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arc101  (Charles River Laboratories)

 
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    Charles River Laboratories arc101
    <t>ARC101</t> overview and target cell binding characteristics. (A) Schematic representation of ARC101, constructed on a human IgG1 Fc backbone incorporating Fc-silencing and knobs-into-holes heterodimerization mutations. The molecule features a monovalent anti-CLDN6 Fab fused to the N-terminus of the “hole” chain and a monovalent anti-CD3 scFv fused to the N-terminus of the “knob” chain. (B) Dose-response binding of ARC101 and reference anti-CLDN6 abs to SKOV3 cells overexpressing CLDN6, CLDN9, and CLDN4 using flow cytometry. The Y-axis represents Fold increase in mean fluorescence intensity (MFI) over the background. (C) Dose-response binding of ARC101 to human pan-T cells from five donors by flow cytometry. The Y-axis represents Fold increase in MFI over the background.
    Arc101, supplied by Charles River Laboratories, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
    https://www.bioz.com/product/arc101/arc101/pmc12977278-382-4-14
    Average 86 stars, based on 1 article reviews
    arc101 - by Bioz Stars, 2026-10
    86/100 stars

    Images

    1) Product Images from "Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma"

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma

    Journal: mAbs

    doi: 10.1080/19420862.2026.2637299

    ARC101 overview and target cell binding characteristics. (A) Schematic representation of ARC101, constructed on a human IgG1 Fc backbone incorporating Fc-silencing and knobs-into-holes heterodimerization mutations. The molecule features a monovalent anti-CLDN6 Fab fused to the N-terminus of the “hole” chain and a monovalent anti-CD3 scFv fused to the N-terminus of the “knob” chain. (B) Dose-response binding of ARC101 and reference anti-CLDN6 abs to SKOV3 cells overexpressing CLDN6, CLDN9, and CLDN4 using flow cytometry. The Y-axis represents Fold increase in mean fluorescence intensity (MFI) over the background. (C) Dose-response binding of ARC101 to human pan-T cells from five donors by flow cytometry. The Y-axis represents Fold increase in MFI over the background.
    Figure Legend Snippet: ARC101 overview and target cell binding characteristics. (A) Schematic representation of ARC101, constructed on a human IgG1 Fc backbone incorporating Fc-silencing and knobs-into-holes heterodimerization mutations. The molecule features a monovalent anti-CLDN6 Fab fused to the N-terminus of the “hole” chain and a monovalent anti-CD3 scFv fused to the N-terminus of the “knob” chain. (B) Dose-response binding of ARC101 and reference anti-CLDN6 abs to SKOV3 cells overexpressing CLDN6, CLDN9, and CLDN4 using flow cytometry. The Y-axis represents Fold increase in mean fluorescence intensity (MFI) over the background. (C) Dose-response binding of ARC101 to human pan-T cells from five donors by flow cytometry. The Y-axis represents Fold increase in MFI over the background.

    Techniques Used: Binding Assay, Construct, Flow Cytometry, Fluorescence

    Binding characterization of ARC10 to human CD3εδ heterodimer. (A) Binding affinity and kinetics measurement by surface plasmon resonance (SPR). Curves represent binding response to serial dilution of CD3εδ, ranging from 100 nM to 0.4 nM in 3-fold dilutions. (B) Competitive binding of ARC101-CD3 and SP34-CD3 to human CD3εδ evaluated using SPR. Blue curves represent responses from a two-step injection separated by a dashed line: the first step with ARC101-CD3 injection over the CD3 surface, followed by injecting either SP34-CD3 (top panel) or ARC101-CD3 (bottom panel) over the bound ARC101-CD3/CD3 surface. The orange curves represent controls in which buffer was injected first, followed by injecting either ARC101-CD3 or SP34-CD3 onto the CD3 surface. An increase in the second-step signal indicates non-competitive binding, whereas no change suggests competitive binding. (C) ARC101 binding epitopes identified by HDX-MS, mapped onto the CD3 structure (PDB: 6JXR) with its subunits colored according to the legend. Primary and peripheral interaction sites on CD3ε are shown in blue and cyan, respectively, and the interaction site on CD3δ is shown in green.
    Figure Legend Snippet: Binding characterization of ARC10 to human CD3εδ heterodimer. (A) Binding affinity and kinetics measurement by surface plasmon resonance (SPR). Curves represent binding response to serial dilution of CD3εδ, ranging from 100 nM to 0.4 nM in 3-fold dilutions. (B) Competitive binding of ARC101-CD3 and SP34-CD3 to human CD3εδ evaluated using SPR. Blue curves represent responses from a two-step injection separated by a dashed line: the first step with ARC101-CD3 injection over the CD3 surface, followed by injecting either SP34-CD3 (top panel) or ARC101-CD3 (bottom panel) over the bound ARC101-CD3/CD3 surface. The orange curves represent controls in which buffer was injected first, followed by injecting either ARC101-CD3 or SP34-CD3 onto the CD3 surface. An increase in the second-step signal indicates non-competitive binding, whereas no change suggests competitive binding. (C) ARC101 binding epitopes identified by HDX-MS, mapped onto the CD3 structure (PDB: 6JXR) with its subunits colored according to the legend. Primary and peripheral interaction sites on CD3ε are shown in blue and cyan, respectively, and the interaction site on CD3δ is shown in green.

    Techniques Used: Binding Assay, SPR Assay, Serial Dilution, Injection

    In vivo efficacy and pharmacokinetic profile of ARC101 in humanized mice bearing OVCAR3 xenografts. (A) Study design for evaluating the in vivo anti-tumor efficacy of ARC101 in a T cell-humanized NSG mouse model bearing subcutaneous OVCAR3 tumors. Tumors reached 92 ± 5 mm 3 before mice were randomized and administered 10 × 10 6 human CD3 + cells intraperitoneally. ARC101 treatment began 30 min after T cell implantation on day 0, followed by weekly dosing on days 7, 14, 21, and 28. Tumor volume, body weight, and clinical signs were monitored throughout the study. (B) Anti-tumor efficacy of ARC101 compared to the vehicle control over time. Tumor volumes were measured three times per week using a digital vernier caliper and calculated using the formula: tumor volume (mm 3 ) = (L x W 2 )/2, where L is tumor length and W is tumor width in millimeters. Lines represent the mean tumor volume ± SEM. P -values were determined using two-way ANOVA followed by Bonferroni’s post-hoc multiple comparison test: ***, p < 0.001; ****, p < 0.0001. Percent tumor growth inhibition (% TGI) was calculated using the formula: %TGI = [(mean TV vehicle – mean TV treatment)/mean TV vehicle] × 100. (C) serum concentrations of ARC101 over time following a single intraperitoneal dose when tumors reached 102 ± 1.92 mm 3 . Concentrations from each time point were measured in triplicate using ELISA. Lines represent mean concentration ± SD. Non-compartmental analysis was used to derive pharmacokinetic parameters (see supplemental table S2).
    Figure Legend Snippet: In vivo efficacy and pharmacokinetic profile of ARC101 in humanized mice bearing OVCAR3 xenografts. (A) Study design for evaluating the in vivo anti-tumor efficacy of ARC101 in a T cell-humanized NSG mouse model bearing subcutaneous OVCAR3 tumors. Tumors reached 92 ± 5 mm 3 before mice were randomized and administered 10 × 10 6 human CD3 + cells intraperitoneally. ARC101 treatment began 30 min after T cell implantation on day 0, followed by weekly dosing on days 7, 14, 21, and 28. Tumor volume, body weight, and clinical signs were monitored throughout the study. (B) Anti-tumor efficacy of ARC101 compared to the vehicle control over time. Tumor volumes were measured three times per week using a digital vernier caliper and calculated using the formula: tumor volume (mm 3 ) = (L x W 2 )/2, where L is tumor length and W is tumor width in millimeters. Lines represent the mean tumor volume ± SEM. P -values were determined using two-way ANOVA followed by Bonferroni’s post-hoc multiple comparison test: ***, p < 0.001; ****, p < 0.0001. Percent tumor growth inhibition (% TGI) was calculated using the formula: %TGI = [(mean TV vehicle – mean TV treatment)/mean TV vehicle] × 100. (C) serum concentrations of ARC101 over time following a single intraperitoneal dose when tumors reached 102 ± 1.92 mm 3 . Concentrations from each time point were measured in triplicate using ELISA. Lines represent mean concentration ± SD. Non-compartmental analysis was used to derive pharmacokinetic parameters (see supplemental table S2).

    Techniques Used: In Vivo, Control, Comparison, Inhibition, Enzyme-linked Immunosorbent Assay, Concentration Assay

    Pharmacokinetic profile of ARC101 in cynomolgus monkeys following a single intravenous administration. Male cynomolgus monkeys ( n = 3 per group) received a single intravenous dose of ARC101 at either 1 mg/kg or 10 mg/kg. Serum concentrations of ARC101 were measured at designated time points post-dose using ELISA. Non-compartmental analysis was used to derive the pharmacokinetic parameters (see ).
    Figure Legend Snippet: Pharmacokinetic profile of ARC101 in cynomolgus monkeys following a single intravenous administration. Male cynomolgus monkeys ( n = 3 per group) received a single intravenous dose of ARC101 at either 1 mg/kg or 10 mg/kg. Serum concentrations of ARC101 were measured at designated time points post-dose using ELISA. Non-compartmental analysis was used to derive the pharmacokinetic parameters (see ).

    Techniques Used: Enzyme-linked Immunosorbent Assay

    Ex vivo dendritic cell (DC):CD4 + T cell restimulation assay for immunogenicity assessment. Peripheral blood mononuclear cells (PBMCs) from 30 donors were incubated with KLH, CEFTA, ARC101, or research-grade trastuzumab or bevacizumab antibodies, and analyzed via flow cytometry for CD4 + live cells expressing CD134 (A, B) or IFN-γ (C, D). (A, C) violin plot of the simulation index (SI) for each of the 30 donors treated with the indicated Antibodies or peptide controls. The SI is defined as the ratio of the percentage of CD4 + CD134 + cells or CD4 + IFN-γ + cells in the treated condition to that in the untreated condition. The horizontal dashed line indicates the threshold for a positive response (SI ≥ 1.84 for CD4 + CD134 + and SI ≥ 1.78 for CD4 + IFN-γ + ). Each dot represents an individual donor for KLH and CEFTA, while two dots per donor (corresponding to two tested concentrations) are shown for each antibody. P -values from pairwise comparisons (Wilcoxon matched-pairs signed rank test) are indicated: ns: not significant, p > 0.05; ** p ≤ 0.01; *** p ≤ 0.001; and **** p ≤ 0.0001. (B, D) Percentage of donors classified as positive responders for each treatment based on SI ≥ 2. P -values (Fisher’s exact test) are shown: ns: not significant and *** p ≤ 0.001.
    Figure Legend Snippet: Ex vivo dendritic cell (DC):CD4 + T cell restimulation assay for immunogenicity assessment. Peripheral blood mononuclear cells (PBMCs) from 30 donors were incubated with KLH, CEFTA, ARC101, or research-grade trastuzumab or bevacizumab antibodies, and analyzed via flow cytometry for CD4 + live cells expressing CD134 (A, B) or IFN-γ (C, D). (A, C) violin plot of the simulation index (SI) for each of the 30 donors treated with the indicated Antibodies or peptide controls. The SI is defined as the ratio of the percentage of CD4 + CD134 + cells or CD4 + IFN-γ + cells in the treated condition to that in the untreated condition. The horizontal dashed line indicates the threshold for a positive response (SI ≥ 1.84 for CD4 + CD134 + and SI ≥ 1.78 for CD4 + IFN-γ + ). Each dot represents an individual donor for KLH and CEFTA, while two dots per donor (corresponding to two tested concentrations) are shown for each antibody. P -values from pairwise comparisons (Wilcoxon matched-pairs signed rank test) are indicated: ns: not significant, p > 0.05; ** p ≤ 0.01; *** p ≤ 0.001; and **** p ≤ 0.0001. (B, D) Percentage of donors classified as positive responders for each treatment based on SI ≥ 2. P -values (Fisher’s exact test) are shown: ns: not significant and *** p ≤ 0.001.

    Techniques Used: Ex Vivo, Immunopeptidomics, Incubation, Flow Cytometry, Expressing

    Related Articles

    other:

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma
    Article Snippet: MFI values were extracted, background-subtracted using secondary antibody control wells, and plotted in Prism (GraphPad, version 10.4) using a four-parameter nonlinear regression.

    Microarray:

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma.
    Article Snippet: .. Retrogenix microarray screening further corroborated this finding, as ARC101 bound CD3ε only when coexpressed with CD3δ or CD3γ, indicating a requirement for heterodimer formation consistent with conformational epitope recognition.54 The conformational nature of CD3 binding was further evaluated using a chemical denaturation approach in human pan T cells, which resulted in substantial reduction in ARC101 binding (47–72%) compared with native conditions (Supplementary Figure S11). ..

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma.
    Article Snippet: MFI values were extracted, background-subtracted using secondary antibody control wells, and plotted in Prism (GraphPad, version 10.4) using a four-parameter nonlinear regression. .. Off-target binding interactions of ARC101 with human membrane and secreted proteins were assessed using Retrogenix® Cell Microarray Technology (Charles River Laboratories). .. Plates were incubated for 1 h at 37°C, washed three times with FACS buffer, and incubated with PE-labeled goat anti-human IgG Fc (Abcam, Cat# ab9859) for 30 min at 4°C.

    Binding Assay:

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma.
    Article Snippet: .. Retrogenix microarray screening further corroborated this finding, as ARC101 bound CD3ε only when coexpressed with CD3δ or CD3γ, indicating a requirement for heterodimer formation consistent with conformational epitope recognition.54 The conformational nature of CD3 binding was further evaluated using a chemical denaturation approach in human pan T cells, which resulted in substantial reduction in ARC101 binding (47–72%) compared with native conditions (Supplementary Figure S11). ..

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma.
    Article Snippet: MFI values were extracted, background-subtracted using secondary antibody control wells, and plotted in Prism (GraphPad, version 10.4) using a four-parameter nonlinear regression. .. Off-target binding interactions of ARC101 with human membrane and secreted proteins were assessed using Retrogenix® Cell Microarray Technology (Charles River Laboratories). .. Plates were incubated for 1 h at 37°C, washed three times with FACS buffer, and incubated with PE-labeled goat anti-human IgG Fc (Abcam, Cat# ab9859) for 30 min at 4°C.

    Screening:

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma
    Article Snippet: .. The specificity of ARC101 for both CLDN6 and CD3 was further confirmed by Retrogenix screening against approximately 6500 human proteins, including plasma membrane proteins, secreted proteins, and heterodimeric complexes, collectively covering > 90% of the known cell surface and secreted proteome. ..

    Clinical Proteomics:

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma
    Article Snippet: .. The specificity of ARC101 for both CLDN6 and CD3 was further confirmed by Retrogenix screening against approximately 6500 human proteins, including plasma membrane proteins, secreted proteins, and heterodimeric complexes, collectively covering > 90% of the known cell surface and secreted proteome. ..

    Membrane:

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma
    Article Snippet: .. The specificity of ARC101 for both CLDN6 and CD3 was further confirmed by Retrogenix screening against approximately 6500 human proteins, including plasma membrane proteins, secreted proteins, and heterodimeric complexes, collectively covering > 90% of the known cell surface and secreted proteome. ..

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma.
    Article Snippet: MFI values were extracted, background-subtracted using secondary antibody control wells, and plotted in Prism (GraphPad, version 10.4) using a four-parameter nonlinear regression. .. Off-target binding interactions of ARC101 with human membrane and secreted proteins were assessed using Retrogenix® Cell Microarray Technology (Charles River Laboratories). .. Plates were incubated for 1 h at 37°C, washed three times with FACS buffer, and incubated with PE-labeled goat anti-human IgG Fc (Abcam, Cat# ab9859) for 30 min at 4°C.



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    <t>ARC101</t> overview and target cell binding characteristics. (A) Schematic representation of ARC101, constructed on a human IgG1 Fc backbone incorporating Fc-silencing and knobs-into-holes heterodimerization mutations. The molecule features a monovalent anti-CLDN6 Fab fused to the N-terminus of the “hole” chain and a monovalent anti-CD3 scFv fused to the N-terminus of the “knob” chain. (B) Dose-response binding of ARC101 and reference anti-CLDN6 abs to SKOV3 cells overexpressing CLDN6, CLDN9, and CLDN4 using flow cytometry. The Y-axis represents Fold increase in mean fluorescence intensity (MFI) over the background. (C) Dose-response binding of ARC101 to human pan-T cells from five donors by flow cytometry. The Y-axis represents Fold increase in MFI over the background.
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    <t>ARC101</t> overview and target cell binding characteristics. (A) Schematic representation of ARC101, constructed on a human IgG1 Fc backbone incorporating Fc-silencing and knobs-into-holes heterodimerization mutations. The molecule features a monovalent anti-CLDN6 Fab fused to the N-terminus of the “hole” chain and a monovalent anti-CD3 scFv fused to the N-terminus of the “knob” chain. (B) Dose-response binding of ARC101 and reference anti-CLDN6 abs to SKOV3 cells overexpressing CLDN6, CLDN9, and CLDN4 using flow cytometry. The Y-axis represents Fold increase in mean fluorescence intensity (MFI) over the background. (C) Dose-response binding of ARC101 to human pan-T cells from five donors by flow cytometry. The Y-axis represents Fold increase in MFI over the background.
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    Image Search Results


    ARC101 overview and target cell binding characteristics. (A) Schematic representation of ARC101, constructed on a human IgG1 Fc backbone incorporating Fc-silencing and knobs-into-holes heterodimerization mutations. The molecule features a monovalent anti-CLDN6 Fab fused to the N-terminus of the “hole” chain and a monovalent anti-CD3 scFv fused to the N-terminus of the “knob” chain. (B) Dose-response binding of ARC101 and reference anti-CLDN6 abs to SKOV3 cells overexpressing CLDN6, CLDN9, and CLDN4 using flow cytometry. The Y-axis represents Fold increase in mean fluorescence intensity (MFI) over the background. (C) Dose-response binding of ARC101 to human pan-T cells from five donors by flow cytometry. The Y-axis represents Fold increase in MFI over the background.

    Journal: mAbs

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma

    doi: 10.1080/19420862.2026.2637299

    Figure Lengend Snippet: ARC101 overview and target cell binding characteristics. (A) Schematic representation of ARC101, constructed on a human IgG1 Fc backbone incorporating Fc-silencing and knobs-into-holes heterodimerization mutations. The molecule features a monovalent anti-CLDN6 Fab fused to the N-terminus of the “hole” chain and a monovalent anti-CD3 scFv fused to the N-terminus of the “knob” chain. (B) Dose-response binding of ARC101 and reference anti-CLDN6 abs to SKOV3 cells overexpressing CLDN6, CLDN9, and CLDN4 using flow cytometry. The Y-axis represents Fold increase in mean fluorescence intensity (MFI) over the background. (C) Dose-response binding of ARC101 to human pan-T cells from five donors by flow cytometry. The Y-axis represents Fold increase in MFI over the background.

    Article Snippet: Off-target binding interactions of ARC101 with human membrane and secreted proteins were assessed using Retrogenix® Cell Microarray Technology (Charles River Laboratories).

    Techniques: Binding Assay, Construct, Flow Cytometry, Fluorescence

    Binding characterization of ARC10 to human CD3εδ heterodimer. (A) Binding affinity and kinetics measurement by surface plasmon resonance (SPR). Curves represent binding response to serial dilution of CD3εδ, ranging from 100 nM to 0.4 nM in 3-fold dilutions. (B) Competitive binding of ARC101-CD3 and SP34-CD3 to human CD3εδ evaluated using SPR. Blue curves represent responses from a two-step injection separated by a dashed line: the first step with ARC101-CD3 injection over the CD3 surface, followed by injecting either SP34-CD3 (top panel) or ARC101-CD3 (bottom panel) over the bound ARC101-CD3/CD3 surface. The orange curves represent controls in which buffer was injected first, followed by injecting either ARC101-CD3 or SP34-CD3 onto the CD3 surface. An increase in the second-step signal indicates non-competitive binding, whereas no change suggests competitive binding. (C) ARC101 binding epitopes identified by HDX-MS, mapped onto the CD3 structure (PDB: 6JXR) with its subunits colored according to the legend. Primary and peripheral interaction sites on CD3ε are shown in blue and cyan, respectively, and the interaction site on CD3δ is shown in green.

    Journal: mAbs

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma

    doi: 10.1080/19420862.2026.2637299

    Figure Lengend Snippet: Binding characterization of ARC10 to human CD3εδ heterodimer. (A) Binding affinity and kinetics measurement by surface plasmon resonance (SPR). Curves represent binding response to serial dilution of CD3εδ, ranging from 100 nM to 0.4 nM in 3-fold dilutions. (B) Competitive binding of ARC101-CD3 and SP34-CD3 to human CD3εδ evaluated using SPR. Blue curves represent responses from a two-step injection separated by a dashed line: the first step with ARC101-CD3 injection over the CD3 surface, followed by injecting either SP34-CD3 (top panel) or ARC101-CD3 (bottom panel) over the bound ARC101-CD3/CD3 surface. The orange curves represent controls in which buffer was injected first, followed by injecting either ARC101-CD3 or SP34-CD3 onto the CD3 surface. An increase in the second-step signal indicates non-competitive binding, whereas no change suggests competitive binding. (C) ARC101 binding epitopes identified by HDX-MS, mapped onto the CD3 structure (PDB: 6JXR) with its subunits colored according to the legend. Primary and peripheral interaction sites on CD3ε are shown in blue and cyan, respectively, and the interaction site on CD3δ is shown in green.

    Article Snippet: Off-target binding interactions of ARC101 with human membrane and secreted proteins were assessed using Retrogenix® Cell Microarray Technology (Charles River Laboratories).

    Techniques: Binding Assay, SPR Assay, Serial Dilution, Injection

    In vivo efficacy and pharmacokinetic profile of ARC101 in humanized mice bearing OVCAR3 xenografts. (A) Study design for evaluating the in vivo anti-tumor efficacy of ARC101 in a T cell-humanized NSG mouse model bearing subcutaneous OVCAR3 tumors. Tumors reached 92 ± 5 mm 3 before mice were randomized and administered 10 × 10 6 human CD3 + cells intraperitoneally. ARC101 treatment began 30 min after T cell implantation on day 0, followed by weekly dosing on days 7, 14, 21, and 28. Tumor volume, body weight, and clinical signs were monitored throughout the study. (B) Anti-tumor efficacy of ARC101 compared to the vehicle control over time. Tumor volumes were measured three times per week using a digital vernier caliper and calculated using the formula: tumor volume (mm 3 ) = (L x W 2 )/2, where L is tumor length and W is tumor width in millimeters. Lines represent the mean tumor volume ± SEM. P -values were determined using two-way ANOVA followed by Bonferroni’s post-hoc multiple comparison test: ***, p < 0.001; ****, p < 0.0001. Percent tumor growth inhibition (% TGI) was calculated using the formula: %TGI = [(mean TV vehicle – mean TV treatment)/mean TV vehicle] × 100. (C) serum concentrations of ARC101 over time following a single intraperitoneal dose when tumors reached 102 ± 1.92 mm 3 . Concentrations from each time point were measured in triplicate using ELISA. Lines represent mean concentration ± SD. Non-compartmental analysis was used to derive pharmacokinetic parameters (see supplemental table S2).

    Journal: mAbs

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma

    doi: 10.1080/19420862.2026.2637299

    Figure Lengend Snippet: In vivo efficacy and pharmacokinetic profile of ARC101 in humanized mice bearing OVCAR3 xenografts. (A) Study design for evaluating the in vivo anti-tumor efficacy of ARC101 in a T cell-humanized NSG mouse model bearing subcutaneous OVCAR3 tumors. Tumors reached 92 ± 5 mm 3 before mice were randomized and administered 10 × 10 6 human CD3 + cells intraperitoneally. ARC101 treatment began 30 min after T cell implantation on day 0, followed by weekly dosing on days 7, 14, 21, and 28. Tumor volume, body weight, and clinical signs were monitored throughout the study. (B) Anti-tumor efficacy of ARC101 compared to the vehicle control over time. Tumor volumes were measured three times per week using a digital vernier caliper and calculated using the formula: tumor volume (mm 3 ) = (L x W 2 )/2, where L is tumor length and W is tumor width in millimeters. Lines represent the mean tumor volume ± SEM. P -values were determined using two-way ANOVA followed by Bonferroni’s post-hoc multiple comparison test: ***, p < 0.001; ****, p < 0.0001. Percent tumor growth inhibition (% TGI) was calculated using the formula: %TGI = [(mean TV vehicle – mean TV treatment)/mean TV vehicle] × 100. (C) serum concentrations of ARC101 over time following a single intraperitoneal dose when tumors reached 102 ± 1.92 mm 3 . Concentrations from each time point were measured in triplicate using ELISA. Lines represent mean concentration ± SD. Non-compartmental analysis was used to derive pharmacokinetic parameters (see supplemental table S2).

    Article Snippet: Off-target binding interactions of ARC101 with human membrane and secreted proteins were assessed using Retrogenix® Cell Microarray Technology (Charles River Laboratories).

    Techniques: In Vivo, Control, Comparison, Inhibition, Enzyme-linked Immunosorbent Assay, Concentration Assay

    Pharmacokinetic profile of ARC101 in cynomolgus monkeys following a single intravenous administration. Male cynomolgus monkeys ( n = 3 per group) received a single intravenous dose of ARC101 at either 1 mg/kg or 10 mg/kg. Serum concentrations of ARC101 were measured at designated time points post-dose using ELISA. Non-compartmental analysis was used to derive the pharmacokinetic parameters (see ).

    Journal: mAbs

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma

    doi: 10.1080/19420862.2026.2637299

    Figure Lengend Snippet: Pharmacokinetic profile of ARC101 in cynomolgus monkeys following a single intravenous administration. Male cynomolgus monkeys ( n = 3 per group) received a single intravenous dose of ARC101 at either 1 mg/kg or 10 mg/kg. Serum concentrations of ARC101 were measured at designated time points post-dose using ELISA. Non-compartmental analysis was used to derive the pharmacokinetic parameters (see ).

    Article Snippet: Off-target binding interactions of ARC101 with human membrane and secreted proteins were assessed using Retrogenix® Cell Microarray Technology (Charles River Laboratories).

    Techniques: Enzyme-linked Immunosorbent Assay

    Ex vivo dendritic cell (DC):CD4 + T cell restimulation assay for immunogenicity assessment. Peripheral blood mononuclear cells (PBMCs) from 30 donors were incubated with KLH, CEFTA, ARC101, or research-grade trastuzumab or bevacizumab antibodies, and analyzed via flow cytometry for CD4 + live cells expressing CD134 (A, B) or IFN-γ (C, D). (A, C) violin plot of the simulation index (SI) for each of the 30 donors treated with the indicated Antibodies or peptide controls. The SI is defined as the ratio of the percentage of CD4 + CD134 + cells or CD4 + IFN-γ + cells in the treated condition to that in the untreated condition. The horizontal dashed line indicates the threshold for a positive response (SI ≥ 1.84 for CD4 + CD134 + and SI ≥ 1.78 for CD4 + IFN-γ + ). Each dot represents an individual donor for KLH and CEFTA, while two dots per donor (corresponding to two tested concentrations) are shown for each antibody. P -values from pairwise comparisons (Wilcoxon matched-pairs signed rank test) are indicated: ns: not significant, p > 0.05; ** p ≤ 0.01; *** p ≤ 0.001; and **** p ≤ 0.0001. (B, D) Percentage of donors classified as positive responders for each treatment based on SI ≥ 2. P -values (Fisher’s exact test) are shown: ns: not significant and *** p ≤ 0.001.

    Journal: mAbs

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma

    doi: 10.1080/19420862.2026.2637299

    Figure Lengend Snippet: Ex vivo dendritic cell (DC):CD4 + T cell restimulation assay for immunogenicity assessment. Peripheral blood mononuclear cells (PBMCs) from 30 donors were incubated with KLH, CEFTA, ARC101, or research-grade trastuzumab or bevacizumab antibodies, and analyzed via flow cytometry for CD4 + live cells expressing CD134 (A, B) or IFN-γ (C, D). (A, C) violin plot of the simulation index (SI) for each of the 30 donors treated with the indicated Antibodies or peptide controls. The SI is defined as the ratio of the percentage of CD4 + CD134 + cells or CD4 + IFN-γ + cells in the treated condition to that in the untreated condition. The horizontal dashed line indicates the threshold for a positive response (SI ≥ 1.84 for CD4 + CD134 + and SI ≥ 1.78 for CD4 + IFN-γ + ). Each dot represents an individual donor for KLH and CEFTA, while two dots per donor (corresponding to two tested concentrations) are shown for each antibody. P -values from pairwise comparisons (Wilcoxon matched-pairs signed rank test) are indicated: ns: not significant, p > 0.05; ** p ≤ 0.01; *** p ≤ 0.001; and **** p ≤ 0.0001. (B, D) Percentage of donors classified as positive responders for each treatment based on SI ≥ 2. P -values (Fisher’s exact test) are shown: ns: not significant and *** p ≤ 0.001.

    Article Snippet: Off-target binding interactions of ARC101 with human membrane and secreted proteins were assessed using Retrogenix® Cell Microarray Technology (Charles River Laboratories).

    Techniques: Ex Vivo, Immunopeptidomics, Incubation, Flow Cytometry, Expressing

    ARC101 overview and target cell binding characteristics. (A) Schematic representation of ARC101, constructed on a human IgG1 Fc backbone incorporating Fc-silencing and knobs-into-holes heterodimerization mutations. The molecule features a monovalent anti-CLDN6 Fab fused to the N-terminus of the “hole” chain and a monovalent anti-CD3 scFv fused to the N-terminus of the “knob” chain. (B) Dose-response binding of ARC101 and reference anti-CLDN6 abs to SKOV3 cells overexpressing CLDN6, CLDN9, and CLDN4 using flow cytometry. The Y-axis represents Fold increase in mean fluorescence intensity (MFI) over the background. (C) Dose-response binding of ARC101 to human pan-T cells from five donors by flow cytometry. The Y-axis represents Fold increase in MFI over the background.

    Journal: mAbs

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma

    doi: 10.1080/19420862.2026.2637299

    Figure Lengend Snippet: ARC101 overview and target cell binding characteristics. (A) Schematic representation of ARC101, constructed on a human IgG1 Fc backbone incorporating Fc-silencing and knobs-into-holes heterodimerization mutations. The molecule features a monovalent anti-CLDN6 Fab fused to the N-terminus of the “hole” chain and a monovalent anti-CD3 scFv fused to the N-terminus of the “knob” chain. (B) Dose-response binding of ARC101 and reference anti-CLDN6 abs to SKOV3 cells overexpressing CLDN6, CLDN9, and CLDN4 using flow cytometry. The Y-axis represents Fold increase in mean fluorescence intensity (MFI) over the background. (C) Dose-response binding of ARC101 to human pan-T cells from five donors by flow cytometry. The Y-axis represents Fold increase in MFI over the background.

    Article Snippet: The binding of ARC101 to claudin family proteins was compared with two publicly disclosed anti-CLDN6 antibodies: Ref CLDN6 Ab1 (US20220289839) (assignee: Xencor) and Ref CLDN6 Ab2 (WO2022096700A1) (assignee: Amgen), both of which are CLDN6xCD3 bsAbs developed as treatments for solid tumors., To evaluate their target specificity for CLDN6, CLDN9, and CLDN4, each protein was overexpressed in SKOV3 cells, and surface antibody binding was assessed using flow cytometry ( ).

    Techniques: Binding Assay, Construct, Flow Cytometry, Fluorescence

    Binding characterization of ARC10 to human CD3εδ heterodimer. (A) Binding affinity and kinetics measurement by surface plasmon resonance (SPR). Curves represent binding response to serial dilution of CD3εδ, ranging from 100 nM to 0.4 nM in 3-fold dilutions. (B) Competitive binding of ARC101-CD3 and SP34-CD3 to human CD3εδ evaluated using SPR. Blue curves represent responses from a two-step injection separated by a dashed line: the first step with ARC101-CD3 injection over the CD3 surface, followed by injecting either SP34-CD3 (top panel) or ARC101-CD3 (bottom panel) over the bound ARC101-CD3/CD3 surface. The orange curves represent controls in which buffer was injected first, followed by injecting either ARC101-CD3 or SP34-CD3 onto the CD3 surface. An increase in the second-step signal indicates non-competitive binding, whereas no change suggests competitive binding. (C) ARC101 binding epitopes identified by HDX-MS, mapped onto the CD3 structure (PDB: 6JXR) with its subunits colored according to the legend. Primary and peripheral interaction sites on CD3ε are shown in blue and cyan, respectively, and the interaction site on CD3δ is shown in green.

    Journal: mAbs

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma

    doi: 10.1080/19420862.2026.2637299

    Figure Lengend Snippet: Binding characterization of ARC10 to human CD3εδ heterodimer. (A) Binding affinity and kinetics measurement by surface plasmon resonance (SPR). Curves represent binding response to serial dilution of CD3εδ, ranging from 100 nM to 0.4 nM in 3-fold dilutions. (B) Competitive binding of ARC101-CD3 and SP34-CD3 to human CD3εδ evaluated using SPR. Blue curves represent responses from a two-step injection separated by a dashed line: the first step with ARC101-CD3 injection over the CD3 surface, followed by injecting either SP34-CD3 (top panel) or ARC101-CD3 (bottom panel) over the bound ARC101-CD3/CD3 surface. The orange curves represent controls in which buffer was injected first, followed by injecting either ARC101-CD3 or SP34-CD3 onto the CD3 surface. An increase in the second-step signal indicates non-competitive binding, whereas no change suggests competitive binding. (C) ARC101 binding epitopes identified by HDX-MS, mapped onto the CD3 structure (PDB: 6JXR) with its subunits colored according to the legend. Primary and peripheral interaction sites on CD3ε are shown in blue and cyan, respectively, and the interaction site on CD3δ is shown in green.

    Article Snippet: The binding of ARC101 to claudin family proteins was compared with two publicly disclosed anti-CLDN6 antibodies: Ref CLDN6 Ab1 (US20220289839) (assignee: Xencor) and Ref CLDN6 Ab2 (WO2022096700A1) (assignee: Amgen), both of which are CLDN6xCD3 bsAbs developed as treatments for solid tumors., To evaluate their target specificity for CLDN6, CLDN9, and CLDN4, each protein was overexpressed in SKOV3 cells, and surface antibody binding was assessed using flow cytometry ( ).

    Techniques: Binding Assay, SPR Assay, Serial Dilution, Injection

    In vivo efficacy and pharmacokinetic profile of ARC101 in humanized mice bearing OVCAR3 xenografts. (A) Study design for evaluating the in vivo anti-tumor efficacy of ARC101 in a T cell-humanized NSG mouse model bearing subcutaneous OVCAR3 tumors. Tumors reached 92 ± 5 mm 3 before mice were randomized and administered 10 × 10 6 human CD3 + cells intraperitoneally. ARC101 treatment began 30 min after T cell implantation on day 0, followed by weekly dosing on days 7, 14, 21, and 28. Tumor volume, body weight, and clinical signs were monitored throughout the study. (B) Anti-tumor efficacy of ARC101 compared to the vehicle control over time. Tumor volumes were measured three times per week using a digital vernier caliper and calculated using the formula: tumor volume (mm 3 ) = (L x W 2 )/2, where L is tumor length and W is tumor width in millimeters. Lines represent the mean tumor volume ± SEM. P -values were determined using two-way ANOVA followed by Bonferroni’s post-hoc multiple comparison test: ***, p < 0.001; ****, p < 0.0001. Percent tumor growth inhibition (% TGI) was calculated using the formula: %TGI = [(mean TV vehicle – mean TV treatment)/mean TV vehicle] × 100. (C) serum concentrations of ARC101 over time following a single intraperitoneal dose when tumors reached 102 ± 1.92 mm 3 . Concentrations from each time point were measured in triplicate using ELISA. Lines represent mean concentration ± SD. Non-compartmental analysis was used to derive pharmacokinetic parameters (see supplemental table S2).

    Journal: mAbs

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma

    doi: 10.1080/19420862.2026.2637299

    Figure Lengend Snippet: In vivo efficacy and pharmacokinetic profile of ARC101 in humanized mice bearing OVCAR3 xenografts. (A) Study design for evaluating the in vivo anti-tumor efficacy of ARC101 in a T cell-humanized NSG mouse model bearing subcutaneous OVCAR3 tumors. Tumors reached 92 ± 5 mm 3 before mice were randomized and administered 10 × 10 6 human CD3 + cells intraperitoneally. ARC101 treatment began 30 min after T cell implantation on day 0, followed by weekly dosing on days 7, 14, 21, and 28. Tumor volume, body weight, and clinical signs were monitored throughout the study. (B) Anti-tumor efficacy of ARC101 compared to the vehicle control over time. Tumor volumes were measured three times per week using a digital vernier caliper and calculated using the formula: tumor volume (mm 3 ) = (L x W 2 )/2, where L is tumor length and W is tumor width in millimeters. Lines represent the mean tumor volume ± SEM. P -values were determined using two-way ANOVA followed by Bonferroni’s post-hoc multiple comparison test: ***, p < 0.001; ****, p < 0.0001. Percent tumor growth inhibition (% TGI) was calculated using the formula: %TGI = [(mean TV vehicle – mean TV treatment)/mean TV vehicle] × 100. (C) serum concentrations of ARC101 over time following a single intraperitoneal dose when tumors reached 102 ± 1.92 mm 3 . Concentrations from each time point were measured in triplicate using ELISA. Lines represent mean concentration ± SD. Non-compartmental analysis was used to derive pharmacokinetic parameters (see supplemental table S2).

    Article Snippet: The binding of ARC101 to claudin family proteins was compared with two publicly disclosed anti-CLDN6 antibodies: Ref CLDN6 Ab1 (US20220289839) (assignee: Xencor) and Ref CLDN6 Ab2 (WO2022096700A1) (assignee: Amgen), both of which are CLDN6xCD3 bsAbs developed as treatments for solid tumors., To evaluate their target specificity for CLDN6, CLDN9, and CLDN4, each protein was overexpressed in SKOV3 cells, and surface antibody binding was assessed using flow cytometry ( ).

    Techniques: In Vivo, Control, Comparison, Inhibition, Enzyme-linked Immunosorbent Assay, Concentration Assay

    Pharmacokinetic profile of ARC101 in cynomolgus monkeys following a single intravenous administration. Male cynomolgus monkeys ( n = 3 per group) received a single intravenous dose of ARC101 at either 1 mg/kg or 10 mg/kg. Serum concentrations of ARC101 were measured at designated time points post-dose using ELISA. Non-compartmental analysis was used to derive the pharmacokinetic parameters (see ).

    Journal: mAbs

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma

    doi: 10.1080/19420862.2026.2637299

    Figure Lengend Snippet: Pharmacokinetic profile of ARC101 in cynomolgus monkeys following a single intravenous administration. Male cynomolgus monkeys ( n = 3 per group) received a single intravenous dose of ARC101 at either 1 mg/kg or 10 mg/kg. Serum concentrations of ARC101 were measured at designated time points post-dose using ELISA. Non-compartmental analysis was used to derive the pharmacokinetic parameters (see ).

    Article Snippet: The binding of ARC101 to claudin family proteins was compared with two publicly disclosed anti-CLDN6 antibodies: Ref CLDN6 Ab1 (US20220289839) (assignee: Xencor) and Ref CLDN6 Ab2 (WO2022096700A1) (assignee: Amgen), both of which are CLDN6xCD3 bsAbs developed as treatments for solid tumors., To evaluate their target specificity for CLDN6, CLDN9, and CLDN4, each protein was overexpressed in SKOV3 cells, and surface antibody binding was assessed using flow cytometry ( ).

    Techniques: Enzyme-linked Immunosorbent Assay

    Ex vivo dendritic cell (DC):CD4 + T cell restimulation assay for immunogenicity assessment. Peripheral blood mononuclear cells (PBMCs) from 30 donors were incubated with KLH, CEFTA, ARC101, or research-grade trastuzumab or bevacizumab antibodies, and analyzed via flow cytometry for CD4 + live cells expressing CD134 (A, B) or IFN-γ (C, D). (A, C) violin plot of the simulation index (SI) for each of the 30 donors treated with the indicated Antibodies or peptide controls. The SI is defined as the ratio of the percentage of CD4 + CD134 + cells or CD4 + IFN-γ + cells in the treated condition to that in the untreated condition. The horizontal dashed line indicates the threshold for a positive response (SI ≥ 1.84 for CD4 + CD134 + and SI ≥ 1.78 for CD4 + IFN-γ + ). Each dot represents an individual donor for KLH and CEFTA, while two dots per donor (corresponding to two tested concentrations) are shown for each antibody. P -values from pairwise comparisons (Wilcoxon matched-pairs signed rank test) are indicated: ns: not significant, p > 0.05; ** p ≤ 0.01; *** p ≤ 0.001; and **** p ≤ 0.0001. (B, D) Percentage of donors classified as positive responders for each treatment based on SI ≥ 2. P -values (Fisher’s exact test) are shown: ns: not significant and *** p ≤ 0.001.

    Journal: mAbs

    Article Title: Overcoming claudin family homology: discovery of ARC101, a highly potent CLDN6-specific T-cell engager with a novel CD3 binder for ovarian adenocarcinoma

    doi: 10.1080/19420862.2026.2637299

    Figure Lengend Snippet: Ex vivo dendritic cell (DC):CD4 + T cell restimulation assay for immunogenicity assessment. Peripheral blood mononuclear cells (PBMCs) from 30 donors were incubated with KLH, CEFTA, ARC101, or research-grade trastuzumab or bevacizumab antibodies, and analyzed via flow cytometry for CD4 + live cells expressing CD134 (A, B) or IFN-γ (C, D). (A, C) violin plot of the simulation index (SI) for each of the 30 donors treated with the indicated Antibodies or peptide controls. The SI is defined as the ratio of the percentage of CD4 + CD134 + cells or CD4 + IFN-γ + cells in the treated condition to that in the untreated condition. The horizontal dashed line indicates the threshold for a positive response (SI ≥ 1.84 for CD4 + CD134 + and SI ≥ 1.78 for CD4 + IFN-γ + ). Each dot represents an individual donor for KLH and CEFTA, while two dots per donor (corresponding to two tested concentrations) are shown for each antibody. P -values from pairwise comparisons (Wilcoxon matched-pairs signed rank test) are indicated: ns: not significant, p > 0.05; ** p ≤ 0.01; *** p ≤ 0.001; and **** p ≤ 0.0001. (B, D) Percentage of donors classified as positive responders for each treatment based on SI ≥ 2. P -values (Fisher’s exact test) are shown: ns: not significant and *** p ≤ 0.001.

    Article Snippet: The binding of ARC101 to claudin family proteins was compared with two publicly disclosed anti-CLDN6 antibodies: Ref CLDN6 Ab1 (US20220289839) (assignee: Xencor) and Ref CLDN6 Ab2 (WO2022096700A1) (assignee: Amgen), both of which are CLDN6xCD3 bsAbs developed as treatments for solid tumors., To evaluate their target specificity for CLDN6, CLDN9, and CLDN4, each protein was overexpressed in SKOV3 cells, and surface antibody binding was assessed using flow cytometry ( ).

    Techniques: Ex Vivo, Immunopeptidomics, Incubation, Flow Cytometry, Expressing