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In 0 peer-reviewten Publikationen zu Chromatographie, organischer Synthese und Kreuzkupplungsreaktionen zitiert.
UNC569 is a potent, reversible, ATP-competitive and orally active Mer kinase inhibitor with an IC 50 of 2.9 nM and a K i of 4.3 nM. UNC569 also inhibits Axl and Tyro3 with IC 50 s of 37 nM and 48 nM, respectively. UNC569 can be used for acute lymphoblastic leukemia (ALL) and atypical teratoid/rhabdoid tumors research
In Vitro
UNC569 (24 hours) induces apoptosis in ALL cell lines, and increases the levels of cleaved Caspase 3 and cleaved PARP. UNC569 (1 µM; 1.5 hours) treatment effectively inhibit the activation of Mer and downstream signaling, including the PI3K/AKT and MAPK/ERK pathways. UNC569 (1 hour) inhibits Mer phosphorylation levels with IC50 values of 141 nM and 193 nM in human B-ALL (acute lymphoblastic leukemia) 697 and Jurkat cell lines, respectively . MCE has not independently confirmed the accuracy of these methods. They are for reference only. Apoptosis AnalysisCell Line: 697 and Jurkat cells Concentration: 0.4 µM, 0.8 µM, 1 µM, 1.2 µM, 1.4 µM, 1.6 µM, 1.8 µM, 2 µM Incubation Time: 24 hours Result: Induced apoptosis in ALL cell lines. Western Blot AnalysisCell Line: 697 and Jurkat cells Concentration: 1 µM Incubation Time: 1.5 hours Result: Inhibited Mer activation and downstream signaling through ERK1/2 and AKT.
In Vivo
The in vivo pharmacokinetic properties of UNC569 (3 mg/kg) are also assessed in mice via both intravenous (IV) and oral (PO) administration. UNC569 has low systemic clearance (19.5 mL/min/kg), high volume of distribution (V ss of 5.83 L/kg), and good oral bioavailability (57%) . Leukemic zebrafish are treated continuously for 2 weeks by immersion in 4 µM UNC569. the result shows that UNC569 induces more than 50% reduction in tumor burden compared with vehicle- and mock-treated fish. MCE has not independently confirmed the accuracy of these methods. They are for reference only.
IC50& Target:IC50: 2.9 nM (Mer), 37 nM (Axl), 48 nM (Tyro3), Ki: 4.3 nM (Mer)
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