Gustavo Martinez,Alexander Smashnov,Mitali Ghose,Seamus Mckinney,Sharon Lin,P. Rod Dunbar,Meghan Travers,Ashish Yeri,Katarina Halpin-veszeleiova,David Thompson,Hugh Gannon,Conor Calnan,Sarah Benn,Glenn J. Hanna,Liam B Oakley,Dipen Sangurdekar,Fiona A McHUGH,Micah J. Benson,Karrie Wong
Tumor Infiltrating Lymphocyte (TIL) therapy is an autologous cell therapy involving the isolation and ex vivo expansion of TIL for the treatment of solid tumors. However, not all patients currently respond to TIL therapy. Seeking to improve the clinical efficacy and durability of TIL therapy, we developed KSQ-004EX, a CRISPR/Cas9 dual-edited engineered TIL (eTILÒ) therapy with inactivation of the genes encoding the SOCS1 and Regnase-1 proteins. We previously reported SOCS1 and Regnase-1 as a top dual-edit target combination able to enhance T cell anti-tumor function by conducting in vivo T cell combinatorial screens in syngeneic mouse models. SOCS1 is a negative regulator of cytokine signaling while Regnase-1 is an RNase targeting the 3' UTR of transcripts encoding proteins involved in inflammation.
Methods
Non-clinical lots of KSQ-004EX were manufactured from core biopsies or surgically-resected tumor fragments obtained from NSCLC, HNSCC, melanoma, breast, or ovarian cancer patient samples. Using ExPRESS, a feeder cell-free, next-gen eTIL manufacturing process, TIL were activated and expanded for 11 days whereupon editing of SOCS1 and Regnase-1 was performed by electroporation (EP) of CRISPR/Cas9 ribonucleoprotein (RNP) complexes. Following an additional 10 days of expansion, KSQ-004EX was harvested, cryopreserved and characterized. The phenotypic and functional attributes of KSQ-004EX were assessed in comparison to single-edit and unedited TIL (No EP).
Results
KSQ-004EX on-target editing efficiency was > 94% for both SOCS1 and Regnase-1 with commensurate protein loss. KSQ-004EX displayed a predominantly CD8+CCR7-CD45RO+ phenotype with a consistently high frequency of CD8+ T cells across tumor samples evaluated. KSQ-004EX retained high diversity of TCR repertoire and exhibited greater cytotoxicity and higher IFNγ production against tumor in comparison to No EP. Upon transfer into NSG mice, KSQ-004EX demonstrated enhanced in vivo function, expansion and persistence relative to No EP controls even upon withdrawal of exogenously provided IL-2. Transcriptional analyses of KSQ-004EX in comparison to No EP and single-edit controls highlighted the dual contributions of the SOCS1 and Regnase-1 pathways.
Conclusions
KSQ-004EX, a SOCS1/Regnase-1 dual CRISPR/Cas9 edited TIL therapy, demonstrated enhanced anti-tumor functionality and in vivo persistence in pre-clinical animal models. These results support the evaluation of KSQ-004EX in a clinical setting in cancer patients with treatment-refractory solid tumors.