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anti trp1 ta99  (Bio X Cell)


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    Structured Review

    Bio X Cell anti trp1 ta99
    A) Immunofluorescent staining of B16F10 WT melanoma with the <t>TRP1-targeting</t> <t>TA99</t> antibody (scale bar = 100 μm). B) B16F10 WT tumour growth upon treatment with TA99 or IgG2a isotype control (n ≥ 4, mean ± SEM, Mann-Whitney test on d11). C) Design of FabTRP-OVA fusion protein and analysis of its production by SDS-PAGE (expected size = 92,3 kDa). D) Illustration of the FabTRP-OVA fusion protein approach for targeting the xenoantigen to the cancer cell membrane. E) Representative flow cytometry plot of FabTRP-OVA, OVA and no OVA (i.e., secondary antibody only) binding to the surface of B16F10 WT cells. F) B16F10 WT tumour growth when treated with FabTRP-OVA in pre-immunised or naïve mice (n ≥ 4, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d12). G) B16F10 WT tumour growth when treated with FabTRP-OVA in combination with anti-PD-1 checkpoint blocade therapy (n ≥ 4, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d12). H) Experimental treatment timeline of xenoantigen delivery (i.e., FabTRP-OVA, OVA or PBS (vehicle only)) and anti-PD-1 checkpoint blockade therapy in B16F10 WT in mice pre-immunised against OVA (Vax) or naïve (No vax). I, J) B16F10 WT tumour growth (I) and associated mouse survival (J) upon treatment with FabTRP-OVA, OVA or PBS in combination with anti-PD-1 checkpoint blockade therapy (n ≥ 5, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d16, log-rank tests for survival).
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    Images

    1) Product Images from "Membrane localisation and checkpoint blockade enhance xenoantigen delivery to redirect pre-existing immunity against tumours"

    Article Title: Membrane localisation and checkpoint blockade enhance xenoantigen delivery to redirect pre-existing immunity against tumours

    Journal: bioRxiv

    doi: 10.64898/2026.03.01.708859

    A) Immunofluorescent staining of B16F10 WT melanoma with the TRP1-targeting TA99 antibody (scale bar = 100 μm). B) B16F10 WT tumour growth upon treatment with TA99 or IgG2a isotype control (n ≥ 4, mean ± SEM, Mann-Whitney test on d11). C) Design of FabTRP-OVA fusion protein and analysis of its production by SDS-PAGE (expected size = 92,3 kDa). D) Illustration of the FabTRP-OVA fusion protein approach for targeting the xenoantigen to the cancer cell membrane. E) Representative flow cytometry plot of FabTRP-OVA, OVA and no OVA (i.e., secondary antibody only) binding to the surface of B16F10 WT cells. F) B16F10 WT tumour growth when treated with FabTRP-OVA in pre-immunised or naïve mice (n ≥ 4, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d12). G) B16F10 WT tumour growth when treated with FabTRP-OVA in combination with anti-PD-1 checkpoint blocade therapy (n ≥ 4, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d12). H) Experimental treatment timeline of xenoantigen delivery (i.e., FabTRP-OVA, OVA or PBS (vehicle only)) and anti-PD-1 checkpoint blockade therapy in B16F10 WT in mice pre-immunised against OVA (Vax) or naïve (No vax). I, J) B16F10 WT tumour growth (I) and associated mouse survival (J) upon treatment with FabTRP-OVA, OVA or PBS in combination with anti-PD-1 checkpoint blockade therapy (n ≥ 5, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d16, log-rank tests for survival).
    Figure Legend Snippet: A) Immunofluorescent staining of B16F10 WT melanoma with the TRP1-targeting TA99 antibody (scale bar = 100 μm). B) B16F10 WT tumour growth upon treatment with TA99 or IgG2a isotype control (n ≥ 4, mean ± SEM, Mann-Whitney test on d11). C) Design of FabTRP-OVA fusion protein and analysis of its production by SDS-PAGE (expected size = 92,3 kDa). D) Illustration of the FabTRP-OVA fusion protein approach for targeting the xenoantigen to the cancer cell membrane. E) Representative flow cytometry plot of FabTRP-OVA, OVA and no OVA (i.e., secondary antibody only) binding to the surface of B16F10 WT cells. F) B16F10 WT tumour growth when treated with FabTRP-OVA in pre-immunised or naïve mice (n ≥ 4, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d12). G) B16F10 WT tumour growth when treated with FabTRP-OVA in combination with anti-PD-1 checkpoint blocade therapy (n ≥ 4, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d12). H) Experimental treatment timeline of xenoantigen delivery (i.e., FabTRP-OVA, OVA or PBS (vehicle only)) and anti-PD-1 checkpoint blockade therapy in B16F10 WT in mice pre-immunised against OVA (Vax) or naïve (No vax). I, J) B16F10 WT tumour growth (I) and associated mouse survival (J) upon treatment with FabTRP-OVA, OVA or PBS in combination with anti-PD-1 checkpoint blockade therapy (n ≥ 5, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d16, log-rank tests for survival).

    Techniques Used: Staining, Control, MANN-WHITNEY, SDS Page, Membrane, Flow Cytometry, Binding Assay



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    A) Immunofluorescent staining of B16F10 WT melanoma with the <t>TRP1-targeting</t> <t>TA99</t> antibody (scale bar = 100 μm). B) B16F10 WT tumour growth upon treatment with TA99 or IgG2a isotype control (n ≥ 4, mean ± SEM, Mann-Whitney test on d11). C) Design of FabTRP-OVA fusion protein and analysis of its production by SDS-PAGE (expected size = 92,3 kDa). D) Illustration of the FabTRP-OVA fusion protein approach for targeting the xenoantigen to the cancer cell membrane. E) Representative flow cytometry plot of FabTRP-OVA, OVA and no OVA (i.e., secondary antibody only) binding to the surface of B16F10 WT cells. F) B16F10 WT tumour growth when treated with FabTRP-OVA in pre-immunised or naïve mice (n ≥ 4, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d12). G) B16F10 WT tumour growth when treated with FabTRP-OVA in combination with anti-PD-1 checkpoint blocade therapy (n ≥ 4, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d12). H) Experimental treatment timeline of xenoantigen delivery (i.e., FabTRP-OVA, OVA or PBS (vehicle only)) and anti-PD-1 checkpoint blockade therapy in B16F10 WT in mice pre-immunised against OVA (Vax) or naïve (No vax). I, J) B16F10 WT tumour growth (I) and associated mouse survival (J) upon treatment with FabTRP-OVA, OVA or PBS in combination with anti-PD-1 checkpoint blockade therapy (n ≥ 5, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d16, log-rank tests for survival).
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    a Crystal structure of human TRP1 (PDB: 5M8L), with the red motif indicating the N-terminal pGlu. b Titration of αTRP1 clone <t>TA99</t> (1:1 dilution, commencing at 40 μg/mL) followed by αmouse IgG APC (1:800) on murine B16F10 wildtype (blue) and QPCTL KO (red) cells. Data represents individual data point and the line is the mean percentage of MFI of αTRP1 clone TA99 staining relative to the MFI of 40 μg/mL αTRP1 clone TA99 on wildtype cells (n = 3). c Flanvotumab (1:200) followed by αhuman clone QA19 (1:100) on B16F10 wildtype (blue) and QPCTL KO (red) cells. Data represents the percentage of MFI, + standard deviation error, bar of flanvotumab staining relative to the MFI flanvotumab on wildtype cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n = 3). d Representative histograms of αTRP1 clone TA99 (1:100) followed by αmouse IgG APC (1:800) or flanvotumab (1:200) followed by αhuman clone QA19 PE (1:100), unstained (gray) or secondary controls (dark gray) staining on B16F10 treated with 10 μM glutaminyl cyclase inhibitors PQ912 (red) or SEN177 (orange) or equal amounts of DMSO (blue) for three days. Bar graphs show the percentage of the MFI of αTRP1 clone TA99 or flanvotumab staining, + standard deviation error bar, relative to the MFI of DMSO control cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n = 3). e Representative histograms of αTRP1 clone TA99 (1:100) followed by αmouse IgG APC (1:800), or flanvotumab (1:50) followed by αhuman clone QA19 PE (1:100), unstained (gray) or secondary controls (dark gray) staining on primary immortalized human melanocytes treated with 10 μM glutaminyl cyclase inhibitors PQ912 (red) or SEN177 (orange) or equal amounts of DMSO (blue) for three days. Bar graphs show the percentage of the MFI of αTRP1 clone TA99 or flanvotumab, + standard deviation error bar, relative to the MFI of DMSO control cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n ≥ 3). Abbreviations: MFI, median fluorescent intensity; KO, knockout; US, unstained; Sec, secondary antibody only; PQ, PQ912; SEN, SEN177.
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    a Crystal structure of human TRP1 (PDB: 5M8L), with the red motif indicating the N-terminal pGlu. b Titration of αTRP1 clone <t>TA99</t> (1:1 dilution, commencing at 40 μg/mL) followed by αmouse IgG APC (1:800) on murine B16F10 wildtype (blue) and QPCTL KO (red) cells. Data represents individual data point and the line is the mean percentage of MFI of αTRP1 clone TA99 staining relative to the MFI of 40 μg/mL αTRP1 clone TA99 on wildtype cells (n = 3). c Flanvotumab (1:200) followed by αhuman clone QA19 (1:100) on B16F10 wildtype (blue) and QPCTL KO (red) cells. Data represents the percentage of MFI, + standard deviation error, bar of flanvotumab staining relative to the MFI flanvotumab on wildtype cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n = 3). d Representative histograms of αTRP1 clone TA99 (1:100) followed by αmouse IgG APC (1:800) or flanvotumab (1:200) followed by αhuman clone QA19 PE (1:100), unstained (gray) or secondary controls (dark gray) staining on B16F10 treated with 10 μM glutaminyl cyclase inhibitors PQ912 (red) or SEN177 (orange) or equal amounts of DMSO (blue) for three days. Bar graphs show the percentage of the MFI of αTRP1 clone TA99 or flanvotumab staining, + standard deviation error bar, relative to the MFI of DMSO control cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n = 3). e Representative histograms of αTRP1 clone TA99 (1:100) followed by αmouse IgG APC (1:800), or flanvotumab (1:50) followed by αhuman clone QA19 PE (1:100), unstained (gray) or secondary controls (dark gray) staining on primary immortalized human melanocytes treated with 10 μM glutaminyl cyclase inhibitors PQ912 (red) or SEN177 (orange) or equal amounts of DMSO (blue) for three days. Bar graphs show the percentage of the MFI of αTRP1 clone TA99 or flanvotumab, + standard deviation error bar, relative to the MFI of DMSO control cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n ≥ 3). Abbreviations: MFI, median fluorescent intensity; KO, knockout; US, unstained; Sec, secondary antibody only; PQ, PQ912; SEN, SEN177.
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    a Crystal structure of human TRP1 (PDB: 5M8L), with the red motif indicating the N-terminal pGlu. b Titration of αTRP1 clone <t>TA99</t> (1:1 dilution, commencing at 40 μg/mL) followed by αmouse IgG APC (1:800) on murine B16F10 wildtype (blue) and QPCTL KO (red) cells. Data represents individual data point and the line is the mean percentage of MFI of αTRP1 clone TA99 staining relative to the MFI of 40 μg/mL αTRP1 clone TA99 on wildtype cells (n = 3). c Flanvotumab (1:200) followed by αhuman clone QA19 (1:100) on B16F10 wildtype (blue) and QPCTL KO (red) cells. Data represents the percentage of MFI, + standard deviation error, bar of flanvotumab staining relative to the MFI flanvotumab on wildtype cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n = 3). d Representative histograms of αTRP1 clone TA99 (1:100) followed by αmouse IgG APC (1:800) or flanvotumab (1:200) followed by αhuman clone QA19 PE (1:100), unstained (gray) or secondary controls (dark gray) staining on B16F10 treated with 10 μM glutaminyl cyclase inhibitors PQ912 (red) or SEN177 (orange) or equal amounts of DMSO (blue) for three days. Bar graphs show the percentage of the MFI of αTRP1 clone TA99 or flanvotumab staining, + standard deviation error bar, relative to the MFI of DMSO control cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n = 3). e Representative histograms of αTRP1 clone TA99 (1:100) followed by αmouse IgG APC (1:800), or flanvotumab (1:50) followed by αhuman clone QA19 PE (1:100), unstained (gray) or secondary controls (dark gray) staining on primary immortalized human melanocytes treated with 10 μM glutaminyl cyclase inhibitors PQ912 (red) or SEN177 (orange) or equal amounts of DMSO (blue) for three days. Bar graphs show the percentage of the MFI of αTRP1 clone TA99 or flanvotumab, + standard deviation error bar, relative to the MFI of DMSO control cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n ≥ 3). Abbreviations: MFI, median fluorescent intensity; KO, knockout; US, unstained; Sec, secondary antibody only; PQ, PQ912; SEN, SEN177.
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    a Crystal structure of human TRP1 (PDB: 5M8L), with the red motif indicating the N-terminal pGlu. b Titration of αTRP1 clone <t>TA99</t> (1:1 dilution, commencing at 40 μg/mL) followed by αmouse IgG APC (1:800) on murine B16F10 wildtype (blue) and QPCTL KO (red) cells. Data represents individual data point and the line is the mean percentage of MFI of αTRP1 clone TA99 staining relative to the MFI of 40 μg/mL αTRP1 clone TA99 on wildtype cells (n = 3). c Flanvotumab (1:200) followed by αhuman clone QA19 (1:100) on B16F10 wildtype (blue) and QPCTL KO (red) cells. Data represents the percentage of MFI, + standard deviation error, bar of flanvotumab staining relative to the MFI flanvotumab on wildtype cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n = 3). d Representative histograms of αTRP1 clone TA99 (1:100) followed by αmouse IgG APC (1:800) or flanvotumab (1:200) followed by αhuman clone QA19 PE (1:100), unstained (gray) or secondary controls (dark gray) staining on B16F10 treated with 10 μM glutaminyl cyclase inhibitors PQ912 (red) or SEN177 (orange) or equal amounts of DMSO (blue) for three days. Bar graphs show the percentage of the MFI of αTRP1 clone TA99 or flanvotumab staining, + standard deviation error bar, relative to the MFI of DMSO control cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n = 3). e Representative histograms of αTRP1 clone TA99 (1:100) followed by αmouse IgG APC (1:800), or flanvotumab (1:50) followed by αhuman clone QA19 PE (1:100), unstained (gray) or secondary controls (dark gray) staining on primary immortalized human melanocytes treated with 10 μM glutaminyl cyclase inhibitors PQ912 (red) or SEN177 (orange) or equal amounts of DMSO (blue) for three days. Bar graphs show the percentage of the MFI of αTRP1 clone TA99 or flanvotumab, + standard deviation error bar, relative to the MFI of DMSO control cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n ≥ 3). Abbreviations: MFI, median fluorescent intensity; KO, knockout; US, unstained; Sec, secondary antibody only; PQ, PQ912; SEN, SEN177.
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    Image Search Results


    A) Immunofluorescent staining of B16F10 WT melanoma with the TRP1-targeting TA99 antibody (scale bar = 100 μm). B) B16F10 WT tumour growth upon treatment with TA99 or IgG2a isotype control (n ≥ 4, mean ± SEM, Mann-Whitney test on d11). C) Design of FabTRP-OVA fusion protein and analysis of its production by SDS-PAGE (expected size = 92,3 kDa). D) Illustration of the FabTRP-OVA fusion protein approach for targeting the xenoantigen to the cancer cell membrane. E) Representative flow cytometry plot of FabTRP-OVA, OVA and no OVA (i.e., secondary antibody only) binding to the surface of B16F10 WT cells. F) B16F10 WT tumour growth when treated with FabTRP-OVA in pre-immunised or naïve mice (n ≥ 4, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d12). G) B16F10 WT tumour growth when treated with FabTRP-OVA in combination with anti-PD-1 checkpoint blocade therapy (n ≥ 4, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d12). H) Experimental treatment timeline of xenoantigen delivery (i.e., FabTRP-OVA, OVA or PBS (vehicle only)) and anti-PD-1 checkpoint blockade therapy in B16F10 WT in mice pre-immunised against OVA (Vax) or naïve (No vax). I, J) B16F10 WT tumour growth (I) and associated mouse survival (J) upon treatment with FabTRP-OVA, OVA or PBS in combination with anti-PD-1 checkpoint blockade therapy (n ≥ 5, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d16, log-rank tests for survival).

    Journal: bioRxiv

    Article Title: Membrane localisation and checkpoint blockade enhance xenoantigen delivery to redirect pre-existing immunity against tumours

    doi: 10.64898/2026.03.01.708859

    Figure Lengend Snippet: A) Immunofluorescent staining of B16F10 WT melanoma with the TRP1-targeting TA99 antibody (scale bar = 100 μm). B) B16F10 WT tumour growth upon treatment with TA99 or IgG2a isotype control (n ≥ 4, mean ± SEM, Mann-Whitney test on d11). C) Design of FabTRP-OVA fusion protein and analysis of its production by SDS-PAGE (expected size = 92,3 kDa). D) Illustration of the FabTRP-OVA fusion protein approach for targeting the xenoantigen to the cancer cell membrane. E) Representative flow cytometry plot of FabTRP-OVA, OVA and no OVA (i.e., secondary antibody only) binding to the surface of B16F10 WT cells. F) B16F10 WT tumour growth when treated with FabTRP-OVA in pre-immunised or naïve mice (n ≥ 4, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d12). G) B16F10 WT tumour growth when treated with FabTRP-OVA in combination with anti-PD-1 checkpoint blocade therapy (n ≥ 4, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d12). H) Experimental treatment timeline of xenoantigen delivery (i.e., FabTRP-OVA, OVA or PBS (vehicle only)) and anti-PD-1 checkpoint blockade therapy in B16F10 WT in mice pre-immunised against OVA (Vax) or naïve (No vax). I, J) B16F10 WT tumour growth (I) and associated mouse survival (J) upon treatment with FabTRP-OVA, OVA or PBS in combination with anti-PD-1 checkpoint blockade therapy (n ≥ 5, mean ± SEM, Kruskal-Wallis with Dunn’s post-test on d16, log-rank tests for survival).

    Article Snippet: Anti-TRP1 TA99 (#BE0151) and IgG2a (clone C1.18.4, #BE0085) (InVivoMab, Bio X Cell, Lebanon, NH, USA), was injected at a dose of 100 μg.

    Techniques: Staining, Control, MANN-WHITNEY, SDS Page, Membrane, Flow Cytometry, Binding Assay

    a Crystal structure of human TRP1 (PDB: 5M8L), with the red motif indicating the N-terminal pGlu. b Titration of αTRP1 clone TA99 (1:1 dilution, commencing at 40 μg/mL) followed by αmouse IgG APC (1:800) on murine B16F10 wildtype (blue) and QPCTL KO (red) cells. Data represents individual data point and the line is the mean percentage of MFI of αTRP1 clone TA99 staining relative to the MFI of 40 μg/mL αTRP1 clone TA99 on wildtype cells (n = 3). c Flanvotumab (1:200) followed by αhuman clone QA19 (1:100) on B16F10 wildtype (blue) and QPCTL KO (red) cells. Data represents the percentage of MFI, + standard deviation error, bar of flanvotumab staining relative to the MFI flanvotumab on wildtype cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n = 3). d Representative histograms of αTRP1 clone TA99 (1:100) followed by αmouse IgG APC (1:800) or flanvotumab (1:200) followed by αhuman clone QA19 PE (1:100), unstained (gray) or secondary controls (dark gray) staining on B16F10 treated with 10 μM glutaminyl cyclase inhibitors PQ912 (red) or SEN177 (orange) or equal amounts of DMSO (blue) for three days. Bar graphs show the percentage of the MFI of αTRP1 clone TA99 or flanvotumab staining, + standard deviation error bar, relative to the MFI of DMSO control cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n = 3). e Representative histograms of αTRP1 clone TA99 (1:100) followed by αmouse IgG APC (1:800), or flanvotumab (1:50) followed by αhuman clone QA19 PE (1:100), unstained (gray) or secondary controls (dark gray) staining on primary immortalized human melanocytes treated with 10 μM glutaminyl cyclase inhibitors PQ912 (red) or SEN177 (orange) or equal amounts of DMSO (blue) for three days. Bar graphs show the percentage of the MFI of αTRP1 clone TA99 or flanvotumab, + standard deviation error bar, relative to the MFI of DMSO control cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n ≥ 3). Abbreviations: MFI, median fluorescent intensity; KO, knockout; US, unstained; Sec, secondary antibody only; PQ, PQ912; SEN, SEN177.

    Journal: Communications Biology

    Article Title: Pyroglutamation of cell surface proteins CD47 and TRP1 by glutaminyl cyclase modulates therapeutic antibody binding

    doi: 10.1038/s42003-025-08938-4

    Figure Lengend Snippet: a Crystal structure of human TRP1 (PDB: 5M8L), with the red motif indicating the N-terminal pGlu. b Titration of αTRP1 clone TA99 (1:1 dilution, commencing at 40 μg/mL) followed by αmouse IgG APC (1:800) on murine B16F10 wildtype (blue) and QPCTL KO (red) cells. Data represents individual data point and the line is the mean percentage of MFI of αTRP1 clone TA99 staining relative to the MFI of 40 μg/mL αTRP1 clone TA99 on wildtype cells (n = 3). c Flanvotumab (1:200) followed by αhuman clone QA19 (1:100) on B16F10 wildtype (blue) and QPCTL KO (red) cells. Data represents the percentage of MFI, + standard deviation error, bar of flanvotumab staining relative to the MFI flanvotumab on wildtype cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n = 3). d Representative histograms of αTRP1 clone TA99 (1:100) followed by αmouse IgG APC (1:800) or flanvotumab (1:200) followed by αhuman clone QA19 PE (1:100), unstained (gray) or secondary controls (dark gray) staining on B16F10 treated with 10 μM glutaminyl cyclase inhibitors PQ912 (red) or SEN177 (orange) or equal amounts of DMSO (blue) for three days. Bar graphs show the percentage of the MFI of αTRP1 clone TA99 or flanvotumab staining, + standard deviation error bar, relative to the MFI of DMSO control cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n = 3). e Representative histograms of αTRP1 clone TA99 (1:100) followed by αmouse IgG APC (1:800), or flanvotumab (1:50) followed by αhuman clone QA19 PE (1:100), unstained (gray) or secondary controls (dark gray) staining on primary immortalized human melanocytes treated with 10 μM glutaminyl cyclase inhibitors PQ912 (red) or SEN177 (orange) or equal amounts of DMSO (blue) for three days. Bar graphs show the percentage of the MFI of αTRP1 clone TA99 or flanvotumab, + standard deviation error bar, relative to the MFI of DMSO control cells. One-way Anova was performed followed by the Dunnett’s multiple comparisons test (n ≥ 3). Abbreviations: MFI, median fluorescent intensity; KO, knockout; US, unstained; Sec, secondary antibody only; PQ, PQ912; SEN, SEN177.

    Article Snippet: Cells were incubated with polyclonal αTRP1 (1:100, # EPR13063 , Abcam) or αTRP1 clone TA99 (1:100, #SC-58438, Santa Cruz), diluted in 50 μL facs buffer supplemented with saponin for 30 minutes on ice shielded from light.

    Techniques: Titration, Staining, Standard Deviation, Control, Knock-Out

    a K D calculation of TRP1 TA99 on B16F10 wildtype and QPCTL KO cells. ODE model fit for titration binding curves of WT and QPCTL KO conditions for the B16F10 cell line utilizing the full model in which K D values are estimated separately. b MFI of αTRP1 clone TA99 (1:50) followed by αmouse IgG APC (1:100) or αHIS PE (1:50) on grazoprevir treated HeLa cells expressing CAR-TRP1 in the presence or absence of 4 day treatment of 30 µM SEN177. Data represents the MFI, + standard deviation error bar. Unpaired T test was performed to assess the two groups (n = 3). c Percentage of CD8 + T-cells positive for the indicated markers that have been cocultured with B16F10 wildtype or QPCTL KO cells in the presence of 1, 0.1 or 0.01 ug/mL TRP1 TA99-CD3-bispecific antibody for 48 hours. Data represents the percentage, + standard deviation error bar. One-way Anova was performed to assess the groups (n = 3). Abbreviations: MFI, median fluorescent intensity; WT, wildtype; KO, knockout; PQ, PQ912; SEN, SEN177.

    Journal: Communications Biology

    Article Title: Pyroglutamation of cell surface proteins CD47 and TRP1 by glutaminyl cyclase modulates therapeutic antibody binding

    doi: 10.1038/s42003-025-08938-4

    Figure Lengend Snippet: a K D calculation of TRP1 TA99 on B16F10 wildtype and QPCTL KO cells. ODE model fit for titration binding curves of WT and QPCTL KO conditions for the B16F10 cell line utilizing the full model in which K D values are estimated separately. b MFI of αTRP1 clone TA99 (1:50) followed by αmouse IgG APC (1:100) or αHIS PE (1:50) on grazoprevir treated HeLa cells expressing CAR-TRP1 in the presence or absence of 4 day treatment of 30 µM SEN177. Data represents the MFI, + standard deviation error bar. Unpaired T test was performed to assess the two groups (n = 3). c Percentage of CD8 + T-cells positive for the indicated markers that have been cocultured with B16F10 wildtype or QPCTL KO cells in the presence of 1, 0.1 or 0.01 ug/mL TRP1 TA99-CD3-bispecific antibody for 48 hours. Data represents the percentage, + standard deviation error bar. One-way Anova was performed to assess the groups (n = 3). Abbreviations: MFI, median fluorescent intensity; WT, wildtype; KO, knockout; PQ, PQ912; SEN, SEN177.

    Article Snippet: Cells were incubated with polyclonal αTRP1 (1:100, # EPR13063 , Abcam) or αTRP1 clone TA99 (1:100, #SC-58438, Santa Cruz), diluted in 50 μL facs buffer supplemented with saponin for 30 minutes on ice shielded from light.

    Techniques: Titration, Binding Assay, Expressing, Standard Deviation, Knock-Out