P1/2, N=32, Active, not recruiting, University of Aarhus | Recruiting --> Active, not recruiting | Trial completion date: Mar 2026 --> Mar 2027 | Trial primary completion date: Mar 2026 --> Mar 2027
3 days ago
Enrollment closed • Trial completion date • Trial primary completion date
P1, N=42, Terminated, BeOne Medicines | N=75 --> 42 | Trial completion date: Dec 2027 --> Apr 2026 | Active, not recruiting --> Terminated | Trial primary completion date: Dec 2027 --> Apr 2026; This decision is due to a company business decision with a strategy change on the BGB-R046 development in Advanced or Metastatic Solid Tumors.
4 days ago
Enrollment change • Trial completion date • Trial termination • Trial primary completion date • First-in-human
Utilizing this workflow, we studied dose-dependent protein degradation patterns induced by pomalidomide, iberdomide, and mezigdomide. Our results indicate that mezigdomide may possess enhanced efficacy in T cells by degrading additional proteins such as IKZF2, thereby boosting anticancer immunity. Together, we developed an ultrahigh-throughput LC-MS/MS method with excellent proteome coverage and quantitation accuracy that is highly suitable for chemoproteomics screening of drug libraries.
PROTAC LNPs were synthesized by modifying F1324 and pomalidomide aptamers onto LNPs via a covalent chemical reaction in a certain proportion...Overall, we developed a PROTAC that exhibited persistent and excellent BCL6 degradation ability in DLBCL, with an excellent safety profile. Thus, our BCL6 degrader provides a complementary approach to existing clinical‑stage candidates.
A photocaged dibenzosilacycloheptyne (photo-DBSH) and the complementary azide were deployed to tag the oncoprotein ligands (i.e., (+)-JQ1 for BRD4 and Olaparib for PARP1) and the E3 ligase ligand (i.e., Pomalidomide for CRBN), respectively, for a proof-of-concept study and potential treatment for triple-negative breast cancer (TNBC). Further in zebrafish models, PCPTAC promoted BRD4 degradation leading to thinner yolk sac extension and achieved 94% tumor inhibition in HeLa xenografts. This split-and-photoclick strategy paves a new avenue for developing safer and more efficacious PROTACs with synergistic antitumor effects.
In combination with rhIL-2, exp_GAIA integrates endogenous NK activity with induction of long-lasting, CD8+T cell-dependent antitumor immunity via a CCR5-CCL3-NK-IFN-γ-CD8 pathway, reinforced ICD with CRT exposure. These findings support exp_GAIA+rhIL-2 as a new NK-based strategy for durable control of solid tumors.