Imipramine (0.5-300 渭M, 3 days) inhibits HCT-116 cell viability[1].
Imipramine (20 渭M) inhibits cell migration (7 h) and invasion (48 h)[1].
Imipramine (50 渭M, 0-240 min) inhibites the PI3K/Akt/mTOR signaling pathway in U-87MG glioma cells[2].
Imipramine (60 渭M, 24 h) stimulates U-87MG glioma cells autophagy[2].
Imipramine (80 渭M, 24 h) induces HL-60 cell apoptosis[3].
Imipramine (20 mg/kg, i.p. or 15 mg/kg, p.o.; daily for 24 days) attenuates neuroinflammatory signaling and reverses stress-induced social avoidance in mice[4].
[1]. Alburquerque-Gonz谩lez B, et al. New role of the antidepressant imipramine as a Fascin1 inhibitor in colorectal cancer cells. Exp Mol Med. 2020 Feb;52(2):281-292.
[2]. Jeon SH, et al. The tricyclic antidepressant imipramine induces autophagic cell death in U-87MG glioma cells. Biochem Biophys Res Commun. 2011 Sep 23;413(2):311-7.
[3]. Xia Z, et al. The antidepressants imipramine, clomipramine, and citalopram induce apoptosis in human acute myeloid leukemia HL-60 cells via caspase-3 activation. J Biochem Mol Toxicol. 1999;13(6):338-47.
[4]. Ramirez K, et al. Imipramine attenuates neuroinflammatory signaling and reverses stress-induced social avoidance. Brain Behav Immun. 2015 May;46:212-20.
[5]. Balkovetz DF, et al. Evidence for an imipramine-sensitive serotonin transporter in human placental brush-border membranes. J Biol Chem. 1989 Feb 5;264(4):2195-8.