Affimed (AFMD) Status Update summary

Clinical program overview and rationale

• Over 450 patients have been studied across three clinical programs, with consistent efficacy as monotherapy and in combination with NK cells or checkpoint inhibitors, maintaining a strong safety profile.

• AFM24 targets CD16A on NK cells and macrophages, with global rights and a strong IP position.

• AFM24's mechanism is distinct from traditional EGFR inhibitors, acting via immune effector cells rather than disrupting EGFR signaling, thus avoiding resistance mutations and classic toxicities.

• Combination with atezolizumab is based on observed upregulation of T cell activation and increased tumor infiltration by immune cells.

• AFM24 is a tetravalent, bispecific innate cell engager (ICE®) that activates innate immune cells to target EGFR-expressing tumors.

EGFR wild-type cohort results

• 17 patients enrolled, heavily pretreated (median 2 prior therapies, up to 5), with most having poor prognosis.

• Disease control rate reached 71%, with 1 complete response, 3 partial responses, and 8 stable diseases among 15 evaluable patients.

• Median progression-free survival was 5.9 months, with 4 objective responses, 3 ongoing for over 7 months.

• Notably, 3 of 4 responders had not achieved objective response with prior checkpoint inhibitors, suggesting efficacy in refractory cases.

• Safety profile was manageable, with most adverse events mild to moderate; only one grade 3 liver toxicity attributed to atezolizumab.

EGFR mutant cohort results

• 21 patients enrolled, all TKI-resistant, 80% also platinum-refractory, with high tumor burden and poor prognosis.

• 13 evaluable patients: 1 complete response, 3 partial responses, and 6 with stable disease; all objective responses ongoing at data cut-off.

• Early dropouts due to rapid progression, not drug-related; inclusion criteria to be refined to exclude very early progressors.

• The patient with complete response was a 67-year-old female with exon 21 L858R mutation, stage 4 disease, and unknown PD-L1 status.

• EGFRmut NSCLC, typically unresponsive to single-agent checkpoint inhibitors, showed encouraging responses with the combination.