Fig. 7

Fig. 7

Fig. 7. Molecular action of L72, both invitro, and invivo. The L72 after entering the plasma membrane causes inhibition of FLT3, IDH2, STAT3, and Flk-1. Meanwhile, it generates reactive oxygen species (ROS) and mitochondrial membrane damage-causing alterations in MMP. This results in the release of cytochrome c and activation of p21. This activation eventually triggers apoptotic gene transcription in the nucleus, causing cellular apoptosis. The fore-mentioned inhibition of STAT3 causes the lack of transcription of cell survival genes. Moreover, inhibition of Flk-1 promotes anti-angiogenesis, inhibiting the formation of new cells or vasculatures. All these events favored cellular apoptosis, after L72 administration.