TRIANA Biomedicines Announces Oral Presentation of TRI-611 and Additional Poster Presentations at the American Association for Cancer Research Annual Meeting 2026

LEXINGTON, Mass.--(BUSINESS WIRE)--#ALK--TRIANA Biomedicines, Inc. (TRIANA), a leading biopharmaceutical company focused on advancing a target-first and proximity-first molecular glue discovery platform to address difficult to drug disease targets, today announced one oral and three poster presentations regarding the Company’s clinical asset, TRI-611, as well as its preclinical asset Cyclin E1 (CCNE1) will be presented at the American Association for Cancer Research (AACR) Annual Meeting 2026, taking place April 17-22, 2026 in San Diego, California.

TRIANA will present data highlighting the first-in-class clinical stage compound TRI-611 as a selective, brain-penetrant molecular glue degrader for the treatment of anaplastic lymphoma kinase–positive (ALK+) non-small cell lung cancer (NSCLC). In pre-clinical ALK+ NSCLC tumor models, TRI-611 promotes the degradation of tyrosine kinase inhibitor (TKI)-sensitive and -resistant ALK fusion proteins and leads to regression of both ALK TKI-refractory subcutaneous and intracranial tumors. TRI-611 demonstrates combinability with ALK TKIs in pre-clinical tumor models, potentially opening additional therapeutic avenues for patients with ALK+ NSCLC.

“We are pleased to provide further preclinical data highlighting the breadth of our molecular glue degrader therapeutics portfolio,” said Dr. Patrick Trojer, President and CEO of TRIANA. “By binding at a site distal to the TKI domain binding site, TRI-611 tethers the E3 ligase complex cereblon to ALK fusion proteins, promoting their destruction by engaging the cell’s own degradation machinery. This mechanism renders potent tumor regression activity, irrespective of mutations in the TKI binding domain.”

About TRI-611

TRI-611 is a novel oral, small-molecule, investigational therapy designed to target and degrade ALK fusion proteins in patients with ALK+ NSCLC. TRI-611 is a potent, brain-penetrant molecular glue degrader that brings ALK fusion proteins and the E3 ligase enzyme cereblon together through a unique binding mechanism that works independently of the ALK 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.

About CCNE1

CCNE1 (cyclin E1) is a key disease driver in CCNE1-amplified tumors and in a subset of HR+/HER2- breast cancers. 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 in cancer. CCNE1 has been difficult to drug with traditional approaches. Our novel oral, small-molecule 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. ​

About TRIANA Biomedicines, Inc.

TRIANA Biomedicines is a private biotechnology company, headquartered in Lexington, Massachusetts, focused on building the leading molecular glue discovery platform to regulate disease targets that are difficult to address with any other modality. TRIANA’s drug discovery engine is powered by bespoke chemical libraries, deep biochemical and biological mechanistic insights in addition to high resolution structural biology. TRIANA’s target-first and proximity-first approach to molecular glue discovery is currently focused on inducing or enhancing the degradation of high-profile disease targets. The therapeutic approach pioneered by TRIANA has the potential to fundamentally change the paradigm of small molecule drug discovery and bring significant therapeutic benefits to patients.

IR@trianabio.com