Day Two

Achieving durable responses in patients remains one of the most important challenges for NK cell therapies. This panel will bring together leaders in academia, biotech, and clinical development to discuss strategies for boosting efficacy, extending persistence, and improving the therapeutic potential of NK-based treatments. Experts will explore how next generation engineering, manufacturing, and clinical insights are shaping the future of innate cell therapies.

• Understanding barriers to efficacy and persistence, examining tumor escape, immunosuppression, and NK cell exhaustion that limit clinical outcomes
• Advancing engineering solutions, exploring cytokine support, gene edits, and checkpoint resistance to strengthen NK cell function in vivo
• Improving translation to the clinic, aligning manufacturing, trial design, and biomarker strategies to achieve more consistent and durable responses

• Comparative characterization of iPSC- and peripheral blood–derived NK cells to define intrinsic phenotypic and metabolic differences
• Functional evaluation of cytotoxicity, persistence, and metabolic adaptability to reveal donor- and source-dependent performance variability
• Metabolic engineering strategies to enhance mitochondrial fitness, delay exhaustion, and improve next-generation NK cell efficacy

• Engineering NK cells with cytokine support to sustain proliferation and activity in hostile tumor environments
• Developing membrane-bound or controlled cytokine expression systems to avoid systemic toxicity while boosting local activity
• Advancing self-renewing NK platforms that maintain long-term cytotoxicity and persistence after infusion

• Developing safer and more effective CAR-NK therapies from cord blood to treat a range of cancers from lymphoma leukaemia to breast cancer
• Enhancing NK cell function through gene editing and checkpoint discovery
• Expanding applications to solid tumors with scalable off-the-shelf products

• Profile of AlloNK, ability to deeply deplete B-cells, and potential advantages over other modalities
• Early clinical insights from ongoing clinical trials in autoimmune disease
• Process strategies enabling consistency and potency at scale

• Will present clinical data consistent with SENTI-202 mechanism of action, including:
• CD33 OR FLT3 logic gated CAR approach for targeting both AML blasts and leukemic stem cell NOT EMCN logic gated inhibitory CAR approach for protection of hematopoietic stem and progenitor cells
• Supporting data for SENTI-202 PK, patient disease characterization, and patient responses

• Developing strategies to enhance NK, persistence, migration, tumor-killing potential and improving safety profiles
• Exploring scalable platforms for making ex vivo cell manufacturing more efficient at reduced cost

• Disarming immune suppression by engineering NK cells to resist inhibitory signals
• Overcoming NK cell-intrinsic checkpoints to boost NK metabolism and functional activity
• Combining multiplex base editing and CAR and cytokine engineering to enhance activity to antigen positive and negative tumors