Lexington, Mass. — TRIANA Biomedicines, Inc. announced the publication of preclinical data supporting the clinical development of TRI-611, its molecular glue degrader being studied for ALK fusion-positive non-small cell lung cancer.
The manuscript, titled “TRI-611, a selective, brain-penetrant molecular glue degrader of ALK,” was published in Nature. TRIANA said the findings support the ongoing Phase 1/2 clinical development of TRI-611.
The company will also present the ongoing study in a Trial-in-Progress poster at the European Society for Medical Oncology Congress 2026, scheduled for Oct. 23-27 in Madrid.
Tyrosine kinase inhibitors targeting anaplastic lymphoma kinase have improved treatment options for ALK fusion-positive non-small cell lung cancer, but their use can be limited by tolerability issues and resistance mutations.
TRI-611 is designed to promote proximity between the ALK kinase domain and the E3 ligase Cereblon, leading to degradation of ALK fusion proteins. According to the published preclinical data, TRI-611 induced degradation of both wild-type and ALK TKI-resistant mutated ALK fusion proteins.
Treatment with TRI-611 led to tumor regression in preclinical cell line-derived and patient-derived subcutaneous and intracranial models of ALK-positive non-small cell lung cancer, the company said.
TRIANA also reported that TRI-611 showed potential for use in combination with ALK tyrosine kinase inhibitors, producing synergistic and durable tumor regressions in preclinical models.
“This publication provides important validation of the scientific rationale supporting TRI-611 and adds to the growing body of preclinical evidence demonstrating the potential of our molecular glue platform,” said Vito Palombella, Ph.D., Chief Scientific Officer of TRIANA.
“We are excited to showcase our scientific leadership in the molecular glue field. Our goal is to build on this body of work and ultimately deliver TRI-611 as a meaningful new option for ALK fusion positive NSCLC patients both in early and later lines of treatment,” said Patrick Trojer, Ph.D., President and CEO of TRIANA. “Due to its new mechanism of action, TRI-611 may constitute a new product class and allow for combination strategies to further increase therapeutic options for patients.”
The ongoing Phase 1/2 study will be highlighted at ESMO with additional details on the program’s clinical development strategy.
