On April 15, 2026 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, reported 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) (Free AACR Whitepaper) Annual Meeting 2026, taking place April 17-22, 2026 in San Diego, California.

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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."

Oral Presentation Details:

Title:

TRI-611, a potent, selective, CNS-penetrant ALK molecular glue degrader for the treatment of ALK-fusion protein positive non-small cell lung cancer

Abstract Number:

ND07

Date and Time:

Sunday, April 19, 2026, 3:45 p.m. – 4:00 p.m. PT

Session Category:

New Drugs on the Horizon: Part 2

Session:

DDT02

Location:

Ballroom 20 CD – Upper Level – Convention Center

Poster Presentation Details:

Title:

TRI-611, a development stage molecular glue degrader of ALK, promotes the degradation of TKI-resistant ALK fusion proteins and leads to regression of ALK TKI-refractory tumors

Abstract Number:

5787 / 14

Date and Time:

Tuesday, April 21, 2026, 2:00 p.m. – 5:00 p.m. PT

Session Category:

Proximity-Induced Drug Discovery 2

Session:

T09.04

Location:

Poster Section 15

Title:

TRI-611, a development stage molecular glue degrader of ALK for the treatment of ALK-positive NSCLC including central nervous system metastases​

Abstract Number:

4618 / 28

Date and Time:

Tuesday, April 21, 2026, 9:00 a.m. – 12:00 p.m. PT

Session Category:

Proximity-Induced Drug Discovery 1

Session:

ET09.03

Location:

Poster Section 18

Title:

Discovery of a selective molecular glue degrader of CCNE1 for the treatment of CCNE1-amplified solid tumors and CDK4/6i-resistant HR+/HER2- breast cancers

Abstract Number:

5789 / 16

Date and Time:

Tuesday, April 21, 2026, 2:00 p.m. – 5:00 p.m. PT

Session Category:

Proximity-Induced Drug Discovery 2

Session:

ET09.04

Location:

Poster Section 15

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.

(Press release, Triana Biomedicines, APR 15, 2026, View Source [SID1234664421])