Catalog No.S7162 Synonyms: Mitochondrial division inhibitor 1

For research use only.

Mdivi-1 (Mitochondrial division inhibitor 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. Mdivi-1 attenuates mitophagy and enhances apoptosis.

Mdivi-1 Chemical Structure

CAS No. 338967-87-6

Selleck's Mdivi-1 has been cited by 42 publications

Purity & Quality Control

Choose Selective Dynamin Inhibitors

Biological Activity

Description Mdivi-1 (Mitochondrial division inhibitor 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. Mdivi-1 attenuates mitophagy and enhances apoptosis.
Features The first selective inhibitor of mitochondrial division dynamins.
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 M1LzXGNmdGxidnnhZoltcXS7IHHzd4F6 NWe4N3BHOTBizszN M{HmcVEhcA>? NXn2OXJ7dWSrdnmtNUBxemW2cnXheI1mdnRiaX7jdoVie2WmIFK1S|EucW6mdXPl[EBieG:ydH;zbZMh[W6mIHPlcIwh\GWjdHigbY4hUGWyR{KvRWROKGOnbHzz M1zJ[VxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzNyOEWwOVg2Lz5|MEi1NFU5PTxxYU6=
R28 MULGeY5kfGmxbjDhd5NigQ>? NX;SXXl2PSEQvF2= MU[yJIg> M4KzXI1qfG:laH;u[JJq[SCrbjDSNlgh[2WubIOgdJJmfHKnYYTl[EB4cXSqIEWg{txOKES{cEGgbY5pcWKrdH;yJG1lcX[rLUGgdoV1[WmwZXSgeIhmKGG4ZYLh[4UhdGWwZ4ToJIFv\CCjcIDlZZJm\CCjczDlcI9v\2G2ZXSgeJVjfWyjcjygeIhz\WGmLXzpb4UhdmW2d3;yb5Mh[W[2ZYKgbZJz[WSrYYTpc44> NH[yfGY9[SC2YYLn[ZQ:L1:kbHHub{chcHKnZk2nbJR1eHN8Lz;weYJu\WRwbnPibU5vdG1wbnnoModwfi9|MEWzPFYzOSd-M{C1N|g3OjF:L3G+
INS-1E MWHGeY5kfGmxbjDhd5NigQ>? NF\Sboc2OCEQvF2= MlzINVIhcA>? NY\SSHBGfHKnYYTt[Y51KHerdHigUYRqfmlvMTDzbYdvcW[rY3HueIx6KGmwaHnibZRm\CCvaYTvZ4hwdmS{aXHsJIZz[WevZX70ZZRqd25iYX7kJINt\WG{bImgbY5kemWjc3XkJJRp\SC4aXHibYxqfHmxZoDhcoNz\WG2aXOgZoV1[SCLTmOtNWUh[2WubIOgeY5l\XJiaInwc5hq[SClb37kbZRqd26| NUnsV282RGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMkm3Olg2OTNpPkK5O|Y5PTF|PD;hQi=>
L1210 M1HqSWZ2dmO2aX;uJIF{e2G7 MUmyMlUtKDViYX7kJFExKM7:TR?= MoK2O|IhcA>? NWC1WoVIVWSrdnmtNUApPSEEtV2pJJNq\26rZnnjZY51dHliYYT0[Y52[XSnZDCwMlQhdWdxbDDv[kBkcXOybHH0bY4ucW6mdXPl[EBk\WyuIHTlZZRpKGmwIFyxNlExKGOnbHzzMEB4cXSqIITo[UBmgGOncITpc44hd2ZiMj61JIFv\CBzMDFCuW0hd2ZiTXTpeokuOQ>? NXTNeXRMRGFidHHy[4V1RSehYnzhcosoKGi{ZX[9K4h1fHC|Oj:vdJVjdWWmLn7jZokvdmyvLn7pbE5od3ZxMki2O|c5OTRpPkK4Olc4QDF2PD;hQi=>
SH-SY5Y MVPGeY5kfGmxbjDhd5NigQ>? NIn4O4oyOCEQvF2= MnHaN|AhdWmw Mn3sTY5pcWKrdHnu[{BFenBzIIDyc5Rm[3S|IHHnZYlve3RiQ2DGMYlv\HWlZXSgbY51emmwc3njJIFxd3C2b4Ppd{BjgSCkbH;jb4lv\yCEYYigeJJidnOub3PheIlwdg>? M{DWOVxiKHSjcnfleF0oZ2KuYX7rK{BpemWoPTfoeJRxezpxL4D1Zo1m\C6wY3LpMo5tdS6waXiu[493NzJ4NUm4Nlk1Lz5{NkW5PFI6PDxxYU6=
Methods Test Index PMID
Western blot p-Chk1 / p-Chk2 / Chk1 / Chk2 / p-ATM / ATM ; COX-2 / p-Drp1 / Drp1 / Mfn2 / ABCG2 / Oct4 24952704 28435473
Immunofluorescence β-tubulin 25458053
Growth inhibition assay Cell viability ; Apoptosis 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 (from reference)

Animal Research:


  • Animal Models: C57BL/6 mice
  • Dosages: 50 mg/kg
  • Administration: IP injection

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.


Chemical Information

Molecular Weight 353.22


CAS No. 338967-87-6
Storage 3 years -20°C powder
2 years -80°C in solvent
Smiles COC1=C(C=C(C(=C1)N2C(=O)C3=CC=CC=C3NC2=S)Cl)Cl

In vivo Formulation Calculator (Clear solution)

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Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O, mix and clarify.

Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.

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Molarity Calculator

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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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