Molecular Weight(MW): 353.22
Mdivi-1 is a selective cell-permeable inhibitor of mitochondrial division DRP1 (dynamin-related GTPase) and mitochondrial division Dynamin I (Dnm1) with IC50 of 1-10 μM.
Cited by 11 Publications
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A. shCon and shPINK1 cells were pretreated with Mdivi-1 (50 μM) for 2 h, followed by treatment with 8 μM PPI for 6 h. Mitochondrial fractions (Mito) were prepared and subjected to western blot analysis. B-C. RFP-mito-expressing cells were treated as indicated in (A), and fluorescence images were evaluated by confocal microscopy. Scale bars: 10 μm. Average mitochondrial length was quantified as previously described. Data are presented as mean ± SD (*P< 0.01 compared to shCon cells treated with PPI, ##P< 0.01 compared to shPINK1 cells treated with PPI). D-E. Cells were treated as indicated in (A); apoptosis was then measured by flow cytometry, and whole-cell lysates were prepared and subjected to western blot analysis. Data are presented as mean ± SD (*P< 0.01 compared to shCon cells treated with PPI, ##P< 0.01 compared to shPINK1 cells treated with PPI).
Oncotarget, 2017, 8(6):10359-10374. Mdivi-1 purchased from Selleck.
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|Description||Mdivi-1 is a selective cell-permeable inhibitor of mitochondrial division DRP1 (dynamin-related GTPase) and mitochondrial division Dynamin I (Dnm1) with IC50 of 1-10 μM.|
|Features||The first selective inhibitor of mitochondrial division dynamins.|
Mdivi-1 is a cell-permeable quinazolinone compound that inhibits yeast (Dnm1) and mammalian (Drp1) division DRPs (dynamin-related GTPases) and effectively induces mitochondrial fusion into net-like structures in a reversible manner. Cell-free studies indicate that mdivi-1 blocks Dnm1 ATPase activity (IC50<10 μM) and self-assembly by an allosteric modulation-based mechanism. Mdivi-1 is shown to effectively suppress STS- as well as C8-Bid-induced MOMP (Mitochondrial Outer Membrane Permeabilization) in HeLa cultures and in cell-free murine liver mitochondria preparations, respectively, as assessed by cytochrome C release. In cells, mdivi-1 retards apoptosis by inhibiting mitochondrial outer membrane permeabilization. In principle, mivi-1 represents a class of therapeutics for stroke, myocardial infarction, and neurodegenerative diseases. 
|In vivo||Drp1 and GFAP protein expression is significantly increased in the early neurodegenerative events of ischemic mouse retina. Mdivi-1 treatment blocks apoptotic cell death in ischemic retina, and significantly increases RGC survival at 2 weeks after ischemia. In the normal mouse retina, Drp1 is expressed in the ganglion cell layer (GCL) as well as the inner plexiform layer, the inner nuclear layer (INL), and the outer plexiform layer (OPL). In the GCL, Drp1 immunoreactivity is strong in RGCs. While Drp1 protein expression is increased in the GCL of vehicle-treated ischemic retina at 12 hours. Mdivi-1 treatment does not change this increase of Drp1 protein expression but significantly decreased GFAP protein expression. |
|In vitro||DMSO||70 mg/mL (198.17 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5% DMSO+40% PEG 300+ddH2O
For best results, use promptly after mixing.
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