Brevilin A
(Synonyms: 短叶老鹳草素A) 目录号 : GC35554
A sesquiterpene lactone with anticancer activity
Cas No.:16503-32-5
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
Brevilin A is a sesquiterpene lactone that has been found in C. minima and has anticancer activity.1 It is an inhibitor of STAT3 signaling (IC50 = 10.6 ?M in A549R cells) that inhibits the tyrosine kinase activity of the JAK1, JAK2, JAK3, and JAK4 JH1 subunit (IC50s = 11.2, 8.4, 10.2, and 11.9 ?M, respectively).2 It inhibits proliferation of a variety of cancer cells, including A549 lung, HepG2 liver, HeLa cervical, A875 melanoma, and CT26 mouse colon carcinoma cells in a concentration-dependent manner.1 Brevilin A (1-4 ?g/ml) decreases the mitochondrial membrane potential, induces apoptosis, and increases the level of reactive oxygen species (ROS) in CT26 cells. It also induces autophagosome formation in CT26 cells, an effect that can be blocked by the PI3K inhibitor 3-methyladenine . Brevilin A (5 mg/kg per day) increases intratumor expression of the autophagy marker LC3-II and reduces tumor growth in a murine CT26 colon cancer model.
1.You, P., Wu, H., Deng, M., et al.Brevilin A induces apoptosis and autophagy of colon adenocarcinoma cell CT26 via mitochondrial pathway and PI3K/AKT/mTOR inactivationBiomed. Pharmacother.98619-625(2018) 2.Chen, X., Du, Y., Nan, J.X., et al.Brevilin A, a novel natural product, inhibits janus kinase activity and blocks STAT3 signaling in cancer cellsPLoS One8(5)e63697(2013)
| Cas No. | 16503-32-5 | SDF | |
| 别名 | 短叶老鹳草素A | ||
| Canonical SMILES | C/C=C(C)\C(O[C@H]1[C@@]([C@@H]2C)([H])[C@@](OC2=O)([H])C[C@@H](C)[C@@]3([H])[C@]1(C(C=C3)=O)C)=O | ||
| 分子式 | C20H26O5 | 分子量 | 346.42 |
| 溶解度 | DMSO: 250 mg/mL (721.67 mM) | 储存条件 | Store at -20°C,protect from light |
| 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 | 2.8867 mL | 14.4333 mL | 28.8667 mL |
| 5 mM | 0.5773 mL | 2.8867 mL | 5.7733 mL |
| 10 mM | 0.2887 mL | 1.4433 mL | 2.8867 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。
Brevilin A Ameliorates Imiquimod-Induced Psoriasis-like Dermatitis and Reduces Th17 Differentiation in Psoriasis Patients
J Pers Med 2022 Nov 10;12(11):1888.PMID:36579613DOI:10.3390/jpm12111888.
Psoriasis is a predominantly Th17 cell-driven chronic autoinflammatory skin disorder. Brevilin A, a natural sesquiterpene lactone extracted from Centipeda minima, has been used as a traditional oriental medicine for allergic diseases for centuries. However, the effects of Brevilin A on psoriasis have yet to be established. In this study, we investigated Brevilin A to elucidate its potential effects on T cell activities in psoriasis, in animal models and patients. An imiquimod (IMQ)-induced psoriasis-like dermatitis murine model was utilized. Experimental mice were administered different doses of Brevilin A (5, 10, 20 mg/kg respectively) for a duration of 5 days. Cutaneous manifestations were measured daily. Under hematoxylin and eosin (H&E) stain and immunohistochemistry (IHC), acanthosis and proinflammatory cytokine expression in the dorsal skin of mice were detected. Enzyme-linked immunosorbent assay (ELISA) was used for the measurement of IL-17A levels in serum samples. Naïve CD4+ T cells, isolated from mice spleen and lymph nodes and from peripheral blood mononuclear cells (PBMCs) of psoriatic patients, were used to evaluate the effects of Brevilin A on Th17 differentiation. In brevilin A-treated mice, Brevilin A significantly reduced skin redness and scaling; acanthosis as well as IL-6, IL-17A, and ki-67 expressions were downregulated in the dorsal skin, and serum levels of IL-17A were lowered. Brevilin A also inhibited Th17 differentiation. In conclusion, Brevilin A demonstrated significant capability in ameliorating skin inflammation in IMQ-induced psoriasis-like dermatitis and could modulate Th17 differentiation. Therefore, Brevilin A is potentially pharmacologically effective in the treatment of psoriasis.
Brevilin A Inhibits VEGF-Induced Angiogenesis through ROS-Dependent Mitochondrial Dysfunction
Oxid Med Cell Longev 2022 Dec 14;2022:5888636.PMID:36567856DOI:10.1155/2022/5888636.
Brevilin A (BA), a sesquiterpene lactone isolated from Centipeda minima herb, has been identified to exhibit potent anticancer activity. However, the potential pharmacological effect and mechanism of BA in regulating endothelial cell (EC) angiogenesis, a key event in tumor growth, is poorly understood. In this study, BA was shown to significantly prevent vascular endothelial growth factor (VEGF) induced EC angiogenic capacities in vitro, ex vivo, and in vivo. Subsequent functional assays revealed that BA dose dependently inhibited VEGF-stimulated survival, proliferation, migration, and triggered apoptosis activity in human umbilical vein endothelial cells (HUVECs), as well as suppressed the expression of antiapoptotic protein Bcl-2, increased the expression of proapoptotic protein caspase-3 and Bax, and suppressed PI3K/AKT pathway. Meanwhile, BA was also able to depolarize mitochondrial membranal permeability (MMP), accelerate mitochondrial superoxide accumulation, induce intracellular reactive oxygen species (ROS) production, and decreased intracellular glutathione (GSH) in HUVECs. Furthermore, both mitochondria-specific superoxide scavenger Mito-TEMPOL and broad-spectrum antioxidant N-acetyl-cysteine (NAC) dramatically abolished BA-induced mitochondrial dysfunction and mitochondrial ROS production, causing the reversion of PI3K/AKT pathway and repression of apoptosis, eventually correcting the impaired endothelial behavior in survival, growth, migration, and angiogenesis. Collectively, our data for the first time identified a new mechanism for antiangiogenic effect of BA in vascular EC, one that is based on the regulation of mitochondrial-dependent ROS overproduction.
Brevilin A Isolated from Centipeda minima Induces Apoptosis in Human Gastric Cancer Cells via an Extrinsic Apoptotic Signaling Pathway
Plants (Basel) 2022 Jun 23;11(13):1658.PMID:35807611DOI:10.3390/plants11131658.
Brevilin A, which has anticancer activities against a range of cancers, is an abundant constituent of the medicinal herb Centipeda minima (L.) A. Braun & Asch, which has also been reported to have anticancer activity against breast cancer cells. However, the anticancer activities of C. minima and Brevilin A against human gastric cancer have yet to be reported. In this study, we aimed to evaluate the cytotoxicity and molecular basis underlying the anticancer activities of extracts of C. minima (CMX) and Brevilin A against human gastric cancer (AGS) cells. We deduced the potential targets and mechanisms underlying the anticancer activity of Brevilin A based on a network pharmacology approach. CCND1, CDK4, and BCL2L1 were identified as the key anticancer genes targeted by Brevilin A. Cytotoxicity analyses revealed that CMX and Brevilin A reduced the viability of AGS cells to levels below 50% (9.73 ± 1.29 µg/mL and 54.69 ± 1.38 μM, respectively). Furthermore, Hoechst 33342, annexin V, and propidium iodide staining and western blot analyses revealed that CMX and Brevilin A promoted a significant induction of apoptotic cell death by upregulating the expression of cleaved caspase-8 and cleaved caspase-3 and reducing the ratio of Bax to Bcl-2, which is partially consistent with the findings of our network pharmacology analysis. Collectively, our observations indicate that CMX and Brevilin A are novel sources of herbal medicine with potential utility as effective agents for the treatment of gastric cancer.
Brevilin A enhances innate immunity and the resistance of oxidative stress in Caenorhabditis elegans via p38 MAPK pathway
Int Immunopharmacol 2022 Dec;113(Pt A):109385.PMID:36330917DOI:10.1016/j.intimp.2022.109385.
The conserved p38/PMK-1 pathway that is an evolutionarily conserved module used by mammals and nematodes in immune response against bacterial infections. Brevilin A (BA), a sesquiterpene lactone compound of Centipeda minima has been shown to exhibit activities such as anti-tumor, anti-bacterial and anti-protozoal. However, whether the Brevilin A influences the immune response and the underlying molecular mechanisms remain obscure. We find that 10 μM Brevilin A increases resistance to not only the Gram-negative pathogens Pseudomonas aeruginosa and Salmonella enterica but also the Gram-positive pathogens Enterococcusfaecalis and Staphylococcus aureus. Meanwhile, Brevilin A enhances the resistance to pathogens by reducing the bacterial burden in the intestine. Through the genetic screening in C. elegans, we find that Brevilin A promotes innate immunity via p38 MAPK pathway. Furthermore, Brevilin A activates the p38/PMK-1 in the intestine for innate immune response. In addition, we also find that Brevilin A increases the resistance of oxidative stress and extends lifespan through p38 MAPK pathway. Our work suggests that Brevilin A may be a viable candidate for the treatment of infectious diseases.
Brevilin A Induces Cell Cycle Arrest and Apoptosis in Nasopharyngeal Carcinoma
Front Pharmacol 2019 May 24;10:594.PMID:31178739DOI:10.3389/fphar.2019.00594.
Nasopharyngeal carcinoma (NPC) is one of the most common malignant cancers in Southeast Asia and Southern China. Centipeda minima extract (CME) had previously demonstrated anti-cancer effects in human NPC. Brevilin A, a sesquiterpene lactone isolated from C. minima, has been reported to exhibit biological activities. In this study, we investigated its anti-NPC effect and further explored its molecular mechanisms. The effects of Brevilin A were tested in the NPC cell lines CNE-1, CNE-2, SUNE-1, HONE1, and C666-1. Effects of Brevilin A on cell viability were determined by MTT assay, and cell cycle and apoptosis were detected by flow cytometry. The molecular mechanism of cell cycle regulation and apoptosis were investigated via Western blot. Results showed that Brevilin A inhibited NPC cell viability in a concentration- and time-dependent manner. Brevilin A induced cell cycle arrest at G2/M and induced apoptosis. Western blot results demonstrated that Brevilin A could down-regulate cyclin D3, cdc2, p-PI3K, p-AKT, p-mTOR, and p-STAT3, while up-regulating cleaved PARP, cleaved caspase 9, and Bax. Regulation of cyclin B1, cdk6, and Bcl-2 expression by Brevilin A showed dynamic changes according to dose and time. In the tumor xenograft model, Brevilin A could reduce tumor growth, at a similar magnitude to cisplatin. However, notably, whereas cisplatin treatment led to significant weight loss in treated mice, treatment with Brevilin A did not, indicating its relative lack of toxicity. Taken together, Brevilin A regulated cell cycle, activated the caspase signaling pathway, and inhibited PI3K/AKT/mTOR and STAT3 signaling pathways in vitro, and exhibited similar efficacy to the common chemotherapeutic cisplatin in vivo, without its associated toxicity. These findings provide a framework for the preclinical development of Brevilin A as a chemotherapeutic for NPC.