Date: 2015-11-06
Type of information: Presentation of results at a congress
phase: preclinical
Announcement: presentation of results at the 30th annual Society for Immunotherapy of Cancer (SITC) conference
Company: Affimed (Germany)
Product: AFM21 and AFM22 (NK- and T-cell TandAbs generated against EGFRvIII)
Action
mechanism: bispecific antibody/fusion protein. AFM21 (T-cell-engager targeting EGFRvIII and CD3) and AFM22 (NK-cell-engager targeting EGFRvIII and CD16A) both specifically bind to Epidermal Growth Factor Receptor variant III (EGFRvIII) on solid tumor 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. It 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. 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.
Disease:
Therapeutic area: Autoimmune diseases
Country:
Trial details:
Latest
news: * On November 6, 2015, Affimed presented first data on its 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 (EGFRvIII TandAbs are specific and highly potent drug candidates for the treatment of solid tumors). 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. * On October 6, 2015, Affimed announced that the Company’s abstract has been chosen for a poster presentation at the 30th annual Society for Immunotherapy of Cancer (SITC) conference, being held November 4-8 in National Harbor, Maryland. This will be the first publication of data on the Company’s proprietary NK- and T-cell TandAbs generated against EGFRvIII.
