Affimed Presents Data on Potency of NK- and T-cell EGFRvIII TandAbs at SITC

Press Release - November 6, 2015

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NK- and T-cell TandAbs Demonstrate Similar Robust Potency

Heidelberg, Germany, November 6, 2015 – Affimed N.V. (Nasdaq: AFMD), a clinical-stage biopharmaceutical company developing highly targeted cancer immunotherapies, yesterday presented first data on the Company’s proprietary NK- and T-cell TandAbs generated against the tumor-specific variant III of the Epidermal Growth Factor Receptor (EGFRvIII), at the annual Society for Immunotherapy of Cancer (SITC) conference in National Harbor, Maryland.

Results showed that the Company’s TandAbs against EGFRvIII, AFM21 (T-cell-engager targeting EGFRvIII and CD3) and AFM22 (NK-cell-engager targeting EGFRvIII and CD16A) were similarly potent as measured in killing assays, displaying cytotoxicity towards EGFRvIII+ F98 glioma, transfected CHO or human DKMG cells with an EC50 in the range of 1 pM – 10 pM. No cytotoxicity was observed on EGFR wild type cells or EGFRvIII-negative cells, demonstrating the high selectivity of EGFRvIII TandAbs for the tumor-specific EGFRvIII variant. Importantly, in vitro, in the absence of EGFRvIII+ target cells, TandAbs did not elicit NK- or T-cell activation, as demonstrated by their lack of proliferation.

Both the NK- and T-cell TandAbs against EGFRvIII will be further investigated for candidate selection, which Affimed anticipates to take place around year-end 2015. IND-enabling studies are expected to begin in 2016.

“EGFRvIII is a highly specific target for a variety of solid tumors and thereby represents a unique option to develop T- and NK-cell based immune cell engagers,” said Martin Treder, Ph.D., CSO of Affimed. “We are particularly excited that the NK-cell TandAb shows a strong potency similar to that of our T-cell-engaging EGFRvIII TandAb, which allows us to approach each solid tumor indication with a choice of attacking via NK-cells or T-cells.”

About AFM21 and AFM22
AFM21 and AFM22 both specifically bind to Epidermal Growth Factor Receptor variant III (EGFRvIII) on solid tumor cells. While AFM21 is a T-cell TandAb targeting CD3, AFM22 is a TandAb targeting CD16A on NK-cells. Both targets are bound with high affinity, whereby T-cells or NK-cells are activated and redirected to kill the cancer cells. EGFRvIII is a mutated variant of the wild type EGFR expressed only in certain tumor cells, whereas the wild type receptor is ubiquitously expressed in healthy epithelial tissues. Importantly, AFM21 and AFM22 both selectively bind to EGFRvIII but not EGFR. Both programs are in preclinical development for the treatment of solid tumors expressing EGFRvIII.

The Epidermal Growth Factor Receptor variant III, or EGFRvIII, has been shown to be a highly specific marker for a portion of certain solid tumors including glioblastoma, prostate cancer and head and neck cancer. Based on current research, EGFRvIII is not expressed by healthy tissues, which makes it a unique target for a highly potent cancer immunotherapy such as Affimed’s T-cell TandAb, AFM21, or the NK-cell engaging TandAb against EGFRvIII, AFM22.

About Affimed N.V.

Affimed (Nasdaq: AFMD) is a clinical-stage biopharmaceutical company focused on discovering and developing highly targeted cancer immunotherapies. Affimed’s product candidates are being developed in the field of immuno-oncology, which represents an innovative approach to cancer treatment that seeks to harness the body’s own immune defenses to fight tumor cells. The most potent cells of the human defense arsenal are types of white blood cells called natural killer cells, or NK-cells, and T-cells. Affimed’s proprietary, next-generation bispecific antibodies, called TandAbs for their tandem antibody structure, are designed to direct and establish a bridge between either NK-cells or T-cells and cancer cells, triggering a signal cascade that leads to the destruction of cancer cells. Affimed has focused its research and development efforts on three proprietary TandAb programs for which it retains global commercial rights. For more information, please visit

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