Our Pipeline

Our lead program in development is TRI-611, a novel oral, small-molecule, investigational therapy designed to target and degrade anaplastic lymphoma kinase (ALK) fusion proteins in patients with ALK-positive non-small cell lung cancer (NSCLC) for which ALK tyrosine kinase inhibitors (TKIs) are now the standard of care.

Although TKI therapies have improved patient outcomes, important challenges remain—including treatment resistance, central nervous system metastases, and tolerability concerns. These unmet needs are particularly impactful in this predominantly younger patient population, underscoring the importance of developing next-generation therapies to further advance care and improve patients’ lives.

TRI-611 is a potent, brain-penetrant molecular glue degrader that brings ALK and cereblon together through a unique binding mechanism that works independently of the kinase active site and harnesses the body’s innate protein degradation machinery to selectively eliminate the ALK fusion protein. TRI-611 is designed to overcome the limitations observed with currently available ALK inhibitors.

As a critical regulator of the cell cycle, CCNE1 protein levels are tightly regulated to maintain control of cell growth in normal cells, while elevation of CCNE1 protein levels can lead to aberrant cell growth or resistance to standard of care therapies.

CCNE1 has been difficult to drug with traditional approaches. Molecular glue degraders of CCNE1 offer a unique approach to targeting this key cancer driver by harnessing the cell’s protein degradation machinery to substantially decrease excess CCNE1 and halt growth of CCNE1-dependent tumor cells.