Mechanistically, Tus inhibited tolimidone-induced Lyn kinase activation and suppressed SP-and Tween 80-induced β-hexosaminidase release, exhibiting an inhibitory profile comparable to that of the Lyn/Btk antagonist bosutinib. Additionally, Tus attenuated the phosphorylation levels of MRGPRX2 downstream signal molecules, including Btk, PLCγ1, PKC, p38 MAPK, IκB-α and NF-κB (p65). In conclusion, Tus attenuates SP-and Tween 80-induced mast cell activation and pseudo-allergic reactions by targeting the Lyn/Btk/PLCγ1 and p38/NF-κB pathways, highlighting its therapeutic potential for pseudo-allergy.

NXP900 also synergized with gemcitabine/cisplatin chemotherapy, enhancing antitumor efficacy in both in vitro and in vivo models. IL13RA-AKT signaling was upregulated in resistant models; NXP900 sensitivity could be restored with AKT or IL13RA2 inhibition. Together, these findings demonstrate the therapeutic potential of NXP900 as a novel YAP inhibitor in CCA and support further investigation in a clinical trial.

CXCL16 promotes macrophage senescence, and senescent CXCL16+ macrophages drive LUAD progression through TGF-β signalling. These findings identify CXCL16+ macrophages as a biologically and therapeutically relevant immune cell population, highlighting a potential target for precision intervention in LUAD.

Betamethasone and levofloxacin ophthalmic solutions were started on the same day. Molecular remission was achieved on day 161 after relapse. Three years later, the patient remains in remission on dasatinib therapy.

μPharma provides rapid (4-h assay), accurate, and automated prediction of drug sensitivity at single-cell resolution using minimal clinical samples, potentially enabling same-day precision oncology decision-making.

Both treatment with the senolytic cocktail dasatinib plus quercetin and treatment with the NF-κB inhibitor resveratrol (RSV) alleviated adipose tissue ageing, improved glucose tolerance and insulin sensitivity, and ultimately decreased OC progression and metastasis. Together, these results indicate an important role of ovarian cancer in adipose tissue ageing, and identify the elimination of senescent ADSCs in adipose tissue as a new potential strategy for the treatment of OC.

Structure-based molecular docking further identified Lenvatinib and Dasatinib as previously unappreciated candidate inhibitors of SERPINE1, suggesting actionable therapeutic opportunities. Its strong prognostic power, combined with newly revealed druggability, positions SERPINE1 as a tractable therapeutic axis for precision immunotherapy and rational drug repurposing. These findings provide a mechanistically grounded and clinically actionable entry point into targeting the inflammatory tumor microenvironment of pancreatic cancer.

Drug sensitivity analyses further suggested that stemness-high tumors may exhibit increased susceptibility to selected kinase inhibitors (Dasatinib, A-770041) and metabolic modulators (Phenformin, Salubrinal). OSA-associated IH is linked to stemness-associated transcriptional plasticity, immune suppression, and adverse clinical outcomes in lung cancer. The identified stemness-based gene signature provides a robust prognostic biomarker and highlights potential therapeutic vulnerabilities, supporting integrative strategies that combine stemness and immune -targeted approaches with immunotherapy in OSA-associated lung cancer.

High-risk patients showed higher sensitivity to dasatinib and staurosporine. The study identified mitophagy-related molecular clusters and developed a prognostic model for PaC. This model may help predict overall survival and guide personalized treatment strategies for PaC patients.

P3, N=280, Completed, Almirall, S.A. | Trial completion date: Apr 2025 --> Nov 2025

Patients remaining on dasatinib maintained elevated NK cells with a more mature phenotype, suggesting a durable effect. These results highlight the greater dasa+blina immune activation, supporting a potential synergistic effect of the drug combination.

P1/2, N=20, Active, not recruiting, Mayo Clinic | Enrolling by invitation --> Active, not recruiting