Mdivi-1

Catalog No.S7162

Mdivi-1 Chemical Structure

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.

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Cited by 12 Publications

5 Customer Reviews

  • a Representative TUNEL/DAPI photomicrographs of ipsilateral cortex in different groups (scale bar = 100 μm).

    Neurochem Res, 2017, 42(5):1449-1458. Mdivi-1 purchased from Selleck.

    Cell necroptosis were detected in cells transfected with PCYT1A siRNA or treated with mitophagy inhibitor Mdivi-1 (50 μm).

    Blood Cancer J, 2017, doi:10.1038/bcj.2017.61. Mdivi-1 purchased from Selleck.

  • Mdivi-1 relaxes ET-1-induced constriction, and mdivi-1 pre-treatment inhibits ET-1-induced constriction in rat mesenteric arteries. (A) Mdi-vi-1 induced concentration-dependent relaxation in endothelium-intact rat mesenteric arteries pre-contracted with ET-1 (4 nM). The relaxation ratio of mdivi-1 was calculated by subtracting the relaxation ratio of corresponding control (DMSO). (B) Mdivi-1 (10 µM) pretreatment inhibited ET-1- induced vasoconstriction in endothelium-intact rat mesenteric arteries. **P<0.01 vs. Control. (C) Mdivi-1 induced vasorelaxation in endothelium-denuded rat mesenteric arteries pre-contracted with ET-1 (4 nM). The relaxation ratio of mdivi-1 was calculated by subtracting the relaxation ratio of corresponding control (DMSO). (D) Mdivi-1 (10 µM) pretreatment inhibited ET-1-induced constriction of rat mesenteric arteries with denuded endothelium. **P<0.01 vs. Control.

    Cell Physiol Biochem, 2017, 42(5):1802-1811. Mdivi-1 purchased from Selleck.

    Neurons were pretreated with kaempferol or Mdivi-1 and then subjected to 2 h of dimethyl succinate or OGD insult. (A) View of mitochondrial localization of HK-II with confocal scanning microscope (Green: HK-II; Red: MitoTracker Red CMXRos; Scale bars: 10 μm).

    Biochim Biophys Acta Mol Basis Dis, 2017, 1863(9):2307-2318. Mdivi-1 purchased from Selleck.

  • 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.

Purity & Quality Control

Choose Selective Dynamin Inhibitors

Biological Activity

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.
Targets
Dnm1 GTPase [1]
(Cell-free assay)
1 μM-10 μM
In vitro

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. [1]

Cell Data
Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HepG2/ADM cells M{DXSWNmdGxidnnhZoltcXS7IHHzd4F6 MnzhNVAh|ryP NHHMWJMyKGh? MYTt[Il3cS1zIIDy[ZRz\WG2bXXueEBqdmO{ZXHz[YQhSjWJMT3pcoR2[2WmIHHwc5B1d3OrczDhcoQh[2WubDDk[YF1cCCrbjDI[ZBIOi:DRF2gZ4VtdHN? NVTi[5U5OzB6NUC1PFU>
R28 NXq5Z5pTTnWwY4Tpc44h[XO|YYm= M4LRVFUh|ryP M4XkT|IhcA>? NF\POnRucXSxY3jvcoRzcWFiaX6gVlI5KGOnbHzzJJBz\XS{ZXH0[YQhf2m2aDC1JO69VSCGcoCxJIlvcGmkaYTvdkBO\Gm4aT2xJJJmfGGrbnXkJJRp\SCjdnXyZYdmKGynbnf0bEBidmRiYYDw[YFz\WRiYYOg[YxwdmejdHXkJJR2[nWuYYKsJJRpemWjZD3sbYtmKG6ndIfvdot{KGGodHXyJIlzemGmaXH0bY9v MWezNFU{QDZ{MR?=
INS-1E NIq3WYJHfW6ldHnvckBie3OjeR?= NIjOZWo2OCEQvF2= MUKxNkBp MV\0doVifG2nboSge4l1cCCPZHn2bU0yKHOrZ37p[olk[W62bImgbY5pcWKrdHXkJI1qfG:laH;u[JJq[WxiZoLh[41mdnSjdHnvckBidmRiY3zlZZJtgSCrbnPy[YF{\WRidHjlJJZq[WKrbHn0fY9neGGwY4LlZZRq[yCkZYThJGlPWy1zRTDj[YxteyC3bnTldkBpgXCxeHnhJINwdmSrdHnvcpM> MmTBNlk4Pjh3MUO=
L1210 MUTGeY5kfGmxbjDhd5NigQ>? NFjiengzNjVuIEWgZY5lKDFyIN88US=> M3GyUFczKGh? MWPN[Il3cS1zIDi1JOK2VSlic3nncolncWOjboTsfUBifHSnboXheIVlKDBwNDDt[{9tKG:oIHPpd5Bt[XSrbj3pcoR2[2WmIHPlcIwh\GWjdHigbY4hVDF{MUCgZ4VtdHNuIIfpeIghfGinIHX4Z4VxfGmxbjDv[kAzNjViYX7kJFExKML3TTDv[kBO\Gm4aT2x NUThOZRSOjh4N{e4NVQ>
SH-SY5Y MmLhSpVv[3Srb36gZZN{[Xl? M2KzOlExKM7:TR?= NEXwc48{OCCvaX6= MlHLTY5pcWKrdHnu[{BFenBzIIDyc5Rm[3S|IHHnZYlve3RiQ2DGMYlv\HWlZXSgbY51emmwc3njJIFxd3C2b4Ppd{BjgSCkbH;jb4lv\yCEYYigeJJidnOub3PheIlwdg>? NXjD[pg3OjZ3OUiyPVQ>

... Click to View More Cell Line Experimental Data

Assay
Methods Test Index PMID
Western blot
p-Chk1 / p-Chk2 / Chk1 / Chk2 / p-ATM / ATM ; 

PubMed: 24952704     


MDA-MB-231 cells were treated with cisplatin alone, mdivi-1 alone or the combination at the indicated concentrations for 4 h Western blot was then performed to detect the phosphorylation status of key proteins involved in DNA damage response.

COX-2 / p-Drp1 / Drp1 / Mfn2 / ABCG2 / Oct4 ; 

PubMed: 28435473     


CNE1 and CNE2 cells were treated with or without various concentrations of Mdivi-1 (0, 10, or 20 μM) for 24 h and the level of COX-2, p-Drp1(Ser616), p-Drp1(Ser637), t-Drp1, Mfn2, ABCG2, and Oct4 in CNE1 and CNE2 cells were measured by WB assay. 

24952704 28435473
Immunofluorescence
β-tubulin; 

PubMed: 25458053     


MDA-MB-231 cells were synchronized at prometaphase by incubation with nocodazole (100 ng/ml) for 16 h, and then released for the indicated time in fresh media in the presence of vehicle DMSO or 50 mM mdivi-1. DNA was then visualized by staining cells with DAPI (blue), and microtubules were visualized by staining cells with Alexa Fluor 555-conjugated anti-b-tubulin antibody (red). Scale bars: 5 μm.

25458053
Growth inhibition assay
Cell viability; 

PubMed: 24952704     


MDA-MB-231 cells were treated with increasing doses of mdivi-1 for 72 h The survival was assessed by MTS assay.

Apoptosis; 

PubMed: 26032958     


A375 and SK-MEL-28 cells were treated with mDIVI-1 (0, 5, 10, 25, 50, 100 μM) for 48 hours before AnnexinV-FITC analysis. 

24952704 26032958
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. [2]

Protocol

Animal Research:

[2]

+ Expand
  • Animal Models: C57BL/6 mice
  • Formulation: dimethyl sulfoxide [DMSO]
  • Dosages: 50 mg/kg
  • Administration: IP injection
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 70 mg/mL (198.17 mM)
Water Insoluble
Ethanol Insoluble
In vivo Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
5% DMSO+40% PEG 300+5% Tween 80+ddH2O
For best results, use promptly after mixing.
7mg/mL

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 353.22
Formula

C15H10Cl2N2O2S

CAS No. 338967-87-6
Storage powder
in solvent
Synonyms N/A

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Tech Support

Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

Handling Instructions

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID