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MOMIPP

Catalog No. T33467 CAS 1363421-46-8

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].

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MOMIPP, CAS 1363421-46-8

Pack Size	Availability	Price/USD
1 mg	In stock	$ 116.00
5 mg	In stock	$ 249.00
10 mg	In stock	$ 397.00
25 mg	In stock	$ 662.00
50 mg	In stock	$ 942.00
100 mg	In stock	$ 1,280.00
1 mL * 10 mM (in DMSO)	In stock	$ 258.00

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Purity: 99.92%

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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 Research	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 Research	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
Formula	C18H16N2O2
CAS No.	1363421-46-8

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 1 year

Solubility Information

DMSO: 15.13 mg/mL (51.74 mM)

References and Literature

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.

Related compound libraries

This product is contained In the following compound libraries：

Inhibitor Library Neural Regeneration Compound Library NO PAINS Compound Library Kinase Inhibitor Library Anti-Pancreatic Cancer Compound Library Anti-Breast Cancer Compound Library Antidepressant Compound Library HIF-1 Signaling Pathway Compound Library Anti-Obesity Compound Library Angiogenesis related Compound Library

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Keywords

MOMIPP 1363421-46-8 PI3K/Akt/mTOR signaling PI3K inhibit Inhibitor JNK1/2 BBB Fab1 c-Jun Bcl-2 PIKfyve Macropinocytosis Bcl-xL inhibitor

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