nilotinib

To our knowledge, this is the first report to document histopathological evaluation of a carotid plaque obtained following CEA in a patient with long-term nilotinib therapy. This case highlights the importance of vascular monitoring in patients receiving nilotinib and provides supportive pathological findings for the hypothesis that nilotinib may accelerate atherosclerotic processes.

These engineered peptides, along with high-affinity small molecules such as nilotinib (KD = 4.83nM), effectively downregulated Pomc expression and inhibited proliferation of AtT-20 tumor cells. Taken together, these findings suggest that the JAZF1-TR4-Pomc axis may serve as a potential therapeutic target for modulating adrenocorticotropic hormone (ACTH) hypersecretion in CD.

P2, N=75, Completed, Georgetown University | Unknown status --> Completed

Among patients with chronic myeloid leukemia (CML) aiming for tyrosine kinase inhibitor (TKI) discontinuation, second-generation TKIs (2G-TKIs) are used as one of the first-line options because they induce faster and deeper molecular responses than imatinib...We analyzed 431 patients enrolled in the phase III Japan Adult Leukemia Study Group (JALSG) CML212 trial, comparing nilotinib at 300 mg twice daily (n = 218) and dasatinib at 100 mg once daily (n = 213) as first-line therapy...In multivariable models, HT(0-3) (subdistribution hazard ratio [HR], 2.23; 95% CI, 1.09-4.55) and the 6-month IS (HR, 0.38; 95% CI, 0.31-0.47) were independent predictors of MR4.5 attainment, whereas only the 6-month IS predicted TDE (odds ratio, 0.37; 95% CI, 0.24-0.56). This study demonstrates that molecular response at 6 months after TKI initiation has important clinical value in early stratification of MR4.5 attainment and TDE in patients receiving 2G-TKI therapy.

Three patients were treated with imatinib (one later switched to nilotinib and then dasatinib), while one patient each received osimertinib and brigatinib. When interstitial pneumonia occurs during TKI administration and does not respond to drug withdrawal and corticosteroid treatment, careful analysis of chest imaging features, along with bronchoalveolar lavage and/or bronchoscopic lung biopsy, is necessary for a definitive diagnosis. This case series and literature review suggest that nebulized GM-CSF or whole lung lavage (WLL) may be effective treatment options for TKI-induced autoimmune PAP.

P2, N=21, Completed, National Cancer Institute (NCI) | Active, not recruiting --> Completed

Taken together, our findings indicate that OTUD5 inhibits TGF-β-induced EMT and NSCLC cell metastasis in a partially TIF1γ-dependent manner and reveal an OTUD5-TIF1γ-SMAD3/4 positive feedback loop for preventing TGF-β-induced EMT. These findings provide new insights into the molecular basis of NSCLC metastasis and suggest that nilotinib may be repositioned as an anti-metastatic drug by targeting OTUD5 in NSCLC treatment.

P2, N=40, Active, not recruiting, National Cancer Institute (NCI) | Trial completion date: Jun 2026 --> Jun 2027 | Trial primary completion date: Jun 2026 --> Jun 2027

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.