nilotinib

In Japan, five agents-imatinib (Glivec®), dasatinib (Sprycel®), nilotinib (Tasigna®), bosutinib (Bosulif®), and STAMP inhibitor asciminib (Scemblix®)-are currently approved for first-line therapy. Looking forward, immunologic determinants of TFR and novel therapeutic approaches, including targeting CML stem cells with agents such as asciminib or demethylating drugs, may offer prospects for cure. This review summarizes the current evidence and practical considerations in selecting first-line therapy for chronic-phase CML, with a focus on optimizing long-term outcomes and advancing toward individualized and potentially curative strategies.

In the event of molecular relapse, carefully considered use of imatinib or nilotinib at the lowest effective dose may be employed exclusively in the second or third trimester following multidisciplinary counseling, whereas dasatinib should be avoided throughout gestation. We emphasize structured algorithms, explicit intervention thresholds, and monthly BCR-ABL1 (IS) testing, as well as collaboration with obstetrics, neonatology, and reproductive medicine, including assisted reproductive technologies. Finally, we discuss practical pathways applicable to resource-limited settings to balance maternal-fetal safety with patient values and to support informed, preference-concordant decision-making.

Conditional knockdown of Pim1 in CD4+ T cells (Pim1 cKO) or using the Pim1 inhibitor AZD1208 alleviated the development of inflammatory arthritis in association with decreasing the proportion of Th17 cells. Through molecular docking and dynamic simulation, nilotinib, a Food-and-Drug-Administration-approved drug, was identified as a selective substitute for the currently clinically nonapproved Pim1 inhibitors, which impeded Th17 cell differentiation and was well tolerated during the treatment of Pim1 cKO mice and 2 inflammatory arthritis mouse models. Our study contributes to a better understanding of the mechanism through which Pim1 promotes Th17 cell differentiation and advances the clinical application of Pim1 as an effective target for treating inflammatory arthritis.

VEGF inhibitors, such as bevacizumab and VEGFR-TKIs (e.g., sorafenib, sunitinib), significantly elevate the risk of ATEs, with hypertension and proteinuria as common comorbidities. BCR-ABL-TKIs, especially nilotinib and ponatinib, are linked to rapid-onset PAD, even in patients without prior cardiovascular risk factors...Hormonal therapies, including tamoxifen and androgen deprivation therapy, also contribute to ATEs through metabolic and vascular mechanisms...Monitoring and prevention strategies, such as regular cardiovascular risk assessments, lipid management, and arterial ultrasound surveillance, are critical for high risk patients. Multidisciplinary onco-vascular teams are essential to mitigate these risks and optimize patient outcomes.

P1, N=47, Completed, National Cancer Institute (NCI) | Recruiting --> Completed | N=70 --> 47 | Trial completion date: Jun 2026 --> Feb 2026 | Trial primary completion date: Jun 2026 --> Apr 2025

P=N/A, N=75, Not yet recruiting, Assiut University

This case underlines the importance of considering rare but severe arterio-occlusive complications, such as retinal artery thrombosis, among the cardiovascular toxicities of nilotinib. Careful cardiovascular monitoring and early recognition of such events are crucial to optimize patient safety and treatment outcomes in CML management.

P2, N=37, Completed, Georgetown University | Unknown status --> Completed

Six thousand six hundred twenty-five dasatinib (age 59.7±15.2 years, 44.0% women), 5205 nilotinib (age 55.4±15.0 years, 44.2% women), 2421 bosutinib (age 63.8±14.2 years, 42.1% women),1358 ponatinib (age 57.3±14.9 years, 46.1% women), and 922 asciminib (age 64.3±13.8 years, 43.7% female) new users were each matched with the maximum of available imatinib users on time-conditional propensity score and on duration of prior imatinib use (prevalent users). This study, designed to emulate a randomized trial, suggests that, in French patients with chronic myeloid leukemia treated with BCR-ABL TKIs, dasatinib use is associated with a higher risk of PAH compared with imatinib, while bosutinib and ponatinib exposure may aggravate or trigger a recurrence of PAH in patients with preexisting dasatinib exposure. Whether bosutinib and ponatinib could induce PAH without preexposure to dasatinib remains to be explored.

A model-informed drug development (MIDD) approach was applied to predict 2L efficacy and supported global regulatory approval of asciminib across treatment lines, despite limited clinical data in 2L.

Biological evaluation using MCF-7 breast cancer cells demonstrated substantially improved cytotoxicity (50% inhibitory concentration = 6.7 µg/mL), enhanced reactive oxygen species generation, pronounced mitochondrial membrane depolarization, stronger apoptosis induction, and significant G0/G1-phase arrest compared with the pure drug. Collectively, these findings demonstrate that the optimized PEGylated nanoliposomal formulation significantly improves solubility, stability, intestinal permeation, and in vitro anticancer activity of nilotinib, supporting its potential as a promising preclinical formulation strategy for further in vivo and clinical evaluation.

Consistent with prior preclinical studies, we demonstrate that dasatinib and ponatinib, unlike SRC sparing TKIs (imatinib, nilotinib), antagonize blinatumomab's T-cell engaging efficacy by potently inhibiting LCK Y394 phosphorylation, a critical step in proximal TCR signaling. We show that TKI-induced T-cell suppression and antagonism can be significantly improved by supplementing co-cultures with common gamma-chain cytokines, particularly IL-7. IL-7 robustly enhances human T-cell proliferation, reduces exhaustion, and significantly improves blinatumomab's cytotoxic efficacy in the presence of Src/BCRABL1 TKIs.