On March 17, 2016 Affimed N.V. (Nasdaq: AFMD), a clinical stage biopharmaceutical company focused on discovering and developing highly targeted cancer immunotherapies, reported that preclinical data from a combination study of Affimed’s lead candidate AFM13 and checkpoint modulators, including checkpoint inhibitor PD-1, as well as data on Affimed’s preclinical programs AFM21/22 and AFM24 will be presented at the American Association for Cancer Research (AACR) (Free AACR Whitepaper) 2016 Annual Meeting being held April 16 – 20, 2016 in New Orleans, LA (Press release, Affimed Therapeutics, MAR 17, 2016, View Source [SID:1234512470]).
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AFM13
On Monday, April 18, "Immune checkpoint inhibition by anti-PD-1 or CD137 co-stimulation enhances cytotoxicity towards CD30+ tumors mediated by the bispecific tetravalent CD30/CD16A TandAb AFM13" (Abstract #2323) will be available in a poster session. The results of this preclinical study, conducted in collaboration with Stanford University, confirm earlier evidence of the synergy of our lead candidate, the CD30/CD16A-specific NK-cell engager AFM13, in combination with PD-1 inhibitors in in vivo PDX models with human CD30+ Hodgkin lymphoma (HL) tumors. Our data demonstrate that this synergy is mediated by tumor-infiltrating lymphocytes, macrophages and dendritic cells, and provide strong evidence for cross-talk between innate and adaptive immunity induced by AFM13-recruited human NK-cells. Together with AFM13’s adequate safety profile in patients, these results further justify the Phase 1b combination study investigating AFM13 in combination with pembrolizumab in relapsed/refractory HL patients which we expect to be initiated in the first half of this year.
AFM21/22
On Sunday, April 17, "Anti-EGFRvIII TandAbs recruiting either T or NK cells are highly specific and potent therapeutic antibody candidates for the treatment of EGFRvIII+ tumors" (Abstract #580) will be available in a poster session. In this preclinical study we report development of tetravalent, bi-specific TandAbs (tandem antibodies) that recognize EGFRvIII, the most prevalent tumor-specific variant of the epidermal growth factor receptor, EGFR. Our TandAbs recruit either T-cells or NK-cells, both of which are highly potent and efficacious immune effector cells, by binding to their activating receptors CD3 (AFM21) and CD16A (AFM22), respectively. This allows for the selective destruction of EGFRvIII-positive tumor cells, while sparing healthy, EGFRvIII-negative cells. The AFM21/22 program further validates the robustness of our proprietary TandAb technology platform, allowing for rapid identification of candidate molecules which are stable, highly expressed, and display significant in vitro and in vivo cytotoxicity to cancer cells.
AFM24
On Sunday, April 17, "Highly cytotoxic EGFR/CD16A TandAbs specifically recruit NK cells to potently kill various types of solid tumors" (Abstract #593) will be available in a poster session. In this preclinical study we describe the development of our novel bispecific, tetravalent EGFR/CD16A-specific NK-cell TandAbs and provide evidence for their therapeutic potential. When constitutively activated through amplification or dysregulation, the EGFR wild type (EGFRwt) plays an important role in the pathophysiology of numerous solid cancers. Specifically utilizing the cytotoxic potential of NK-cells for the elimination of EGFR-overexpressing cancer cells, we engineered a set of EGFR/CD16A TandAbs and selected ideal candidates based on their binding, thermostability and cytotoxic properties. Our data suggest that EGFR/CD16A TandAbs are novel, highly potent drug candidates suitable for the treatment of EGFR-overexpressing malignancies and suited to overcome the intrinsic or acquired resistance to other EGFR-targeting treatments such as tyrosine kinase inhibitors or monoclonal antibodies, which has been observed in a large number of patients.
Full abstracts of the presentations can be accessed on the AACR (Free AACR Whitepaper) website at www.aacr.org.