We are currently focusing our development efforts on nanvuranlat for second-line treatment of biliary tract cancer as a monotherapy and for first-line treatment in combination with immune checkpoint inhibitors, as well as on JPH034 for non-relapsing secondary progressive multiple sclerosis. In addition, we are advancing development programs for KRAS-mutant colorectal cancer with nanvuranlat and for glioma with JPH034.

Based on both non-clinical and clinical data, nanvuranlat has shown potential for indication expansion in colorectal cancer. In particular, existing therapies have limited efficacy in KRAS-mutant colorectal cancer, which accounts for approximately 40 percent of metastatic colorectal cancer cases, while clinical data have reported a strong association between high LAT1 expression and poor patient prognosis. Non-clinical studies have also demonstrated that nanvuranlat significantly inhibits the proliferation of KRAS-mutant colorectal cancer cell lines. Furthermore, in our Phase I clinical trial involving multiple solid tumors, two out of six colorectal cancer patients achieved stable disease (SD), providing encouraging signals to support future development. Building on these findings and our internal assessment of nanvuranlat’s potential in KRAS-mutant colorectal cancer, we received a proposal for joint development from a U.S. university, which is now preparing a grant application to initiate an investigator-initiated clinical study.

Meanwhile, for glioma, we initiated development following a proposal from a major U.S. research institution. This decision was supported by multiple reports highlighting the involvement of LAT1 in glioma and by the high brain penetrance of JPH034. We are currently supplying our investigational compound to the institution, where preclinical studies are actively underway.

We prioritize the development of nanvuranlat for first- and second-line treatment of biliary tract cancer and JPH034 for non-relapsing secondary progressive multiple sclerosis. Other clinical development programs will be advanced in a phased manner, subject to funding availability, cost considerations, and appropriate risk management.

Certain rare amino acid–metabolism disorders are caused by abnormalities in amino acid transporters within the SLC family, including LAT1. These conditions arise from impaired amino acid transport in the intestine, kidney, and liver, which constitutes a primary pathogenic mechanism.

We have focused on the unique biodistribution profile of nanvuranlat, which shows high concentrations in the liver, bile ducts, and colon. In an animal model of a certain rare disease, nanvuranlat demonstrated findings suggestive of therapeutic efficacy. Based on these results, we are in the process of filing a use patent covering this indication and are exploring new opportunities for expanding the therapeutic potential of nanvuranlat.