Affimed Presents Data on Innate Cell Engagers AFM24 and AFM28 at 19th Meeting of the Society for Natural Immunity
Correlative science data from AFM24-101 clinical study support the rationale to develop AFM24 as monotherapy and in combination therapies
First preclinical data set on the combination of AFM28 with natural killer cells, both in co-administration or pre-complexed, demonstrates cytotoxic activity against CD123-positive tumor cells
HEIDELBERG, Germany, May 16, 2022 (GLOBE NEWSWIRE) -- Affimed N.V. (Nasdaq: AFMD) (“Affimed”, or the “Company”), a clinical-stage immuno-oncology company committed to giving patients back their innate ability to fight cancer, has announced the presentation of new data on AFM24 and AFM28 in two posters at the 19th Meeting of the Society for Natural Immunity (NK2022).
The AFM24 presentation showed correlative science data of the exposure and pharmacodynamic effects of the compound in patients with epidermal growth factor receptor (EGFR)-expressing solid tumors from the ongoing phase 1/2a study. The poster featured an analysis of the longitudinal effects of AFM24, a CD16A/EGFR-targeting bispecific innate cell engager (ICE®), in patients treated in the AFM24-101 phase 1/2a clinical study, confirming the mechanism of action of AFM24 on the innate immune system.
The correlative science data further supports the rationale for combining different therapeutic approaches in patients with EGFR-expressing solid tumors. AFM24 engages CD16A on natural killer (NK) cells and macrophages with higher affinity than monoclonal antibodies, and triggers antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), respectively, directed at EGFR-expressing cancer cells. Preclinical data have shown that AFM24 can induce NK cell-mediated killing of EGFR-positive solid tumor cell lines, independent of EGFR mutational status.
The analysis also showed activation of cytotoxic T cells in the periphery, and infiltration of T cells into the tumor bed, suggesting stimulation of anti-cancer immunity beyond the innate immune system and the possible engagement of the adaptive immune system. These data support the rationale for AFM24 as monotherapy and the two combinations that are currently under way in separate phase 1/2a studies – with autologous NK cell therapy and with immune checkpoint inhibition.
The AFM28 poster featured preclinical data on the anti-leukemic activity of the compound when pre-complexed and co-administered with allogeneic NK cells.
AFM28 is a novel ICE® binding to CD16A on NK cells, and CD123 on acute myeloid leukemia (AML) and myelodysplastic syndrome (MDS) tumor cells. The novel bispecific engager binds with high affinity to NK cells stimulating them to destroy CD123-positive tumor cells via ADCC. In addition, AFM28 exhibits greater cell surface retention than conventional monoclonal antibodies, including Fc-enhanced IgG1.
Furthermore, the data presented at the conference demonstrate that AFM28 stimulates lysis of CD123-positive tumor cells in both formats, pre-complexed or when co-administered with NK cells. The poster also demonstrated the feasibility of cryopreserving AFM28 pre-complexed with NK cells whilst maintaining anti-tumor activity suggesting the promise for an off-the-shelf therapy targeting leukemic blasts and leukemic stem cells in patients with AML and MDS.