Filanesib TFA

Filanesib TFA inhibits human KSP with an IC₅₀ of 6 nM by a mechanism demonstrated to be uncompetitive with respect to ATP and noncompetitive with respect to tubulin^[1].
Filanesib TFA induces mitotic arrest in multiple cell lines^[1].
Filanesib TFA exhibits anti-proliferative against a broad range of human and rodent tumor cell lines^[1].
Filanesib TFA (0.001-0.1 nM; 36 hours) induces apoptosis, by a mechanism that is independent of p53 status, as defined by formation of nucleosomes and activation of caspases 3 and 7, as well as accumulation in SubG0/1 by FACS ^[1].
Filanesib TFA (0.1-100 nM; 18 hours) induces the accumulation of phospho-Histone H3 (a marker of mitosis, and an indicator of mitotic arrest) in HeLa cells^[1].
Filanesib TFA (0.78-6.25 nM; 44 hours) treatment results in G2/M arrest^[1].
Filanesib TFA (10 nM; 16 hours) treatment results in the formation of monopolar spindles^[1].
Filanesib TFA potently induces cell cycle block and subsequent death in leukemic cells via the mitochondrial pathway and has potential to eradicate AML progenitor cells^[2].
Filanesib TFA (3 μM; 6-24 hours) is able to induce caspase-2 activation^[3].
Filanesib TFA (0.003-3 μM; 24-48 hours) is cytotoxic in Type II EOC cells^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.