TRIANA Biomedicines Announces Publication of Preclinical Data Supporting Clinical Advancement of TRI-611

• Publication in Nature supports TRI-611’s potential to expand the arsenal of therapeutic options for ALK+ NSCLC patients, both as a single agent and in combination with other ALK TKI therapies
• TRI-611 administration results in degradation of ALK fusion proteins, including wild-type and ALK TKI-resistant mutated versions
• The Trial-in-Progress presentation at ESMO will provide an overview of the ongoing phase 1/2 study and underscore the clinical advancement of TRI-611

LEXINGTON, Mass.--(BUSINESS WIRE)--TRIANA Biomedicines, Inc. (TRIANA), a clinical-stage biopharmaceutical company focused on developing innovative molecular glue therapies for difficult-to-drug disease targets, leveraging its target-first and proximity-first molecular glue discovery platform, today announced the publication of a manuscript titled “TRI-611, a selective, brain-penetrant molecular glue degrader of ALK,” in the international peer-reviewed scientific journal, Nature. These preclinical results support the ongoing clinical development of TRI-611, which will be featured in a Trial-in-Progress poster presentation at European Society of Medical Oncology (ESMO) Congress 2026, taking place October 23-27, 2026, in Madrid, Spain.

Tyrosine kinase inhibitors (TKIs) targeting Anaplastic Lymphoma Kinase (ALK) have made noteworthy contributions to the treatment of ALK fusion-positive non-small cell lung cancer (ALK+ NSCLC), but are limited by tolerability issues and resistance mutations. TRI-611 represents the first example of a clinical-stage molecular glue degrader targeting an oncogenic gene fusion and has the potential to expand the arsenal of therapeutic options for ALK+ NSCLC patients.

TRI-611 is an innovative product candidate discovered through TRIANA’s proximity-first approach to finding molecular glues to compelling disease targets. As a molecular glue degrader, TRI-611 promotes the proximity of the ALK kinase domain and the E3 Ligase Cereblon via a unique binding site distal from the kinase active site. Published data support the potency and selectivity of TRI-611 in targeting ALK oncogenic gene fusions. Treatment with TRI-611 induces degradation of ALK fusion proteins, including wild-type and ALK TKI-resistant mutated versions, leading to tumor regression in preclinical cell line-derived and patient-derived subcutaneous and intracranial tumor models of ALK+ NSCLC. TRI-611’s novel mechanism of action also offers therapeutic potential in combination with ALK TKI, resulting in synergistic and durable tumor regressions.

“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 Dr. Vito Palombella, 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 Dr. Patrick Trojer, 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 featured in a Trial-in-Progress poster at ESMO, further detailing the program’s clinical development strategy.

Poster presentation

• Title: TRI-611-101: A Phase 1/2 Trial of TRI-611 in ALK Fusion Positive Non-small Cell Lung Cancer (NSCLC) Patients
• Presentation Number: 2872 eTIP

About TRIANA Biomedicines, Inc.

TRIANA Biomedicines is a private, clinical-stage 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.

To learn more about the clinical program of TRI-611 visit clinicaltrials.gov (NCT07491497).