Tasigna (nilotinib)

P3, N=406, Active, not recruiting, Novartis Pharmaceuticals | Trial completion date: Jan 2031 --> Jan 2028

Furthermore, virtual screening identified several promising therapeutic candidates, including Ecteinascidin, Avodart, and Nilotinib, which demonstrated high binding affinity to pivotal molecular targets such as AIM2, HK3, ATP1A1, and ZAP70. This study provides novel insights into the carcinogenic mechanisms of PFAS in ccRCC and proposes new avenues for targeted therapy. However, further experimental and clinical validation is necessary to confirm these findings and translate them into improved patient outcomes, while also addressing broader environmental health concerns related to PFAS exposure.

TKIs, including flumatinib, may cause AKI; however, FAERS-based disproportionality analysis does not indicate an increased renal safety signal compared to non-TKIs. Among TKIs, dasatinib and nilotinib have lower reporting disproportionality than imatinib does, suggesting a potential therapeutic advantage of their use for patients with kidney diseases.

We evaluated their effects on resistance to five TKIs (imatinib, nilotinib, bosutinib, ponatinib and asciminib), spanning all four TKI generations by using K562 cells. We identified 361 pairs of resistance-conferring single amino acid variants and the corresponding TKIs. Our comprehensive resistance map will complement clinical guidelines in drug selection for patients with chronic myeloid leukaemia based on ABL1 mutations, facilitating precision medicine.

P2, N=124, Active, not recruiting, Novartis Pharmaceuticals | Trial completion date: Dec 2026 --> Jul 2026 | Trial primary completion date: Nov 2026 --> Jul 2026

We assessed EV release and BCR::ABL1 content before and after treatment with imatinib, nilotinib, or dasatinib, alongside Ki67 expression to gauge proliferation. KCL22 cells showed earlier reduction in Ki67 expression. These findings highlight model-dependent EV behaviour, reflecting patient heterogeneity and reinforcing the need for careful model selection in CML research.

P=N/A, N=13, Completed, American University of Beirut Medical Center | N=25 --> 13 | Recruiting --> Completed

P3, N=200, Completed, Hospices Civils de Lyon | Unknown status --> Completed

The patient continues nilotinib therapy with ongoing CML remission and remains under observation for CLL, underscoring a conservative management approach given the indolent nature of his CLL. This case adds to the sparse literature on CML and CLL co-occurrence and raises awareness of secondary hematologic malignancies in TKI-treated CML patients.

This study introduces a microfluidic cell culture array for the comparative analysis of six BCR::ABL1 TKIs, namely imatinib, nilotinib, bosutinib, ponatinib, dasatinib, and asciminib, using CML-related cell lines. We further validated the device with a CML patient-derived bone marrow sample, requiring only minimal adjustments to the experimental conditions. The proposed microfluidic single-cell-based screening array could refine treatment regimens and advance personalized medicine in CML.

Notably, the TLS_H group demonstrated enhanced sensitivity to chemotherapeutics including AZD8055, axitinib, vorinostat, nilotinib, camptothecin and paclitaxel. Real-time fluorescent quantitative PCR (RT-qPCR) validation in Mia PaCa2 and Jurkat cells indicated that LAT, RBP5 and SKAP1 may play important roles in modulating sensitivity to these chemotherapeutics. These findings establish TLS as a potential biomarker for PAAD, enabling personalised chemotherapy selection by integrating immune contexture and genomic drivers to improve clinical outcomes.

In this study, we employed molecular dynamics simulation to observe the synergistic interactions of BCR-ABL1 by the allosteric inhibitor asciminib and ATP competitive inhibitors nilotinib and ponatinib. Our study reveals the allosteric communication pathway between asciminib and ponatinib, providing more detailed insights into the effectiveness of combination therapy. These findings provide valuable insights into combination therapies, aiding in the rational use of medications and guiding the design of novel inhibitors.