Affimed Presents Data on First-in-Class BCMA-Targeting Immune Cell Engager AFM26 at ASCO Annual Meeting 2017

Heidelberg, Germany, June 6, 2017 - Affimed N.V. (Nasdaq: AFMD), a clinical stage biopharmaceutical company focused on discovering and developing highly targeted cancer immunotherapies, announced today that the Company presented data on its preclinical AFM26 program to treat multiple myeloma (MM) at the American Society of Clinical Oncology (ASCO) 2017 Annual Meeting being held in Chicago, IL, June 2-6, 2017.

"NK-cells have been described to play a major role in the control of multiple myeloma, however the recognition and elimination of malignant cells remain challenging," said Dr. Martin Treder, CSO of Affimed. "Our bispecific tetravalent NK-cell engager AFM26, a targeted therapeutic specifically binding BCMA on tumor cells, promises to address this need by unlocking NK-cell cytotoxicity in myeloma."

Affimed's first-in-class tetravalent, bispecific antibody AFM26 binds to the tumor-specific B-cell maturation antigen (BCMA) on MM cells and to CD16A on NK-cells, thereby specifically directing NK-cell anti-tumor activity towards cells expressing BCMA.

In a poster presented June 5, 2017, the Company demonstrated that AFM26 engages NK-cell-mediated lysis of primary myeloma cells and myeloma cell lines more potently than both daratumumab and elotuzumab, two monoclonal antibodies (mAbs) currently approved for myeloma treatment. AFM26 engages NK-cells with markedly higher avidity compared to classical mAbs. This translates into potent and efficacious target cell lysis and retained activity against cell lines that express very low BCMA levels (BCMA-low). Further differentiating Affimed's NK-cell engager, the Company presented data showing that AFM26 potently induced lysis of BCMA-low cell lines that have been described as not sensitive to treatment with GSK2857916, a BCMA-targeting antibody drug conjugate currently in clinical development. Importantly, unlike daratumumab and elotuzumab, AFM26 did not elicit NK-cell depletion in vitro.

MM is characterized by high level production of monoclonal immunoglobulin (M-protein), which competes with classical mAbs for NK-cell binding. Affimed demonstrated that both NK-cell binding affinity and cell surface retention of AFM26 were largely unaffected by serum IgG, suggesting retained cytotoxic activity of the NK-cell engager in patients with high M-protein serum levels.

In addition, the Company presented data showing that AFM26, while effectively lysing target cells, elicited substantially lower cytokine release compared to a BCMA/CD3-specific T-cell engager (BiTE), indicating a potentially superior safety profile.

Addressing minimal residual disease (MRD) following high-dose therapy (HDT) and autologous stem cell transplant (ASCT) remains a significant unmet need in MM treatment as the majority of patients relapse. NK-cells are the first lymphocyte population to reappear after HDT/ASCT providing a specific treatment window for NK-cell-based immunotherapeutic approaches to target MRD shortly after transplant. Furthermore, adoptive transfer of NK-cells has recently been clinically investigated in the transplant setting suggesting a unique combination opportunity for AFM26 with this approach.

In summary, the data presented at ASCO highlight AFM26 as a promising first-in-class therapeutic with particular potential to address the unmet need in ASCT-eligible MM.

About Affimed N.V.

Affimed (Nasdaq: AFMD) engineers targeted immunotherapies, seeking to cure patients by harnessing the power of innate and adaptive immunity (NK- and T-cells). We are developing single and combination therapies to treat cancers and other life-threatening diseases. For more information, please visit


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