Name: Mdivi 1
Price: 188.00 USD

- Overview
  - Please contact us at for specific academic pricing.
    
    Background
    
    Mdivi-1 is a selective cell-permeable inhibitor of mitochondrial division DRP1 (dynamin-related GTPase) and mitochondrial division Dynamin I (Dnm1). DRP1, a member of the dynamin family of large GTPases, mediates mitochondrial fission.
    In vitro: The most efficacious inhibitor, mdivi-1 attenuates mitochondrial division in yeast and mammalian cells by selectively inhibiting the mitochondrial Drp1-mediated division dynamin. Mdivi-1 potently blocks Bid-activated Bax/Bak-dependent cytochrome c release from mitochondria [1].
    In vivo: Mdivi-1 treatment blocked apoptotic cell death in ischemic retina, and significantly increased RGC survival at 2 weeks after ischemia. Moreover, Mdivi-1 treatment did not change this increase of Drp1 protein expression but significantly decreased GFAP protein expression [2].
    Clinical trial: Currently no clinical data are available.
    
    [1] Cassidy-Stone A, Chipuk JE, Ingerman E, Song C, Yoo C, Kuwana T, Kurth MJ, Shaw JT, Hinshaw JE, Green DR, Nunnari J. Chemical inhibition of the mitochondrial division dynamin reveals its role in Bax/Bak-dependent mitochondrial outer membrane permeabilization. Dev Cell. 2008;14(2):193-204.
    [2] Park SW, Kim KY, Lindsey JD, Dai Y, Heo H, Nguyen DH, Ellisman MH, Weinreb RN, Ju WK. A selective inhibitor of drp1, mdivi-1, increases retinal ganglion cell survival in acute ischemic mouse retina. Invest Ophthalmol Vis Sci. 2011;52(5):2837-43.
- Properties
  - Alternative Name
    
    3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanylidene-1H-quinazolin-4-one
    
    CAS Number
    
    338967-87-6
    
    Molecular Formula
    
    C15H10Cl2N2O2S
    
    Molecular Weight
    
    353.22
    
    Appearance
    
    A solid
    
    Purity
    
    99.21%
    
    Solubility
    
    insoluble in H2O; insoluble in EtOH; ≥17.65 mg/mL in DMSO
    
    Storage
    
    Store at -20°C
    
    * For Research Use Only
- Reference
  - 1. Weiwei Qin, Xiyang Tong, et al. "Preservation of mitochondrial homeostasis is responsible for the ameliorative effects of Suhuang antitussive capsule on non-resolving inflammation via inhibition of NF-κB signaling and NLRP3 inflammasome activation." J Ethnopharmacol. 2021 May 10;271:113827. PMID:33460751
    2. Qin W, Wu X, et al. "Suhuang antitussive capsule inhibits NLRP3 inflammasome activation and ameliorates pulmonary dysfunction via suppression of endoplasmic reticulum stress in cough variant asthma." Biomed Pharmacother. 2019 Jul 14;118:109188. PMID:31315072
    3. Chien L, Liang MZ, et al. "Mitochondrial therapy promotes regeneration of injured hippocampal neurons." Biochim Biophys Acta. 2018 Jun 15. pii: S0925-4439(18)30216-3. PMID:29913215

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