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.
2024-06-25 · Series C (including extension; full-round total) · $100 million total Series C ($20 million in this extension) ↗
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.
Technology, programs & evidence
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
Related news & literature
Company-name matches are discovery leads; verify entity identity and transaction roles in the original source.
No cataloged update explicitly mentions this company.
A Nature Materials study describes mRNA-loaded LNPs that reprogram tumor-associated macrophages into Claudin18.2-targeting CAR macrophages. The lipid formulation also promotes TREM2 internalization and degradation, reshaping immune responses. The original abstract reports tumor suppression and longer survival with PD-1 blockade in mice, plus ex vivo patient-sample findings. These findings do not demonstrate clinical efficacy in treated patients.
A Frontiers in Pharmacology review compares direct MCL-1 inhibition with approaches that reduce its abundance, including transcriptional interventions and targeted degradation. The original abstract highlights limited single-agent activity and cardiac safety concerns with inhibitors, while positioning degradation as an unvalidated clinical strategy. Biomarker-guided combinations and dynamic BH3 profiling are discussed; this review does not report a new clinical trial.
Evommune licensed EVO570, formerly HC118, from Hinova for development and commercialization outside Greater China. Upfront consideration totals $30 million: $20 million cash and $10 million in pre-funded warrants. Additional development, regulatory, and commercial milestones could reach approximately $1.1 billion, plus royalties. Phase 1 was expected to begin shortly; the announcement does not establish human efficacy.
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