Mdivi-1

Catalog No.S7162 Batch:S716208

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Technical Data

Formula

C15H10Cl2N2O2S
Molecular Weight 353.22 CAS No. 338967-87-6
Solubility (25°C)* In vitro DMSO 71 mg/mL (201.0 mM)
Water Insoluble
Ethanol Insoluble
In vivo (Add solvents to the product individually and in order)
Clear solution
5%DMSO 40%PEG300 5%Tween80 50%ddH2O
1.87mg/ml Taking the 1 mL working solution as an example, add 50 μL of 37.4 mg/ml clarified DMSO stock solution to 400 μL of PEG300, mix evenly to clarify it; add 50 μL of Tween80 to the above system, mix evenly to clarify; then continue to add 500 μL of ddH2O to make it clear. Volume up to 1 mL. The mixed solution should be used immediately for optimal results. 
* <1 mg/ml means slightly soluble or insoluble.
* 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.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

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.
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]
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]
Features The first selective inhibitor of mitochondrial division dynamins.

Protocol (from reference)

Animal Study:

[3]
  • Animal Models

    Male Sprague Dawley rats

  • Dosages

    3 mg/kg

  • Administration

    IP injection

Customer Product Validation

, , Neurochem Res, 2017, 42(5):1449-1458

Data from [Data independently produced by , , Blood Cancer J, 2017, doi:10.1038/bcj.2017.61]

Data from [Data independently produced by , , Cell Physiol Biochem, 2017, 42(5):1802-1811]

Data from [Data independently produced by , , Biochim Biophys Acta Mol Basis Dis, 2017, 1863(9):2307-2318]

Selleck's Mdivi-1 has been cited by 87 publications

Signaling via a CD27-TRAF2-SHP-1 axis during naive T cell activation promotes memory-associated gene regulatory networks [ Immunity, 2024, 57(2):287-302.e12] PubMed: 38354704
Gonococcal OMV-delivered PorB induces epithelial cell mitophagy [ Nat Commun, 2024, 15(1):1669] PubMed: 38396029
MANF facilitates breast cancer cell survival under glucose-starvation conditions via PRKN-mediated mitophagy regulation [ Autophagy, 2024, 1-22.] PubMed: 39147386
The DNA-dependent protein kinase catalytic subunit exacerbates endotoxemia-induced myocardial microvascular injury by disrupting the MOTS-c/JNK pathway and inducing profilin-mediated lamellipodia degradation [ Theranostics, 2024, 14(4):1561-1582] PubMed: 38389837
Rictor/mTORC2 signalling contributes to renal vascular endothelial-to-mesenchymal transition and renal allograft interstitial fibrosis by regulating BNIP3-mediated mitophagy [ Clin Transl Med, 2024, 14(5):e1686] PubMed: 38769658
Targeting PARP14 with lomitapide suppresses drug resistance through the activation of DRP1-induced mitophagy in multiple myeloma [ Cancer Lett, 2024, 588:216802] PubMed: 38467180
lncRNA Oip5-as1 inhibits excessive mitochondrial fission in myocardial ischemia/reperfusion injury by modulating DRP1 phosphorylation [ Cell Mol Biol Lett, 2024, 29(1):72] PubMed: 38745296
PDGF-BB accelerates TSCC via fibroblast lactates limiting miR-26a-5p and boosting mitophagy [ Cancer Cell Int, 2024, 24(1):5] PubMed: 38169376
Inhibition of OGG1 ameliorates pulmonary fibrosis via preventing M2 macrophage polarization and activating PINK1-mediated mitophagy [ Mol Med, 2024, 30(1):72] PubMed: 38822247
Deciphering the neuroprotective mechanisms of RACK1 in cerebral ischemia-reperfusion injury: Pioneering insights into mitochondrial autophagy and the PINK1/Parkin axis [ CNS Neurosci Ther, 2024, 30(8):e14836] PubMed: 39097918

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.