Hanmi R&D becomes stronger through cooperation with partners.
- efocipegtrutide (LAPSTriple agonist)
- sonefpeglutide (LAPSGLP-2 analog)
- efpegerglucagon (LAPSGlucagon analog)
- HM97662 (EZH1/2 inhibitor)
- BH3120 (PD-L1/4-1BB BsAb)
- HM15275 (LA-GLP/GIP/GCG)
- HM16390 (LAPSIL-2 analog)
- HM17321 (LA-UCN2)
- HM101207 (SOS1 inhibitor)
- LAPS Glucagon Combo
HM16390 (LAPSIL-2 analog)
Oncology
Phase 1
Overview
Long-acting IL-2 analog with enhanced CD122 binding affinity to
elicit potent anti-tumor efficacy
Description
elicit potent anti-tumor efficacy
HM16390 is a long-acting interleukin-2 (IL-2) analog chemically conjugated with constant region of human immunoglobulin G4 (IgG4 Fc) via flexible non-peptidyl linker
Currently, novel IL-2 analogs are being developed by the two different strategies. Some analogs with the reduced affinity to IL-2Rα could reduce adverse events such as vesicular leak syndrome (VLS), but have low anti-tumor efficacy. The other strategy is to intensify affinity to IL-2Rβ and eliminate IL-2Rα affinity. In this case IL-2 analog shows potent anti-tumor efficacy, but it has potential safety concern such as cytokine release syndrome (CRS) by attenuated regulatory T cells.
HM16390 has the modified rhIL-2 analog which shows both a powerful anti-tumor efficacy by the preferential binding to IL-2 Rβ and an improved safety profile by the balanced IL-2Rα binding affinity. The optimal affinity ratio was determined through the evaluation of various IL-2 analogs which have different IL-2R binding profiles.
In nonclinical studies, HM16390 showed the remarkable anti-tumor efficacy in the various syngeneic models and elicited synergistic action when administered with the immune check point inhibitor (ICI) by modulating tumor-microenvironment.
It is being developed for both the treatment of solid tumors and for combination with other immune-oncology drugs, such as ICIs.
Currently, novel IL-2 analogs are being developed by the two different strategies. Some analogs with the reduced affinity to IL-2Rα could reduce adverse events such as vesicular leak syndrome (VLS), but have low anti-tumor efficacy. The other strategy is to intensify affinity to IL-2Rβ and eliminate IL-2Rα affinity. In this case IL-2 analog shows potent anti-tumor efficacy, but it has potential safety concern such as cytokine release syndrome (CRS) by attenuated regulatory T cells.
HM16390 has the modified rhIL-2 analog which shows both a powerful anti-tumor efficacy by the preferential binding to IL-2 Rβ and an improved safety profile by the balanced IL-2Rα binding affinity. The optimal affinity ratio was determined through the evaluation of various IL-2 analogs which have different IL-2R binding profiles.
In nonclinical studies, HM16390 showed the remarkable anti-tumor efficacy in the various syngeneic models and elicited synergistic action when administered with the immune check point inhibitor (ICI) by modulating tumor-microenvironment.
It is being developed for both the treatment of solid tumors and for combination with other immune-oncology drugs, such as ICIs.
IL-2 agonism
- Powerful tumor-killing efficacy by intensified IL-2 Rβ binding
- Favorable safety and tolerability by optimal IL-2 Rα binding
- Long-acting IL-2 medication
- Convenient dosing by subcutaneous administration
Clinical Development
- A phase 1 study is ongoing in United States and Korea NCT06724016
Publications