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necrostatin 1  (MedChemExpress)


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    MedChemExpress necrostatin 1
    Necrostatin 1, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 786 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/necrostatin+1/Necrostatin-1/pmc13633971-361-12-25
    Average 99 stars, based on 786 article reviews
    necrostatin 1 - by Bioz Stars, 2026-10
    99/100 stars

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    Article Title: Epinecidin-1 Induces Distinct Oncosis and Pyroptosis Responses in Osteosarcoma Cells and Enhances Methotrexate-associated Cytotoxicity.
    Article Snippet: Necrostatin-1 (Nec-1, Cat. No. HY-15760), Rhod2-AM (Cat. No. HY-D0989), Fluo4AM (Cat. No. HY-101896), MitoTEMPO (MitoT, Cat. No. HY112879), VX-765 (Cat. No. HY-13205), DiBAC4 (3) (Cat. No. HY-101892), pifithrin-α (Cat. No. HY-15484), and methotrexate (MTX, Cat. No. HY-14519) were purchased from MedChemExpress (United States).

    Article Title: PCK2 Inhibition Reverses Cisplatin Resistance of Non‐Small Cell Lung Cancer by Triggering Ferroptosis
    Article Snippet: Cisplatin (DDP), Necrostatin‐1, Z‐VAD‐FMK, Ferrostatin‐1, and Chloroquine were purchased from MedChemexpress (USA).

    Article Title: Diallyl trisulfide activates Nrf2 by promoting S-sulfhydration of Keap1 to attenuate acute hypobaric hypoxia-induced lung injury.
    Article Snippet: Background: Acute lung injury triggered by rapid ascent to high altitude represents a significant clinical challenge in high-altitude medicine.. Its pathological progression is primarily driven by excessive oxidative stress and the subsequent induction of ferroptosis.. Purpose: This study investigated the therapeutic potential of Diallyl Trisulfide (DATS), a natural sulfur-containing compound from garlic, in mitigating Acute lung injury induced by acute hypobaric hypoxia.

    Article Title: Targeting KIF11 degradation: Oxypeucedanin inhibits lung adenocarcinoma progression by disrupting the MCM2-CDK1 signaling pathway.
    Article Snippet: Background and purpose: Lung adenocarcinoma (LUAD) is the most prevalent subtype of lung cancer and a leading cause of cancer-related mortality worldwide.. Current targeted therapies are limited by acquired resistance, highlighting the urgent need for novel therapeutic agents and targets.. The aim of this study is to investigate the anti-tumor efficacy of oxypeucedanin (OPD) against LUAD and elucidate its underlying molecular mechanism.

    Article Title: Purine salvage pathway protects CD8 + T cells from metabolic stress.
    Article Snippet: Masaki Tajima , He Hao, Baihao Zhang , Yuta Matsuoka , Kazuhiro Sonomura, Koshi Imami , Yosuke Isobe, Rae Maeda, Yu-Hsien Lin , Akihiro Shimba, Ryoma Kato, Pedro Henrique Costa Cruz, Sayaka Washizu, Yosuke Ikejiri, Akiyo Morinibu, Clive Steven Barker, Jun Seita , Yibo Wu, Satomi Ito, Seiko Narushima, Rei Nakano , Mikako Maruya, Wakana Kobayashi, Sai Shanmukha Priya Narayanan , Jumana Shaheen , Hiroyuki Neyama, Ken-ichi Yamada , Makoto Arita , Yuki Sugiura & S i d o n ia F a g a r a s an 1,3

    Article Title: Ru3: a novel ruthenium-based compound overcomes cisplatin resistance in non-small cell lung cancer via the E2F2-IGFBP3-GPX4 pathway
    Article Snippet: NAC (HY-B0215), Mito-TEMPO (HY-112879), HLM006474 (HY-16667), Z-VAD-FAK (HY-16658B), irinotecan (HY-13001), docetaxel (HY-13065), Necrostatin-1 (HY-15760), NLRP3-IN-78 (HY-144623), 4-PBA (HY-100457), Fer-1 (HY-100579), RSL3 (HY-100218) were purchased from MCE.

    Article Title: Yunnan Baiyao inhibits EBV-positive nasopharyngeal carcinoma via ferritinophagy-dependent ferroptosis.
    Article Snippet: Z-VAD(OMe)-FMK (Z-VAD), necrostatin− 1 (Nec− 1), liproxstatin− 1 (Lip− 1), deferoxamine mesylate (DFO), erastin, RSL3, ammonium iron(III) citrate (FAC), Hoechst 33342, Q-VD-OPh, and bafilomycin A1 (BAF) were purchased from MedChemExpress (MCE, Monmouth Junction, NJ, USA).

    Activity Assay:

    Article Title: ALOX12 suppresses colon cancer progression by promoting p53-mediated ferroptosis through upregulating ROS-induced stress
    Article Snippet: TBH (B802372; Macklin, Shanghai, China) served as ROS generator while Nutlin-3 (HY-50696; MCE, Shanghai, China) was used to activate p53. .. Specific cell death inhibitors and ALOX12 activity inhibitor used in our work were as follows: 3-methyladenine (3-MA, autophagy inhibitor) (HY-19312; MCE, Shanghai, China), Z-VAD-FMK (Z-VAD, apoptosis inhibitor) (HY-16658B; MCE, Shanghai, China), necrostatin-1 (Nec-1, necroptosis inhibitor) (HY-15760; MCE, Shanghai, China), ferrostatin-1 (Fer-1, ferroptosis inhibitor) (SJ-MX0049; SparkJade, Shandong, China), liproxstatin-1 (Lip-1, ferroptosis inhibitor) (HY-12726; MCE, Shanghai, China) and ML355 (ALOX12 inhibitor) (HY-12341; MCE, Shanghai, China). ..



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    ( A ) Volcano plot of differentially expressed genes (DEGs) in MFC cells (Control versus DDP + Zn 2+ ). ( B ) KEGG pathway enrichment of DEGs. ( C ) Quantification of extracellular dsDNA. ( D ) JC-1 staining assessed by fluorescence microscopy and flow cytometry. ( E ) γ-H2AX immunofluorescence staining. Scale bar, 20 μm. ( F ) ASC speck colocalization with AIM2, Caspase-1, Caspase-8, and RIPK1. Scale bars, 5 μm (overview) and 1 μm (enlarged). ( G ) Western blot analysis of necroptosis markers (RIPK1, p-RIPK1, MLKL, and p-MLKL) and PANoptosis-related proteins (AIM2 and ZBP1). ( H ) Western blot analysis of apoptosis executors (Caspase-8, Caspase-3, and cleaved forms). ( I ) Western blot analysis of pyroptosis markers (Caspase-1, GSDMD, and cleaved forms). ( J ) Cell viability after DDP + Zn 2+ combined with VX-765, Ac-DEVD-CHO, or <t>Nec-1.</t> ( K ) PANoptosis-related proteins in si AIM2 cells. ( L and M ) cGAS activity (L) and expression (M) under Zn 2+ treatment. ( N ) Violin plot of cGAS expression. ( O ) Western blot analysis of STING pathway (STING, p-STING, TBK1, p-TBK1, IRF3, and p-IRF3). ( P ) CIBERSORT analysis of immune cell infiltration. ( Q ) BMDC maturation (CD80 + CD86 + ) after different treatments. ( R ) Schematic of the DDP + Zn 2+ –induced ICD. Data in (C), (J), and (L) are mean ± SD. Statistical analysis for (C), (J), (L), (N), and (P) used a two-tailed unpaired Student’s t test. (R) was created in BioRender. Fei, G. (2026) https://BioRender.com/8ri399r . * P < 0.05.
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    Direct validation of SLC7A11 expression and exclusionary pharmacological assessment of cell death in PCOS granulosa cells (A) Representative immunofluorescence (IF) staining images showing the expression and localization of SLC7A11 (red) in the ovary of a DHEA-induced PCOS mouse. Nuclei were counterstained with DAPI (blue). White boxes highlight the specific enrichment of SLC7A11 in the granulosa cell layer of the follicles. Magnification: 100×. Images are representative of n = 6 individual mice per experimental group. Scale bars, 100 μm. (B) western blot analysis of SLC7A11 protein expression levels in primary mouse granulosa cells (mGCs) isolated from three independent DHEA-induced PCOS mice (DHEA 1#, 2#, 3#). Tubulin was used as the internal loading control. (C) Flow cytometry analysis (upper panels) and corresponding quantitative bar graph (lower panel) of the cell death rate (PI-positive percentage). LRPPRC-knockdown KGN cells (Sh LRPPRC) were cultured under glucose-sufficient (+Glc) or glucose-deprived (-Glc) conditions, and subsequently treated with or without specific cell death inhibitors: DFO (ferroptosis inhibitor), Z-VAD-FMK (pan-caspase apoptosis inhibitor), <t>or</t> <t>Nec-1</t> (necroptosis inhibitor). Data are presented as the mean ± SD of n = 3 independent biological replicates. ∗∗∗ p < 0.001 compared with the Sh LRPPRC+Glc group; ∗ p < 0.05, ns = not significant compared with the Sh LRPPRC-Glc group.
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    MedChemExpress necrostatin-1
    Direct validation of SLC7A11 expression and exclusionary pharmacological assessment of cell death in PCOS granulosa cells (A) Representative immunofluorescence (IF) staining images showing the expression and localization of SLC7A11 (red) in the ovary of a DHEA-induced PCOS mouse. Nuclei were counterstained with DAPI (blue). White boxes highlight the specific enrichment of SLC7A11 in the granulosa cell layer of the follicles. Magnification: 100×. Images are representative of n = 6 individual mice per experimental group. Scale bars, 100 μm. (B) western blot analysis of SLC7A11 protein expression levels in primary mouse granulosa cells (mGCs) isolated from three independent DHEA-induced PCOS mice (DHEA 1#, 2#, 3#). Tubulin was used as the internal loading control. (C) Flow cytometry analysis (upper panels) and corresponding quantitative bar graph (lower panel) of the cell death rate (PI-positive percentage). LRPPRC-knockdown KGN cells (Sh LRPPRC) were cultured under glucose-sufficient (+Glc) or glucose-deprived (-Glc) conditions, and subsequently treated with or without specific cell death inhibitors: DFO (ferroptosis inhibitor), Z-VAD-FMK (pan-caspase apoptosis inhibitor), <t>or</t> <t>Nec-1</t> (necroptosis inhibitor). Data are presented as the mean ± SD of n = 3 independent biological replicates. ∗∗∗ p < 0.001 compared with the Sh LRPPRC+Glc group; ∗ p < 0.05, ns = not significant compared with the Sh LRPPRC-Glc group.
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    Direct validation of SLC7A11 expression and exclusionary pharmacological assessment of cell death in PCOS granulosa cells (A) Representative immunofluorescence (IF) staining images showing the expression and localization of SLC7A11 (red) in the ovary of a DHEA-induced PCOS mouse. Nuclei were counterstained with DAPI (blue). White boxes highlight the specific enrichment of SLC7A11 in the granulosa cell layer of the follicles. Magnification: 100×. Images are representative of n = 6 individual mice per experimental group. Scale bars, 100 μm. (B) western blot analysis of SLC7A11 protein expression levels in primary mouse granulosa cells (mGCs) isolated from three independent DHEA-induced PCOS mice (DHEA 1#, 2#, 3#). Tubulin was used as the internal loading control. (C) Flow cytometry analysis (upper panels) and corresponding quantitative bar graph (lower panel) of the cell death rate (PI-positive percentage). LRPPRC-knockdown KGN cells (Sh LRPPRC) were cultured under glucose-sufficient (+Glc) or glucose-deprived (-Glc) conditions, and subsequently treated with or without specific cell death inhibitors: DFO (ferroptosis inhibitor), Z-VAD-FMK (pan-caspase apoptosis inhibitor), <t>or</t> <t>Nec-1</t> (necroptosis inhibitor). Data are presented as the mean ± SD of n = 3 independent biological replicates. ∗∗∗ p < 0.001 compared with the Sh LRPPRC+Glc group; ∗ p < 0.05, ns = not significant compared with the Sh LRPPRC-Glc group.
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    ( A ) Volcano plot of differentially expressed genes (DEGs) in MFC cells (Control versus DDP + Zn 2+ ). ( B ) KEGG pathway enrichment of DEGs. ( C ) Quantification of extracellular dsDNA. ( D ) JC-1 staining assessed by fluorescence microscopy and flow cytometry. ( E ) γ-H2AX immunofluorescence staining. Scale bar, 20 μm. ( F ) ASC speck colocalization with AIM2, Caspase-1, Caspase-8, and RIPK1. Scale bars, 5 μm (overview) and 1 μm (enlarged). ( G ) Western blot analysis of necroptosis markers (RIPK1, p-RIPK1, MLKL, and p-MLKL) and PANoptosis-related proteins (AIM2 and ZBP1). ( H ) Western blot analysis of apoptosis executors (Caspase-8, Caspase-3, and cleaved forms). ( I ) Western blot analysis of pyroptosis markers (Caspase-1, GSDMD, and cleaved forms). ( J ) Cell viability after DDP + Zn 2+ combined with VX-765, Ac-DEVD-CHO, or Nec-1. ( K ) PANoptosis-related proteins in si AIM2 cells. ( L and M ) cGAS activity (L) and expression (M) under Zn 2+ treatment. ( N ) Violin plot of cGAS expression. ( O ) Western blot analysis of STING pathway (STING, p-STING, TBK1, p-TBK1, IRF3, and p-IRF3). ( P ) CIBERSORT analysis of immune cell infiltration. ( Q ) BMDC maturation (CD80 + CD86 + ) after different treatments. ( R ) Schematic of the DDP + Zn 2+ –induced ICD. Data in (C), (J), and (L) are mean ± SD. Statistical analysis for (C), (J), (L), (N), and (P) used a two-tailed unpaired Student’s t test. (R) was created in BioRender. Fei, G. (2026) https://BioRender.com/8ri399r . * P < 0.05.

    Journal: Science Advances

    Article Title: Chemo-metallo nanodrivers for spatiotemporally controlled in situ vaccination

    doi: 10.1126/sciadv.aee4577

    Figure Lengend Snippet: ( A ) Volcano plot of differentially expressed genes (DEGs) in MFC cells (Control versus DDP + Zn 2+ ). ( B ) KEGG pathway enrichment of DEGs. ( C ) Quantification of extracellular dsDNA. ( D ) JC-1 staining assessed by fluorescence microscopy and flow cytometry. ( E ) γ-H2AX immunofluorescence staining. Scale bar, 20 μm. ( F ) ASC speck colocalization with AIM2, Caspase-1, Caspase-8, and RIPK1. Scale bars, 5 μm (overview) and 1 μm (enlarged). ( G ) Western blot analysis of necroptosis markers (RIPK1, p-RIPK1, MLKL, and p-MLKL) and PANoptosis-related proteins (AIM2 and ZBP1). ( H ) Western blot analysis of apoptosis executors (Caspase-8, Caspase-3, and cleaved forms). ( I ) Western blot analysis of pyroptosis markers (Caspase-1, GSDMD, and cleaved forms). ( J ) Cell viability after DDP + Zn 2+ combined with VX-765, Ac-DEVD-CHO, or Nec-1. ( K ) PANoptosis-related proteins in si AIM2 cells. ( L and M ) cGAS activity (L) and expression (M) under Zn 2+ treatment. ( N ) Violin plot of cGAS expression. ( O ) Western blot analysis of STING pathway (STING, p-STING, TBK1, p-TBK1, IRF3, and p-IRF3). ( P ) CIBERSORT analysis of immune cell infiltration. ( Q ) BMDC maturation (CD80 + CD86 + ) after different treatments. ( R ) Schematic of the DDP + Zn 2+ –induced ICD. Data in (C), (J), and (L) are mean ± SD. Statistical analysis for (C), (J), (L), (N), and (P) used a two-tailed unpaired Student’s t test. (R) was created in BioRender. Fei, G. (2026) https://BioRender.com/8ri399r . * P < 0.05.

    Article Snippet: The pharmacological inhibitors VX-765, Ac-DEVD-CHO, and Nec-1 were purchased from MedChemExpress (USA).

    Techniques: Control, Staining, Fluorescence, Microscopy, Flow Cytometry, Immunofluorescence, Western Blot, Analysis, Activity Assay, Expressing, Immune Cell, Two Tailed Test

    Direct validation of SLC7A11 expression and exclusionary pharmacological assessment of cell death in PCOS granulosa cells (A) Representative immunofluorescence (IF) staining images showing the expression and localization of SLC7A11 (red) in the ovary of a DHEA-induced PCOS mouse. Nuclei were counterstained with DAPI (blue). White boxes highlight the specific enrichment of SLC7A11 in the granulosa cell layer of the follicles. Magnification: 100×. Images are representative of n = 6 individual mice per experimental group. Scale bars, 100 μm. (B) western blot analysis of SLC7A11 protein expression levels in primary mouse granulosa cells (mGCs) isolated from three independent DHEA-induced PCOS mice (DHEA 1#, 2#, 3#). Tubulin was used as the internal loading control. (C) Flow cytometry analysis (upper panels) and corresponding quantitative bar graph (lower panel) of the cell death rate (PI-positive percentage). LRPPRC-knockdown KGN cells (Sh LRPPRC) were cultured under glucose-sufficient (+Glc) or glucose-deprived (-Glc) conditions, and subsequently treated with or without specific cell death inhibitors: DFO (ferroptosis inhibitor), Z-VAD-FMK (pan-caspase apoptosis inhibitor), or Nec-1 (necroptosis inhibitor). Data are presented as the mean ± SD of n = 3 independent biological replicates. ∗∗∗ p < 0.001 compared with the Sh LRPPRC+Glc group; ∗ p < 0.05, ns = not significant compared with the Sh LRPPRC-Glc group.

    Journal: iScience

    Article Title: Disulfidptosis in PCOS pathogenesis: Multi-omics identification of LRPPRC as a diagnostic biomarker and therapeutic target

    doi: 10.1016/j.isci.2026.116561

    Figure Lengend Snippet: Direct validation of SLC7A11 expression and exclusionary pharmacological assessment of cell death in PCOS granulosa cells (A) Representative immunofluorescence (IF) staining images showing the expression and localization of SLC7A11 (red) in the ovary of a DHEA-induced PCOS mouse. Nuclei were counterstained with DAPI (blue). White boxes highlight the specific enrichment of SLC7A11 in the granulosa cell layer of the follicles. Magnification: 100×. Images are representative of n = 6 individual mice per experimental group. Scale bars, 100 μm. (B) western blot analysis of SLC7A11 protein expression levels in primary mouse granulosa cells (mGCs) isolated from three independent DHEA-induced PCOS mice (DHEA 1#, 2#, 3#). Tubulin was used as the internal loading control. (C) Flow cytometry analysis (upper panels) and corresponding quantitative bar graph (lower panel) of the cell death rate (PI-positive percentage). LRPPRC-knockdown KGN cells (Sh LRPPRC) were cultured under glucose-sufficient (+Glc) or glucose-deprived (-Glc) conditions, and subsequently treated with or without specific cell death inhibitors: DFO (ferroptosis inhibitor), Z-VAD-FMK (pan-caspase apoptosis inhibitor), or Nec-1 (necroptosis inhibitor). Data are presented as the mean ± SD of n = 3 independent biological replicates. ∗∗∗ p < 0.001 compared with the Sh LRPPRC+Glc group; ∗ p < 0.05, ns = not significant compared with the Sh LRPPRC-Glc group.

    Article Snippet: Necrostatin-1 (Nec-1) , MedChemExpress , Cat# HY-15760.

    Techniques: Biomarker Discovery, Expressing, Immunofluorescence, Staining, Western Blot, Isolation, Control, Flow Cytometry, Knockdown, Cell Culture