LEXINGTON, Mass. — TRIANA Biomedicines, Inc. will present new clinical and preclinical data on its lead asset TRI-611 and additional pipeline programs at the American Association for Cancer Research Annual Meeting 2026, scheduled for April 17–22 in San Diego.
The company said it will deliver one oral presentation and three poster presentations highlighting TRI-611, a molecular glue degrader targeting anaplastic lymphoma kinase–positive (ALK+) non-small cell lung cancer, along with early-stage research on its Cyclin E1 (CCNE1) program.
Preclinical findings show TRI-611 selectively targets and degrades both treatment-sensitive and treatment-resistant ALK fusion proteins. In tumor models of ALK+ non-small cell lung cancer, including those resistant to tyrosine kinase inhibitors (TKIs), the therapy demonstrated tumor regression in both subcutaneous and intracranial settings. The company also reported that TRI-611 may be used in combination with existing ALK inhibitors, potentially expanding treatment options for patients.
“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.”
The oral presentation will focus on TRI-611 as a selective, brain-penetrant degrader designed to treat ALK-fusion protein–positive non-small cell lung cancer. It is scheduled for April 19 in a session on emerging cancer therapies.
Additional poster presentations will detail TRI-611’s activity in TKI-resistant tumors, its potential role in treating brain metastases, and the company’s work developing a molecular glue degrader targeting CCNE1. That program aims to address CCNE1-amplified solid tumors and certain hormone receptor-positive, HER2-negative breast cancers that have developed resistance to CDK4/6 inhibitors.
TRI-611 is an investigational oral therapy designed to eliminate ALK fusion proteins by recruiting the E3 ligase cereblon, triggering the body’s natural protein degradation processes. Unlike conventional inhibitors, its mechanism operates independently of the ALK kinase active site, which may help overcome resistance seen with current treatments.
The company’s CCNE1 program targets a key regulator of the cell cycle that is frequently amplified in cancer and has historically been difficult to treat with traditional drug approaches. TRIANA said its molecular glue strategy enables selective degradation of the protein, potentially slowing or stopping tumor growth in cancers driven by CCNE1 overexpression.
