COMPANY RESEARCHA March 2026 announcement reports the first patient treated in Phase 1/2 TRI-611. A September 2026 Nature paper describes its distinctive ALK–CRBN interface and preclinical intracranial tumor models.
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Profile review: 2026-11-04 · Fields retain their individual source dates. Undisclosed values are not zero; early or historical events do not establish the latest financing. Awards and acquisitions are distinguished from equity rounds.
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A March 2026 announcement reports the first patient treated in Phase 1/2 TRI-611. A September 2026 Nature paper describes its distinctive ALK–CRBN interface and preclinical intracranial tumor models.
| Program / service | Target / indication | Representative stage | Evidence & scope |
|---|---|---|---|
| TRI-611 | ALK fusion proteins · See individual trial / indication; not individually confirmed in this review | Phase 1/2 | IND / clinical entry disclosed; public human results not confirmed in this review |
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Amphista announced an ASH oral presentation on AMX-883-mediated BRD9 degradation, describing disruption of hematopoietic transcriptional programs, myeloid differentiation, and reduced leukemic stem-cell frequency in experimental work. A separate abstract outlines the ongoing Phase 1 BRAMLIE study in AML and high-risk myelodysplastic syndrome. The announcement does not establish clinical efficacy for AMX-883.
Nurix announced updated Phase 1a/1b findings for its oral BTK degrader bexobrutideg (NX-5948) in relapsed or refractory CLL/SLL. The ASH presentation will include patients previously exposed to covalent BTK inhibitors and data at the recommended Phase 2 dose of 600 mg once daily. The release describes durable activity without providing numerical response rates.
A PNAS study reports RHV, a tetravalent bispecific protein designed to internalize and lysosomally degrade VCAM-1 and VEGFR on pathological vessels. The original abstract describes activity in mouse choroidal neovascularization models, including efficacy comparable to aflibercept at one-quarter of the molar dose. This is preclinical extracellular receptor degradation, distinct from an intracellular small-molecule PROTAC.
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