475859
Mitochondrial Fusion Promoter, M1
A cell-permeable phenylhydrazone that restores mitochondrial tubular network formation in MEF lacking either of the two outer mitochondrial membrane.
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Mitochondrial Fusion Promoter, M1, ( E)-4-Chloro-2-(1-(2-(2,4,6-trichlorophenyl)hydrazono)ethyl)phenol
C14H10Cl4N2O
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Quality Level
Assay
≥98% (HPLC)
form
solid
manufacturer/tradename
Calbiochem®
storage condition
OK to freeze
protect from light
color
off-white
solubility
DMSO: 25 mg/mL
shipped in
ambient
storage temp.
2-8°C
SMILES string
ClC1=CC(/C(C)=N/NC2=C(Cl)C=C(Cl)C=C2Cl)=C(O)C=C1
General description
A cell-permeable phenylhydrazone compound that restores mitochondrial tubular network formation from the fragmented mitochondria seen in MEF lacking either one of the two outer mitochondrial membrane (OMM) mitofusins (EC50 = 5.3 and 4.42 µM, respectively, in Mfn1 or Mfn2 knockout MEF cells) or MPP+-treated SH-SY5Y cells (5 µM 24 h), while displaying no effect on ER or lysosome morphology in Mfn1 knockout MEF. The effect of M1 is limited to enhancing weakened mitochondrial fusion machinery and M1 cannot by itself rebuild interconnected tubular mitochondria in MEF lacking both Mfn1/2 or the inner mitochondrial membrane (IMM) fusion mediator Opa1 (optic atrophy1). M1 (5 µM 24 h) is reported to boost the downregulated ATP5A and ATP5B protein level in either Mfn1 or Mfn2 knockout MEF to the wild-type MEF level and ATPase inhibitor oligomycin (Cat. No. 495455) at 5 µM is shown to completely offset the mitochondrial fusion effect by 5 µM M1 in Mfn1 knockout MEF. Both M1 and Z-VAD-FMK (Cat. No. 219007) are shown to protect SH-SY5Y against MPP+-induced neuronal toxicity and additive protection can be achieved via a combined treatment (62%, 73%, 77%, and 89% survival rate, respectively, with DMSO, 5 µM M1, 1 µM Z-VAD-FMK, and combined treatment). Comparing to mdivi-1 (Cat. No. 475856), M1 exerts its effect via promoting fusion rather than inhibiting fission or division.
A cell-permeable phenylhydrazone that restores mitochondrial tubular network formation in MEF lacking either of the two outer mitochondrial membrane (OMM) mitofusins (EC50 = 5.3 and 4.42 µM, respectively, in Mfn1 or Mfn2 knockout MEF cells) or in MPP+-treated SH-SY5Y cells (5 µM 24 h), but not in MEF lacking both Mfn1/2 or the inner mitochondrial membrane (IMM) fusion mediator Opa1 (optic atrophy1). M1 (5 µM 24 h) is reported to boost the downregulated ATP5A & ATP5B protein level in Mfn1 or Mfn2 knockout MEF to the wild-type MEF level and ATPase inhibitor oligomycin (Cat. No. 495455) at 5 µM is shown to completely offset the mitochondrial fusion effect by 5 µM M1 in Mfn1 knockout MEF. Comparing to mdivi-1 (Cat. No. 475856), M1 exerts its effect via promoting fusion rather than inhibiting fission or division.
Biochem/physiol Actions
Cell permeable: yes
Reversible: yes
Packaging
Packaged under inert gas
Warning
Toxicity: Standard Handling (A)
Reconstitution
Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 6 months at -20°C.
Other Notes
Wang, D., et al. 2012. Angew. Chem. Int. Ed.51, 9302.
Legal Information
CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany
WGK
WGK 3
Flash Point(F)
Not applicable
Flash Point(C)
Not applicable
Certificates of Analysis (COA)
Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.
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Find documentation for the products that you have recently purchased in the Document Library.
A small molecule promotes mitochondrial fusion in mammalian cells.
Angewandte Chemie (International ed. in English), 51(37), 9302-9305 (2012-08-22)
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