Celyad Oncology announces the publication of data from its Phase 1 THINK study of CYAD-01
Mont-Saint-Guibert, Belgium - Celyad Oncology (Euronext & Nasdaq: CYAD) (the “Company”), a biotechnology company focused on the discovery and development of innovative technologies for chimeric antigen receptor (CAR) T-cell therapies, today announces the publication of the data from the haematological arm of the THINK study which evaluated CYAD-01 in relapsed or refractory (r/r) acute myeloid leukaemia (AML) and myelodysplastic syndromes (MDS) or multiple myeloma (MM) patients. The findings were published in the journal The Lancet Haematology.
CYAD-01 is the Company’s first autologous CAR T-cell candidate, based on the natural killer receptor NKG2D, assessed clinically. The completed THINK study was an open-label, dose-escalation Phase 1 study for patients with r/r AML, MDS, or MM, after at least one previous line of therapy. Patients were recruited from five hospitals in the USA and Belgium.
The Lancet Haematology publication includes data from the 16 patients treated with CYAD-01 in the dose escalation segment of the study, which evaluated three dose levels of CYAD-01 using a schedule of three infusions at two-week intervals in the absence of any preconditioning chemotherapy. Overall, CYAD-01 showed favourable safety data with signs of clinical activity with three of the 12 evaluable AML/MDS patients presenting an objective response.
Importantly, the THINK study is one of the first completed dose-escalation CAR T-cell studies in r/r AML/MDS. Unlike the majority of the studies evaluating CAR T-cell therapy candidates, the THINK study evaluated multiple infusions of CYAD-01 as a stand-alone product candidate (i.e., without prior bridging or preconditioning chemotherapy). This feature is of particular interest considering the median older age and the poorer general condition of patients with r/r AML or MDS at diagnosis.
Although the need to improve the anti-tumour activity is warranted, these data in a difficult-to-treat patient population potentially provide the proof-of-concept of targeting NKG2D ligands by a CAR T-cell product candidate, and support the further development of NKG2D-based CAR T-cell therapies