COMPANY RESEARCHAn October 2025 company announcement and original structural study establish DCAF2 as an E3 for PROTAC-mediated degradation. This does not make the company's other clinical small molecules degraders.
This is the full-round total and must not be added again to the $80 million announced in February.
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.
Disease tags match recorded text mentions and require program-level verification.
An October 2025 company announcement and original structural study establish DCAF2 as an E3 for PROTAC-mediated degradation. This does not make the company's other clinical small molecules degraders.
| Program / service | Target / indication | Representative stage | Evidence & scope |
|---|---|---|---|
| DCAF2-recruiting degrader research | DCAF2 E3 ligand; model PROTAC · Determined by the collaboration program | Platform / services | This record does not claim platform-wide human validation |
Company-name matches are discovery leads; verify entity identity and transaction roles in the original source.
No cataloged update explicitly mentions this company.
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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