Oleoylcarnitine |
| (Synonyms: CAR 18:1, C18:1 Carnitine, L-Carnitine oleoyl ester, L-Oleoylcarnitine) Catalog No.: GC38560 |
A long-chain acylcarnitine
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.:38677-66-6
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
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Purity: >96.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Oleoylcarnitine is an endogenous metabolite.
| Cas No. | 38677-66-6 | SDF | |
| Synonyms | CAR 18:1, C18:1 Carnitine, L-Carnitine oleoyl ester, L-Oleoylcarnitine | ||
| Canonical SMILES | CCCCCCCC/C=C\CCCCCCCC(O[C@H](CC([O-])=O)C[N+](C)(C)C)=O | ||
| Formula | C25H47NO4 | M.Wt | 425.64 |
| Solubility | Methanol: slightly soluble | Storage | Store at -20°C |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. | ||
| Shipping Condition | Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request |
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Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )
Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL saline, mix and clarify.
Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
3. All of the above co-solvents are available for purchase on the GlpBio website.
CPT2 downregulation adapts HCC to lipid-rich environment and promotes carcinogenesis via acylcarnitine accumulation in obesity
Gut 2018 Aug;67(8):1493-1504.PMID:29437870DOI:10.1136/gutjnl-2017-315193.
Objective: Metabolic reprogramming of tumour cells that allows for adaptation to their local environment is a hallmark of cancer. Interestingly, obesity-driven and non-alcoholic steatohepatitis (NASH)-driven hepatocellular carcinoma (HCC) mouse models commonly exhibit strong steatosis in tumour cells as seen in human steatohepatitic HCC (SH-HCC), which may reflect a characteristic metabolic alteration. Design: Non-tumour and HCC tissues obtained from diethylnitrosamine-injected mice fed either a normal or a high-fat diet (HFD) were subjected to comprehensive metabolome analysis, and the significance of obesity-mediated metabolic alteration in hepatocarcinogenesis was evaluated. Results: The extensive accumulation of acylcarnitine species was seen in HCC tissues and in the serum of HFD-fed mice. A similar increase was found in the serum of patients with NASH-HCC. The accumulation of acylcarnitine could be attributed to the downregulation of carnitine palmitoyltransferase 2 (CPT2), which was also seen in human SH-HCC. CPT2 downregulation induced the suppression of fatty acid β-oxidation, which would account for the steatotic changes in HCC. CPT2 knockdown in HCC cells resulted in their resistance to lipotoxicity by inhibiting the Src-mediated JNK activation. Additionally, Oleoylcarnitine enhanced sphere formation by HCC cells via STAT3 activation, suggesting that acylcarnitine accumulation was a surrogate marker of CPT2 downregulation and directly contributed to hepatocarcinogenesis. HFD feeding and carnitine supplementation synergistically enhanced HCC development accompanied by acylcarnitine accumulation in vivo. Conclusion: In obesity-driven and NASH-driven HCC, metabolic reprogramming mediated by the downregulation of CPT2 enables HCC cells to escape lipotoxicity and promotes hepatocarcinogenesis.
Inhibition of adenine nucleotide translocase by Oleoylcarnitine, oleoylcoa and oleate in isolated arterial mitochondria
Atherosclerosis 1980 Sep;37(1):21-32.PMID:6252909DOI:10.1016/0021-9150(80)90090-8.
Adenine nucleotide translocase (AdNT) activity was studied in isolated mitochondria from normal rabbit aortas. The enzyme was inhibited by oleic acid, oleoylCoA, and Oleoylcarnitine with 50% inhibition occurring at 5 muM, 6 muM and 14 muM, respectively (corresponding to 8, 10, and 23 nmol/mg protein). PalmitoylCoA and palmitoylcarnitine displayed similar potency to oleylCoA and Oleoylcarnitine. The possibility that inhibition by fatty acid, acylCoA, and acylcarnitine could be attributed to non-specific detergency effects seems remote in that these compounds were more potent inhibitors of AdNT than equimolar concentrations of laurylsulfate. In addition, by use of the fluorescent probe N-phenyl-1-naphthylamine, it was shown that under the experimental conditions, inhibition of AdNT occurred at concentrations not exceeding a critical micelle concentration (CMC). Specificity was also suggested in that octanoylCoA was a weak inhibitor of AdNT and acetylcarnitine, butyrylcarnitine, cholesteryl oleate, and sphingomyelin were not inhibitory to the enzyme. In contrast to the observed inhibition of arterial AdNT by oleoylCoA and Oleoylcarnitine, AdNT in isolated rabbit and rat heart mitochondria was inhibited only by oleoylCoA.
Systemic inflammatory markers in patients with polyneuropathies
Front Immunol 2023 Feb 13;14:1067714.PMID:36860843DOI:10.3389/fimmu.2023.1067714.
Introduction: In patients with peripheral neuropathies (PNP), neuropathic pain is present in 50% of the cases, independent of the etiology. The pathophysiology of pain is poorly understood, and inflammatory processes have been found to be involved in neuro-degeneration, -regeneration and pain. While previous studies have found a local upregulation of inflammatory mediators in patients with PNP, there is a high variability described in the cytokines present systemically in sera and cerebrospinal fluid (CSF). We hypothesized that the development of PNP and neuropathic pain is associated with enhanced systemic inflammation. Methods: To test our hypothesis, we performed a comprehensive analysis of the protein, lipid and gene expression of different pro- and anti-inflammatory markers in blood and CSF from patients with PNP and controls. Results: While we found differences between PNP and controls in specific cytokines or lipids, such as CCL2 or Oleoylcarnitine, PNP patients and controls did not present major differences in systemic inflammatory markers in general. IL-10 and CCL2 levels were related to measures of axonal damage and neuropathic pain. Lastly, we describe a strong interaction between inflammation and neurodegeneration at the nerve roots in a specific subgroup of PNP patients with blood-CSF barrier dysfunction. Conclusion: In patients with PNP systemic inflammatory, markers in blood or CSF do not differ from controls in general, but specific cytokines or lipids do. Our findings further highlight the importance of CSF analysis in patients with peripheral neuropathies.
A plasma long-chain acylcarnitine predicts cardiovascular mortality in incident dialysis patients
J Am Heart Assoc 2013 Dec 5;2(6):e000542.PMID:24308938DOI:10.1161/JAHA.113.000542.
Background: The marked excess in cardiovascular mortality that results from uremia remains poorly understood. Methods and results: In 2 independent, nested case-control studies, we applied liquid chromatography-mass spectrometry-based metabolite profiling to plasma obtained from participants of a large cohort of incident hemodialysis patients. First, 100 individuals who died of a cardiovascular cause within 1 year of initiating hemodialysis (cases) were randomly selected along with 100 individuals who survived for at least 1 year (controls), matched for age, sex, and race. Four highly intercorrelated long-chain acylcarnitines achieved the significance threshold adjusted for multiple testing (P<0.0003). Oleoylcarnitine, the long-chain acylcarnitine with the strongest association with cardiovascular mortality in unadjusted analysis, remained associated with 1-year cardiovascular death after multivariable adjustment (odds ratio per SD 2.3 [95% confidence interval, 1.4 to 3.8]; P=0.001). The association between Oleoylcarnitine and 1-year cardiovascular death was then replicated in an independent sample (n=300, odds ratio per SD 1.4 [95% confidence interval, 1.1 to 1.9]; P=0.008). Addition of Oleoylcarnitine to clinical variables improved cardiovascular risk prediction using net reclassification (NRI, 0.38 [95% confidence interval, 0.20 to 0.56]; P<0.0001). In physiologic profiling studies, we demonstrate that the fold change in plasma acylcarnitine levels from the aorta to renal vein and from pre- to posthemodialysis samples exclude renal or dialytic clearance of long-chain acylcarnitines as confounders in our analysis. Conclusions: Our data highlight clinically meaningful alterations in acylcarnitine homeostasis at the time of dialysis initiation, which may represent an early marker, effector, or both of uremic cardiovascular risk.
A Metabolomic Approach in Search of Neurobiomarkers of Perinatal Asphyxia: A Review of the Current Literature
Front Pediatr 2021 Jun 25;9:674585.PMID:34249811DOI:10.3389/fped.2021.674585.
Perinatal asphyxia and the possible sequelae of hypoxic-ischemic encephalopathy (HIE), are associated with high morbidity and mortality rates. The use of therapeutic hypothermia (TH) commencing within the first 6 h of life-currently the only treatment validated for the management of HIE-has been proven to reduce the mortality rate and disability seen at follow up at 18 months. Although there have been attempts to identify neurobiomarkers assessing the severity levels in HIE; none have been validated in clinical use to date, and the lack thereof limits the optimal treatment for these vulnerable infants. Metabolomics is a promising field of the "omics technologies" that may: identify neurobiomarkers, help improve diagnosis, identify patients prone to developing HIE, and potentially improve targeted neuroprotection interventions. This review focuses on the current evidence of metabolomics, a novel tool which may prove to be a useful in the diagnosis, management and treatment options for this multifactorial complex disease. Some of the most promising metabolites analyzed are the group of acylcarnitines: Hydroxybutyrylcarnitine (Malonylcarnitine) [C3-DC (C4-OH)], Tetradecanoylcarnitine [C14], L-Palmitoylcarnitine [C16], Hexadecenoylcarnitine [C16:1], Stearoylcarnitine [C18], and Oleoylcarnitine [C18:1]. A metabolomic "fingerprint" or "index," made up of 4 metabolites (succinate × glycerol/(β-hydroxybutyrate × O-phosphocholine)), seems promising in identifying neonates at risk of developing severe HIE.
Average Rating: 5 (Based on Reviews and 27 reference(s) in Google Scholar.)
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