Mont-Saint-Guibert, Belgium – Celyad Oncology SA (Euronext & Nasdaq: CYAD), a clinical-stage biotechnology company focused on the discovery and development of chimeric antigen receptor T cell (CAR T) therapies for cancer, announced today that the Company has entered into a clinical trial collaboration with MSD, a tradename of Merck & Co., Inc., Kenilworth, NJ., USA, through a subsidiary.
Celyad Oncology will conduct the Phase 1b KEYNOTE-B79 clinical trial, which will evaluate Celyad Oncology’s investigational non-gene edited allogeneic CAR T candidate, CYAD-101, following FOLFIRI (combination of 5-fluorouracil, leucovorin and irinotecan) preconditioning chemotherapy, with MSD’s anti-PD-1 therapy, KEYTRUDA® (pembrolizumab) in refractory metastatic colorectal cancer (mCRC) patients with microsatellite stable (MSS) / mismatch-repair proficient (pMMR) disease.
“We are extremely pleased to enter into this clinical collaboration with MSD, as we believe the mechanism of actions of CYAD-101 and KEYTRUDA are highly complementary and could help to drive meaningful clinical benefit in patients with advanced metastatic colorectal cancer, in particular with microsatellite stable disease where a high unmet medical need exists” said Filippo Petti, Chief Executive Officer of Celyad Oncology. “In addition, the collaboration with MSD adds an important dimension to our clinical program for CYAD-101 for the treatment of mCRC and provides us with the opportunity to build upon the encouraging clinical activity we’ve reported to date from the ongoing alloSHRINK trial.”
KEYTRUDA® is a registered trademark of Merck Sharp & Dohme Corp, a subsidiary of Merck & Co., Inc., Kenilworth, NJ, USA.
About CYAD-101
CYAD-101 is an investigational, non-gene edited, allogeneic (healthy donor derived) CAR T candidate engineered to co-express a chimeric antigen receptor based on NKG2D, a receptor expressed on natural killer (NK) cells that binds to eight stress-induced ligands and the novel inhibitory peptide TIM (TCR Inhibitory Molecule). The expression of TIM reduces signaling of the TCR complex, which is responsible for graft-versus host disease.
