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Key Documents

475856

Sigma-Aldrich

Mitochondrial Division Inhibitor, mdivi-1

The Mitochondrial Division Inhibitor, mdivi-1, also referenced under CAS 338967-87-6, controls the biological activity of yeast Dnm1 and mammalian Drp1.

Sinónimos:

Mitochondrial Division Inhibitor, mdivi-1, Mitochondrial Division Dnm1/Drp1 ATPase Inhibitor, 3-(2,4-Dichloro-5-methoxy-phenyl)-2-thioxo-1H-quinazolin-4-one

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About This Item

Fórmula empírica (notación de Hill):
C15H10Cl2N2O2S
Número de CAS:
338967-87-6
Peso molecular:
353.22
MDL number:
MFCD00974506
UNSPSC Code:
12352200
NACRES:
NA.77

Quality Level

100

assay

≥95% (HPLC)

form

solid

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
protect from light

color

white

solubility

DMSO: 10 mg/mL

shipped in

wet ice

storage temp.

−20°C

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

General description

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 (IC50 = 10 and 50 M in yeast and COS cultures, respectively) in a reversible manner. Cell-free studies indicate that mdivi-1 blocks Dnm1 ATPase activity (IC50<10 M) 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.

Packaging

Packaged under inert gas

Warning

Toxicity: Standard Handling (A)

Other Notes

Cassidy-Stone A., et al. 2008. Dev. Cell14, 193.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Storage Class

11 - Combustible Solids

wgk_germany

WGK 3

flash_point_f

Not applicable

flash_point_c

Not applicable

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Henna Myllymäki et al.
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Otto Warburg described tumour cells as displaying enhanced aerobic glycolysis whilst maintaining defective oxidative phosphorylation (OXPHOS) for energy production almost 100 years ago [1, 2]. Since then, the 'Warburg effect' has been widely accepted as a key feature of rapidly
Ann Cassidy-Stone et al.
Developmental cell, 14(2), 193-204 (2008-02-13)
Mitochondrial fusion and division play important roles in the regulation of apoptosis. Mitochondrial fusion proteins attenuate apoptosis by inhibiting release of cytochrome c from mitochondria, in part by controlling cristae structures. Mitochondrial division promotes apoptosis by an unknown mechanism. We
Afzal Misrani et al.
Frontiers in aging neuroscience, 13, 748388-748388 (2021-12-28)
Alzheimer's disease (AD) is the most common neurodegenerative disorder worldwide. Mitochondrial dysfunction is thought to be an early event in the onset and progression of AD; however, the precise underlying mechanisms remain unclear. In this study, we investigated mitochondrial proteins
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Journal of diabetes research, 2022, 3555889-3555889 (2022-04-12)
Mitochondria play a central role in the development of diabetic retinopathy and in the metabolic memory associated with its continued progression. Mitochondria have a regulated fusion fission process, which is essential for their homeostasis. One of the major fission proteins
Yongqi Zhen et al.
Cell death & disease, 13(4), 375-375 (2022-04-21)
Breast cancer is still one of the most common malignancies worldwide and remains a major clinical challenge. We previously reported that the anthelmintic drug flubendazole induced autophagy and apoptosis via upregulation of eva-1 homolog A (EVA1A) in triple-negative breast cancer

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