P1, N=36, Recruiting, Memorial Sloan Kettering Cancer Center | Trial completion date: Feb 2026 --> Feb 2027 | Trial primary completion date: Feb 2026 --> Feb 2027

P2, N=60, Recruiting, Chengdu Zenitar Biomedical Technology Co., Ltd | Active, not recruiting --> Recruiting

P3, N=105, Recruiting, Chengdu Zenitar Biomedical Technology Co., Ltd | Not yet recruiting --> Recruiting

P2, N=64, Not yet recruiting, Chengdu Zenitar Biomedical Technology Co., Ltd

Functional plausibility was assessed in pre-stasis human mammary epithelial cells (HMECs) exposed for 24 h to clinically relevant EGFR (lapatinib) or KIT (ripretinib) inhibitors. Together, matched normal tissue and primary-cell data indicate a coordinated EGFR/KIT-linked proliferative bias in NHBW epithelium that is rapidly reversible in vitro. These findings motivate composition-aware validation in larger normal-tissue cohorts and pharmacodynamic window studies to test whether short-term RTK modulation can reset proliferation-biased states in at-risk breast epithelium.

Dual targeting of FLT3/SYK (TAK-659) and the proteasome (Ixazomib) showed strong synergy across genetically defined AML subsets, irrespective of FLT3 mutant status. These findings define a therapeutically targetable axis linking FLT3/SYK/β-catenin signaling to stress adaptation, provide a mechanistic basis for combinatorial targeting in high-risk AML. Trial registration: NCT04079738, Date of registration 03 September 2019.

Fedratinib is the second drug approved by the FDA for adult patients with myelofibrosis (MF) following ruxolitinib; however, the mechanism of its dose-limiting toxicity, particularly hepatotoxicity, remains poorly unclear. The results of risk assessment indicated that clinically relevant doses of fedratinib could significantly increase the area under curve (AUC) of drugs mainly metabolized by UGT1A1 and UGT1A3, suggesting a potential risk of clinically significant drug-drug interactions (DDIs). The current research provides useful information for the possible hepatotoxicity mechanism and clinical safe medication of fedratinib.

This PMS showed that the safety profile of quizartinib in routine clinical practice in Japanese patients with R/R FLT3-ITD-positive AML did not differ from the known safety profile of quizartinib. QT interval prolongation was manageable with current risk minimization measures.

Herein, we develop an MRX-2843 (MerTK inhibitor) and Mn2+ codelivered defective metal-organic framework (copper-2,3,6,7,10,11-hexaiminotriphenylene (Cu-HITP))-based single-site nanozyme (Ir@D-Cu-HITP-MMP) for antitumor immunotherapy via innate immune-checkpoint blockade...This synergizes with Mn2+ to enhance the stimulator of interferon genes (STING) activation, triggering robust immune responses. Overall, Ir@D-Cu-HITP-MMP demonstrates potent antitumor effects by activating powerful innate and adaptive immune responses.

P1, N=35, Active, not recruiting, Biomea Fusion Inc. | Trial completion date: Jan 2026 --> Apr 2026 | Trial primary completion date: Jan 2026 --> Apr 2026

P2/3, N=230, Not yet recruiting, European Organisation for Research and Treatment of Cancer - EORTC

FLT3 inhibitors - midostaurin (first-generation), gilteritinib and quizartinib (second-generation) - have been developed to block FLT3 activation. The only exception was an higher risk of ALT increased with gilteritinib (RR = 2.40, 95% CI: 1.16-4.95). Future studies should stratify safety outcomes by demographic and clinical characteristics and incorporate long-term follow-up for a more comprehensive safety assessment in clinical practice.