Affimed Announces Positive Early Efficacy and Progression Free Survival Results of AFM24-102 Study in EGFR Wild-Type Non-Small Cell Lung Cancer at the Annual Meeting of the American Society of Clinical Oncology 2024

On May 23, 2024 Affimed N.V. (Nasdaq: AFMD), a clinical-stage immuno-oncology company committed to giving patients back their innate ability to fight cancer, reported that an update from the Company’s AFM24-102 study in advanced EGFR wild-type (EGFRwt) non-small cell lung cancer (NSCLC) will be presented at the annual meeting of the American Society of Clinical Oncology (ASCO) (Free ASCO Whitepaper) to be held in Chicago on May 31 – June 4, 2024 (Press release, Affimed, MAY 23, 2024, View Source [SID1234643619]). Patients in the study are treated with the combination of AFM24, Affimed’s innate cell engager (ICE), and atezolizumab, Roche’s checkpoint inhibitor (CPI).

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As of the March 18 cut-off for the poster, 17 patients with EGFRwt NSCLC received the combination treatment and 15 patients were response evaluable. One patient showed a confirmed complete response, and three patients showed confirmed partial responses (PR). In addition, seven patients achieved stable disease, resulting in a disease control rate of 73.3% (11/15 patients). Median progression-free survival was 5.9 months.

All responders were resistant to checkpoint inhibitor treatment prior to the study, which supports the hypothesis that combining AFM24 with atezolizumab may enhance the cancer-immunity cycle and provide an alternative strategy to overcome resistance to existing therapies for EGFR-expressing tumors.

AFM24 and atezolizumab were given at their respective single agent doses. Treatment in these heavily pretreated patients was well tolerated. Side effects were consistent with the known safety profiles of these agents. The most frequent side effects observed were mild to moderate infusion related reactions and transient mild to moderate increase in liver enzymes.

"We are very encouraged to see objective and lasting responses in patients who have failed multiple lines of therapy including platinum doublets and checkpoint inhibitors," said Dr. Andreas Harstrick, Chief Medical and acting Chief Executive Officer of Affimed. "These data support our hypothesis that the combination of AFM24 and PD-1 targeting may act synergistically on the immunity cycle. It is remarkable that this can be achieved with a chemotherapy-free approach. We are committed to continuing clinical development of this therapy and are enrolling additional patients for both EGFRwt and EGFRmut NSCLC."

The EGFRwt NSCLC cohort of the study will enroll up to 40 patients and the EGFRmut NSCLC cohort will enroll up to 25 patients.

The full data set will be presented by Dr. Hye Ryun Kim, Professor at Yonsei University College of Medicine, Seoul, Korea, at ASCO (Free ASCO Whitepaper) on June 1, 2024, during the poster session on Developmental Therapeutics—Immunotherapy (9:00 a.m.—12:00 p.m. CDT).

The abstract and more details about the ASCO (Free ASCO Whitepaper) conference are available online at Attend | ASCO (Free ASCO Whitepaper) Annual Meeting. The poster will be available online at View Source the presentation.

Conference Call and Webcast Information

Affimed will host a conference call and webcast for the financial community on June 1, 2024, at 6:00 p.m. CDT / 7:00 p.m. EDT.

The conference call will be available via phone and webcast. The live audio webcast of the call will be available in the "Webcasts" section on the "Investors" page of the Affimed website at View Source To access the call by phone, please use link:

https://register.vevent.com/register/BIff607338e5d247f99b548240be2ad413, and you will be provided with dial-in details and a pin number.

About AFM24

AFM24 is a tetravalent, bispecific ICE that activates the innate immune system by binding to CD16A on innate immune cells and epidermal growth factor receptors (EGFR), a protein widely expressed on solid tumors, to kill cancer cells. Generated by Affimed’s fit-for-purpose ROCK platform, AFM24 represents a distinctive mechanism of action that uses EGFR as a docking site to engage innate immune cells for tumor cell killing through antibody-dependent cellular cytotoxicity and antibody-dependent cellular phagocytosis.