. Data are shown as mean ± SEM of three biological replicates.

Article Snippet: For drug treatments, cells were treated with vehicle (0.01% DMSO), VIC-1911 (VITRAC), adavosertib (MedChemExpress, HY-10993), erlotinib (MedChemExpress, E-4997), or afatinib (MedChemExpress, HY-10261).

Techniques: Derivative Assay, Clonogenic Cell Survival Assay, Concentration Assay, Comparison

Expression of PSA in erlotinib-treated LNCaP cells cultured on a collagen-coated surface RNA was isolated from LNCaP cells cultured either on a plain surface or collagen-coated and treated with±10 nM EGF, ± 5 μM flutamide, or ± 5 μM erlotinib for 48hrs. The extracted RNA was converted into cDNA using reverse transcriptase and used as a template to perform qRT-PCR. The bar represents the relative expression levels of PSA with respect to vehicle ± S.E.M., normalized to RPL35. The experiments were repeated three times and figures represents average of three experiments. A significance of difference was analyzed using 2-way ANOVA test.

Journal: Biochemistry and Biophysics Reports

Article Title: ECM (collagen) mediated signaling drives the emergence of androgen independence in prostate cancer cells

doi: 10.1016/j.bbrep.2026.102580

Figure Lengend Snippet: Expression of PSA in erlotinib-treated LNCaP cells cultured on a collagen-coated surface RNA was isolated from LNCaP cells cultured either on a plain surface or collagen-coated and treated with±10 nM EGF, ± 5 μM flutamide, or ± 5 μM erlotinib for 48hrs. The extracted RNA was converted into cDNA using reverse transcriptase and used as a template to perform qRT-PCR. The bar represents the relative expression levels of PSA with respect to vehicle ± S.E.M., normalized to RPL35. The experiments were repeated three times and figures represents average of three experiments. A significance of difference was analyzed using 2-way ANOVA test.

Article Snippet: Erlotinib , Cayman Chemicals , 10483 , Erlo , 5 μM.

Techniques: Expressing, Cell Culture, Isolation, Reverse Transcription, Quantitative RT-PCR

Effect of collagen on cell proliferation A total of 5000 cells/well were treated with or without 10 nM DHT, ± 5 μM erlotinib, ± 5 μM flutamide, ± 10 nM FAK inhibitor, ± 10 nM EGF for 72 h. Cell proliferation was assessed using an MTT assay. The student t-test was performed to determine the significance between the groups. Each sample was in triplicate. The experiment was repeated twice. A significance of difference was analyzed using 2-way ANOVA test.

Journal: Biochemistry and Biophysics Reports

Article Title: ECM (collagen) mediated signaling drives the emergence of androgen independence in prostate cancer cells

doi: 10.1016/j.bbrep.2026.102580

Figure Lengend Snippet: Effect of collagen on cell proliferation A total of 5000 cells/well were treated with or without 10 nM DHT, ± 5 μM erlotinib, ± 5 μM flutamide, ± 10 nM FAK inhibitor, ± 10 nM EGF for 72 h. Cell proliferation was assessed using an MTT assay. The student t-test was performed to determine the significance between the groups. Each sample was in triplicate. The experiment was repeated twice. A significance of difference was analyzed using 2-way ANOVA test.

Article Snippet: Erlotinib , Cayman Chemicals , 10483 , Erlo , 5 μM.

Techniques: MTT Assay