P1/2, N=70, Recruiting, Ellipses Pharma | Trial completion date: Dec 2026 --> Dec 2027 | Trial primary completion date: Oct 2025 --> Dec 2027

P1/2, N=32, Active, not recruiting, M.D. Anderson Cancer Center | Trial completion date: Jun 2026 --> Jun 2028 | Trial primary completion date: Jun 2026 --> Jun 2028

P2, N=120, Recruiting, Puma Biotechnology, Inc. | N=80 --> 120 | Trial completion date: Oct 2027 --> Apr 2028 | Trial primary completion date: Apr 2027 --> Oct 2027

These findings propose that TGT targets AURKA/KEAP1/NRF2 axis to exert anti-breast cancer effect, and AURKA inhibition represents a potential strategy for breast cancer treatment through inducing cell cycle arrest and driving ferroptosis.

P=N/A, N=5, Terminated, RenJi Hospital | N=30 --> 5

Collectively, our findings systematically reveal that Alisertib exerts significant AURKA-independent antitumor effects in colon cancer, likely mediated through alternative mechanisms such as the regulation of ZAP70 and associated immune pathways. This study provides a novel perspective on the pharmacological action of Alisertib and its clinical application.

Importantly, TCHP inhibition not only suppresses tumor growth directly but also sensitizes liver cancer cells to the AURKA inhibitor alisertib, allowing tumor suppression at reduced drug doses and mitigating toxicity risks. Collectively, our findings establish TCHP as a potential oncogenic driver and therapeutic vulnerability in liver cancer and highlight the TCHP-AURKA axis as a promising target for synergistic treatment strategies.

P=N/A, N=30, Terminated, RenJi Hospital | Recruiting --> Terminated; The study was terminated because the originally planned VIC-1911 dose-escalation scheme (100 mg, 150 mg, 200 mg BID) was scientifically unjustified, lacking prior clinical safety data to support such starting doses when combined with lenvatinib in HC

P=N/A, N=15, Active, not recruiting, RenJi Hospital | Recruiting --> Active, not recruiting | Trial primary completion date: Jul 2025 --> Dec 2025

Mechanistically, VIC-1911 disabled HR-mediated repair of DSBs in otherwise HR-proficient PC cells, leading to a "BRCAness" phenotype and pronounced accumulation of DNA damage and mitotic catastrophe. In summary, our study uncovers what we believe a novel mechanism to functional "BRCAness" by inducing mitotic arrest and highlights VIC-1911 as a promising therapeutic agent for advanced PC, either as a single agent or in combination, sensitizing HR-proficient tumors to PARP inhibitors.

These findings highlight the superiority of scL-ALI in overcoming delivery barriers and enhancing therapeutic efficacy of alisertib, while possibly minimizing undesirable side effects in normal tissues. The scL-ALI nanocomplex shows enhanced therapeutic potential for treating AURKA-driven malignancies, particularly in combination with radiation therapy.

P2, N=50, Not yet recruiting, Puma Biotechnology, Inc.