AURKB contributes to LUAD progression by modulating MYC-driven oncogenic programs. Consequently, targeting the AURKB/MYC axis may represent a potential therapeutic strategy for MYC-dependent lung adenocarcinoma.

This study identifies Aurora B as a therapeutically actionable vulnerability in HCC, whose inhibition induces senescence and enhances tumor immunogenicity. The combination of Aurora B inhibitor with anti-PD-1 therapy yields synergistic anti-tumor effects, supporting its potential as a promising strategy to improve immunotherapy outcomes in HCC.

P2, N=80, Recruiting, Advenchen Pharmaceuticals, LLC. | N=36 --> 80 | Trial completion date: Dec 2026 --> Dec 2028 | Trial primary completion date: Dec 2025 --> Dec 2027 | Active, not recruiting --> Recruiting

P2, N=50, Active, not recruiting, Advenchen Pharmaceuticals, LLC. | N=30 --> 50 | Recruiting --> Active, not recruiting

HCC cells with low S100P expression showed significantly greater sensitivity to the AURKB inhibitor AZD1152-HQPA than control cells, with a 61% decrease in IC₅₀. This study reveals the S100P/MYBL2/AURKB axis as a key driver of HCC and a predictor of targeted therapy response, supporting precision treatment strategies.

A personalised surveillance strategy may provide a novel avenue to monitor SCLC, supporting further investigation and potential broader clinical application.

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