| Bioactivity | MOPIPP is a novel indolebased chalcone, and vacuolin-1, is a non-lethal vacuoleinducing 2-propyl analog of MOMIPP (HY-148114). MOPIPP induces cellular vacuolization and increases autophagosomes numbers. MOPIPP also triggers methuosis, and interrupts glucose uptake and glycolytic metabolism. MOPIPP can cross the blood-brain barrier and shows efficacy in suppressing tumor progression agaisnt glioblastoma cells[1][2][3]. |
| Invitro | MOPIPP (10 μM; 48 h) induces cellular vacuolization but does not cause cell death in U251 glioblastoma cells， exhibiting characteristics of late endosomes[1][2].MOPIPP (10 μM; 24 h) results an increasing LC3 fluorescence associated with the number of autophagosomes and inhibits fusion of autophagosomes with lysosomes[1]. MOPIPP (10 μM; 24 h) increases the amounts of exosomal marker proteins in vesicle fractions recovered from 293T cells[2].MOMIPP (10 μM; 24 h and 5 h, respectively) causes early disruptions of glucose uptake and glycolytic metabolism, induces methuosis, a form of non-apoptotic cell death, in glioblastoma and other cancer cell lines[3].MOMIPP (10 μM; 4 h and 24 h) selectively activates the JNK1/2 stress kinase pathway, resulting in phosphorylation of c-Jun, Bcl-2 and Bcl-xL[3]. Immunofluorescence[1] Cell Line: |
| In Vivo | MOMIPP (80 mg/kg; i.p.; single dose) readily penetrates the bloodbrain barrier in female Swiss Webster Mice and (80 mg/kg; i.p.; every 24 h; 15 d) is effective in suppressing progression of intracerebral glioblastoma xenografts in female NCR-Foxn1 mice[3]. Animal Model: |
| Name | MOPIPP |
| CAS | 1485521-76-3 |
| Formula | C20H20N2O2 |
| Molar Mass | 320.39 |
| Transport | Room temperature in continental US; may vary elsewhere. |
| Storage | Please store the product under the recommended conditions in the Certificate of Analysis. |
| Reference | [1]. Mbah NE, et al. Disruption of endolysosomal trafficking pathways in glioma cells by methuosis-inducing indole-based chalcones. Cell Biol Toxicol. 2017 Jun;33(3):263-282. [2]. Li Z, et al. Vacuole-inducing compounds that disrupt endolysosomal trafficking stimulate production of exosomes by glioblastoma cells. Mol Cell Biochem. 2018 Feb;439(1-2):1-9. [3]. Li Z, 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. |