HM16390

B16F10 mice were sacrificed at days 1, 3, and 8 following single subcutaneous administration of HM16390 or 5 consecutive daily administrations of aldesleukin. In conclusion, HM16390 effectively induced tumor growth inhibition through the activation and tumor infiltration of cytotoxic lymphocytes. This favorable immune alteration in tumor elicited a TME remodeling in which CPI could sufficiently respond.

Although recombinant IL-2 (aldesleukin) was approved for the treatment of metastatic renal cell carcinoma and melanoma, its suboptimal ligand binding affinity required high-dose administrations, resulting in dose-limiting toxicity such as vascular leak syndrome. Of note, at doses ≥17 mg/kg, CR was observed in up to 22% of the mice. To sum up with the results, HM16390 has a dose-dependent and potent anti-tumor efficacy in murine models with the broad range of the immunogenic condition via CD122-enhanced IL-2 agonism.