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iap inhibitor birinapant  (MedChemExpress)


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    MedChemExpress iap inhibitor birinapant
    (A) Schematic of the Fas signaling pathway highlighting key regulatory proteins and corresponding pharmacologic inhibitors. (B) Representative flow cytometry plots showing cleaved caspase-3 and Annexin V staining of CD19⁻Fas⁺ and CD19⁻Fas⁻ bystander tumor cells co-cultured with CAR-T cells in the presence or absence of <t>birinapant</t> (Bir). (C) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with CAR-T across increasing birinapant doses. n = 5 independent experiments. (D) Synergy analysis using Bliss scoring. The x-axis shows increasing effector-to-target (E:T) ratios, the y-axis shows birinapant doses, and the z-axis shows delta-scores. A Bliss synergy score >10 indicates a greater-than-additive effect. (E) Schematic of the experimental design to assess birinapant potentiation of CAR-T bystander killing in mixed-antigen tumors. (F) Survival curves for mice bearing 80:20 Fas⁺ mixed tumors treated with or without CAR-T in the presence or absence of birinapant. Mice received 2 Gy TBI on day 9 and CAR-T transfer on day 10; birinapant (15 mg/kg) was dosed twice weekly for 10 doses starting on day 9. No CAR-T cohorts, n=8 per group; CAR-T cohorts, n=28 (no birinapant) and n=27 (birinapant). Statistical significance was determined by log-rank test; 95% CI shown by shaded area above and below survival line. (G) Individual tumor growth curves for mice in (F). “No tumor” indicates the number of mice without palpable tumors at the end of the experiment, shown separately for no birinapant (top) or birinapant-treated (bottom) groups. (H) Schematic of FasL shedding by ADAM10 and its inhibition by GI254023X (GIX). (I) Surface FasL expression on CAR-T cells with or without GIX treatment in the presence of CD19 + , CD19⁻, or mixed target cell populations. (J) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with CAR-T across increasing GIX doses. n = 3 independent experiments. (K) Schematic of non-cleavable mutFasL resisting ADAM10-mediated shedding. (L) Schematic of retroviral vectors for αCD19 CAR constructs overexpressing either wild-type FasL (WTFasL, orange) or non-cleavable mutant FasL (mutFasL, teal). The amino acid sequence of the ADAM10 cleavage domain is shown below the constructs. (M) FasL protein expression in CAR-T cells. mutFasL migrates at slightly higher molecular weight due to non-cleavable modification. (N) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with WTFasL CAR-T versus mutFasL CAR-T. n = 3 independent experiments. Dots represent technical replicates, bars indicate mean ± s.e.m. Statistical significance determined by two-way ANOVA with Tukey’s multiple comparisons. *p < 0.03, **p < 0.002, ***p < 0.0002, ****p < 0.0001.
    Iap Inhibitor Birinapant, supplied by MedChemExpress, used in various techniques. Bioz Stars score: 93/100, based on 44 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/iap inhibitor birinapant/product/MedChemExpress
    Average 93 stars, based on 44 article reviews
    iap inhibitor birinapant - by Bioz Stars, 2026-02
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    1) Product Images from "Potentiating CAR-T bystander killing by enhanced Fas/FasL signaling mitigates antigen escape in heterogeneous tumors"

    Article Title: Potentiating CAR-T bystander killing by enhanced Fas/FasL signaling mitigates antigen escape in heterogeneous tumors

    Journal: bioRxiv

    doi: 10.1101/2025.09.22.677496

    (A) Schematic of the Fas signaling pathway highlighting key regulatory proteins and corresponding pharmacologic inhibitors. (B) Representative flow cytometry plots showing cleaved caspase-3 and Annexin V staining of CD19⁻Fas⁺ and CD19⁻Fas⁻ bystander tumor cells co-cultured with CAR-T cells in the presence or absence of birinapant (Bir). (C) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with CAR-T across increasing birinapant doses. n = 5 independent experiments. (D) Synergy analysis using Bliss scoring. The x-axis shows increasing effector-to-target (E:T) ratios, the y-axis shows birinapant doses, and the z-axis shows delta-scores. A Bliss synergy score >10 indicates a greater-than-additive effect. (E) Schematic of the experimental design to assess birinapant potentiation of CAR-T bystander killing in mixed-antigen tumors. (F) Survival curves for mice bearing 80:20 Fas⁺ mixed tumors treated with or without CAR-T in the presence or absence of birinapant. Mice received 2 Gy TBI on day 9 and CAR-T transfer on day 10; birinapant (15 mg/kg) was dosed twice weekly for 10 doses starting on day 9. No CAR-T cohorts, n=8 per group; CAR-T cohorts, n=28 (no birinapant) and n=27 (birinapant). Statistical significance was determined by log-rank test; 95% CI shown by shaded area above and below survival line. (G) Individual tumor growth curves for mice in (F). “No tumor” indicates the number of mice without palpable tumors at the end of the experiment, shown separately for no birinapant (top) or birinapant-treated (bottom) groups. (H) Schematic of FasL shedding by ADAM10 and its inhibition by GI254023X (GIX). (I) Surface FasL expression on CAR-T cells with or without GIX treatment in the presence of CD19 + , CD19⁻, or mixed target cell populations. (J) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with CAR-T across increasing GIX doses. n = 3 independent experiments. (K) Schematic of non-cleavable mutFasL resisting ADAM10-mediated shedding. (L) Schematic of retroviral vectors for αCD19 CAR constructs overexpressing either wild-type FasL (WTFasL, orange) or non-cleavable mutant FasL (mutFasL, teal). The amino acid sequence of the ADAM10 cleavage domain is shown below the constructs. (M) FasL protein expression in CAR-T cells. mutFasL migrates at slightly higher molecular weight due to non-cleavable modification. (N) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with WTFasL CAR-T versus mutFasL CAR-T. n = 3 independent experiments. Dots represent technical replicates, bars indicate mean ± s.e.m. Statistical significance determined by two-way ANOVA with Tukey’s multiple comparisons. *p < 0.03, **p < 0.002, ***p < 0.0002, ****p < 0.0001.
    Figure Legend Snippet: (A) Schematic of the Fas signaling pathway highlighting key regulatory proteins and corresponding pharmacologic inhibitors. (B) Representative flow cytometry plots showing cleaved caspase-3 and Annexin V staining of CD19⁻Fas⁺ and CD19⁻Fas⁻ bystander tumor cells co-cultured with CAR-T cells in the presence or absence of birinapant (Bir). (C) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with CAR-T across increasing birinapant doses. n = 5 independent experiments. (D) Synergy analysis using Bliss scoring. The x-axis shows increasing effector-to-target (E:T) ratios, the y-axis shows birinapant doses, and the z-axis shows delta-scores. A Bliss synergy score >10 indicates a greater-than-additive effect. (E) Schematic of the experimental design to assess birinapant potentiation of CAR-T bystander killing in mixed-antigen tumors. (F) Survival curves for mice bearing 80:20 Fas⁺ mixed tumors treated with or without CAR-T in the presence or absence of birinapant. Mice received 2 Gy TBI on day 9 and CAR-T transfer on day 10; birinapant (15 mg/kg) was dosed twice weekly for 10 doses starting on day 9. No CAR-T cohorts, n=8 per group; CAR-T cohorts, n=28 (no birinapant) and n=27 (birinapant). Statistical significance was determined by log-rank test; 95% CI shown by shaded area above and below survival line. (G) Individual tumor growth curves for mice in (F). “No tumor” indicates the number of mice without palpable tumors at the end of the experiment, shown separately for no birinapant (top) or birinapant-treated (bottom) groups. (H) Schematic of FasL shedding by ADAM10 and its inhibition by GI254023X (GIX). (I) Surface FasL expression on CAR-T cells with or without GIX treatment in the presence of CD19 + , CD19⁻, or mixed target cell populations. (J) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with CAR-T across increasing GIX doses. n = 3 independent experiments. (K) Schematic of non-cleavable mutFasL resisting ADAM10-mediated shedding. (L) Schematic of retroviral vectors for αCD19 CAR constructs overexpressing either wild-type FasL (WTFasL, orange) or non-cleavable mutant FasL (mutFasL, teal). The amino acid sequence of the ADAM10 cleavage domain is shown below the constructs. (M) FasL protein expression in CAR-T cells. mutFasL migrates at slightly higher molecular weight due to non-cleavable modification. (N) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with WTFasL CAR-T versus mutFasL CAR-T. n = 3 independent experiments. Dots represent technical replicates, bars indicate mean ± s.e.m. Statistical significance determined by two-way ANOVA with Tukey’s multiple comparisons. *p < 0.03, **p < 0.002, ***p < 0.0002, ****p < 0.0001.

    Techniques Used: Flow Cytometry, Staining, Cell Culture, Co-Culture Assay, Inhibition, Expressing, Retroviral, Construct, Mutagenesis, Sequencing, Molecular Weight, Modification

    (A) Schematic of a CD3 + T cell engaging a CD20 + tumor cell through a CD20xCD3 bispecific antibody (BsAb) leading to Fas-mediated bystander killing on an adjacent CD20-cell. (B) Normalized viable cell counts of CD20 + , CD20⁻Fas + , and CD20⁻Fas⁻ OCI-Ly8 human lymphoma cells following co-culture with increasing doses of CD20xCD3 BsAb Epcoritamab. Bystander killing of CD20⁻Fas + cells is highlighted in red. Multiple t-tests were conducted on pre-specified comparisons, without correction. (C) Surface expression of CD19, CD20, and Fas in two human lymphoma cell lines OCI-Ly8 and Raji. (D) Mean fluorescence intensity (MFI) fold-change of surface expression in (C) . (E) Heatmap of normalized viable cell counts of OCI-Ly8 and Raji cells following 72 h co-culture with αFas agonist antibody. Boxes represent mean values. n=3 technical replicates. (F) Normalized viable cell counts of CD20 + and CD20⁻ Raji cells after 48 h co-culture with Epcoritamab in the presence or absence of birinapant. Bystander killing of CD20⁻ cells is highlighted in red. Dots indicate replicates; bars show mean ± s.e.m. Statistical significance was determined by two-way ANOVA with correction for multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
    Figure Legend Snippet: (A) Schematic of a CD3 + T cell engaging a CD20 + tumor cell through a CD20xCD3 bispecific antibody (BsAb) leading to Fas-mediated bystander killing on an adjacent CD20-cell. (B) Normalized viable cell counts of CD20 + , CD20⁻Fas + , and CD20⁻Fas⁻ OCI-Ly8 human lymphoma cells following co-culture with increasing doses of CD20xCD3 BsAb Epcoritamab. Bystander killing of CD20⁻Fas + cells is highlighted in red. Multiple t-tests were conducted on pre-specified comparisons, without correction. (C) Surface expression of CD19, CD20, and Fas in two human lymphoma cell lines OCI-Ly8 and Raji. (D) Mean fluorescence intensity (MFI) fold-change of surface expression in (C) . (E) Heatmap of normalized viable cell counts of OCI-Ly8 and Raji cells following 72 h co-culture with αFas agonist antibody. Boxes represent mean values. n=3 technical replicates. (F) Normalized viable cell counts of CD20 + and CD20⁻ Raji cells after 48 h co-culture with Epcoritamab in the presence or absence of birinapant. Bystander killing of CD20⁻ cells is highlighted in red. Dots indicate replicates; bars show mean ± s.e.m. Statistical significance was determined by two-way ANOVA with correction for multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Techniques Used: Co-Culture Assay, Expressing, Fluorescence

    (A) Viable CD4⁺ and CD8⁺ CAR-T counts after 48 h co-culture with CD19⁺ or CD19⁻ target cells in the presence of increasing doses of birinapant. (B) Surface Fas expression on CD4⁺ and CD8⁺ CAR-T after birinapant treatment. (C) Percentage of cleaved caspase-3⁺ CD4⁺ and CD8⁺ CAR-T after co-culture ± birinapant. Increased apoptosis is observed in CD4⁺ cells. (D) Viable cell counts of CD4⁺ and CD8⁺ CAR-T after co-culture with increasing doses of birinapant. (E) Schematic of the mechanism of CD4⁺ T cell fratricide via Fas-FasL and the Fas knockout (FasKO) strategy to preserve T cell viability. (F) Surface Fas expression on scramble gRNA control (ScrKO) versus FasKO CAR-T. (G) Viable CD4⁺ and CD8⁺ CAR-T counts after co-culture with ScrKO or FasKO CAR-T in the presence or absence of birinapant. CD4 + CAR-T FasKO with birinapant is highlighted in red. n = 2 independent experiments. (H) Normalized viable cell counts of CD19⁻Fas + tumor cells following 48 h co-culture with ScrKO or FasKO CAR-T in the presence or absence of birinapant (5 µM). n = 2 independent experiments. (I) Bystander killing index of CAR-T overexpressing wild-type Fasl (WTFasL) or non-cleavable mutant FasL (mutFasL), with or without FasKO, in the presence or absence of birinapant (5 µM). Dots indicate technical replicates; bars show mean ± s.e.m. Statistical significance was determined by two-way ANOVA with Tukey’s multiple comparisons (A-D, I) or by pre-specified t-test comparisons (G-H). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
    Figure Legend Snippet: (A) Viable CD4⁺ and CD8⁺ CAR-T counts after 48 h co-culture with CD19⁺ or CD19⁻ target cells in the presence of increasing doses of birinapant. (B) Surface Fas expression on CD4⁺ and CD8⁺ CAR-T after birinapant treatment. (C) Percentage of cleaved caspase-3⁺ CD4⁺ and CD8⁺ CAR-T after co-culture ± birinapant. Increased apoptosis is observed in CD4⁺ cells. (D) Viable cell counts of CD4⁺ and CD8⁺ CAR-T after co-culture with increasing doses of birinapant. (E) Schematic of the mechanism of CD4⁺ T cell fratricide via Fas-FasL and the Fas knockout (FasKO) strategy to preserve T cell viability. (F) Surface Fas expression on scramble gRNA control (ScrKO) versus FasKO CAR-T. (G) Viable CD4⁺ and CD8⁺ CAR-T counts after co-culture with ScrKO or FasKO CAR-T in the presence or absence of birinapant. CD4 + CAR-T FasKO with birinapant is highlighted in red. n = 2 independent experiments. (H) Normalized viable cell counts of CD19⁻Fas + tumor cells following 48 h co-culture with ScrKO or FasKO CAR-T in the presence or absence of birinapant (5 µM). n = 2 independent experiments. (I) Bystander killing index of CAR-T overexpressing wild-type Fasl (WTFasL) or non-cleavable mutant FasL (mutFasL), with or without FasKO, in the presence or absence of birinapant (5 µM). Dots indicate technical replicates; bars show mean ± s.e.m. Statistical significance was determined by two-way ANOVA with Tukey’s multiple comparisons (A-D, I) or by pre-specified t-test comparisons (G-H). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Techniques Used: Co-Culture Assay, Expressing, Knock-Out, Control, Mutagenesis

    (A) Schematic of tumor microenvironment antigen (TME-Ag)-directed bystander killing. Anti-FOLR2 CAR-T cells target FOLR2⁺ tumor-associated macrophages (TAMs), leading to Fas-dependent killing of adjacent FOLR2⁻ tumor cells. (B) Normalized viable cell counts of FOLR2⁺ Raw264.7 macrophages and FOLR2⁻ A20 tumor cells after 48 h co-culture with anti-FOLR2 CAR-T in the presence or absence of birinapant (5 µM). Bystander killing of FOLR2⁻Fas + A20 cells is highlighted in red. n = 2 independent experiments. (C) Heatmap of ID8 ovarian cancer cell viability after treatment with increasing doses of anti-Fas agonist, birinapant, or both. (D) Normalized viable cell counts of FOLR2⁺ Raw264.7 macrophages and FOLR2⁻ ID8 tumor cells after 48 h co-culture with anti-FOLR2 CAR-T in the presence or absence of birinapant (1 µM). Bystander killing of FOLR2⁻Fas + ID8 cells is highlighted in red. n = 3 technical replicates. (E) Representative flow cytometry dot plots from the co-culture experiment in (D). (F) Experimental timeline for tracking Luc + anti-FOLR2 CAR-T in mice bearing FOLR2⁻ A20 lymphoma tumors. (G) IVIS images of Luc + anti-FOLR2 CAR-T localizing to FOLR2⁻ A20 lymphoma tumor. (H) Quantification of Luc + anti-FOLR2 CAR-T from (G). Dots indicate replicates; bars show mean ± s.e.m. Statistical significance was determined by two-way ANOVA with Tukey’s multiple-comparisons test. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.
    Figure Legend Snippet: (A) Schematic of tumor microenvironment antigen (TME-Ag)-directed bystander killing. Anti-FOLR2 CAR-T cells target FOLR2⁺ tumor-associated macrophages (TAMs), leading to Fas-dependent killing of adjacent FOLR2⁻ tumor cells. (B) Normalized viable cell counts of FOLR2⁺ Raw264.7 macrophages and FOLR2⁻ A20 tumor cells after 48 h co-culture with anti-FOLR2 CAR-T in the presence or absence of birinapant (5 µM). Bystander killing of FOLR2⁻Fas + A20 cells is highlighted in red. n = 2 independent experiments. (C) Heatmap of ID8 ovarian cancer cell viability after treatment with increasing doses of anti-Fas agonist, birinapant, or both. (D) Normalized viable cell counts of FOLR2⁺ Raw264.7 macrophages and FOLR2⁻ ID8 tumor cells after 48 h co-culture with anti-FOLR2 CAR-T in the presence or absence of birinapant (1 µM). Bystander killing of FOLR2⁻Fas + ID8 cells is highlighted in red. n = 3 technical replicates. (E) Representative flow cytometry dot plots from the co-culture experiment in (D). (F) Experimental timeline for tracking Luc + anti-FOLR2 CAR-T in mice bearing FOLR2⁻ A20 lymphoma tumors. (G) IVIS images of Luc + anti-FOLR2 CAR-T localizing to FOLR2⁻ A20 lymphoma tumor. (H) Quantification of Luc + anti-FOLR2 CAR-T from (G). Dots indicate replicates; bars show mean ± s.e.m. Statistical significance was determined by two-way ANOVA with Tukey’s multiple-comparisons test. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Techniques Used: Co-Culture Assay, Flow Cytometry



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    (A) Schematic of the Fas signaling pathway highlighting key regulatory proteins and corresponding pharmacologic inhibitors. (B) Representative flow cytometry plots showing cleaved caspase-3 and Annexin V staining of CD19⁻Fas⁺ and CD19⁻Fas⁻ bystander tumor cells co-cultured with CAR-T cells in the presence or absence of <t>birinapant</t> (Bir). (C) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with CAR-T across increasing birinapant doses. n = 5 independent experiments. (D) Synergy analysis using Bliss scoring. The x-axis shows increasing effector-to-target (E:T) ratios, the y-axis shows birinapant doses, and the z-axis shows delta-scores. A Bliss synergy score >10 indicates a greater-than-additive effect. (E) Schematic of the experimental design to assess birinapant potentiation of CAR-T bystander killing in mixed-antigen tumors. (F) Survival curves for mice bearing 80:20 Fas⁺ mixed tumors treated with or without CAR-T in the presence or absence of birinapant. Mice received 2 Gy TBI on day 9 and CAR-T transfer on day 10; birinapant (15 mg/kg) was dosed twice weekly for 10 doses starting on day 9. No CAR-T cohorts, n=8 per group; CAR-T cohorts, n=28 (no birinapant) and n=27 (birinapant). Statistical significance was determined by log-rank test; 95% CI shown by shaded area above and below survival line. (G) Individual tumor growth curves for mice in (F). “No tumor” indicates the number of mice without palpable tumors at the end of the experiment, shown separately for no birinapant (top) or birinapant-treated (bottom) groups. (H) Schematic of FasL shedding by ADAM10 and its inhibition by GI254023X (GIX). (I) Surface FasL expression on CAR-T cells with or without GIX treatment in the presence of CD19 + , CD19⁻, or mixed target cell populations. (J) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with CAR-T across increasing GIX doses. n = 3 independent experiments. (K) Schematic of non-cleavable mutFasL resisting ADAM10-mediated shedding. (L) Schematic of retroviral vectors for αCD19 CAR constructs overexpressing either wild-type FasL (WTFasL, orange) or non-cleavable mutant FasL (mutFasL, teal). The amino acid sequence of the ADAM10 cleavage domain is shown below the constructs. (M) FasL protein expression in CAR-T cells. mutFasL migrates at slightly higher molecular weight due to non-cleavable modification. (N) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with WTFasL CAR-T versus mutFasL CAR-T. n = 3 independent experiments. Dots represent technical replicates, bars indicate mean ± s.e.m. Statistical significance determined by two-way ANOVA with Tukey’s multiple comparisons. *p < 0.03, **p < 0.002, ***p < 0.0002, ****p < 0.0001.
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    iap inhibitor birinapant  (Selleck Chemicals)
    94
    Selleck Chemicals iap inhibitor birinapant
    (A) Schematic of the Fas signaling pathway highlighting key regulatory proteins and corresponding pharmacologic inhibitors. (B) Representative flow cytometry plots showing cleaved caspase-3 and Annexin V staining of CD19⁻Fas⁺ and CD19⁻Fas⁻ bystander tumor cells co-cultured with CAR-T cells in the presence or absence of <t>birinapant</t> (Bir). (C) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with CAR-T across increasing birinapant doses. n = 5 independent experiments. (D) Synergy analysis using Bliss scoring. The x-axis shows increasing effector-to-target (E:T) ratios, the y-axis shows birinapant doses, and the z-axis shows delta-scores. A Bliss synergy score >10 indicates a greater-than-additive effect. (E) Schematic of the experimental design to assess birinapant potentiation of CAR-T bystander killing in mixed-antigen tumors. (F) Survival curves for mice bearing 80:20 Fas⁺ mixed tumors treated with or without CAR-T in the presence or absence of birinapant. Mice received 2 Gy TBI on day 9 and CAR-T transfer on day 10; birinapant (15 mg/kg) was dosed twice weekly for 10 doses starting on day 9. No CAR-T cohorts, n=8 per group; CAR-T cohorts, n=28 (no birinapant) and n=27 (birinapant). Statistical significance was determined by log-rank test; 95% CI shown by shaded area above and below survival line. (G) Individual tumor growth curves for mice in (F). “No tumor” indicates the number of mice without palpable tumors at the end of the experiment, shown separately for no birinapant (top) or birinapant-treated (bottom) groups. (H) Schematic of FasL shedding by ADAM10 and its inhibition by GI254023X (GIX). (I) Surface FasL expression on CAR-T cells with or without GIX treatment in the presence of CD19 + , CD19⁻, or mixed target cell populations. (J) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with CAR-T across increasing GIX doses. n = 3 independent experiments. (K) Schematic of non-cleavable mutFasL resisting ADAM10-mediated shedding. (L) Schematic of retroviral vectors for αCD19 CAR constructs overexpressing either wild-type FasL (WTFasL, orange) or non-cleavable mutant FasL (mutFasL, teal). The amino acid sequence of the ADAM10 cleavage domain is shown below the constructs. (M) FasL protein expression in CAR-T cells. mutFasL migrates at slightly higher molecular weight due to non-cleavable modification. (N) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with WTFasL CAR-T versus mutFasL CAR-T. n = 3 independent experiments. Dots represent technical replicates, bars indicate mean ± s.e.m. Statistical significance determined by two-way ANOVA with Tukey’s multiple comparisons. *p < 0.03, **p < 0.002, ***p < 0.0002, ****p < 0.0001.
    Iap Inhibitor Birinapant, supplied by Selleck Chemicals, used in various techniques. Bioz Stars score: 94/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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    birinapant smac mimetic and iap inhibitor  (SMAC Corp)
    90
    SMAC Corp birinapant smac mimetic and iap inhibitor
    Ongoing phase 2 and 3 studies investigating late-line therapies in ovarian cancer
    Birinapant Smac Mimetic And Iap Inhibitor, supplied by SMAC Corp, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/result/birinapant smac mimetic and iap inhibitor/product/SMAC Corp
    Average 90 stars, based on 1 article reviews
    birinapant smac mimetic and iap inhibitor - by Bioz Stars, 2026-02
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    (A) Schematic of the Fas signaling pathway highlighting key regulatory proteins and corresponding pharmacologic inhibitors. (B) Representative flow cytometry plots showing cleaved caspase-3 and Annexin V staining of CD19⁻Fas⁺ and CD19⁻Fas⁻ bystander tumor cells co-cultured with CAR-T cells in the presence or absence of birinapant (Bir). (C) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with CAR-T across increasing birinapant doses. n = 5 independent experiments. (D) Synergy analysis using Bliss scoring. The x-axis shows increasing effector-to-target (E:T) ratios, the y-axis shows birinapant doses, and the z-axis shows delta-scores. A Bliss synergy score >10 indicates a greater-than-additive effect. (E) Schematic of the experimental design to assess birinapant potentiation of CAR-T bystander killing in mixed-antigen tumors. (F) Survival curves for mice bearing 80:20 Fas⁺ mixed tumors treated with or without CAR-T in the presence or absence of birinapant. Mice received 2 Gy TBI on day 9 and CAR-T transfer on day 10; birinapant (15 mg/kg) was dosed twice weekly for 10 doses starting on day 9. No CAR-T cohorts, n=8 per group; CAR-T cohorts, n=28 (no birinapant) and n=27 (birinapant). Statistical significance was determined by log-rank test; 95% CI shown by shaded area above and below survival line. (G) Individual tumor growth curves for mice in (F). “No tumor” indicates the number of mice without palpable tumors at the end of the experiment, shown separately for no birinapant (top) or birinapant-treated (bottom) groups. (H) Schematic of FasL shedding by ADAM10 and its inhibition by GI254023X (GIX). (I) Surface FasL expression on CAR-T cells with or without GIX treatment in the presence of CD19 + , CD19⁻, or mixed target cell populations. (J) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with CAR-T across increasing GIX doses. n = 3 independent experiments. (K) Schematic of non-cleavable mutFasL resisting ADAM10-mediated shedding. (L) Schematic of retroviral vectors for αCD19 CAR constructs overexpressing either wild-type FasL (WTFasL, orange) or non-cleavable mutant FasL (mutFasL, teal). The amino acid sequence of the ADAM10 cleavage domain is shown below the constructs. (M) FasL protein expression in CAR-T cells. mutFasL migrates at slightly higher molecular weight due to non-cleavable modification. (N) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with WTFasL CAR-T versus mutFasL CAR-T. n = 3 independent experiments. Dots represent technical replicates, bars indicate mean ± s.e.m. Statistical significance determined by two-way ANOVA with Tukey’s multiple comparisons. *p < 0.03, **p < 0.002, ***p < 0.0002, ****p < 0.0001.

    Journal: bioRxiv

    Article Title: Potentiating CAR-T bystander killing by enhanced Fas/FasL signaling mitigates antigen escape in heterogeneous tumors

    doi: 10.1101/2025.09.22.677496

    Figure Lengend Snippet: (A) Schematic of the Fas signaling pathway highlighting key regulatory proteins and corresponding pharmacologic inhibitors. (B) Representative flow cytometry plots showing cleaved caspase-3 and Annexin V staining of CD19⁻Fas⁺ and CD19⁻Fas⁻ bystander tumor cells co-cultured with CAR-T cells in the presence or absence of birinapant (Bir). (C) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with CAR-T across increasing birinapant doses. n = 5 independent experiments. (D) Synergy analysis using Bliss scoring. The x-axis shows increasing effector-to-target (E:T) ratios, the y-axis shows birinapant doses, and the z-axis shows delta-scores. A Bliss synergy score >10 indicates a greater-than-additive effect. (E) Schematic of the experimental design to assess birinapant potentiation of CAR-T bystander killing in mixed-antigen tumors. (F) Survival curves for mice bearing 80:20 Fas⁺ mixed tumors treated with or without CAR-T in the presence or absence of birinapant. Mice received 2 Gy TBI on day 9 and CAR-T transfer on day 10; birinapant (15 mg/kg) was dosed twice weekly for 10 doses starting on day 9. No CAR-T cohorts, n=8 per group; CAR-T cohorts, n=28 (no birinapant) and n=27 (birinapant). Statistical significance was determined by log-rank test; 95% CI shown by shaded area above and below survival line. (G) Individual tumor growth curves for mice in (F). “No tumor” indicates the number of mice without palpable tumors at the end of the experiment, shown separately for no birinapant (top) or birinapant-treated (bottom) groups. (H) Schematic of FasL shedding by ADAM10 and its inhibition by GI254023X (GIX). (I) Surface FasL expression on CAR-T cells with or without GIX treatment in the presence of CD19 + , CD19⁻, or mixed target cell populations. (J) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with CAR-T across increasing GIX doses. n = 3 independent experiments. (K) Schematic of non-cleavable mutFasL resisting ADAM10-mediated shedding. (L) Schematic of retroviral vectors for αCD19 CAR constructs overexpressing either wild-type FasL (WTFasL, orange) or non-cleavable mutant FasL (mutFasL, teal). The amino acid sequence of the ADAM10 cleavage domain is shown below the constructs. (M) FasL protein expression in CAR-T cells. mutFasL migrates at slightly higher molecular weight due to non-cleavable modification. (N) Normalized viable cell counts of CD19⁻Fas⁺ and CD19⁻Fas⁻ tumor cells in mixed co-culture with WTFasL CAR-T versus mutFasL CAR-T. n = 3 independent experiments. Dots represent technical replicates, bars indicate mean ± s.e.m. Statistical significance determined by two-way ANOVA with Tukey’s multiple comparisons. *p < 0.03, **p < 0.002, ***p < 0.0002, ****p < 0.0001.

    Article Snippet: The IAP inhibitor birinapant (TL32711, MedChemExpress, cat no. HY-16591) was resuspended in DMSO for a stock solution of 10mM.

    Techniques: Flow Cytometry, Staining, Cell Culture, Co-Culture Assay, Inhibition, Expressing, Retroviral, Construct, Mutagenesis, Sequencing, Molecular Weight, Modification

    (A) Schematic of a CD3 + T cell engaging a CD20 + tumor cell through a CD20xCD3 bispecific antibody (BsAb) leading to Fas-mediated bystander killing on an adjacent CD20-cell. (B) Normalized viable cell counts of CD20 + , CD20⁻Fas + , and CD20⁻Fas⁻ OCI-Ly8 human lymphoma cells following co-culture with increasing doses of CD20xCD3 BsAb Epcoritamab. Bystander killing of CD20⁻Fas + cells is highlighted in red. Multiple t-tests were conducted on pre-specified comparisons, without correction. (C) Surface expression of CD19, CD20, and Fas in two human lymphoma cell lines OCI-Ly8 and Raji. (D) Mean fluorescence intensity (MFI) fold-change of surface expression in (C) . (E) Heatmap of normalized viable cell counts of OCI-Ly8 and Raji cells following 72 h co-culture with αFas agonist antibody. Boxes represent mean values. n=3 technical replicates. (F) Normalized viable cell counts of CD20 + and CD20⁻ Raji cells after 48 h co-culture with Epcoritamab in the presence or absence of birinapant. Bystander killing of CD20⁻ cells is highlighted in red. Dots indicate replicates; bars show mean ± s.e.m. Statistical significance was determined by two-way ANOVA with correction for multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Journal: bioRxiv

    Article Title: Potentiating CAR-T bystander killing by enhanced Fas/FasL signaling mitigates antigen escape in heterogeneous tumors

    doi: 10.1101/2025.09.22.677496

    Figure Lengend Snippet: (A) Schematic of a CD3 + T cell engaging a CD20 + tumor cell through a CD20xCD3 bispecific antibody (BsAb) leading to Fas-mediated bystander killing on an adjacent CD20-cell. (B) Normalized viable cell counts of CD20 + , CD20⁻Fas + , and CD20⁻Fas⁻ OCI-Ly8 human lymphoma cells following co-culture with increasing doses of CD20xCD3 BsAb Epcoritamab. Bystander killing of CD20⁻Fas + cells is highlighted in red. Multiple t-tests were conducted on pre-specified comparisons, without correction. (C) Surface expression of CD19, CD20, and Fas in two human lymphoma cell lines OCI-Ly8 and Raji. (D) Mean fluorescence intensity (MFI) fold-change of surface expression in (C) . (E) Heatmap of normalized viable cell counts of OCI-Ly8 and Raji cells following 72 h co-culture with αFas agonist antibody. Boxes represent mean values. n=3 technical replicates. (F) Normalized viable cell counts of CD20 + and CD20⁻ Raji cells after 48 h co-culture with Epcoritamab in the presence or absence of birinapant. Bystander killing of CD20⁻ cells is highlighted in red. Dots indicate replicates; bars show mean ± s.e.m. Statistical significance was determined by two-way ANOVA with correction for multiple comparisons. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Article Snippet: The IAP inhibitor birinapant (TL32711, MedChemExpress, cat no. HY-16591) was resuspended in DMSO for a stock solution of 10mM.

    Techniques: Co-Culture Assay, Expressing, Fluorescence

    (A) Viable CD4⁺ and CD8⁺ CAR-T counts after 48 h co-culture with CD19⁺ or CD19⁻ target cells in the presence of increasing doses of birinapant. (B) Surface Fas expression on CD4⁺ and CD8⁺ CAR-T after birinapant treatment. (C) Percentage of cleaved caspase-3⁺ CD4⁺ and CD8⁺ CAR-T after co-culture ± birinapant. Increased apoptosis is observed in CD4⁺ cells. (D) Viable cell counts of CD4⁺ and CD8⁺ CAR-T after co-culture with increasing doses of birinapant. (E) Schematic of the mechanism of CD4⁺ T cell fratricide via Fas-FasL and the Fas knockout (FasKO) strategy to preserve T cell viability. (F) Surface Fas expression on scramble gRNA control (ScrKO) versus FasKO CAR-T. (G) Viable CD4⁺ and CD8⁺ CAR-T counts after co-culture with ScrKO or FasKO CAR-T in the presence or absence of birinapant. CD4 + CAR-T FasKO with birinapant is highlighted in red. n = 2 independent experiments. (H) Normalized viable cell counts of CD19⁻Fas + tumor cells following 48 h co-culture with ScrKO or FasKO CAR-T in the presence or absence of birinapant (5 µM). n = 2 independent experiments. (I) Bystander killing index of CAR-T overexpressing wild-type Fasl (WTFasL) or non-cleavable mutant FasL (mutFasL), with or without FasKO, in the presence or absence of birinapant (5 µM). Dots indicate technical replicates; bars show mean ± s.e.m. Statistical significance was determined by two-way ANOVA with Tukey’s multiple comparisons (A-D, I) or by pre-specified t-test comparisons (G-H). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Journal: bioRxiv

    Article Title: Potentiating CAR-T bystander killing by enhanced Fas/FasL signaling mitigates antigen escape in heterogeneous tumors

    doi: 10.1101/2025.09.22.677496

    Figure Lengend Snippet: (A) Viable CD4⁺ and CD8⁺ CAR-T counts after 48 h co-culture with CD19⁺ or CD19⁻ target cells in the presence of increasing doses of birinapant. (B) Surface Fas expression on CD4⁺ and CD8⁺ CAR-T after birinapant treatment. (C) Percentage of cleaved caspase-3⁺ CD4⁺ and CD8⁺ CAR-T after co-culture ± birinapant. Increased apoptosis is observed in CD4⁺ cells. (D) Viable cell counts of CD4⁺ and CD8⁺ CAR-T after co-culture with increasing doses of birinapant. (E) Schematic of the mechanism of CD4⁺ T cell fratricide via Fas-FasL and the Fas knockout (FasKO) strategy to preserve T cell viability. (F) Surface Fas expression on scramble gRNA control (ScrKO) versus FasKO CAR-T. (G) Viable CD4⁺ and CD8⁺ CAR-T counts after co-culture with ScrKO or FasKO CAR-T in the presence or absence of birinapant. CD4 + CAR-T FasKO with birinapant is highlighted in red. n = 2 independent experiments. (H) Normalized viable cell counts of CD19⁻Fas + tumor cells following 48 h co-culture with ScrKO or FasKO CAR-T in the presence or absence of birinapant (5 µM). n = 2 independent experiments. (I) Bystander killing index of CAR-T overexpressing wild-type Fasl (WTFasL) or non-cleavable mutant FasL (mutFasL), with or without FasKO, in the presence or absence of birinapant (5 µM). Dots indicate technical replicates; bars show mean ± s.e.m. Statistical significance was determined by two-way ANOVA with Tukey’s multiple comparisons (A-D, I) or by pre-specified t-test comparisons (G-H). *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Article Snippet: The IAP inhibitor birinapant (TL32711, MedChemExpress, cat no. HY-16591) was resuspended in DMSO for a stock solution of 10mM.

    Techniques: Co-Culture Assay, Expressing, Knock-Out, Control, Mutagenesis

    (A) Schematic of tumor microenvironment antigen (TME-Ag)-directed bystander killing. Anti-FOLR2 CAR-T cells target FOLR2⁺ tumor-associated macrophages (TAMs), leading to Fas-dependent killing of adjacent FOLR2⁻ tumor cells. (B) Normalized viable cell counts of FOLR2⁺ Raw264.7 macrophages and FOLR2⁻ A20 tumor cells after 48 h co-culture with anti-FOLR2 CAR-T in the presence or absence of birinapant (5 µM). Bystander killing of FOLR2⁻Fas + A20 cells is highlighted in red. n = 2 independent experiments. (C) Heatmap of ID8 ovarian cancer cell viability after treatment with increasing doses of anti-Fas agonist, birinapant, or both. (D) Normalized viable cell counts of FOLR2⁺ Raw264.7 macrophages and FOLR2⁻ ID8 tumor cells after 48 h co-culture with anti-FOLR2 CAR-T in the presence or absence of birinapant (1 µM). Bystander killing of FOLR2⁻Fas + ID8 cells is highlighted in red. n = 3 technical replicates. (E) Representative flow cytometry dot plots from the co-culture experiment in (D). (F) Experimental timeline for tracking Luc + anti-FOLR2 CAR-T in mice bearing FOLR2⁻ A20 lymphoma tumors. (G) IVIS images of Luc + anti-FOLR2 CAR-T localizing to FOLR2⁻ A20 lymphoma tumor. (H) Quantification of Luc + anti-FOLR2 CAR-T from (G). Dots indicate replicates; bars show mean ± s.e.m. Statistical significance was determined by two-way ANOVA with Tukey’s multiple-comparisons test. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Journal: bioRxiv

    Article Title: Potentiating CAR-T bystander killing by enhanced Fas/FasL signaling mitigates antigen escape in heterogeneous tumors

    doi: 10.1101/2025.09.22.677496

    Figure Lengend Snippet: (A) Schematic of tumor microenvironment antigen (TME-Ag)-directed bystander killing. Anti-FOLR2 CAR-T cells target FOLR2⁺ tumor-associated macrophages (TAMs), leading to Fas-dependent killing of adjacent FOLR2⁻ tumor cells. (B) Normalized viable cell counts of FOLR2⁺ Raw264.7 macrophages and FOLR2⁻ A20 tumor cells after 48 h co-culture with anti-FOLR2 CAR-T in the presence or absence of birinapant (5 µM). Bystander killing of FOLR2⁻Fas + A20 cells is highlighted in red. n = 2 independent experiments. (C) Heatmap of ID8 ovarian cancer cell viability after treatment with increasing doses of anti-Fas agonist, birinapant, or both. (D) Normalized viable cell counts of FOLR2⁺ Raw264.7 macrophages and FOLR2⁻ ID8 tumor cells after 48 h co-culture with anti-FOLR2 CAR-T in the presence or absence of birinapant (1 µM). Bystander killing of FOLR2⁻Fas + ID8 cells is highlighted in red. n = 3 technical replicates. (E) Representative flow cytometry dot plots from the co-culture experiment in (D). (F) Experimental timeline for tracking Luc + anti-FOLR2 CAR-T in mice bearing FOLR2⁻ A20 lymphoma tumors. (G) IVIS images of Luc + anti-FOLR2 CAR-T localizing to FOLR2⁻ A20 lymphoma tumor. (H) Quantification of Luc + anti-FOLR2 CAR-T from (G). Dots indicate replicates; bars show mean ± s.e.m. Statistical significance was determined by two-way ANOVA with Tukey’s multiple-comparisons test. *p < 0.05, **p < 0.01, ***p < 0.001, ****p < 0.0001.

    Article Snippet: The IAP inhibitor birinapant (TL32711, MedChemExpress, cat no. HY-16591) was resuspended in DMSO for a stock solution of 10mM.

    Techniques: Co-Culture Assay, Flow Cytometry

    Ongoing phase 2 and 3 studies investigating late-line therapies in ovarian cancer

    Journal: Gynecologic Oncology Research and Practice

    Article Title: Bringing new medicines to women with epithelial ovarian cancer: what is the unmet medical need?

    doi: 10.1186/s40661-017-0050-0

    Figure Lengend Snippet: Ongoing phase 2 and 3 studies investigating late-line therapies in ovarian cancer

    Article Snippet: Birinapant (SMAC mimetic and IAP inhibitor) , , , , , .

    Techniques: Mutagenesis