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  • Poster presentation
  • Open Access

The CD40 agonistic monoclonal antibody APX005M has potent immune stimulatory capabilities

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Journal for ImmunoTherapy of Cancer20153 (Suppl 2) :P198

https://doi.org/10.1186/2051-1426-3-S2-P198

  • Published:

Keywords

  • Tumor Necrosis Factor Receptor
  • CD40 Antibody
  • IgG1 Monoclonal Antibody
  • Agonistic Effect
  • Agonistic Antibody

The co-stimulatory receptor CD40 is a member of the tumor necrosis factor receptor (TNFR) superfamily and plays an important role in the control and regulation of immune activation, especially in crosstalk between T cells and antigen presenting cells (APCs). The natural ligand for CD40 (CD40L, CD154) is expressed on activated T cells and provides a major component of T cell “help” for the immune response. Agonistic CD40 antibodies can substitute for the function of CD154 on T cells to boost immunity by stimulating antigen presentation and co-stimulation to T cells and have been shown to be potent boosters of anti-tumor immune responses. Anti-CD40 can directly inhibit tumor growth in CD40 expressing tumor cells.

APX005M is a humanized IgG1 monoclonal antibody that binds CD40 with high affinity and blocks the binding of CD40 to CD40L. APX005M activates dendritic cells, B cells and monocytes, and promotes antigen-specific T cell responses. APX005M demonstrates potent anti-tumor activity via ADCC and induction of apoptosis in CD40 expressing tumor cells. In comparison with other CD40 agonistic antibodies such as CP-870, 893 and SGN-40 analogs, APX005M has more potent CD40 agonistic effects and antibody effector function.

Authors’ Affiliations

(1)
Apexigen, Inc., San Carlos, CA, USA

Copyright

© Bjorck et al. 2015

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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