arGEN-X Partners with University of Bern to Develop Combination Cancer Therapies

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ARGX-110-based combination therapies have demonstrated potential in treatment-resistant cancers.

arGEN-X, a clinical-stage biopharmaceutical company, and the Clinical Research Department of the University of Bern announced that they have entered into an agreement to develop and commercialize ARGX-110-based therapies for treatment-resistant cancers.

ARGX-110 is a monoclonal antibody that potently blocks CD70-induced tumor cell proliferation and tumor escape from immune surveillance. CD70 is overexpressed in the majority of cancer patients.  In addition to modulating CD70 signaling, the enhanced antibody-dependent cellular cytotoxicity (ADCC) of ARGX-110 enables selective destruction of CD70-positive tumor cells.

The license agreement follows a productive collaboration between the two groups, announced in December 2014 at the annual American Society of Hematology conference. Ongoing preclinical work shows the potential of ARGX-110 in treating imatinib resistance in chronic myelogenous leukemia (CML).

“The multi-faceted clinical potential of ARGX-110 in CD70 positive tumors is unfolding rapidly as we progress through preclinical and clinical development. Together with our collaborators in Bern, our discovery that CD70 blockade overcomes resistance to tyrosine kinase inhibitor treatment in CML patients offers an exciting in-road into combination therapy with ARGX-110. Through this collaboration, we have built a deeper understanding of the role of leukemia stem cells (LSCs) in CML and how CD70 plays a role in establishment of resistance to standard of care therapies,” commented Hans de Haard, chief scientific officer of arGEN-X, in a press release.


“LSCs are responsible for the development of imatinib resistance. This resistance is caused by imatinib-dependent increase of CD70 expression which signals through its known receptor, CD27, resulting in the alternative activation of the Wnt signaling pathway. Combination therapy of imatinib and CD70 blockade has been shown to eliminate LSCs both in a murine CML model and in CML tumor xenografts,” said Carsten Riether and Adrian Ochsenbein, who are leading the research project at the University of Bern.

Source: arGEN-X