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eprenetapopt apr 246  (MedChemExpress)


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    MedChemExpress eprenetapopt apr 246
    Pharmacological and genetic inhibition of CEBPA synergizes with VEN-induced apoptosis in TP53mut/mut-like AMLs (A) MOLM13 (VEN-sensitive) and KG1 (VEN-resistant) cells were treated for 72 h with increasing concentrations of VEN and GFC. Synergy was determined by Bliss coefficient (ZIP score >10 indicates synergism). (B and C) Drug-induced apoptosis (B) and viable cell counts (C) in MOLM13 shCEBPA/shScr cells treated with VEN alone or in combination with GFC (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D and E) Apoptosis was detected by flow cytometry in gated human CD45 dim CD34 + (or CD117 + cells for CD34 − AMLs) of ex vivo -treated AML samples categorized as TP53 mut-like ( n = 8) (D) and TP53 mut ( n = 9) (E) in a co-culture system using an FITC-annexin V/DAPI staining method. Cells were treated with vehicle, VEN (100 and 500 nM), and VEN+Aza (VEN 100 nM + 5′ Aza 1.5 μM), in the presence or absence of GFC (30 μM) for 72 h. Bar graphs represent the mean ± SEM of all the independent patients screened; each point represents a patient. (F and G) Mitochondrial membrane potential (F) (measured by TMRE staining, n = 18) and total cytoplasmatic ROS levels (G) (measured using the CellROX Red probe, via flow cytometry, n = 6) for the data included in (D) and (E). TP53 mut AMLs are depicted in red, and TP53 mut-like AMLs are depicted in black. <t>APR-246,</t> eprenetapopt. Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.
    Eprenetapopt Apr 246, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 94/100, based on 18 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    Average 94 stars, based on 18 article reviews
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    1) Product Images from "ΔNp73 isoform defines a TP53 -mutant-like poor-risk subgroup of acute myeloid leukemia"

    Article Title: ΔNp73 isoform defines a TP53 -mutant-like poor-risk subgroup of acute myeloid leukemia

    Journal: Cell Reports Medicine

    doi: 10.1016/j.xcrm.2025.102540

    Pharmacological and genetic inhibition of CEBPA synergizes with VEN-induced apoptosis in TP53mut/mut-like AMLs (A) MOLM13 (VEN-sensitive) and KG1 (VEN-resistant) cells were treated for 72 h with increasing concentrations of VEN and GFC. Synergy was determined by Bliss coefficient (ZIP score >10 indicates synergism). (B and C) Drug-induced apoptosis (B) and viable cell counts (C) in MOLM13 shCEBPA/shScr cells treated with VEN alone or in combination with GFC (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D and E) Apoptosis was detected by flow cytometry in gated human CD45 dim CD34 + (or CD117 + cells for CD34 − AMLs) of ex vivo -treated AML samples categorized as TP53 mut-like ( n = 8) (D) and TP53 mut ( n = 9) (E) in a co-culture system using an FITC-annexin V/DAPI staining method. Cells were treated with vehicle, VEN (100 and 500 nM), and VEN+Aza (VEN 100 nM + 5′ Aza 1.5 μM), in the presence or absence of GFC (30 μM) for 72 h. Bar graphs represent the mean ± SEM of all the independent patients screened; each point represents a patient. (F and G) Mitochondrial membrane potential (F) (measured by TMRE staining, n = 18) and total cytoplasmatic ROS levels (G) (measured using the CellROX Red probe, via flow cytometry, n = 6) for the data included in (D) and (E). TP53 mut AMLs are depicted in red, and TP53 mut-like AMLs are depicted in black. APR-246, eprenetapopt. Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.
    Figure Legend Snippet: Pharmacological and genetic inhibition of CEBPA synergizes with VEN-induced apoptosis in TP53mut/mut-like AMLs (A) MOLM13 (VEN-sensitive) and KG1 (VEN-resistant) cells were treated for 72 h with increasing concentrations of VEN and GFC. Synergy was determined by Bliss coefficient (ZIP score >10 indicates synergism). (B and C) Drug-induced apoptosis (B) and viable cell counts (C) in MOLM13 shCEBPA/shScr cells treated with VEN alone or in combination with GFC (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D and E) Apoptosis was detected by flow cytometry in gated human CD45 dim CD34 + (or CD117 + cells for CD34 − AMLs) of ex vivo -treated AML samples categorized as TP53 mut-like ( n = 8) (D) and TP53 mut ( n = 9) (E) in a co-culture system using an FITC-annexin V/DAPI staining method. Cells were treated with vehicle, VEN (100 and 500 nM), and VEN+Aza (VEN 100 nM + 5′ Aza 1.5 μM), in the presence or absence of GFC (30 μM) for 72 h. Bar graphs represent the mean ± SEM of all the independent patients screened; each point represents a patient. (F and G) Mitochondrial membrane potential (F) (measured by TMRE staining, n = 18) and total cytoplasmatic ROS levels (G) (measured using the CellROX Red probe, via flow cytometry, n = 6) for the data included in (D) and (E). TP53 mut AMLs are depicted in red, and TP53 mut-like AMLs are depicted in black. APR-246, eprenetapopt. Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.

    Techniques Used: Inhibition, Flow Cytometry, Ex Vivo, Co-Culture Assay, Staining, Membrane



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    Pharmacological and genetic inhibition of CEBPA synergizes with VEN-induced apoptosis in TP53mut/mut-like AMLs (A) MOLM13 (VEN-sensitive) and KG1 (VEN-resistant) cells were treated for 72 h with increasing concentrations of VEN and GFC. Synergy was determined by Bliss coefficient (ZIP score >10 indicates synergism). (B and C) Drug-induced apoptosis (B) and viable cell counts (C) in MOLM13 shCEBPA/shScr cells treated with VEN alone or in combination with GFC (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D and E) Apoptosis was detected by flow cytometry in gated human CD45 dim CD34 + (or CD117 + cells for CD34 − AMLs) of ex vivo -treated AML samples categorized as TP53 mut-like ( n = 8) (D) and TP53 mut ( n = 9) (E) in a co-culture system using an FITC-annexin V/DAPI staining method. Cells were treated with vehicle, VEN (100 and 500 nM), and VEN+Aza (VEN 100 nM + 5′ Aza 1.5 μM), in the presence or absence of GFC (30 μM) for 72 h. Bar graphs represent the mean ± SEM of all the independent patients screened; each point represents a patient. (F and G) Mitochondrial membrane potential (F) (measured by TMRE staining, n = 18) and total cytoplasmatic ROS levels (G) (measured using the CellROX Red probe, via flow cytometry, n = 6) for the data included in (D) and (E). TP53 mut AMLs are depicted in red, and TP53 mut-like AMLs are depicted in black. <t>APR-246,</t> eprenetapopt. Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.
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    Pharmacological and genetic inhibition of CEBPA synergizes with VEN-induced apoptosis in TP53mut/mut-like AMLs (A) MOLM13 (VEN-sensitive) and KG1 (VEN-resistant) cells were treated for 72 h with increasing concentrations of VEN and GFC. Synergy was determined by Bliss coefficient (ZIP score >10 indicates synergism). (B and C) Drug-induced apoptosis (B) and viable cell counts (C) in MOLM13 shCEBPA/shScr cells treated with VEN alone or in combination with GFC (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D and E) Apoptosis was detected by flow cytometry in gated human CD45 dim CD34 + (or CD117 + cells for CD34 − AMLs) of ex vivo -treated AML samples categorized as TP53 mut-like ( n = 8) (D) and TP53 mut ( n = 9) (E) in a co-culture system using an FITC-annexin V/DAPI staining method. Cells were treated with vehicle, VEN (100 and 500 nM), and VEN+Aza (VEN 100 nM + 5′ Aza 1.5 μM), in the presence or absence of GFC (30 μM) for 72 h. Bar graphs represent the mean ± SEM of all the independent patients screened; each point represents a patient. (F and G) Mitochondrial membrane potential (F) (measured by TMRE staining, n = 18) and total cytoplasmatic ROS levels (G) (measured using the CellROX Red probe, via flow cytometry, n = 6) for the data included in (D) and (E). TP53 mut AMLs are depicted in red, and TP53 mut-like AMLs are depicted in black. <t>APR-246,</t> eprenetapopt. Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.
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    Pharmacological and genetic inhibition of CEBPA synergizes with VEN-induced apoptosis in TP53mut/mut-like AMLs (A) MOLM13 (VEN-sensitive) and KG1 (VEN-resistant) cells were treated for 72 h with increasing concentrations of VEN and GFC. Synergy was determined by Bliss coefficient (ZIP score >10 indicates synergism). (B and C) Drug-induced apoptosis (B) and viable cell counts (C) in MOLM13 shCEBPA/shScr cells treated with VEN alone or in combination with GFC (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D and E) Apoptosis was detected by flow cytometry in gated human CD45 dim CD34 + (or CD117 + cells for CD34 − AMLs) of ex vivo -treated AML samples categorized as TP53 mut-like ( n = 8) (D) and TP53 mut ( n = 9) (E) in a co-culture system using an FITC-annexin V/DAPI staining method. Cells were treated with vehicle, VEN (100 and 500 nM), and VEN+Aza (VEN 100 nM + 5′ Aza 1.5 μM), in the presence or absence of GFC (30 μM) for 72 h. Bar graphs represent the mean ± SEM of all the independent patients screened; each point represents a patient. (F and G) Mitochondrial membrane potential (F) (measured by TMRE staining, n = 18) and total cytoplasmatic ROS levels (G) (measured using the CellROX Red probe, via flow cytometry, n = 6) for the data included in (D) and (E). TP53 mut AMLs are depicted in red, and TP53 mut-like AMLs are depicted in black. APR-246, eprenetapopt. Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.

    Journal: Cell Reports Medicine

    Article Title: ΔNp73 isoform defines a TP53 -mutant-like poor-risk subgroup of acute myeloid leukemia

    doi: 10.1016/j.xcrm.2025.102540

    Figure Lengend Snippet: Pharmacological and genetic inhibition of CEBPA synergizes with VEN-induced apoptosis in TP53mut/mut-like AMLs (A) MOLM13 (VEN-sensitive) and KG1 (VEN-resistant) cells were treated for 72 h with increasing concentrations of VEN and GFC. Synergy was determined by Bliss coefficient (ZIP score >10 indicates synergism). (B and C) Drug-induced apoptosis (B) and viable cell counts (C) in MOLM13 shCEBPA/shScr cells treated with VEN alone or in combination with GFC (concentrations indicated in the plots, 72 h) detected by flow cytometry ( n = 4). (D and E) Apoptosis was detected by flow cytometry in gated human CD45 dim CD34 + (or CD117 + cells for CD34 − AMLs) of ex vivo -treated AML samples categorized as TP53 mut-like ( n = 8) (D) and TP53 mut ( n = 9) (E) in a co-culture system using an FITC-annexin V/DAPI staining method. Cells were treated with vehicle, VEN (100 and 500 nM), and VEN+Aza (VEN 100 nM + 5′ Aza 1.5 μM), in the presence or absence of GFC (30 μM) for 72 h. Bar graphs represent the mean ± SEM of all the independent patients screened; each point represents a patient. (F and G) Mitochondrial membrane potential (F) (measured by TMRE staining, n = 18) and total cytoplasmatic ROS levels (G) (measured using the CellROX Red probe, via flow cytometry, n = 6) for the data included in (D) and (E). TP53 mut AMLs are depicted in red, and TP53 mut-like AMLs are depicted in black. APR-246, eprenetapopt. Data are reported as mean ± SEM for (B)–(G). The p values and cell types are indicated in the graphs; ∗ p < 0.05; ∗∗ p < 0.01; ∗∗∗ p < 0.001; ANOVA and Bonferroni post-test.

    Article Snippet: Eprenetapopt (APR-246) , MedChemExpress , HY-19980.

    Techniques: Inhibition, Flow Cytometry, Ex Vivo, Co-Culture Assay, Staining, Membrane

    Journal: bioRxiv

    Article Title: APR-246 & COTI-2 increase chemoradiotherapy sensitivity via ROS-induced DNA damage and ferroptosis in p53 mutant HPV negative head and neck squamous cell carcinoma

    doi: 10.1101/2024.12.23.630069

    Figure Lengend Snippet:

    Article Snippet: APR-246, Buthionine sulfoximine (BSO), cisplatin, COTI-2 and erastin were purchased at Bioconnect, Netherlands.

    Techniques: Standard Deviation