| Description | MOMIPP is a PIKfyve inhibitor and a macropinocytosis inducer. MOMIPP readily penetrates the blood-brain barrier and is moderately effective in suppressing progression of intracerebral glioblastoma xenografts[1][2]. |
| In vitro | MOMIPP can induce intense macropinocytosis, leading to methuosis in cultured glioblastoma cells at low micromolar concentrations[1]. MOMIPP(3 μM) induces cell vacuolization in U373 and Hs683 cell lines[1]. The cytotoxic IPP compound, MOMIPP, causes early disruptions of glucose uptake and glycolytic metabolism. Coincident with these metabolic changes, MOMIPP selectively activates the JNK1/2 stress kinase pathway, resulting in phosphorylation of c-Jun, Bcl-2 and Bcl-xL[2]. |
| In vivo | MOMIPP (80 mg/kg; i.p.; once daily; for 15 consecutive days) shows result that MOMIPP is moderately effective in suppressing progression of intracerebral glioblastoma xenografts. |
| Cell experiments | When JNK activation (phosphorylation) was assessed by western blot analysis after 24 h, MOMIPP(10 μM)has been found that induced major increases in JNK1/2 phosphorylation[2]. |
| Animal experiments | MOMIPP (Athymic CrTac:NCR-Foxn1 mice (female, 7-8 weeks); 80 mg/kg; i.p.; once daily; for 15 consecutive days) suppressed progression of intracerebral glioblastoma xenografts[2]. |
| molecular weight | 292.33 |
| Molecular formula | C18H16N2O2 |
| CAS | 1363421-46-8 |
| Storage | Powder: -20°C for 3 years | In solvent: -80°C for 1 year |
| Solubility | DMSO: 15.13 mg/mL (51.74 mM) |
| References | 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. 3. Trabbic CJ, Overmeyer JH, Alexander EM, Crissman EJ, Kvale HM, Smith MA, Erhardt PW, Maltese WA. Synthesis and biological evaluation of indolyl-pyridinyl-propenones having either methuosis or microtubule disruption activity. J Med Chem. 2015 Mar 12;58(5):2489-512. doi: 10.1021/jm501997q. Epub 2015 Feb 19. PubMed PMID: 25654321; PubMed Central PMCID: PMC4360382. 4. Trabbic CJ, Dietsch HM, Alexander EM, Nagy PI, Robinson MW, Overmeyer JH, Maltese WA, Erhardt PW. Differential Induction of Cytoplasmic Vacuolization and Methuosis by Novel 2-Indolyl-Substituted Pyridinylpropenones. ACS Med Chem Lett. 2014 Jan 9;5(1):73-77. PubMed PMID: 24527179; PubMed Central PMCID: PMC3918887. |