nilotinib

P2, N=17, Active, not recruiting, Baylor College of Medicine | N=100 --> 17 | Recruiting --> Active, not recruiting

This led to development of tyrosine kinase inhibitors (TKIs) such as Imatinib, Nilotinib, and Ponatinib. Asciminib does not appear to induce a prothrombotic or proinflammatory state under the conditions studied, which may be advantageous for CML patients. However, the observed increase in thrombin generation over time suggests a potential effect on secondary haemostasis that warrants further investigation in controlled studies.

In this setting, Peg-IFN combined with nilotinib induced higher initial rates of MR4·5 compared to TKI monotherapy, despite additional side effects. The onset of psychiatric events might promote immediate cease of Peg-IFN and psychiatrist advice Whether this early molecular response translates into sustained treatment-free survival should be studied in a randomised trial sufficiently powered for this outcome.

Cycloheximide chase assays indicated accelerated AIRE protein degradation, while MG132 partially rescued AIRE levels, implicating proteasome-dependent degradation. Overall, Nilotinib suppresses ESCC progression by inhibiting ILK and destabilising AIRE, suggesting its potential as a targeted therapy for ILK-positive ESCC.

These findings establish MPERSRGs as key determinants of tumor-immune interactions and provide actionable biomarkers for risk stratification and precision therapy selection in cancer.

P3, N=603, Completed, Institut National de la Santé Et de la Recherche Médicale, France | Active, not recruiting --> Completed

P2, N=82, Recruiting, National Cancer Institute (NCI) | Trial completion date: Apr 2026 --> Apr 2027 | Trial primary completion date: Apr 2026 --> Apr 2027

TKI-associated bone marrow aplasia has been reported with agents such as imatinib, dasatinib, and nilotinib. This case supports the potential role of ponatinib as an effective salvage option following severe TKI-related marrow toxicity, particularly in patients who are not candidates for allogeneic transplantation. Further clinical experience and larger studies are needed to better define optimal management strategies for this rare but serious complication.

Curcumin did not sensitize HepG2-DR cells to doxorubicin, whereas verapamil and simvastatin enhanced doxorubicin cytotoxicity only at toxic concentrations. In contrast, several TKIs, including nilotinib, tivozanib, and, to a lesser extent, cabozantinib, exhibited synergistic effects with doxorubicin in HepG2-DR cells...Third-generation MDR1 inhibitors (tariquidar, elacridar, and zosuquidar) sensitized HepG2-DR and HB-303 cells at non-toxic nanomolar concentrations in vitro...MDR1 inhibitors, such as zosuquidar, may enable dose reductions of chemotherapeutic agents, whereas the use of synergistic TKIs, such as tivozanib, may improve therapeutic outcomes and minimize adverse effects in children with HB. TG100-115, a TRPM7 kinase inhibitor, provides neuroprotection and attenuates NLRP3 inflammasome-mediated neuroinflammation in a neonatal mouse model of hypoxic-ischemic brain injury.

During follow-up, improvements in tricuspid regurgitant pressure gradient, brain natriuretic peptide values, and hypertension were observed after reducing the dose of the same TKI, interrupting the TKI treatment, and switching from the newer-generation TKIs to imatinib (IM) or bosutinib (BOS). These findings highlight the importance of blood pressure control and cardiovascular monitoring for CVE prevention in high-risk CML patients. Switching to IM or BOS, TKI dose reduction, or treatment discontinuation was observed to be associated with improvement in cardiovascular parameters in selected patients achieving deep molecular response.

FTO inhibitors (e.g., CS1, FB23-2) appreciably impair the growth of resistant cells either alone or in combination with nilotinib...These findings offer new insights into cancer drug resistance and advance the application of RNA nanotechnology for treating leukemia. The research provides a foundation for developing novel, targeted therapies for resistant leukemia.

Both imatinib and nilotinib therapies lead to significant increases in BP, with nilotinib showing a greater hypertensive effect. Monitoring BP is crucial, especially for patients on second-generation TKIs, to manage cardiovascular risks associated with long-term treatment.