Mink Therapeutics, Inc. · NASDAQ:INKT
Mink Therapeutics — Technical Presentation (February 2025)
12 slides from Mink Therapeutics's technical presentation, February 2025
Slide 1: Biomarker Analysis From a Phase II Study of AgenT-797 with Botensilimab and Balstilimab
Biomarker Analysis From a Phase II Study of AgenT-797 (invariant natural killer T cells) with Botensilimab (Fc-enhanced CTLA-4 inhibitor) and Balstilimab (anti-PD-1) in PD-1 Refractory Gastroesophageal Cancer Samuel L. Cytryn,1 Patrick Evans, 1 June Song, 2 Sophie Hieronymi, 2 Michal Segal, 1 Charlt
Slide 2: Disclosure Information
Disclosure Information I have the following relevant financial relationships to disclose: Research support from Stand Up to Cancer Consulting services for Bristol Myers Squibb, Gilead, Amgen Advisory board for Bristol Myers Squibb, Henlius Honoraria for educational services for Kaplan, HMP Education
Slide 3: Background
Background ▪ PD-1 inhibitors, combined with chemotherapy, are approved for frontline treatment of advanced gastroesophageal cancer, but most patients develop disease progression1-3. Standard second-line therapy with ramucirumab (anti-VEGF) and paclitaxel has poor outcomes4. ▪ AgenT-797 is an allogen
Slide 4: Methods: Trial Schema
Methods: Trial Schema ▪ Investigator-initiated phase II study of agenT-797, botensilimab, and balstilimab in combination with ramucirumab and paclitaxel in refractory gastroesophageal cancer Cycle 1 Cycle 2+ AgenT-797 Induction Primary Endpoint AgenT-797 Botensilimab (3 total doses) + • Objective re
Slide 5: Baseline Clinical Characteristics
Baseline Clinical Characteristics Characteristics Number of Patients (N = 15) Median age (IQR), years 63 (39-73) Male 11 (73%) Female 4 (27%) Esophageal / GEJ 11 (73%) Gastric 4 (27%) Number metastatic sites 1 5 (33%) ≥ 2 10 (67%) Liver metastases 9 (60%) Peritoneal metastases 5 (33%) F
Slide 6: Increased Immune Cell Infiltration
Increased Immune Cell Infiltration ▪ Tumor immune infiltration and activation of cytotoxic T cells ▪ Enhanced antigen presenting activity within tumor CD8+Ki67+ CD11c+HLA-DR+ CD86+HLA-DR+ CD3+CD4+ CD3+CD8+ CD8+GranzymeB+ 0.0371 0.0039 250 60 40 60 200 0.0059 50 Density (Cells/mm2) Density (Cells/mm2
Slide 7: Increased Immune Cell Infiltration
Increased Immune Cell Infiltration ▪ Tumor immune infiltration and formation of tertiary lymphoid structures (TLS) ▪ Enhanced antigen presenting activity within tumor Induction: agenT-797+BOT/BAL
Slide 8: T cell Activation in Peripheral Blood
T cell Activation in Peripheral Blood ▪ Activation of central and effector memory T cells CD4 Tn CD4 Tcm CD4 Tem CD4 Teff CD8 Tn CD8 Tcm CD8 Tem CD8 Teff 0.6523 0.0488 1.00 30 30 0.0020 2.0 1.00 15 15 2.0 0.2500 0.0215 0.75 0.0488 1.5 0.75 0.0371 1.5 % ICOS+ % ICOS+ % ICOS+ % ICOS+ % ICOS+ % ICOS+ %
Slide 9: Increase in Peripheral Immune Activation
Increase in Peripheral Immune Activation ▪ Proinflammatory biomarkers indicating increased activity of cytotoxic lymphocytes IFN-γ TNF-α IL-15 GranzymeB 0.0005 0.0005 0.0015 0.0049 600 150 500 8 400 6 400 100 300 pg/ml pg/ml pg/ml pg/ml 4 200 200 50 2 100 0 0 0 0 PreTx onTx PreTx onTx PreTx onTx Pre
Slide 10: Sustained Increase of IFN-γ
Sustained Increase of IFN-γ ▪ Pronounced IFN-γ response with agenT-797/BOT/BAL combination than was seen with BOT/BAL alone ▪ Prolonged IFN-γ response than was seen with agenT-797 monotherapy ▪ Secondary IFN-γ response observed upon BOT/BAL re-dosing IFN-γ 100 NCT06251793 (MSKCC) Bot/Bal+agenT-797 ±
Slide 11: Key Takeaways and Future Directions
Key Takeaways and Future Directions ▪ The combination of agenT-797, botensilimab, and balstilimab with ramucirumab and paclitaxel induces immune modulation in patients with PD-1 refractory gastroesophageal cancer. This is characterized by: • Tumor infiltration of T cells and antigen presenting cells
Slide 12: Acknowledgements
Acknowledgements ▪ The patients and families who made this study possible ▪ The Memorial Sloan Kettering Cancer Center cellular therapy and GI oncology clinical trial teams ▪ Agenus Inc and MiNK Therapeutics for their support
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