Oligomycin A (MCH 32)

製品コードS1478 バッチS147808

印刷

化学情報

Synonyms

MCH 32

Storage
(From the date of receipt)

3 years -20°C powder
1 years -80°C in solvent

化学式

C₄₅H₇₄O₁₁

分子量

791.06

CAS No.

579-13-5

Solubility (25°C)*

体外

DMSO

100 mg/mL (126.41 mM)

Water

Insoluble

Ethanol

Insoluble

体内（毎回新しく調製した物を用意してください）

Homogeneous suspension	CMC-NA	≥5mg/ml	Taking the 1 mL working solution as an example, add 5 mg of this product to 1 ml of CMC-Na solution, mix evenly to obtain a homogeneous suspension with a final concentration of 5 mg/ml.
Clear solution	5%DMSO 1 40%PEG300 2 5%Tween80 3 50%ddH2O この製剤はselleckのラボで検証済みです。上記の溶解方法がご要望を満たさない場合、selleckの営業担当までお問い合わせ頂ければ、個別の試験を行います。	5.000mg/ml (6.32mM)	Taking the 1 mL working solution as an example, add 50 μL of 100 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 adjust the volume 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.

溶剤液（一定の濃度）を調合する

生物活性

製品説明	Oligomycin A (MCH 32), a dominant analog of the isomers, is an inhibitor of mitochondrial F1FO ATP synthase which inhibits oxidative phosphorylation and all the ATP-dependent processes occurring on the coupling membrane of mitochondria. It inhibits ATP synthase by blocking its proton channel (Fo subunit), which is necessary for oxidative phosphorylation of ADP to ATP. It also induces apoptosis in a variety of cell types.
in vitro	Oligomycin A is an inhibitor of ATP synthase, inhibits oxidative phosphorylation and all the ATP-dependent processes occurring on the coupling membrane of mitochondria.This compound inhibits ATP synthase by blocking its proton channel (Fo subunit), which is necessary for oxidative phosphorylation of ADP to ATP. The inhibition of ATP synthesis by this chemical will significantly reduce electron flow through the electron transport chain; however, electron flow is not stopped completely due to a process known as proton leak or mitochondrial uncoupling. ^[1] In a group of cancer cells, this compound at 100 ng/ml completely inhibits oxidative phosphorylation activity in 1 h and induces various levels of glycolysis gains by 6 h. ^[2] This inhibitor, of the F0 part of H⁺-ATP-synthase, suppresses the TNF-induced apoptosis. ^[3] This chemical inhibits mitochondrial respiration in melanoma, sensitizes melanoma cells to therapy, blocks the emergence of the slow-cycling, long-term tumor-maintaining melanoma cells. ^[4]
in vivo	Oligomycin A (MCH 32) is an inhibitor of mitochondrial F0F1-ATPase.

製品説明

Oligomycin A (MCH 32), a dominant analog of the isomers, is an inhibitor of mitochondrial F1FO ATP synthase which inhibits oxidative phosphorylation and all the ATP-dependent processes occurring on the coupling membrane of mitochondria. It inhibits ATP synthase by blocking its proton channel (Fo subunit), which is necessary for oxidative phosphorylation of ADP to ATP. It also induces apoptosis in a variety of cell types.

in vitro

Oligomycin A is an inhibitor of ATP synthase, inhibits oxidative phosphorylation and all the ATP-dependent processes occurring on the coupling membrane of mitochondria.This compound inhibits ATP synthase by blocking its proton channel (Fo subunit), which is necessary for oxidative phosphorylation of ADP to ATP. The inhibition of ATP synthesis by this chemical will significantly reduce electron flow through the electron transport chain; however, electron flow is not stopped completely due to a process known as proton leak or mitochondrial uncoupling. ^[1]

In a group of cancer cells, this compound at 100 ng/ml completely inhibits oxidative phosphorylation activity in 1 h and induces various levels of glycolysis gains by 6 h. ^[2]

This inhibitor, of the F0 part of H⁺-ATP-synthase, suppresses the TNF-induced apoptosis. ^[3]

This chemical inhibits mitochondrial respiration in melanoma, sensitizes melanoma cells to therapy, blocks the emergence of the slow-cycling, long-term tumor-maintaining melanoma cells. ^[4]

in vivo

Oligomycin A (MCH 32) is an inhibitor of mitochondrial F0F1-ATPase.

プロトコル(参考用のみ)

細胞アッセイ	細胞株	H1229
	濃度	100 ng/ml
	反応時間	1 h
	実験の流れ	ATP and Oligomycin A Dose-Response Growth Measurement. Cellular ATP changes are measured by CellTiter-Glo reagent. To measure this compound dose-response curves, the cells are plated in 96-well plates at about 400–500 cells/well in 100 μl of culture, dosed the next day, and grown for 4 additional days followed by assaying with Cell-Titer-Glo reagent. The dose-response curves are plotted with nonlinear regression analysis of GraphPad Prism.
動物実験	動物モデル	Male Sprague-Dawley rats
	投薬量	0.5 mg/kg
	投与方法	i.v.

参考

https://pubmed.ncbi.nlm.nih.gov/20533900/
https://pubmed.ncbi.nlm.nih.gov/20110356/
https://pubmed.ncbi.nlm.nih.gov/12444550/

https://pubmed.ncbi.nlm.nih.gov/23764003/
https://pubmed.ncbi.nlm.nih.gov/28495827/
https://pubmed.ncbi.nlm.nih.gov/15833846/

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カスタマーフィードバック

: Data from [Data independently produced by , , Sci Rep, 2016, 6:24641.]

: Data from [Data independently produced by , , Int J Oncol, 2018, 53(6):2590-2604]

: Data from [Data independently produced by , , PLoS One, 2017, 12(4):e0176355]

Selleckの高級品が、幾つかの出版された研究調査結果（以下を含む）で使われた：

Mitochondrial-cytochrome c oxidase II promotes glutaminolysis to sustain tumor cell survival upon glucose deprivation [ Nat Commun, 2025, 16(1):212]	PubMed: 39747079
Aberrant activation of adenine nucleotide translocase 3 promotes progression and chemoresistance in multiple myeloma dependent on PINK1 transport [ Int J Biol Sci, 2025, 21(1):233-250]	PubMed: 39744418
CAR-T cells containing CD28 versus 4-1BB co-stimulatory domains show distinct metabolic profiles in patients [ Cell Rep, 2025, 44(7):115973]	PubMed: 40650909
Non-canonical hepatic androgen receptor mediates glucagon sensitivity in female mice through the PGC1α/ERRα/mitochondria axis [ Cell Rep, 2025, 44(1):115188]	PubMed: 39792556
Pharmacologic activation of integrated stress response kinases inhibits pathologic mitochondrial fragmentation [ Elife, 2025, 13RP100541]	PubMed: 39937095
PEBP1 amplifies mitochondrial dysfunction-induced integrated stress response [ Elife, 2025, 13RP102852]	PubMed: 39878441
Autophagic flux-lipid droplet biogenesis cascade sustains mitochondrial fitness in colorectal cancer cells adapted to acidosis [ Cell Death Discov, 2025, 11(1):21]	PubMed: 39856069
TGF-β secreted by cancer cells-platelets interaction activates cancer metastasis potential by inducing metabolic reprogramming and bioenergetic adaptation [ J Cancer, 2025, 16(4):1310-1323]	PubMed: 39895802
Metabolic Plasticity and Transcriptomic Reprogramming Orchestrate Hypoxia Adaptation in Yak [ Animals (Basel), 2025, 15(14)2084]	PubMed: 40723548
Drug Repurposing Screen Identifies an HRI Activating Compound that Promotes Adaptive Mitochondrial Remodeling in MFN2-deficient Cells [ bioRxiv, 2025, 2025.06.23.660251]	PubMed: 40666974

長期の保管のために-20°Cの下で製品を保ってください。

人間や獣医の診断であるか治療的な使用のためにでない。

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