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z vad fmk  (MedChemExpress)


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    MedChemExpress z vad fmk
    Z Vad Fmk, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 99/100, based on 1014 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/z+vad+fmk/Z-VAD-FMK/pm42595780-48-35-37
    Average 99 stars, based on 1014 article reviews
    z vad fmk - by Bioz Stars, 2026-10
    99/100 stars

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    other:

    Article Title: Bisphenol A induces ototoxic injury by ferroptosis pathway: integrated analysis of network toxicology, RNA-sequencing and experimental validation
    Article Snippet: Liproxstatin-1 (HY-12726), Ferrostatin-1 (HY-100579) and Z-VAD-FMK (HY-16658B) were purchased from MedChemExpress.

    Activity Assay:

    Article Title: Andrographolide alleviates type 2 diabetic nephropathy through suppressing PI3K/AKT1/RRM2-triggered oxeiptosis
    Article Snippet: To activate or inhibit the PI3K/AKT1 signaling pathway, MDCK cells were treated with Recilisib (HY-101625, MCE, China) or Miltefosine (HY-13685, MCE, China), respectively. .. Moreover, Z-VAD-FMK (Z-VAD; HY-16658B, MCE, China) was used to inhibit pan-caspase activity, Necrostatin-1 (Nec-1; HY-15760, MCE, China) to inhibit necroptosis, and Hydroxyurea (HU; HY-B0313, MCE, China) to inhibit RRM2 enzymatic activity. ..



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    Induction of ferroptosis-like phenotype by JIB-04 drives synergism with VEN. (A-C) OCI-AML3 and MOLM-1 cells were treated with 40nM/50nM JIB-04, 8mM/4mM NAC <t>(antioxidant),</t> <t>25μM</t> <t>Z-VAD-FMK</t> <t>(caspase</t> inhibitor), or the combination JIB-04+NAC and JIB-04+Z-VAD-FMK for up to 48 hours (mean ± SD; n = 3). Cells were stained for ferroptosis markers and analyzed by flow cytometry. JIB-04 treatment group was normalized to the DMSO group. Statistical significance was calculated by 2-way ANOVA with Tukey multiple-comparison test. (A) MitoSOX red for mitochondrial ROS at 24 hours. (B) MitoPerOx for mitochondrial lipid peroxidation at 24 hours. (C) BODIPY C11 for lipid peroxidation at 48 hours. (D) HMOX1 protein levels were visualized by immunoblotting in AML cell lines treated with DMSO, JIB-04, or JIB-04+NAC for 24 hours. (E-F) Quantification of apoptosis by annexin V/PI staining in OCI-AML3 and MOLM-13 cells after treatment with 40nM/50nM JIB-04, 1μM/1nM VEN, 8mM/4mM NAC, or the indicated drug combinations. Statistical significance was calculated by ordinary 1-way ANOVA with Tukey multiple-comparison test. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001. Z-VAD, Z-VAD-FMK.
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    Induction of ferroptosis-like phenotype by JIB-04 drives synergism with VEN. (A-C) OCI-AML3 and MOLM-1 cells were treated with 40nM/50nM JIB-04, 8mM/4mM NAC <t>(antioxidant),</t> <t>25μM</t> <t>Z-VAD-FMK</t> <t>(caspase</t> inhibitor), or the combination JIB-04+NAC and JIB-04+Z-VAD-FMK for up to 48 hours (mean ± SD; n = 3). Cells were stained for ferroptosis markers and analyzed by flow cytometry. JIB-04 treatment group was normalized to the DMSO group. Statistical significance was calculated by 2-way ANOVA with Tukey multiple-comparison test. (A) MitoSOX red for mitochondrial ROS at 24 hours. (B) MitoPerOx for mitochondrial lipid peroxidation at 24 hours. (C) BODIPY C11 for lipid peroxidation at 48 hours. (D) HMOX1 protein levels were visualized by immunoblotting in AML cell lines treated with DMSO, JIB-04, or JIB-04+NAC for 24 hours. (E-F) Quantification of apoptosis by annexin V/PI staining in OCI-AML3 and MOLM-13 cells after treatment with 40nM/50nM JIB-04, 1μM/1nM VEN, 8mM/4mM NAC, or the indicated drug combinations. Statistical significance was calculated by ordinary 1-way ANOVA with Tukey multiple-comparison test. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001. Z-VAD, Z-VAD-FMK.
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    Induction of ferroptosis-like phenotype by JIB-04 drives synergism with VEN. (A-C) OCI-AML3 and MOLM-1 cells were treated with 40nM/50nM JIB-04, 8mM/4mM NAC <t>(antioxidant),</t> <t>25μM</t> <t>Z-VAD-FMK</t> <t>(caspase</t> inhibitor), or the combination JIB-04+NAC and JIB-04+Z-VAD-FMK for up to 48 hours (mean ± SD; n = 3). Cells were stained for ferroptosis markers and analyzed by flow cytometry. JIB-04 treatment group was normalized to the DMSO group. Statistical significance was calculated by 2-way ANOVA with Tukey multiple-comparison test. (A) MitoSOX red for mitochondrial ROS at 24 hours. (B) MitoPerOx for mitochondrial lipid peroxidation at 24 hours. (C) BODIPY C11 for lipid peroxidation at 48 hours. (D) HMOX1 protein levels were visualized by immunoblotting in AML cell lines treated with DMSO, JIB-04, or JIB-04+NAC for 24 hours. (E-F) Quantification of apoptosis by annexin V/PI staining in OCI-AML3 and MOLM-13 cells after treatment with 40nM/50nM JIB-04, 1μM/1nM VEN, 8mM/4mM NAC, or the indicated drug combinations. Statistical significance was calculated by ordinary 1-way ANOVA with Tukey multiple-comparison test. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001. Z-VAD, Z-VAD-FMK.
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    Induction of ferroptosis-like phenotype by JIB-04 drives synergism with VEN. (A-C) OCI-AML3 and MOLM-1 cells were treated with 40nM/50nM JIB-04, 8mM/4mM NAC (antioxidant), 25μM Z-VAD-FMK (caspase inhibitor), or the combination JIB-04+NAC and JIB-04+Z-VAD-FMK for up to 48 hours (mean ± SD; n = 3). Cells were stained for ferroptosis markers and analyzed by flow cytometry. JIB-04 treatment group was normalized to the DMSO group. Statistical significance was calculated by 2-way ANOVA with Tukey multiple-comparison test. (A) MitoSOX red for mitochondrial ROS at 24 hours. (B) MitoPerOx for mitochondrial lipid peroxidation at 24 hours. (C) BODIPY C11 for lipid peroxidation at 48 hours. (D) HMOX1 protein levels were visualized by immunoblotting in AML cell lines treated with DMSO, JIB-04, or JIB-04+NAC for 24 hours. (E-F) Quantification of apoptosis by annexin V/PI staining in OCI-AML3 and MOLM-13 cells after treatment with 40nM/50nM JIB-04, 1μM/1nM VEN, 8mM/4mM NAC, or the indicated drug combinations. Statistical significance was calculated by ordinary 1-way ANOVA with Tukey multiple-comparison test. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001. Z-VAD, Z-VAD-FMK.

    Journal: Blood Neoplasia

    Article Title: The KDM-family inhibitor JIB-04 sensitizes AML cells to venetoclax by inducing a ferroptosis-like phenotype

    doi: 10.1016/j.bneo.2026.100236

    Figure Lengend Snippet: Induction of ferroptosis-like phenotype by JIB-04 drives synergism with VEN. (A-C) OCI-AML3 and MOLM-1 cells were treated with 40nM/50nM JIB-04, 8mM/4mM NAC (antioxidant), 25μM Z-VAD-FMK (caspase inhibitor), or the combination JIB-04+NAC and JIB-04+Z-VAD-FMK for up to 48 hours (mean ± SD; n = 3). Cells were stained for ferroptosis markers and analyzed by flow cytometry. JIB-04 treatment group was normalized to the DMSO group. Statistical significance was calculated by 2-way ANOVA with Tukey multiple-comparison test. (A) MitoSOX red for mitochondrial ROS at 24 hours. (B) MitoPerOx for mitochondrial lipid peroxidation at 24 hours. (C) BODIPY C11 for lipid peroxidation at 48 hours. (D) HMOX1 protein levels were visualized by immunoblotting in AML cell lines treated with DMSO, JIB-04, or JIB-04+NAC for 24 hours. (E-F) Quantification of apoptosis by annexin V/PI staining in OCI-AML3 and MOLM-13 cells after treatment with 40nM/50nM JIB-04, 1μM/1nM VEN, 8mM/4mM NAC, or the indicated drug combinations. Statistical significance was calculated by ordinary 1-way ANOVA with Tukey multiple-comparison test. ∗ P < .05; ∗∗ P < .01; ∗∗∗ P < .001; ∗∗∗∗ P < .0001. Z-VAD, Z-VAD-FMK.

    Article Snippet: AML cells were treated with JIB-04, the antioxidant NAC, the pan caspase inhibitor Z-VAD-FMK (MedChemExpress), or indicated combinations for up to 48 hours.

    Techniques: Staining, Flow Cytometry, Comparison, Western Blot