Oligomycin A
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| Category | Antibiotics |
| Catalog number | BBF-02618 |
| CAS | 579-13-5 |
| Molecular Weight | 791.06 |
| Molecular Formula | C45H74O11 |
| Purity | >98% |
Ordering Information
| Catalog Number | Size | Price | Stock | Quantity |
|---|---|---|---|---|
| BBF-02618 | 10 mg | $268 | In stock |
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Add to cartDescription
Oligomycin A, an ATP synthase inhibitor and a macrolide antibiotic with fungicidal activity isolated from Streptomyces species, inhibits oxidative phosphorylation and all the ATP-dependent processes occurring on the coupling membrane of mitochondria.
Specification
| Related CAS | 11030-76-5 (Deleted CAS) 21307-25-5 (Deleted CAS) 31422-20-5 (Deleted CAS) 1255037-37-6 (Deleted CAS) |
| Synonyms | Spiro[2,26-dioxabicyclo[23.3.1]nonacosa-4,18,20-triene-27,2'-[2H]pyran]-3,9,13-trione, 22-ethyl-3',4',5',6'-tetrahydro-7,11,14,15-tetrahydroxy-6'-[(2R)-2-hydroxypropyl]-5',6,8,10,12,14,16,28,29-nonamethyl-, (1R,2'R,4E,5'S,6S,6'S,7R,8S,10R,11R,12S,14R,15S,16R,18E,20E,22R,25S,28S,29R)-; (1R,2'R,4E,5'S,6S,6'S,7R,8S,10R,11R,12S,14R,15S,16R,18E,20E,22R,25S,28S,29R)-22-Ethyl-3',4',5',6'-tetrahydro-7,11,14,15-tetrahydroxy-6'-[(2R)-2-hydroxypropyl]-5',6,8,10,12,14,16,28,29-nonamethylspiro[2,26-dioxabicyclo[23.3.1]nonacosa-4,18,20-triene-27,2'-[2H]pyran]-3,9,13-trione; MCH 32 |
| Storage | Store at -20°C |
| IUPAC Name | (1R,4E,5'S,6S,6'S,7R,8S,10R,11R,12S,14R,15S,16R,18Z,20E,22R,25S,27R,28S,29R)-22-ethyl-7,11,14,15-tetrahydroxy-6'-[(2R)-2-hydroxypropyl]-5',6,8,10,12,14,16,28,29-nonamethylspiro[2,26-dioxabicyclo[23.3.1]nonacosa-4,18,20-triene-27,2'-oxane]-3,9,13-trione |
| Canonical SMILES | CCC1CCC2C(C(C(C3(O2)CCC(C(O3)CC(C)O)C)C)OC(=O)C=CC(C(C(C(=O)C(C(C(C(=O)C(C(C(CC=CC=C1)C)O)(C)O)C)O)C)C)O)C)C |
| InChI | InChI=1S/C45H74O11/c1-12-34-17-15-13-14-16-27(4)42(51)44(11,53)43(52)32(9)40(50)31(8)39(49)30(7)38(48)26(3)18-21-37(47)54-41-29(6)35(20-19-34)55-45(33(41)10)23-22-25(2)36(56-45)24-28(5)46/h13-15,17-18,21,25-36,38,40-42,46,48,50-51,53H,12,16,19-20,22-24H2,1-11H3/b14-13-,17-15+,21-18+/t25-,26-,27+,28+,29+,30-,31-,32-,33-,34-,35-,36-,38+,40+,41+,42-,44+,45-/m0/s1 |
| InChI Key | MNULEGDCPYONBU-UQFNUYRPSA-N |
| Source | Streptomyces sp. |
Properties
| Appearance | Needle Crystals |
| Antibiotic Activity Spectrum | fungi; neoplastics (Tumor) |
| Boiling Point | 886.3±65.0°C at 760 mmHg |
| Melting Point | 140-141°C |
| Density | 1.116 g/cm3 |
| Solubility | Soluble in ethanol, methanol, DMF or DMSO. Poor water solubility. |
Reference Reading
1.Oligomycins as inhibitors of K-Ras plasma membrane localisation.
Salim AA1, Tan L2, Huang XC1, Cho KJ2, Lacey E3, Hancock JF2, Capon RJ1. Org Biomol Chem. 2016 Jan 14;14(2):711-5. doi: 10.1039/c5ob02020d.
Frequently present in pancreatic, colorectal and non-small cell lung carcinomas, oncogenic mutant K-Ras must be localised to the plasma membrane (PM) to be functional. Inhibitors of K-Ras PM localisation are therefore putative cancer chemotherapeutics. By screening a microbial extract library in a high content cell-based assay we detected the rare oligomycin class of Streptomyces polyketides as inhibitors of K-Ras PM localisation. Cultivation and fractionation of three unique oligomycin producing Streptomyces strains yielded oligomycins A-E (1-5) and 21-hydroxy-oligomycin A (6), together with the new 21-hydroxy-oligomycin C (7) and 40-hydroxy-oligomycin B (8). Structures for 1-8 were assigned by detailed spectroscopic analysis. Cancer cell viability screening confirmed 1-8 were cytotoxic to human colorectal carcinoma cells (IC50 > 3 μM), and were inhibitors of the ABC transporter efflux pump P-glycoprotein (P-gp), with 5 being comparable in potency to the positive control verapamil.
2.Impaired oxidative phosphorylation regulates necroptosis in human lung epithelial cells.
Koo MJ1, Rooney KT1, Choi ME2, Ryter SW1, Choi AM1, Moon JS3. Biochem Biophys Res Commun. 2015 Aug 28;464(3):875-80. doi: 10.1016/j.bbrc.2015.07.054. Epub 2015 Jul 14.
Cellular metabolism can impact cell life or death outcomes. While metabolic dysfunction has been linked to cell death, the mechanisms by which metabolic dysfunction regulates the cell death mode called necroptosis remain unclear. Our study demonstrates that mitochondrial oxidative phosphorylation (OXPHOS) activates programmed necrotic cell death (necroptosis) in human lung epithelial cells. Inhibition of mitochondrial respiration and ATP synthesis induced the phosphorylation of mixed lineage kinase domain-like protein (MLKL) and necroptotic cell death. Furthermore, we demonstrate that the activation of AMP-activated protein kinase (AMPK), resulting from impaired mitochondrial OXPHOS, regulates necroptotic cell death. These results suggest that impaired mitochondrial OXPHOS contributes to necroptosis in human lung epithelial cells.
3.Mitochondrial biogenesis is required for the anchorage-independent survival and propagation of stem-like cancer cells.
De Luca A1,2,3, Fiorillo M1,2,3, Peiris-Pagès M1,2, Ozsvari B1,2, Smith DL4, Sanchez-Alvarez R1,2, Martinez-Outschoorn UE5, Cappello AR3, Pezzi V3, Lisanti MP1,2, Sotgia F1,2. Oncotarget. 2015 Jun 20;6(17):14777-95.
Here, we show that new mitochondrial biogenesis is required for the anchorage independent survival and propagation of cancer stem-like cells (CSCs). More specifically, we used the drug XCT790 as an investigational tool, as it functions as a specific inhibitor of the ERRα-PGC1 signaling pathway, which governs mitochondrial biogenesis. Interestingly, our results directly demonstrate that XCT790 efficiently blocks both the survival and propagation of tumor initiating stem-like cells (TICs), using the MCF7 cell line as a model system. Mechanistically, we show that XCT790 suppresses the activity of several independent signaling pathways that are normally required for the survival of CSCs, such as Sonic hedgehog, TGFβ-SMAD, STAT3, and Wnt signaling. We also show that XCT790 markedly reduces oxidative mitochondrial metabolism (OXPHOS) and that XCT790-mediated inhibition of CSC propagation can be prevented or reversed by Acetyl-L-Carnitine (ALCAR), a mitochondrial fuel.
4.Changes in the Proteome of Langat-Infected Ixodes scapularis ISE6 Cells: Metabolic Pathways Associated with Flavivirus Infection.
Grabowski JM1,2, Perera R2, Roumani AM3, Hedrick VE3, Inerowicz HD3, Hill CA1, Kuhn RJ2,3. PLoS Negl Trop Dis. 2016 Feb 9;10(2):e0004180. doi: 10.1371/journal.pntd.0004180. eCollection 2016.
BACKGROUND: Ticks (Family Ixodidae) transmit a variety of disease causing agents to humans and animals. The tick-borne flaviviruses (TBFs; family Flaviviridae) are a complex of viruses, many of which cause encephalitis and hemorrhagic fever, and represent global threats to human health and biosecurity. Pathogenesis has been well studied in human and animal disease models. Equivalent analyses of tick-flavivirus interactions are limited and represent an area of study that could reveal novel approaches for TBF control.
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Bio Calculators
* Our calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
It is commonly abbreviated as: C1V1 = C2V2
* Total Molecular Weight:
g/mol
Tip: Chemical formula is case sensitive. C22H30N4O √ c22h30n40 ╳
