N-Arachidonoyl Taurine
目录号 : GC44317
An arachidonoyl amino acid
Cas No.:119959-65-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
N-Arachidonoyl taurine is an arachidonoyl amino acid. It is oxygenated by 12(S)- and 15(S)-lipoxygenase and is converted to 12-HETE-taurine (12-HETE-T) in murine resident peritoneal macrophages. N-Arachidonoyl taurine is an activator of the transient receptor potential vanilloid (TRPV) channels TRPV1 and TRPV4 (EC50s = 28 and 21 µM, respectively). It increases calcium flux in HIT-T15 pancreatic β-cells and INS-1 rat islet cells when used at a concentration of 10 µM and increases insulin secretion from 832/13 INS-1 pancreatic β-cells. The levels of N-arachidonoyl taurine are changed in mouse brain following administration of δ9-tetrahydrocannabinol (δ9-THC).
| Cas No. | 119959-65-8 | SDF | |
| Canonical SMILES | CCCCC/C=C\C/C=C\C/C=C\C/C=C\CCCC(N(CCS(=O)(O)=O)[H])=O | ||
| 分子式 | C22H37NO4S | 分子量 | 411.6 |
| 溶解度 | DMF: 10 mg/ml,DMSO: 20 mg/ml,PBS (pH 7.2): 1.5 mg/ml | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.4295 mL | 12.1477 mL | 24.2954 mL |
| 5 mM | 0.4859 mL | 2.4295 mL | 4.8591 mL |
| 10 mM | 0.243 mL | 1.2148 mL | 2.4295 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Essential roles of exosome and circRNA_101093 on ferroptosis desensitization in lung adenocarcinoma
Cancer Commun (Lond) 2022 Apr;42(4):287-313.PMID:35184419DOI:10.1002/cac2.12275.
Background: Resistance to ferroptosis, a regulated cell death caused by iron-dependent excessive accumulation of lipid peroxides, has recently been linked to lung adenocarcinoma (LUAD). Intracellular antioxidant systems are required for protection against ferroptosis. The purpose of the present study was to investigate whether and how extracellular system desensitizes LUAD cells to ferroptosis. Methods: Established human lung fibroblasts MRC-5, WI38, and human LUAD H1650, PC9, H1975, H358, A549, and H1299 cell lines, tumor and matched normal adjacent tissues of LUAD, and plasma from healthy individuals and LUAD patients were used in this study. Immunohistochemistry and immunoblotting were used to analyze protein expression, and quantitative reverse transcription-PCR was used to analyze mRNA expression. Cell viability, cell death, and the lipid reactive oxygen species generation were measured to evaluate the responses to ferroptosis. Exosomes were observed using transmission electron microscope. The localization of arachidonic acid (AA) was detected using click chemistry labeling followed by confocal microscopy. Interactions between RNAs and proteins were detected using RNA pull-down, RNA immunoprecipitation and photoactivatable ribonucleoside-enhanced crosslinking and immunoprecipitation methods. Proteomic analysis was used to investigate RNA-regulated proteins, and metabolomic analysis was performed to analyze metabolites. Cell-derived xenograft, patient-derived xenograft, cell-implanted intrapulmonary LUAD mouse models and plasma/tissue specimens from LUAD patients were used to validate the molecular mechanism. Results: Plasma exosome from LUAD patients specifically reduced lipid peroxidation and desensitized LUAD cells to ferroptosis. A potential explanation is that exosomal circRNA_101093 (cir93) maintained an elevation in intracellular cir93 in LUAD to modulate AA, a poly-unsaturated fatty acid critical for ferroptosis-associated increased peroxidation in the plasma membrane. Mechanistically, cir93 interacted with and increased fatty acid-binding protein 3 (FABP3), which transported AA and facilitated its reaction with taurine. Thus, global AA was reduced, whereas N-Arachidonoyl Taurine (NAT, the product of AA and taurine) was induced. Notably, the role of NAT in suppressing AA incorporation into the plasma membrane was also revealed. In pre-clinical in vivo models, reducing exosome improved ferroptosis-based treatment. Conclusion: Exosome and cir93 are essential for desensitizing LUAD cells to ferroptosis, and blocking exosome may be helpful for future LUAD treatment.
Fatty acid analogue N-Arachidonoyl Taurine restores function of IKs channels with diverse long QT mutations
Elife 2016 Sep 30;5:e20272.PMID:27690226DOI:10.7554/eLife.20272.
About 300 loss-of-function mutations in the IKs channel have been identified in patients with Long QT syndrome and cardiac arrhythmia. How specific mutations cause arrhythmia is largely unknown and there are no approved IKs channel activators for treatment of these arrhythmias. We find that several Long QT syndrome-associated IKs channel mutations shift channel voltage dependence and accelerate channel closing. Voltage-clamp fluorometry experiments and kinetic modeling suggest that similar mutation-induced alterations in IKs channel currents may be caused by different molecular mechanisms. Finally, we find that the fatty acid analogue N-Arachidonoyl Taurine restores channel gating of many different mutant channels, even though the mutations are in different domains of the IKs channel and affect the channel by different molecular mechanisms. N-Arachidonoyl Taurine is therefore an interesting prototype compound that may inspire development of future IKs channel activators to treat Long QT syndrome caused by diverse IKs channel mutations.
Effects of TRPV1 Activation by Capsaicin and Endogenous N-Arachidonoyl Taurine on Synaptic Transmission in the Prefrontal Cortex
Front Neurosci 2020 Feb 7;14:91.PMID:32116530DOI:10.3389/fnins.2020.00091.
While the transient receptor potential vanilloid 1 (TRPV1) ion channel, a non-selective calcium-permeable cation channel with high Ca2+ permeability, mainly integrates physical and chemical stimuli for nociception, recent studies suggest that it has a role beyond a noxious thermal sensor. In fact, TRPV1 is presently being considered as a target for treating pathophysiological processes including pain, fear, and anxiety disorders. Although this ion channel has many potential roles, its underlying mechanism of action remains elusive. Here we show in mice that activation of TRPV1-, by the exogenous agonist capsaicin-, regulates synaptic activity in both glutamatergic and GABAergic synaptic transmission. Moreover, activation by the endogenous activator N-Arachidonoyl Taurine (NAT), induced similar effects as capsaicin. On the other hand, taurine, the decomposition product of NAT, strongly depressed the evoked glutamatergic synaptic transmission. In addition to these findings, we also show the immunohistochemical distribution of TRPV1 in the prefrontal cortex (PFC) of mice, as such studies are currently less frequent in the PFC. Overall, these observations allow for a better understanding of how TRPV1 helps regulate excitatory and inhibitory synaptic activity in the PFC of mice.
N-acyl taurines are anti-proliferative in prostate cancer cells
Lipids 2012 Apr;47(4):355-61.PMID:22160494DOI:10.1007/s11745-011-3639-9.
Endocannabinoids have been implicated in cancer development and cause heterogenous effects in tumor cells, by inducing apoptosis, reducing migration, causing anti-angiogenic activity and alterations in the cell cycle resulting in growth arrest. Recently, several novel amides of fatty acids that are structurally related to endocannabinoids have been isolated from mammalian sources, although the functions of these fatty amides are not well studied. One group of these novel fatty acid amides are the N-acyl taurines (fatty acids conjugated to the amino acid taurine). This study examined if N-acyl taurines, specifically N-Arachidonoyl Taurine and N-oleoyl taurine could function in a similar way to endocannabinoids and result in cell cycle alterations or growth arrest in the human prostate adenocarcinoma cell line PC-3. PC-3 cells were treated with various concentrations of N-Arachidonoyl Taurine and N-oleoyl taurine and cell proliferation and viability was measured using resazurin and colony formation assays. Effects of N-acyl taurines on the cell cycle was measured using FACS analysis. Treatment with N-Arachidonoyl Taurine and N-oleoyl taurine resulted in a significant reduction in proliferation of PC-3 cells, even at concentrations as low as 1 μM. Treatment with N-oleoyl taurine resulted in an increased number of cells in the subG1 population, suggesting apoptosis, and a lower number of cells in S-phase of the cell cycle. In summary, our results show that novel biologically active lipids, the N-acyl taurines, result in reduced proliferation in PC-3 cells.
N-Acyl taurines trigger insulin secretion by increasing calcium flux in pancreatic β-cells
Biochem Biophys Res Commun 2013 Jan 4;430(1):54-9.PMID:23159632DOI:10.1016/j.bbrc.2012.11.026.
Pancreatic β-cells secrete insulin in response to various stimuli to control blood glucose levels. This insulin release is the result of a complex interplay between signaling, membrane potential and intracellular calcium levels. Various nutritional and hormonal factors are involved in regulating this process. N-Acyl taurines are a group of fatty acids which are amidated (or conjugated) to taurine and little is known about their physiological functions. In this study, treatment of pancreatic β-cell lines (HIT-T15) and rat islet cell lines (INS-1) with N-acyl taurines (N-Arachidonoyl Taurine and N-oleoyl taurine), induced a high frequency of calcium oscillations in these cells. Treatment with N-Arachidonoyl Taurine and N-oleoyl taurine also resulted in a significant increase in insulin secretion from pancreatic β-cell lines as determined by insulin release assay and immunofluorescence (p<0.05). Our data also show that the transient receptor potential vanilloid 1 (TRPV1) channel is involved in insulin secretion in response to N-Arachidonoyl Taurine and N-oleoyl taurine treatment. However our data also suggest that receptors other than TRPV1 are involved in the insulin secretion response to treatment with N-oleoyl taurine.