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

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.

Echinococcal infection promotes pathological osteoclastogenesis and osteolysis through IL-1β/c-Fos/NFATc1 signaling activation.

Data from this interim analysis support the long-term effectiveness and safety of canakinumab for the treatment of TRAPS.

Mechanistically, TPM3-TRKA degradation by compound 9 was dependent on CRBN-mediated polyubiquitination and proteasomal degradation; accordingly, it was hindered by inhibitors of the proteasome (MG132) or Cullins (MLN4924), by dominant negative Cullin 4A mutant, and by free pomalidomide. Finally, a compound 9 derivative, compound 20, induced in vivo degradation of TMP3-TRKA in KM12 cells mouse xenografts. In conclusion, our study indicated that PROTAC-mediated degradation is an efficient strategy to intercept RET and TRKA oncogenic signaling.

By directly modulating inflammatory pathways, canakinumab significantly lowered the incidence of major adverse cardiovascular events (MACE) independent of lipid levels. Similarly, colchicine, an ancient anti-inflammatory drug, has gained renewed interest due to its efficacy in reducing cardiovascular events in patients with chronic coronary disease and recent myocardial infarction...In conclusion, targeted anti-inflammatory therapy represents a promising adjunct to traditional CVD treatments, potentially revolutionizing the management of cardiovascular events. Future studies are essential to optimize these strategies and fully integrate them into clinical practice, enhancing outcomes for patients with CVD.

P2, N=250, Active, not recruiting, Avalo Therapeutics, Inc. | Recruiting --> Active, not recruiting | Trial completion date: Jul 2026 --> Apr 2026 | Trial primary completion date: Jun 2026 --> Mar 2026

Given the immune-enhancing effects and excellent safety profile, pomalidomide should be further investigated as an immune-enhancing strategy for an HIV cure.

P2, N=20, Recruiting, Novartis Pharmaceuticals | Not yet recruiting --> Recruiting

Our findings suggest that CU06-1004 inhibits inflammation-induced tumorigenesis by modulating the inflammatory response in the colon. Consequently, CU06-1004 could represent a promising therapeutic candidate for the prevention of colorectal cancer through modulation of inflammation.

P=N/A, N=46, Recruiting, The First Affiliated Hospital of Zhejiang University School of Medicine; The First Affiliated Hospital of Zhejiang University School of Medicine

P2, N=15, Active, not recruiting, Weill Medical College of Cornell University | Trial completion date: Sep 2027 --> Jan 2028 | Trial primary completion date: Sep 2025 --> Jan 2026