| Bioactivity | MOMIPP, a macropinocytosis inducer, is a PIKfyve inhibitor. MOMIPP penetrates the blood-brain barrier (BBB)[1][2]. | |||||||||
| Invitro | MOMIPP can induce intense macropinocytosis, leading to methuosis in cultured glioblastoma cells at low micromolar concentrations[1]. In U373 and Hs683 cell lines, 3 µM for MOMIPP induces cell vacuolization[1].MOMIPP (10 μM) causes early disruptions of glucose uptake and glycolytic metabolism. MOMIPP selectively activates the JNK1/2 stress kinase pathway, resulting in phosphorylation of c-Jun, Bcl-2 and Bcl-xL[2]. Western Blot Analysis[2] Cell Line: | |||||||||
| In Vivo | MOMIPP (80 mg/kg; i.p.; once daily; for 15 consecutive days) shows moderately effective in suppressing progression of intracerebral glioblastoma xenografts[2]. Animal Model: | |||||||||
| Name | MOMIPP | |||||||||
| CAS | 1363421-46-8 | |||||||||
| Formula | C18H16N2O2 | |||||||||
| Molar Mass | 292.33 | |||||||||
| Appearance | Solid | |||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | |||||||||
| Storage |
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| Reference | [1]. Margaux Colin, et al. Dysregulation of Macropinocytosis Processes in Glioblastomas May Be Exploited to Increase Intracellular Anti-Cancer Drug Levels: The Example of Temozolomide. Cancers (Basel). 2019 Mar 22;11(3):411. [2]. Zehui Li, et al. The JNK signaling pathway plays a key role in methuosis (non-apoptotic cell death) induced by MOMIPP in glioblastoma. BMC Cancer. 2019 Jan 16;19(1):77. |