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injection  (MedChemExpress)


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    Structured Review

    MedChemExpress injection
    Injection, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 95/100, based on 73 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ag+1478/AG-1478/pmc13289659-77-22-33
    Average 95 stars, based on 73 article reviews
    injection - by Bioz Stars, 2026-09
    95/100 stars

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    MedChemExpress egfr inhibitor ag1478
    IL-37/IL-1R8 protects HaCaT cells from keratinocyte dissociation and apoptosis through the ADAM17/EGFR pathway. (A) Protein expression levels of ADAM17, p-EGFR, total EGFR as well as EGFR downstream protein p-AKT, p-ERK1/2 and p-STAT3 levels were determined by western blotting. HaCaT cells were treated with EGFR activator NSC228155. (B) Cell dissociation was analyzed by cell dissociation assay. (C) Cell apoptosis was analyzed by flow cytometry. (D) Protein expression levels of Bcl-2 and Bax were analyzed by western blotting. (E) HaCaT was transfected with ADAM17 siRNA and the transfection efficiency was detected by western blotting. HaCaT cells were transfected with ADAM17 siRNA or treated with 1 μ M of EGFR inhibitor <t>AG1478</t> for 30 min followed by treated with AK23. (F) Cell dissociation was analyzed by cell dissociation assay. (G) Cell apoptosis was analyzed by flow cytometry. # P<0.05 vs. Control group; & P<0.05 vs. anti-Dsg3 group; @ P<0.05 vs. anti- Dsg3 + IL-37 + si-NC group; * P<0.05; Data are presented as mean ± SD, n=3 biological indepen- dent replicates. One-way ANOVA with Bonferroni's post-hoc test was used for multiple group comparisons. IL, interleukin; ADAM17, TNF-alpha-converting enzyme; EGFR, epidermal growth factor receptor; p- phosphorylated; STAT, signal transducer and activator of transcription; si, short interfering.
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    MedChemExpress ag 1478
    IL-37/IL-1R8 protects HaCaT cells from keratinocyte dissociation and apoptosis through the ADAM17/EGFR pathway. (A) Protein expression levels of ADAM17, p-EGFR, total EGFR as well as EGFR downstream protein p-AKT, p-ERK1/2 and p-STAT3 levels were determined by western blotting. HaCaT cells were treated with EGFR activator NSC228155. (B) Cell dissociation was analyzed by cell dissociation assay. (C) Cell apoptosis was analyzed by flow cytometry. (D) Protein expression levels of Bcl-2 and Bax were analyzed by western blotting. (E) HaCaT was transfected with ADAM17 siRNA and the transfection efficiency was detected by western blotting. HaCaT cells were transfected with ADAM17 siRNA or treated with 1 μ M of EGFR inhibitor <t>AG1478</t> for 30 min followed by treated with AK23. (F) Cell dissociation was analyzed by cell dissociation assay. (G) Cell apoptosis was analyzed by flow cytometry. # P<0.05 vs. Control group; & P<0.05 vs. anti-Dsg3 group; @ P<0.05 vs. anti- Dsg3 + IL-37 + si-NC group; * P<0.05; Data are presented as mean ± SD, n=3 biological indepen- dent replicates. One-way ANOVA with Bonferroni's post-hoc test was used for multiple group comparisons. IL, interleukin; ADAM17, TNF-alpha-converting enzyme; EGFR, epidermal growth factor receptor; p- phosphorylated; STAT, signal transducer and activator of transcription; si, short interfering.
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    Selleck Chemicals tyrphostin ag 1478 ag
    IL-37/IL-1R8 protects HaCaT cells from keratinocyte dissociation and apoptosis through the ADAM17/EGFR pathway. (A) Protein expression levels of ADAM17, p-EGFR, total EGFR as well as EGFR downstream protein p-AKT, p-ERK1/2 and p-STAT3 levels were determined by western blotting. HaCaT cells were treated with EGFR activator NSC228155. (B) Cell dissociation was analyzed by cell dissociation assay. (C) Cell apoptosis was analyzed by flow cytometry. (D) Protein expression levels of Bcl-2 and Bax were analyzed by western blotting. (E) HaCaT was transfected with ADAM17 siRNA and the transfection efficiency was detected by western blotting. HaCaT cells were transfected with ADAM17 siRNA or treated with 1 μ M of EGFR inhibitor <t>AG1478</t> for 30 min followed by treated with AK23. (F) Cell dissociation was analyzed by cell dissociation assay. (G) Cell apoptosis was analyzed by flow cytometry. # P<0.05 vs. Control group; & P<0.05 vs. anti-Dsg3 group; @ P<0.05 vs. anti- Dsg3 + IL-37 + si-NC group; * P<0.05; Data are presented as mean ± SD, n=3 biological indepen- dent replicates. One-way ANOVA with Bonferroni's post-hoc test was used for multiple group comparisons. IL, interleukin; ADAM17, TNF-alpha-converting enzyme; EGFR, epidermal growth factor receptor; p- phosphorylated; STAT, signal transducer and activator of transcription; si, short interfering.
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    Selleck Chemicals ag1478 s2728
    IL-37/IL-1R8 protects HaCaT cells from keratinocyte dissociation and apoptosis through the ADAM17/EGFR pathway. (A) Protein expression levels of ADAM17, p-EGFR, total EGFR as well as EGFR downstream protein p-AKT, p-ERK1/2 and p-STAT3 levels were determined by western blotting. HaCaT cells were treated with EGFR activator NSC228155. (B) Cell dissociation was analyzed by cell dissociation assay. (C) Cell apoptosis was analyzed by flow cytometry. (D) Protein expression levels of Bcl-2 and Bax were analyzed by western blotting. (E) HaCaT was transfected with ADAM17 siRNA and the transfection efficiency was detected by western blotting. HaCaT cells were transfected with ADAM17 siRNA or treated with 1 μ M of EGFR inhibitor <t>AG1478</t> for 30 min followed by treated with AK23. (F) Cell dissociation was analyzed by cell dissociation assay. (G) Cell apoptosis was analyzed by flow cytometry. # P<0.05 vs. Control group; & P<0.05 vs. anti-Dsg3 group; @ P<0.05 vs. anti- Dsg3 + IL-37 + si-NC group; * P<0.05; Data are presented as mean ± SD, n=3 biological indepen- dent replicates. One-way ANOVA with Bonferroni's post-hoc test was used for multiple group comparisons. IL, interleukin; ADAM17, TNF-alpha-converting enzyme; EGFR, epidermal growth factor receptor; p- phosphorylated; STAT, signal transducer and activator of transcription; si, short interfering.
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    MedChemExpress inhibitors egfr inhibitor
    S100A8/A9 heterodimer promotes platelet adhesion and aggregation via <t>EGFR/PI3K/AKT</t> and EGFR/p38 MAPK axes ( A ) Representative images of the morphological changes observed by TEM in washed human platelets treated with vehicle (DMSO), 10 µg/mL S100A8/A9 heterodimer, <t>AG1478</t> or LY294002. ( B ) Representative images of the platelet adhesion test of washed human platelets treated with vehicle (DMSO), 1 µg/mL S100A8/A9 heterodimer, AG1478 or LY294002. The statistics are shown in the histogram below. ( C ) Platelet aggregation induced by ADP, AA or EPI in PRP treated with vehicle (DMSO), 1 µg/mL S100A8/A9 heterodimer, AG1478 or LY294002. The statistics are shown in the histogram below. ( D ) Expression of p-p38 and p38 in the platelets harvested from the reaction cells of the platelet aggregometer. The statistics are shown in the histogram below. ( E ) Expression of p-PI3K, PI3K, p-AKT and AKT in the platelets harvested from the reaction cells of the platelet aggregometer. The statistics are shown in the histogram below. n = 3 independent experiments. Significant results are presented as * p <0.05, ** P <0.01, or *** P <0.001.
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    Image Search Results


    IL-37/IL-1R8 protects HaCaT cells from keratinocyte dissociation and apoptosis through the ADAM17/EGFR pathway. (A) Protein expression levels of ADAM17, p-EGFR, total EGFR as well as EGFR downstream protein p-AKT, p-ERK1/2 and p-STAT3 levels were determined by western blotting. HaCaT cells were treated with EGFR activator NSC228155. (B) Cell dissociation was analyzed by cell dissociation assay. (C) Cell apoptosis was analyzed by flow cytometry. (D) Protein expression levels of Bcl-2 and Bax were analyzed by western blotting. (E) HaCaT was transfected with ADAM17 siRNA and the transfection efficiency was detected by western blotting. HaCaT cells were transfected with ADAM17 siRNA or treated with 1 μ M of EGFR inhibitor AG1478 for 30 min followed by treated with AK23. (F) Cell dissociation was analyzed by cell dissociation assay. (G) Cell apoptosis was analyzed by flow cytometry. # P<0.05 vs. Control group; & P<0.05 vs. anti-Dsg3 group; @ P<0.05 vs. anti- Dsg3 + IL-37 + si-NC group; * P<0.05; Data are presented as mean ± SD, n=3 biological indepen- dent replicates. One-way ANOVA with Bonferroni's post-hoc test was used for multiple group comparisons. IL, interleukin; ADAM17, TNF-alpha-converting enzyme; EGFR, epidermal growth factor receptor; p- phosphorylated; STAT, signal transducer and activator of transcription; si, short interfering.

    Journal: International Journal of Molecular Medicine

    Article Title: IL-37/IL-1R8 blocks keratinocyte acantholysis via suppressing ADAM17/EGFR

    doi: 10.3892/ijmm.2026.5793

    Figure Lengend Snippet: IL-37/IL-1R8 protects HaCaT cells from keratinocyte dissociation and apoptosis through the ADAM17/EGFR pathway. (A) Protein expression levels of ADAM17, p-EGFR, total EGFR as well as EGFR downstream protein p-AKT, p-ERK1/2 and p-STAT3 levels were determined by western blotting. HaCaT cells were treated with EGFR activator NSC228155. (B) Cell dissociation was analyzed by cell dissociation assay. (C) Cell apoptosis was analyzed by flow cytometry. (D) Protein expression levels of Bcl-2 and Bax were analyzed by western blotting. (E) HaCaT was transfected with ADAM17 siRNA and the transfection efficiency was detected by western blotting. HaCaT cells were transfected with ADAM17 siRNA or treated with 1 μ M of EGFR inhibitor AG1478 for 30 min followed by treated with AK23. (F) Cell dissociation was analyzed by cell dissociation assay. (G) Cell apoptosis was analyzed by flow cytometry. # P<0.05 vs. Control group; & P<0.05 vs. anti-Dsg3 group; @ P<0.05 vs. anti- Dsg3 + IL-37 + si-NC group; * P<0.05; Data are presented as mean ± SD, n=3 biological indepen- dent replicates. One-way ANOVA with Bonferroni's post-hoc test was used for multiple group comparisons. IL, interleukin; ADAM17, TNF-alpha-converting enzyme; EGFR, epidermal growth factor receptor; p- phosphorylated; STAT, signal transducer and activator of transcription; si, short interfering.

    Article Snippet: For EGFR inhibition assay, HaCaT cells were pre-treated with 1 μ M of EGFR inhibitor AG1478 (MedChemExpress) at 37°C for 30 min followed by treatment with AK23 for 24 h at 37°C.

    Techniques: Expressing, Western Blot, Flow Cytometry, Transfection, Control

    S100A8/A9 heterodimer promotes platelet adhesion and aggregation via EGFR/PI3K/AKT and EGFR/p38 MAPK axes ( A ) Representative images of the morphological changes observed by TEM in washed human platelets treated with vehicle (DMSO), 10 µg/mL S100A8/A9 heterodimer, AG1478 or LY294002. ( B ) Representative images of the platelet adhesion test of washed human platelets treated with vehicle (DMSO), 1 µg/mL S100A8/A9 heterodimer, AG1478 or LY294002. The statistics are shown in the histogram below. ( C ) Platelet aggregation induced by ADP, AA or EPI in PRP treated with vehicle (DMSO), 1 µg/mL S100A8/A9 heterodimer, AG1478 or LY294002. The statistics are shown in the histogram below. ( D ) Expression of p-p38 and p38 in the platelets harvested from the reaction cells of the platelet aggregometer. The statistics are shown in the histogram below. ( E ) Expression of p-PI3K, PI3K, p-AKT and AKT in the platelets harvested from the reaction cells of the platelet aggregometer. The statistics are shown in the histogram below. n = 3 independent experiments. Significant results are presented as * p <0.05, ** P <0.01, or *** P <0.001.

    Journal: Clinical and Experimental Medicine

    Article Title: The mechanism of S100A8/A9 heterodimer promoting atherosclerotic thrombosis

    doi: 10.1007/s10238-025-02016-z

    Figure Lengend Snippet: S100A8/A9 heterodimer promotes platelet adhesion and aggregation via EGFR/PI3K/AKT and EGFR/p38 MAPK axes ( A ) Representative images of the morphological changes observed by TEM in washed human platelets treated with vehicle (DMSO), 10 µg/mL S100A8/A9 heterodimer, AG1478 or LY294002. ( B ) Representative images of the platelet adhesion test of washed human platelets treated with vehicle (DMSO), 1 µg/mL S100A8/A9 heterodimer, AG1478 or LY294002. The statistics are shown in the histogram below. ( C ) Platelet aggregation induced by ADP, AA or EPI in PRP treated with vehicle (DMSO), 1 µg/mL S100A8/A9 heterodimer, AG1478 or LY294002. The statistics are shown in the histogram below. ( D ) Expression of p-p38 and p38 in the platelets harvested from the reaction cells of the platelet aggregometer. The statistics are shown in the histogram below. ( E ) Expression of p-PI3K, PI3K, p-AKT and AKT in the platelets harvested from the reaction cells of the platelet aggregometer. The statistics are shown in the histogram below. n = 3 independent experiments. Significant results are presented as * p <0.05, ** P <0.01, or *** P <0.001.

    Article Snippet: The roles of S100A8/A9 heterodimer and EGFR signaling pathway in platelet shape, adhesion and aggregation were investigated using recombinant S100A8/A9 heterodimer (Sino Biological, Beijing, China, Cat: CT002-H0822B) or specific inhibitors EGFR inhibitor (AG1478, 10 μM, MedChem Express, Monnouth Junction, NJ, USA, Cat: HY-13524) and PI3K inhibitor (LY294002, 10 μM, MedChem Express, Monnouth Junction, NJ, USA, Cat: HY-10108).

    Techniques: Expressing

    S100A8/A9 heterodimer promotes platelet αⅡbβ3 activation and TXB 2 secretion via EGFR signaling pathway ( A ) Activity of CD62P in washed human platelets treated with Vehicle (DMSO), ADP, ADP + S100A8/A9, ADP + S100A8/A9 + AG1478 or ADP + S100A8/A9 + LY294002. The statistics are shown in the histogram below. ( B ) Representative phalloidin-stained images of washed human platelets treated with vehicle (DMSO), 1 µg/mL S100A8/A9 heterodimer, AG1478 or LY294002 spreading on immobilized fibrinogen for every 20 min. The statistics are shown in the histogram below. ( C ) Clot retraction of human platelets treated with vehicle (DMSO), 1 µg/mL S100A8/A9 heterodimer, AG1478 or LY294002. The statistics are shown in the histogram below. ( D ) TXB 2 secretion detected with ELISA in human platelets treated with Vehicle (DMSO), ADP, ADP + S100A8/A9, AG1478 or LY294002. n = 3 independent experiments. Significant results are presented as * P <0.05, ** P <0.01, or *** P <0.001. Non-significant results are presented as ns.

    Journal: Clinical and Experimental Medicine

    Article Title: The mechanism of S100A8/A9 heterodimer promoting atherosclerotic thrombosis

    doi: 10.1007/s10238-025-02016-z

    Figure Lengend Snippet: S100A8/A9 heterodimer promotes platelet αⅡbβ3 activation and TXB 2 secretion via EGFR signaling pathway ( A ) Activity of CD62P in washed human platelets treated with Vehicle (DMSO), ADP, ADP + S100A8/A9, ADP + S100A8/A9 + AG1478 or ADP + S100A8/A9 + LY294002. The statistics are shown in the histogram below. ( B ) Representative phalloidin-stained images of washed human platelets treated with vehicle (DMSO), 1 µg/mL S100A8/A9 heterodimer, AG1478 or LY294002 spreading on immobilized fibrinogen for every 20 min. The statistics are shown in the histogram below. ( C ) Clot retraction of human platelets treated with vehicle (DMSO), 1 µg/mL S100A8/A9 heterodimer, AG1478 or LY294002. The statistics are shown in the histogram below. ( D ) TXB 2 secretion detected with ELISA in human platelets treated with Vehicle (DMSO), ADP, ADP + S100A8/A9, AG1478 or LY294002. n = 3 independent experiments. Significant results are presented as * P <0.05, ** P <0.01, or *** P <0.001. Non-significant results are presented as ns.

    Article Snippet: The roles of S100A8/A9 heterodimer and EGFR signaling pathway in platelet shape, adhesion and aggregation were investigated using recombinant S100A8/A9 heterodimer (Sino Biological, Beijing, China, Cat: CT002-H0822B) or specific inhibitors EGFR inhibitor (AG1478, 10 μM, MedChem Express, Monnouth Junction, NJ, USA, Cat: HY-13524) and PI3K inhibitor (LY294002, 10 μM, MedChem Express, Monnouth Junction, NJ, USA, Cat: HY-10108).

    Techniques: Activation Assay, Activity Assay, Staining, Enzyme-linked Immunosorbent Assay

    The role of S100A8/A9 heterodimer produced by endothelial cells stimulated by NETs in thrombosis is shown. Neutrophil extracellular traps (NETs) induce pyroptosis and increase S100A8/A9 heterodimer expression in HUVECs via ROS/NF-κB/Caspase-1 axis and S100A8/A9 heterodimer activates platelets via the EGFR/PI3K/AKT and EGFR/p38 MAPK signaling pathways, driving thrombus formation.

    Journal: Clinical and Experimental Medicine

    Article Title: The mechanism of S100A8/A9 heterodimer promoting atherosclerotic thrombosis

    doi: 10.1007/s10238-025-02016-z

    Figure Lengend Snippet: The role of S100A8/A9 heterodimer produced by endothelial cells stimulated by NETs in thrombosis is shown. Neutrophil extracellular traps (NETs) induce pyroptosis and increase S100A8/A9 heterodimer expression in HUVECs via ROS/NF-κB/Caspase-1 axis and S100A8/A9 heterodimer activates platelets via the EGFR/PI3K/AKT and EGFR/p38 MAPK signaling pathways, driving thrombus formation.

    Article Snippet: The roles of S100A8/A9 heterodimer and EGFR signaling pathway in platelet shape, adhesion and aggregation were investigated using recombinant S100A8/A9 heterodimer (Sino Biological, Beijing, China, Cat: CT002-H0822B) or specific inhibitors EGFR inhibitor (AG1478, 10 μM, MedChem Express, Monnouth Junction, NJ, USA, Cat: HY-13524) and PI3K inhibitor (LY294002, 10 μM, MedChem Express, Monnouth Junction, NJ, USA, Cat: HY-10108).

    Techniques: Produced, Expressing, Protein-Protein interactions