Aurantiamide
(Synonyms: 橙黄胡椒酰胺乙酸酯) 目录号 : GC60060
Aurantiamide是马齿苋的一种活性成分，具有口服活性，具有多种生物活性，包括抗氧化、抗血小板、抗炎、抗肿瘤活性等。
Cas No.:58115-31-4
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
Aurantiamide is an orally active constituent of Portulaca oleracea L and has various biological activities, including antioxidant, antiplatelet, anti-inflammatory, and antitumor activities[1].
[1]. Lijiang Chen, et al. Pharmacokinetics and Biodistribution of Aurantiamide and Aurantiamide Acetate in Rats After Oral Administration of Portulaca Oleracea L. Extracts. J Agric Food Chem. 2016 May 4;64(17):3445-55.
| Cas No. | 58115-31-4 | SDF | |
| 别名 | 橙黄胡椒酰胺乙酸酯 | ||
| Canonical SMILES | O=C(N[C@H](CO)CC1=CC=CC=C1)[C@@H](NC(C2=CC=CC=C2)=O)CC3=CC=CC=C3 | ||
| 分子式 | C25H26N2O3 | 分子量 | 402.49 |
| 溶解度 | 储存条件 | ||
| 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 | 2.4845 mL | 12.4227 mL | 24.8453 mL |
| 5 mM | 0.4969 mL | 2.4845 mL | 4.9691 mL |
| 10 mM | 0.2485 mL | 1.2423 mL | 2.4845 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。
Aurantiamide Acetate Ameliorates Lung Inflammation in Lipopolysaccharide-Induced Acute Lung Injury in Mice
Biomed Res Int 2022 Aug 22;2022:3510423.PMID:36046440DOI:10.1155/2022/3510423.
Purpose: Aurantiamide acetate (AA) is a dipeptide derivative with complex pharmacological activities and remarkable effects on preventing and treating various diseases. In the current study, we aimed to investigate whether AA can exert protective effects in a mouse model of ALI induced by LPS. Materials and methods: In this model, mice were given intranasal LPS for 3 days prior to receiving AA (2.5, 5, and 10 mg/kg) via oral gavage. An assessment of histopathological changes was performed by hematoxylin and eosin (HE). Proinflammatory cytokines were detected in bronchoalveolar lavage fluids (BALFs) by enzyme-linked immunosorbent assays (ELISAs). The effects of AA on protein expression of NF-κB and PI3K/AKT signaling pathways were determined by Western blot. In addition, lung wet/dry (W/D) weight ratio, myeloperoxidase (MPO) activity, cell counts, and protein content were also measured. Results: According to results, AA pretreatment significantly reduced lung pathological changes, W/D ratio, MPO activity, and protein content. Additionally, AA resulted in a significant reduction in the number of total cells, neutrophils, and proinflammatory cytokines in the BALF after LPS stimulation. The subsequent study revealed that pretreatment with AA dose dependently suppressed LPS-induced activation of NF-κB as well as PI3K/AKT phosphorylation. Conclusion: The results indicated that the AA had a protective effect on LPS-induced ALI in mice and could be a potential drug for ALI.
Aurantiamide acetate suppresses the growth of malignant gliomas in vitro and in vivo by inhibiting autophagic flux
J Cell Mol Med 2015 May;19(5):1055-64.PMID:25704599DOI:10.1111/jcmm.12498.
We aim to investigate the effect of Aurantiamide acetate isolated from the aerial parts of Clematis terniflora DC against gliomas. Human malignant glioma U87 and U251 cells were incubated with different concentrations (0-100 μM) of Aurantiamide acetate. Aurantiamide acetate greatly decreased the cell viability in a dose- and time-dependent manner. It induced moderate mitochondrial fragmentation and the loss of mitochondrial membrane potential. No significant difference was found in the alternation of other intracellular organelles, although F-actin structure was slightly disturbed. Apparent ultrastructure alternation with increased autophagosome and autolysosome accumulation was observed in Aurantiamide acetate-treated cells. The expression of LC3-II was greatly up-regulated in cells exposed to Aurantiamide acetate (P < 0.05 compared with control). The cytoplasmic accumulation of autophagosomes and autolysosomes induced by Aurantiamide acetate treatment was confirmed by fluorescent reporter protein labelling. Administration of chloroquine (CQ), which inhibits the fusion step of autophagosomes, further increased the accumulation of autophagosomes in the cytoplasm of U87 cells. Autophagy inhibition by 3-methyladenine, Bafilomycin A1 or CQ had no influence on Aurantiamide acetate-induced cytotoxicity, whereas autophagy stimulator rapamycin significantly suppressed Aurantiamide acetate-induced cell death. The anti-tumour effects of Aurantiamide acetate were further evaluated in tumour-bearing nude mice. Intratumoural injection of Aurantiamide acetate obviously suppressed tumour growth, and increased number of autophagic vacuoles was observed in tumour tissues of animals receiving Aurantiamide acetate. Our findings suggest that Aurantiamide acetate may suppress the growth of malignant gliomas by blocking autophagic flux.
Aurantiamide-related dipeptide derivatives are formyl peptide receptor 1 antagonists
Medchemcomm 2019 Oct 7;10(12):2078-2088.PMID:32206242DOI:10.1039/c9md00336c.
Formyl peptide receptor 1 (FPR1) is expressed on a variety of immune system cells and is a key regulator of the inflammatory environment. Therefore, the development of FPR1 antagonists may represent a novel approach for modulating innate immunity and treating inflammatory diseases. Starting from a dipeptide scaffold that is structurally related to the natural product Aurantiamide, we investigated the structure-activity relationships of the dipeptide (2R,2'S)-6, which was reported as an FPR1 antagonist. We found that the absolute configuration 2R,2'S was preferred to obtain potent and selective FPR1 antagonists. The structural modifications performed on the terminal fragments of the molecule suggest that the size of the substituents can greatly influence the interaction with FPR1. These compounds behaved as antagonists in human neutrophils and were able to inhibit formyl peptide-induced chemotaxis. Since FPR1 is a key regulator of the inflammatory environment, the dipeptide derivatives described here may represent important leads for the development of new potent and selective FPR1 antagonists for the treatment of neutrophil-mediated inflammatory diseases.
Hybrids of Aurantiamide acetate and isopropylated genipin as potential anti-inflammatory agents: The design, synthesis, and biological evaluation
Chem Biol Drug Des 2021 Apr;97(4):797-808.PMID:33219736DOI:10.1111/cbdd.13809.
A novel series of hybrids designed on the basis of Aurantiamide acetate and isopropylated genipin were synthesized and biologically evaluated as anti-inflammatory agents. Among them, compound 7o exhibited the best inhibitory activity against TNF-α secretion (IC50 = 16.90 μM) and was selected for further in vitro and in vivo functional study. The results demonstrated that 7o was capable of suppressing the expression of LPS-induced iNOS and COX-2, as well as reducing the production of NO at the concentration of 5 μM, which may be resulted from its regulation of NF-κB signaling and MAPK signaling. Moreover, compound 7o exhibited favorable in vivo anti-inflammatory activity with an inhibition rate of 53.32% against xylene-induced ear swelling in mice at the dose of 5 mg/kg.
Aurantiamide promotes M2 polarization of microglial cells to improve the cognitive ability of mice with Alzheimer's disease
Phytother Res 2023 Jan;37(1):101-110.PMID:36062448DOI:10.1002/ptr.7597.
This work aimed to investigate the effect of Aurantiamide (Aur) in promoting the M2 polarization of microglial cells to improve the cognitive ability of mice with Alzheimer's disease (AD). The M2 polarization of BV2 cells was induced by interleukin-4 (IL-4) treatment.Aur promoted the M2 polarization of BV2 cells, and up-regulated the expression of CD206 and SOCS3. In the meantime, it increased TGF-β1, Arg-1 and IL-10 levels, and promoted the polarization of JAK1-STAT6. Treatment with STAT6 inhibitor antagonized the effect of Aur. Besides, the cognitive ability of AD mice was improved after Aur treatment, meanwhile, the expression of CD206 was up-regulated, while that of IBA-1 was down-regulated. Aur promotes the M2 polarization of microglial cells to improve the cognitive ability of AD mice, and such effect is related to the STAT6 signal.