Antagonistic Anti-CD40 mAb YH015

YH015 is a fully human anti-CD40 IgG1 antagonistic monoclonal antibody. YH015 was generated by our fully human antibody RenMice platform. It was screened out by our unique in vivo strategy and it has good in vivo and in vitro inhibitory activity and physicochemical properties.

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  • Highlights of antagonistic anti-CD40 mAb
  • In Vitro: YH015 has higher affinity for CD40
  • In Vivo: YH015 is superior in inhibition in the OVA antibody suppression screening experiment based on B-hCD40/FcRn double humanized mice
  • About CD40

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    Highlights of antagonistic anti-CD40 mAb
    • Superior affinity and in vivo efficacy of immune suppression as opposed to bleselumab. Bleselumab was chosen as the primary benchmark antibody.
    • Fc effector null.
    • Engineered with half-life extension to reduce frequency of clinical administration and improve patient compliance.
    • Excellent physicochemical properties suitable for CMC development and high concentration formulation for subcutaneous administration.
    • PCT formal application has been submitted in April 2023.
    • Stage: preclinical, CMC to be initiated
    In Vitro: YH015 has higher affinity for CD40
    In Vivo:YH015 is superior in inhibition in the OVA antibody suppression screening experiment based on B-hCD40/FcRn double humanized mice
    About CD40

    CD40 is a transmembrane protein belonging to the tumor necrosis factor receptor (TNFR) superfamily, broadly expressed on antigen-presenting cells such as dendritic cells, macrophages, and B cells. It plays a crucial role in mediating immune responses by facilitating T cell activation, cytokine production, and the development of memory B cells. Engagement of CD40 with its natural ligand, CD40L (CD154), triggers a cascade of signaling events that promote inflammation and immune cell proliferation. Dysregulation of the CD40-CD40L pathway has been implicated in various autoimmune diseases, chronic inflammation, and cancer, making CD40 a promising therapeutic target. CD40 inhibitors aim to modulate this pathway, reducing pathological immune activation while preserving essential immune functions.

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