Oligomycin
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| Category | Enzyme inhibitors |
| Catalog number | BBF-04131 |
| CAS | 1404-19-9 |
| Molecular Weight | 791.06 |
| Molecular Formula | C45H74O11 |
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Description
Oligomycin, a mixture of A, B, and C Oligomycin isomers, has been found to be a macrolide compound and could exhibit effect in restraining mitochondrial ATP-synthase. It is isolated from Streptomyces diastatochromogenes.
Specification
| Synonyms | RK3325000; Oligomycin A |
| Storage | Store at -20°C (dark) |
| IUPAC Name | (1S,4E,5'R,6R,6'R,7S,8R,10S,11S,12R,14S,15R,16S,18E,20E,22S,25R,27S,28R,29S)-22-ethyl-7,11,14,15-tetrahydroxy-6'-[(2S)-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-/m1/s1 |
| InChI Key | MNULEGDCPYONBU-DJRUDOHVSA-N |
| Source | Streptomyces diastatochromogenes |
Properties
| Appearance | White Powder |
| Application | Used as a tool in cytochemistry. |
| Boiling Point | 886.3°C at 760 mmHg |
| Melting Point | 84-100°C |
| Density | 1.14 g/cm3 |
| Solubility | Soluble in Dichloromethane, DMSO, Ethanol, Acetone |
Reference Reading
1.ANT1-mediated fatty acid-induced uncoupling as a target for improving myocellular insulin sensitivity.
Sparks LM1,2, Gemmink A3, Phielix E1, Bosma M1,4, Schaart G3, Moonen-Kornips E1, Jörgensen JA1, Nascimento EB1, Hesselink MK3, Schrauwen P1, Hoeks J5. Diabetologia. 2016 May;59(5):1030-9. doi: 10.1007/s00125-016-3885-8. Epub 2016 Feb 17.
AIMS/HYPOTHESIS: Dissipating energy via mitochondrial uncoupling has been suggested to contribute to enhanced insulin sensitivity. We hypothesised that skeletal muscle mitochondria of endurance-trained athletes have increased sensitivity for fatty acid (FA)-induced uncoupling, which is driven by the mitochondrial protein adenine nucleotide translocase 1 (ANT1).
2.Leptin contributes to long-term stabilization of HIF-1α in cancer cells subjected to oxygen limiting conditions.
Calgani A1, Delle Monache S1, Cesare P2, Vicentini C2, Bologna M2, Angelucci A3. Cancer Lett. 2016 Mar 17. pii: S0304-3835(16)30177-X. doi: 10.1016/j.canlet.2016.03.027. [Epub ahead of print]
Leptin, a cytokine produced by the adipose tissue in response to food intake, is a key player in the regulation of energy balance and body weight control. Physiological action of leptin in modulating the metabolic adaptation of different peripheral tissues supports the hypothesis that it could also exert a direct effect on cancer cells. In vitro, treatment with leptin up-regulated HIF-1α and stimulated adhesion and invasion of prostate cancer cells cultured in hypoxia. Leptin action was effective in both low and high glycolytic cancer cell lines, and determined the up-regulation of lactate exporter MCT4 and its associated protein CD147. HIF-1α stabilization was oligomycin-independent and was associated with an important modulation of mitochondrial homeostasis. In fact, leptin treatment produced mitochondrial biogenesis, stabilization of mitochondrial membrane potential and increased uncoupled respiration through the up-regulation of UCP2.
3.Underestimation of the Maximal Capacity of the Mitochondrial Electron Transport System in Oligomycin-Treated Cells.
Ruas JS1, Siqueira-Santos ES1, Amigo I2, Rodrigues-Silva E1, Kowaltowski AJ2, Castilho RF1. PLoS One. 2016 Mar 7;11(3):e0150967. doi: 10.1371/journal.pone.0150967. eCollection 2016.
The maximal capacity of the mitochondrial electron transport system (ETS) in intact cells is frequently estimated by promoting protonophore-induced maximal oxygen consumption preceded by inhibition of oxidative phosphorylation by oligomycin. In the present study, human glioma (T98G and U-87MG) and prostate cancer (PC-3) cells were titrated with different concentrations of the protonophore CCCP to induce maximal oxygen consumption rate (OCR) within respirometers in a conventional growth medium. The results demonstrate that the presence of oligomycin or its A-isomer leads to underestimation of maximal ETS capacity. In the presence of oligomycin, the spare respiratory capacity (SRC), i.e., the difference between the maximal and basal cellular OCR, was underestimated by 25 to 45%. The inhibitory effect of oligomycin on SRC was more pronounced in T98G cells and was observed in both suspended and attached cells. Underestimation of SRC also occurred when oxidative phosphorylation was fully inhibited by the ATP synthase inhibitor citreoviridin.
4.Arsenite Regulates Prolongation of Glycan Residues of Membrane Glycoprotein: A Pivotal Study via Wax Physisorption Kinetics and FTIR Imaging.
Lee CH1, Hsu CY2, Huang PY3, Chen CI4, Lee YC5,6, Yu HS7,8. Int J Mol Sci. 2016 Mar 22;17(3). pii: E427. doi: 10.3390/ijms17030427.
Arsenic exposure results in several human cancers, including those of the skin, lung, and bladder. As skin cancers are the most common form, epidermal keratinocytes (KC) are the main target of arsenic exposure. The mechanisms by which arsenic induces carcinogenesis remains unclear, but aberrant cell proliferation and dysregulated energy homeostasis play a significant role. Protein glycosylation is involved in many key physiological processes, including cell proliferation and differentiation. To evaluate whether arsenite exposure affected protein glycosylation, the alteration of chain length of glycan residues in arsenite treated skin cells was estimated. Herein we demonstrated that the protein glycosylation was adenosine triphosphate (ATP)-dependent and regulated by arsenite exposure by using Fourier transform infrared (FTIR) reflectance spectroscopy, synchrotron-radiation-based FTIR (SR-FTIR) microspectroscopy, and wax physisorption kinetics coupled with focal-plane-array-based FTIR (WPK-FPA-FTIR) imaging.
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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 ╳
