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Tandutinib

CAS No. : 387867-13-2

MCE 國(guó)際站：Tandutinib

產(chǎn)品活性：Tandutinib (MLN518) 是一種有效和選擇性的 FLT3 的抑制劑，其 IC₅₀ 為 0.22 μM，并且還抑制 c-Kit 和 PDGFR，其 IC₅₀ 分別為 0.17 μM 和 0.20 μM。Tandutinib 可用于急性骨髓性白血病，并具有穿越血腦屏障的能力。

研究領(lǐng)域：Protein Tyrosine Kinase/RTK  |  Apoptosis

作用靶點(diǎn)：FLT3  |  c-Kit  |  PDGFR  |  Apoptosis

In Vitro: Tandutinib (0-3 μM; 30 minutes; Ba/F3 cells) treatment inhibits IL-3-independent cell growth and FLT3-ITD autophosphorylation with an IC₅₀ of 10-100 nM in Ba/F3 cells expressing different FLT3-ITD mutants.
Tandutinib (1 μM; 24-96 hours; Molm-14 and THP-1 AML cells) treatment induces apoptosis in FLT3-ITD-positive AML cells.
In human FLT3-ITD-positive AML cell lines, Tandutinib inhibits FLT3-ITD phosphorylation (IC₅₀ of ~30 nM). As with Erk2, a constitutively high level of Akt phosphorylation is readily detected and is efficiently blocked by pretreatment of the Molm-14 cells with 100-300 nM Tandutinib.
Tandutinib inhibits cell proliferation of the FLT3-ITD-positive Molm-13 and Molm-14 with an IC₅₀ of 10 nM. And signaling through the MAP kinase and PI3 kinase pathways.

In Vivo: Tandutinib (60 mg/kg; oral gavage; daily; for 35 days; athymic nude mice) treatment causes a statistically significant increase in survival that was extended on average by 20 days.

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