P2, N=42, Active, not recruiting, Chipscreen Biosciences, Ltd. | Recruiting --> Active, not recruiting | Trial completion date: Jul 2026 --> Oct 2026 | Trial primary completion date: Feb 2026 --> May 2026

Guided by a scaffold-hopping strategy based on G-749 (denfivontinib), a series of quinazoline-based derivatives was designed and synthesized to explore structure-activity relationships (SAR)...Mechanism studies indicated that W4 induced G0/G1 cell cycle arrest and apoptosis, accompanied by a reduction in intracellular reactive oxygen species levels and a loss of mitochondrial membrane potential. Collectively, these results identified W4 as a potent FLT3 inhibitor and provided valuable SAR insights for further scaffold optimization.

P3, N=558, Not yet recruiting, Chipscreen Biosciences, Ltd.

P1/2, N=228, Recruiting, Advenchen Laboratories, LLC

Computational analysis suggests that the high-risk group is potentially sensitive to targeted drugs such as ZM447439. Furthermore, in vitro experiments confirmed that FN1 silencing significantly suppresses the migration and proliferation of PTC cells. This study systematically deciphers the functional adaptive reprogramming during PTC LNM, providing novel insights and tools for LNM prediction and targeted therapy.

P2, N=31, Active, not recruiting, AstraZeneca | Trial completion date: Dec 2025 --> Dec 2026

P1/2, N=70, Recruiting, Ellipses Pharma | Trial completion date: Dec 2025 --> Dec 2026

Lung adenocarcinoma patients have poorer prognosis due to higher levels of CPCs, TMPO-AS1, and E2F1. A sponge complex between TMPO-AS1 and hsa-let-7b-5p may contribute to the tumor progression, and targeting CPCs with natural compounds could offer therapeutic potential. Highlights 1. The overexpression of chromosomal passenger complex genes, AURKB, BIRC5, CDCA8, and INCENP is significantly associated with poor prognosis in lung adenocarcinoma (LUAD), particularly among smokers. 2. The competing endogenous RNA (ceRNA) axis, which involves the long non-coding RNA TMPO-AS1 and the miRNA hsa-let-7b-5p, regulates the expression of these CPC genes. TMPO-AS1 shows a positive correlation with CPC genes, while hsa-let-7b-5p shows a negative correlation. 3. Survival analysis indicates that the combined expression of CPC genes, TMPO-AS1, hsa-let-7b-5p, and E2F1 may serve as a reliable prognostic biomarker panel for LUAD in smokers. 4. Hesperidin exhibits a strong binding affinity to CPC proteins, particularly AURKB, when compared to Barasertib, Docetaxel, and Paclitaxel, highlighting its potential as a therapeutic agent. 5. The overexpression of CPC genes, E2F1, and TMPO-AS1 in LUAD is strongly associated with reduced infiltration of CD4⁺ T cells, indicating their role in promoting an immunosuppressive tumor microenvironment.

Besides, downregulating the levels of c-Myc, BCL-xL and MCL-1 also contributed to the synergistic effects of the combined regimen on t-FL. Taken together, these findings suggest that the synergy between the DGKα inhibitor ritanserin and multi-targeted inhibitor chiauranib might represent a promising option for the treatment of t-FL.

P2, N=36, Active, not recruiting, Advenchen Pharmaceuticals, LLC. | Recruiting --> Active, not recruiting | Trial completion date: Dec 2025 --> Dec 2026 | Trial primary completion date: Dec 2024 --> Dec 2025

Collectively, this study elucidates a novel anticancer mechanism associated with Aurora B inhibition, revealing that AZD1152-HQPA not only impairs mitotic fidelity and promotes polyploidization but also compromises the telomere/telomerase maintenance system. These findings highlight the therapeutic potential of Aurora B inhibitors in targeting telomere-associated vulnerabilities in polyploid cancer cells.

Overall, compound 18 is a valuable chemical biology tool and a potential therapeutic. Our findings suggest that pharmacological degradation of AURKB could offer an alternative therapeutic approach for treating AURKB-dependent tumors.