TRI-611 entered Phase 1/2 evaluation for ALK-positive non-small cell lung cancer after receiving FDA Fast Track designation. The candidate is described as a CNS-penetrant CRBN-mediated molecular glue degrader designed to recruit a non–G-loop degron distal to the ALK orthosteric site. The program targets a key unmet need in ALK-positive NSCLC, particularly resistance to tyrosine kinase inhibitors and limited options after progression. The molecule’s mechanism is intended to deliver an active-site-independent degradation strategy, distinguishing it from conventional ALK inhibitors. TRI-611 was disclosed at the 2026 AACR New Drugs on the Horizon session, indicating early clinical interest and setting expectations for initial safety and preliminary pharmacodynamic data. For the ALK field, a new degradation modality could expand the treatment sequence for patients who fail TKIs, provided early results demonstrate meaningful target engagement and clinical activity.