M0199
Mdivi-1
≥98% (HPLC), powder, mitochondrial division DRP inhibitor
Synonym(s):
3-(2,4-Dichloro-5-methoxyphenyl)-2,3-dihydro-2-thioxo-4(1H)-quinazolinone, 3-(2,4-Dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinone
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About This Item
Empirical Formula (Hill Notation):
C15H10Cl2N2O2S
CAS Number:
Molecular Weight:
353.22
UNSPSC Code:
12352200
PubChem Substance ID:
NACRES:
NA.77
MDL number:
Product Name
Mdivi-1, ≥98% (HPLC), powder
SMILES string
COc1cc(N2C(S)=Nc3ccccc3C2=O)c(Cl)cc1Cl
InChI
1S/C15H10Cl2N2O2S/c1-21-13-7-12(9(16)6-10(13)17)19-14(20)8-4-2-3-5-11(8)18-15(19)22/h2-7H,1H3,(H,18,22)
InChI key
NZJKEVWTYMOYOR-UHFFFAOYSA-N
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: >20 mg/mL
shipped in
wet ice
storage temp.
−20°C
Quality Level
Application
Mdivi-1 has been used:
- in embryonic thoracic aorta A7r5 cells to inhibit cell migration and proliferation
- in mitochondrial network reshaping and reactive oxygen species (ROS) production studies in oligodendrocyte precursor cells (OPCs)
- to induce mitochondrial damage in lung fibroblasts
Biochem/physiol Actions
Mdivi-1 is a cell-permeable selective inhibitor of mitochondrial division DRP (dynamin-related GTPase) and inhibitor of the mitochondrial division dynamin (Dnm1). Mitochondrial fusion and division play important roles in the regulation of apoptosis. Mdivi-1 is the first selective inhibitor of mitochondrial division dynamins. In principle, Mdivi-1 represents a class of therapeutics for stroke, myocardial infarction, and neurodegenerative diseases.
Mdivi-1 is a selective inhibitor of mitochondrial division DRP (dynamin-related GTPase); inhibitor of the mitochondrial division dynamin (Dnm1).
Features and Benefits
This compound is a featured product for Apoptosis research. Click here to discover more featured Apoptosis products. Learn more about bioactive small molecules for other areas of research at sigma.com/discover-bsm.
General description
Mitochondrial Division Inhibitor 1 (Mdivi-1) is a quinazolinone derivative and is cell permeable. It traverses blood-brain barrier and elicits protective functionality in heart and brain ischemia-reperfusion injury.
Storage Class
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
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To mdivi-1 or not to mdivi-1: Is that the question?
Smith G and Gallo G
Developmental neurobiology, 77(11), 1260-1268 (2017)
Impaired mitophagy leads to cigarette smoke stress-induced cellular senescence: implications for chronic obstructive pulmonary disease
Ahmad T, et al.
Faseb Journal, 29(7), 2912-2929 (2015)
Ze Liu et al.
Antioxidants & redox signaling, 30(15), 1797-1816 (2018-06-13)
Mitochondrial fragmentation is a crucial mechanism contributing to tubular cell apoptosis during acute kidney injury (AKI). However, the mechanism of modulating mitochondrial dynamics during AKI remains unclear. Numb is a multifunction adaptor protein that is expressed in renal tubules. The
Jia Sun et al.
The Journal of endocrinology (2019-01-09)
The molecular signaling mechanisms of Coenzyme Q10 (CoQ10) in diabetic nephropathy (DN) remain poorly understood. We verified that mitochondrial abnormalities, like defective mitophagy, the generation of mitochondrial reactive oxygen species (mtROS) and the reduction of mitochondrial membrane potential, occurred in
K Magalon et al.
Neuropharmacology, 111, 293-303 (2016-09-14)
Multiple sclerosis (MS) is a neurodegenerative disease characterized by episodes of immune attacks and oligodendrocyte death leading to demyelination and progressive functional deficits. New therapeutic strategies are needed to stimulate the spontaneous regenerative process observed in some patients. Spontaneous myelin
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