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ferrostatin 1  (MedChemExpress)


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    Structured Review

    MedChemExpress ferrostatin 1
    Ferrostatin 1, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 2534 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/ferrostatin+1/Ferrostatin-1/pmc13695081-47-0-32
    Average 99 stars, based on 2534 article reviews
    ferrostatin 1 - by Bioz Stars, 2026-11
    99/100 stars

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    Recombinant:

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    Article Snippet: Temporomandibular joint osteoarthritis (TMJ-OA) is a progressive degenerative joint disease characterized by cartilage destruction, extracellular matrix (ECM) degradation, and chronic inflammation, yet effective disease-modifying therapeutic targets and pharmacological interventions remain limited.. Using a monosodium iodoacetate (MIA)-induced rat TMJ-OA model and interleukin-1β (IL-1β)-stimulated chondrocytes, we integrated transcriptomic analysis, chromatin accessibility profiling, and molecular screening to elucidate disease mechanisms and identify candidate compounds.. Integrated RNA sequencing (RNA-seq) analysis revealed Wnt family member 5a (Wnt5a) as a critical upstream regulator significantly associated with TMJ-OA progression, while assay for transposase-accessible chromatin using sequencing (ATAC-seq) uncovered an inflammatory chromatin landscape characterized by enhanced activator protein-1 (AP-1) activity and JUN-dependent transcriptional regulation of matrix metalloproteinase 9 (Mmp9).

    other:

    Article Title: STING engages PKR to drive lysosomal cell death in lung ischemia-reperfusion injury.
    Article Snippet: REAGENT or RESOURCE SOURCE IDENTIFIER Goat anti-Mouse IgG (H+L) Highly Cross-Adsorbed Secondary Antibody, Cy3 Beyotime Cat# A0521; RRID: AB_2923334 Goat anti-Rabbit IgG (H+L) Highly Cross-Adsorbed Secondary Antibody, FITC Beyotime Cat# A0562; RRID: AB_2923335 Goat anti-Rabbit IgG (H+L) Highly Cross-Adsorbed Secondary Antibody, Cy3 Beyotime Cat# A0516; RRID: AB_2893015 Goat anti-Rabbit IgG (H+L) Highly Cross-Adsorbed Secondary Antibody, Alexa Fluor 647 Beyotime Cat# A0473; RRID: AB_2891322 Donkey anti-Goat IgG (H+L) Highly Cross-Adsorbed Secondary Antibody, Cy3 Beyotime Cat# A0502; RRID: AB_3065047 InVivoSIM anti-human IFNAR1 (Anifrolumab Biosimilar) BioXcell Cat# SIM0022; RRID: AB_3696361 Chemicals, Peptides, and Recombinant Proteins Phosphatase inhibitor cocktail Sigma-Aldrich Cat# P5726 Methyl Cellulose Sigma-Aldrich Cat# M0512 Protease inhibitor cocktail Sigma-Aldrich Cat# P8340 Lipofectamine 2000 Reagent ThermoFisher Scientific Cat# L11668019 Lipofectamine 3000 Reagent ThermoFisher Scientific Cat# L3000001 Lipo8000 Transfection Reagent Beyotime Cat# C0533 2’3′-cGAMP Invivogen Cat# tlrl-nacga23-02 DNase I Roche Cat# 9003-98-9 Collagenase Type I ThermoFisher Scientific Cat# 17100017 Dispase Roche Cat# 40104ES80 Palbociclib MedChemExpress Cat# HY-50767 Amlexanox MedChemExpress Cat# HY-B0713 BAY 11-7082 MedChemExpress Cat# HY-13453 2’,3’-dideoxycytidine MedChemExpress Cat# HY-17392 GSK2606414 MedChemExpress Cat# HY-18072 Brefeldin A MedChemExpress Cat# HY-16592 5Z-7-Oxozeaenol MedChemExpress Cat#HY-12686 TUDCA MedChemExpress Cat#HY-19696 LLOMe MedChemExpress Cat#HY-129905 Bafilomycin A1 MedChemExpress Cat#HY-100558 E64d MedChemExpress Cat#HY-100229 CA-074Me MedChemExpress Cat#HY-100350 Z-VAD-FMK MedChemExpress Cat#HY-16658B Ferrostatin-1 MedChemExpress Cat#HY-100579 Recombinant Human IFN-β Peprotech Cat#300-02BC Triton X-100 Sigma-Aldrich Cat#T8787 Digitonin Sigma-Aldrich Cat# 300410 Cls IV Sigma-Aldrich Cat# C4BIOC Anti-FLAG M2 Affinity Gel Sigma-Aldrich Cat# A2220 Critical Commercial Assay TRIzol Reagent ThermoFisher Scientific Cat# 15596-018 TB Green Premix Ex Taq Takara Cat# RR420B Pierce Co-immunoprecipitation kit ThermoFisher Scientific Cat# 26149 (Continued on next page) ll Article Molecular Cell 86, 1–19.e1–e11, November 5, 2026 e2

    Apoptosis Assay:

    Article Title: The m 6 A reader HNRNPC drives osteosarcoma metastasis and cisplatin resistance by stabilizing MTDH to coordinately regulate EMT and ferroptosis.
    Article Snippet: .. Apoptosis assay Cells were pretreated with 2 μM ferrostatin-1 (Ferr-1; HY-100579; MCE, Monmouth Junction, USA) for 12 h, followed by co-treatment with 10 μM cisplatin for an additional 24 h. The cells were resuspended in 1× binding buffer at a density of 1 × 106 cells/mL and subsequently stained with the Annexin V-FITC/PI kit (20-6410-KIT; 4A Biotech, Beijing, China). ..

    Binding Assay:

    Article Title: The m 6 A reader HNRNPC drives osteosarcoma metastasis and cisplatin resistance by stabilizing MTDH to coordinately regulate EMT and ferroptosis.
    Article Snippet: .. Apoptosis assay Cells were pretreated with 2 μM ferrostatin-1 (Ferr-1; HY-100579; MCE, Monmouth Junction, USA) for 12 h, followed by co-treatment with 10 μM cisplatin for an additional 24 h. The cells were resuspended in 1× binding buffer at a density of 1 × 106 cells/mL and subsequently stained with the Annexin V-FITC/PI kit (20-6410-KIT; 4A Biotech, Beijing, China). ..

    Staining:

    Article Title: The m 6 A reader HNRNPC drives osteosarcoma metastasis and cisplatin resistance by stabilizing MTDH to coordinately regulate EMT and ferroptosis.
    Article Snippet: .. Apoptosis assay Cells were pretreated with 2 μM ferrostatin-1 (Ferr-1; HY-100579; MCE, Monmouth Junction, USA) for 12 h, followed by co-treatment with 10 μM cisplatin for an additional 24 h. The cells were resuspended in 1× binding buffer at a density of 1 × 106 cells/mL and subsequently stained with the Annexin V-FITC/PI kit (20-6410-KIT; 4A Biotech, Beijing, China). ..



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    Neutrophil extracellular traps (NETs)-mediated intraplaque hemorrhage drives rapid plaque progression in nonculprit lesions following myocardial infarction (MI), potentially via macrophage ferroptosis. (A) Representative images of intraplaque CD31, TER119 immunofluorescence staining (scale bar = 100 μm), and Prussian blue staining (scale bar = 50 μm) in brachiocephalic artery (BCA) lesions from the sham and MI groups at 4 weeks postsurgery. (B and C) Quantification of TER119 + and CD31 + area relative to plaque area in (A) ( n = 6 per group). (D) Quantification of the Prussian blue positive area in (A) ( n = 6 per group). (E) Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showing enrichment of the ferroptosis signaling pathway. (F) Quantification of the mean fluorescence intensity (MFI) of Bodipy C11 in RAW264.7 cells across the indicated groups ( n = 3 per group). (G) Quantification of PI-positive RAW264.7 cells across the indicated groups ( n = 3 per group). (H and I) Immunoblotting and quantification of the relative protein levels of SLC7A11, HMOX1, FTH1, and GPX4 in RAW264.7 cells across the indicated groups ( n = 3 per group). (J) Representative images and quantification of 4-hydroxynonenal (4-HNE) immunofluorescence staining in BCA lesions from the sham and MI groups at 4 weeks postsurgery (scale bar = 100 μm, n = 6 per group). (K) Representative images and quantification of 4-HNE immunofluorescence staining in BCA lesions from the control and deoxyribonuclease I (DNase I) groups at 4 weeks post-MI (scale bar = 100 μm, n = 6 per group). Statistical analyses were performed using unpaired Student t test (B, C, D, J, and K) and 1-way analysis of variance (ANOVA) with Bonferroni posttest (F, G, and I).
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    Selleck Chemicals ferrostatin 1
    Ferroptosis-specific validation of GINS1 knockdown-induced cell death in neuroblastoma cells. (A) Western blot analysis of GPX4 and SLC7A11 protein levels in SH-SY5Y and SK-N-SH cells transfected with shNC, shGINS1-1, and shGINS1-2. (B-C) CCK-8 assay assessing cell viability in SH-SY5Y (B) and SK-N-SH (C) cells transfected with shNC or shGINS1, treated with erastin (5 μM), RSL3 (1 μM), <t>and/or</t> <t>ferrostatin-1</t> (Fer-1, 1 μM) as indicated. (D-E) Glutathione (GSH) levels in SH-SY5Y (D) and SK-N-SH (E) cells under the indicated conditions. (F-G) Intracellular ROS levels in SH-SY5Y (F) and SK-N-SH (G) cells under the indicated conditions. (H-I) Malondialdehyde (MDA) content in SH-SY5Y (H) and SK-N-SH (I) cells under the indicated conditions. (J-K) Fe 2+ levels in SH-SY5Y (J) and SK-N-SH (K) cells under the indicated conditions. Data are presented as mean ± SD from three independent experiments. Statistical significance was determined using one-way ANOVA. * p < 0.05; ** p < 0.01; *** p < 0.001; ns, not significant.
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    MedChemExpress errostatin 1
    Ferroptosis-specific validation of GINS1 knockdown-induced cell death in neuroblastoma cells. (A) Western blot analysis of GPX4 and SLC7A11 protein levels in SH-SY5Y and SK-N-SH cells transfected with shNC, shGINS1-1, and shGINS1-2. (B-C) CCK-8 assay assessing cell viability in SH-SY5Y (B) and SK-N-SH (C) cells transfected with shNC or shGINS1, treated with erastin (5 μM), RSL3 (1 μM), <t>and/or</t> <t>ferrostatin-1</t> (Fer-1, 1 μM) as indicated. (D-E) Glutathione (GSH) levels in SH-SY5Y (D) and SK-N-SH (E) cells under the indicated conditions. (F-G) Intracellular ROS levels in SH-SY5Y (F) and SK-N-SH (G) cells under the indicated conditions. (H-I) Malondialdehyde (MDA) content in SH-SY5Y (H) and SK-N-SH (I) cells under the indicated conditions. (J-K) Fe 2+ levels in SH-SY5Y (J) and SK-N-SH (K) cells under the indicated conditions. Data are presented as mean ± SD from three independent experiments. Statistical significance was determined using one-way ANOVA. * p < 0.05; ** p < 0.01; *** p < 0.001; ns, not significant.
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    Image Search Results


    Neutrophil extracellular traps (NETs)-mediated intraplaque hemorrhage drives rapid plaque progression in nonculprit lesions following myocardial infarction (MI), potentially via macrophage ferroptosis. (A) Representative images of intraplaque CD31, TER119 immunofluorescence staining (scale bar = 100 μm), and Prussian blue staining (scale bar = 50 μm) in brachiocephalic artery (BCA) lesions from the sham and MI groups at 4 weeks postsurgery. (B and C) Quantification of TER119 + and CD31 + area relative to plaque area in (A) ( n = 6 per group). (D) Quantification of the Prussian blue positive area in (A) ( n = 6 per group). (E) Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showing enrichment of the ferroptosis signaling pathway. (F) Quantification of the mean fluorescence intensity (MFI) of Bodipy C11 in RAW264.7 cells across the indicated groups ( n = 3 per group). (G) Quantification of PI-positive RAW264.7 cells across the indicated groups ( n = 3 per group). (H and I) Immunoblotting and quantification of the relative protein levels of SLC7A11, HMOX1, FTH1, and GPX4 in RAW264.7 cells across the indicated groups ( n = 3 per group). (J) Representative images and quantification of 4-hydroxynonenal (4-HNE) immunofluorescence staining in BCA lesions from the sham and MI groups at 4 weeks postsurgery (scale bar = 100 μm, n = 6 per group). (K) Representative images and quantification of 4-HNE immunofluorescence staining in BCA lesions from the control and deoxyribonuclease I (DNase I) groups at 4 weeks post-MI (scale bar = 100 μm, n = 6 per group). Statistical analyses were performed using unpaired Student t test (B, C, D, J, and K) and 1-way analysis of variance (ANOVA) with Bonferroni posttest (F, G, and I).

    Journal: Research

    Article Title: Neutrophil Extracellular Traps-Mediated Intraplaque Angiogenesis and Microvascular Permeability Promote Rapid Plaque Progression following Myocardial Infarction

    doi: 10.34133/research.1451

    Figure Lengend Snippet: Neutrophil extracellular traps (NETs)-mediated intraplaque hemorrhage drives rapid plaque progression in nonculprit lesions following myocardial infarction (MI), potentially via macrophage ferroptosis. (A) Representative images of intraplaque CD31, TER119 immunofluorescence staining (scale bar = 100 μm), and Prussian blue staining (scale bar = 50 μm) in brachiocephalic artery (BCA) lesions from the sham and MI groups at 4 weeks postsurgery. (B and C) Quantification of TER119 + and CD31 + area relative to plaque area in (A) ( n = 6 per group). (D) Quantification of the Prussian blue positive area in (A) ( n = 6 per group). (E) Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis showing enrichment of the ferroptosis signaling pathway. (F) Quantification of the mean fluorescence intensity (MFI) of Bodipy C11 in RAW264.7 cells across the indicated groups ( n = 3 per group). (G) Quantification of PI-positive RAW264.7 cells across the indicated groups ( n = 3 per group). (H and I) Immunoblotting and quantification of the relative protein levels of SLC7A11, HMOX1, FTH1, and GPX4 in RAW264.7 cells across the indicated groups ( n = 3 per group). (J) Representative images and quantification of 4-hydroxynonenal (4-HNE) immunofluorescence staining in BCA lesions from the sham and MI groups at 4 weeks postsurgery (scale bar = 100 μm, n = 6 per group). (K) Representative images and quantification of 4-HNE immunofluorescence staining in BCA lesions from the control and deoxyribonuclease I (DNase I) groups at 4 weeks post-MI (scale bar = 100 μm, n = 6 per group). Statistical analyses were performed using unpaired Student t test (B, C, D, J, and K) and 1-way analysis of variance (ANOVA) with Bonferroni posttest (F, G, and I).

    Article Snippet: To inhibit ferroptosis, mice were treated with intraperitoneal injections of Fer-1 (5 mg/kg/d; MCE, HY-100579) for 4 weeks following MI, with the initial dose administered 8 h prior to MI induction [ ].

    Techniques: Immunofluorescence, Staining, Analysis, Fluorescence, Western Blot, Control

    Ferroptosis-specific validation of GINS1 knockdown-induced cell death in neuroblastoma cells. (A) Western blot analysis of GPX4 and SLC7A11 protein levels in SH-SY5Y and SK-N-SH cells transfected with shNC, shGINS1-1, and shGINS1-2. (B-C) CCK-8 assay assessing cell viability in SH-SY5Y (B) and SK-N-SH (C) cells transfected with shNC or shGINS1, treated with erastin (5 μM), RSL3 (1 μM), and/or ferrostatin-1 (Fer-1, 1 μM) as indicated. (D-E) Glutathione (GSH) levels in SH-SY5Y (D) and SK-N-SH (E) cells under the indicated conditions. (F-G) Intracellular ROS levels in SH-SY5Y (F) and SK-N-SH (G) cells under the indicated conditions. (H-I) Malondialdehyde (MDA) content in SH-SY5Y (H) and SK-N-SH (I) cells under the indicated conditions. (J-K) Fe 2+ levels in SH-SY5Y (J) and SK-N-SH (K) cells under the indicated conditions. Data are presented as mean ± SD from three independent experiments. Statistical significance was determined using one-way ANOVA. * p < 0.05; ** p < 0.01; *** p < 0.001; ns, not significant.

    Journal: Molecular & Cellular Oncology

    Article Title: GINS1 suppresses ferroptosis by inhibiting the Hippo pathway in neuroblastoma

    doi: 10.1080/23723556.2026.2715868

    Figure Lengend Snippet: Ferroptosis-specific validation of GINS1 knockdown-induced cell death in neuroblastoma cells. (A) Western blot analysis of GPX4 and SLC7A11 protein levels in SH-SY5Y and SK-N-SH cells transfected with shNC, shGINS1-1, and shGINS1-2. (B-C) CCK-8 assay assessing cell viability in SH-SY5Y (B) and SK-N-SH (C) cells transfected with shNC or shGINS1, treated with erastin (5 μM), RSL3 (1 μM), and/or ferrostatin-1 (Fer-1, 1 μM) as indicated. (D-E) Glutathione (GSH) levels in SH-SY5Y (D) and SK-N-SH (E) cells under the indicated conditions. (F-G) Intracellular ROS levels in SH-SY5Y (F) and SK-N-SH (G) cells under the indicated conditions. (H-I) Malondialdehyde (MDA) content in SH-SY5Y (H) and SK-N-SH (I) cells under the indicated conditions. (J-K) Fe 2+ levels in SH-SY5Y (J) and SK-N-SH (K) cells under the indicated conditions. Data are presented as mean ± SD from three independent experiments. Statistical significance was determined using one-way ANOVA. * p < 0.05; ** p < 0.01; *** p < 0.001; ns, not significant.

    Article Snippet: For ferroptosis induction and inhibition experiments, cells were treated with erastin (5 μM, Selleck, S7242), RSL3 (1 μM, Selleck, S8155), or ferrostatin-1 (Fer-1, 1 μM, Selleck, S7243) for 24 hours.

    Techniques: Biomarker Discovery, Knockdown, Western Blot, Analysis, Transfection, CCK-8 Assay