dasatinib

We identified FDA-approved compounds acting through these pathways, three of which, Ribociclib, Ponatinib, and Dasatinib, showed superior efficacy to current therapies across renal cancer cell lines in preclinical screens. By acting through mechanisms distinct from current therapies, they represent promising candidates for combination strategies aimed at overcoming resistance and improving clinical outcomes in ccRCC.

This specific clone persisted after discontinuation, suggesting a role in the sustained immune surveillance of residual leukemia stem cells. These findings suggest that the quality of immune reconstitution, specifically the induction of innate-like effector T-cell clones, may be a more critical determinant of TFR success than the absolute duration of therapy.

Clinically available SFK inhibitors, particularly dasatinib, synergistically enhance ATRA-induced myeloid differentiation of NB4 APL cells and are more effective than the conventional ATRA plus ATO combination in this in vitro model. These findings support further preclinical and clinical evaluation of SFK inhibitor plus ATRA combinations as differentiation-oriented strategies and potential alternatives or complements to ATO-containing regimens in APL.

Proto-oncogene SRC (SRC) overexpression, BCLAF1 knockdown, dasatinib treatment, and hypoxia inducible factor 1 subunit α (HIF-1α) inhibition were employed to elucidate regulatory mechanisms...BCLAF1 knockdown diminished nuclear HIF-1α, and HIF-1α inhibition abrogated BCLAF1-induced tumorsphere formation. BCLAF1 enhances radioresistance and CSC properties in TNBC via SRC-HIF-1α signaling, suggesting that BCLAF1 is a potential therapeutic target to overcome radioresistance in TNBC.

Furthermore, the senolytic Src inhibitor dasatinib reduced senescence and fibrosis markers and attenuated β-catenin activity, suggesting that Src acts upstream of β-catenin in this context. Inhibition of β-catenin using ICG001 or PRI724 suppressed senescence and fibrosis markers and reduced downstream targets including CTGF and cyclin D1. These findings reveal a mechanistic link between mechanical stiffness, cellular senescence, and fibrosis in uterine fibroids, and identify Src and β-catenin as potential therapeutic targets.

P=N/A, N=1000, Recruiting, Novartis Pharmaceuticals | Not yet recruiting --> Recruiting

She was started on hydroxyurea, but her platelet count continued to rise, requiring hospitalization for close monitoring, where she was initiated on dasatinib, a tyrosine kinase inhibitor (TKI). As her platelets peaked above 4,000 × 109/L (Reference Range [RR]: 150-450 × 109/L), given the high risk of both thrombotic and bleeding complications, she underwent plateletpheresis, which effectively reduced counts before TKI therapy could achieve disease control. This case highlights the importance of considering the diagnosis of CML in patients with isolated thrombocytosis, particularly in women, and emphasizes the role of plateletpheresis as a potential preventive bridge until TKI therapy takes effect.

Cellular Ki values of dasatinib and imatinib for 25 kinases by FPCBA were broadly concordant with kinobead LC/MS measurements in cancer cell lysates but diverged substantially from recombinant KINOMEscan values, with divergences attributable to competition with ATP, autoinhibition, and membrane-dependent conformational states in living cells. FPCBA enables profiling of native protein-small molecule interactions in a physiologically relevant cellular context.

Imatinib & Dasatinib Are Two Most Commonly Used Tyrosine Kinase Inhibitor (TKI) for Chronic Myeloid Leukemia (CML) in Chronic Phase (CP). One (1) patient developed grade 3 pleural effusion & succumbed to complication. 20% patients failed to achieve optimum molecular response at 6 month with most common adverse effect being neutropenia.

This study analyzed 5-year follow-up data and immune profiling from two independent phase 2 trials, JALSG N-STOP216 (nilotinib [NIL], n=51) and D-STOP216 (dasatinib [DAS], n=49), involving patients who discontinued frontline 2G-TKIs after sustaining deep molecular response (DMR) for ≥2 years. These findings suggest that 2G-TKI-specific off-target effects influence TFR sustainability by modulating the immune microenvironment and the CD4+ helper cell status. JALSG N-STOP216 (UMIN000024984); JALSG D-STOP216 (UMIN000024985).

Drug sensitivity prediction suggested differential therapeutic vulnerabilities, with high-risk patients showing increased predicted sensitivity to JAK inhibitors, dasatinib, and nutlin-3a. An LLPS-related three-gene RiskScore identifies GC subgroups with different prognosis, immune features, and therapeutic sensitivity.

P1, N=30, Recruiting, Mayo Clinic | N=10 --> 30