P=N/A, N=900, Completed, Second Affiliated Hospital of Wenzhou Medical University

One quarter of IBD patients requiring intensified anti-TNFa therapie were successfully deescalated to standard dosing, after a median of 16.0 (IQR: 8.0-36.0) months.

After induction therapy with the lenalidomide-dexamethasone (RD) regimen, ASCT is performed and partial remission is achieved. The pathogenesis of secondary MDS in POEMS syndrome is discussed from three aspects: cytotoxic therapy, genetic predisposition, and SARS-CoV-2 infection. This case underscores the importance of prolonged surveillance for secondary myeloid neoplasms (sMN) in POEMS patients and suggests that early genomic profiling and individualized treatment may improve outcomes.

The efficacy and safety of IFX-BS after NMS are high. In addition, its trough concentration is serologically non-inferior to baseline values.

P1/2, N=30, Not yet recruiting, University Medical Center Groningen

P=N/A, N=14, Not yet recruiting, M.D. Anderson Cancer Center

P2, N=35, Not yet recruiting, Sun Yat-sen University

Together, we established a proof of concept for PROTAC in the DC vaccine design by linking E3 ligase to a protein model antigen, which can be readily replaced with other identified pathogenic antigens to elicit robust cytotoxic immune responses against tumors or viral diseases, and thus has serious implications in the clinics.

P2, N=26, Completed, AIDS Malignancy Consortium | Trial completion date: Jan 2026 --> Apr 2025 | Active, not recruiting --> Completed

While novel agents continue to expand treatment options, ASCT2 remains a viable therapeutic strategy in appropriately selected patients, especially those with durable responses to prior therapy.

Moreover, SLC7A11 inhibitors, particularly sulfasalazine and erastin, effectively reversed resistance, in 18 clinical trials (Phase I-III) completed over the last decade. Targeting SLC7A11 presents a promising therapeutic strategy to modulate redox balance, metabolism, and ferroptosis, towards efficient cancer treatments.

In the present study, we established a modular synthetic platform to systematically generate a set of PROTAC degrader candidates consisting of the CK1δ-specific inhibitor scaffold, alkyl and PEG linker motifs with various lengths, and Cereblon (CRBN)-engaging pomalidomide and thalidomide derivatives as E3 ligase binders. The most potent PROTAC P1d inhibits the phosphorylation of downstream substrates through CK1δ/ε degradation. We establish the requirement of CUL4ACRBN and the proteasome for the P1d-mediated degradation of CK1δ/ε.