Bavachinin
(Synonyms: 补骨脂二氢黄酮甲醚; 7-O-Methylbavachin; Bavachinin A) 目录号 : GC41158
A pan-PPAR agonist
Cas No.:19879-30-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Bavachinin(7-O-Methylbavachin) is a natural compound isolated from the Chinese herb Fructus Psoraleae;has potent anti-angiogenic activity.IC50 value:Target:in vitro: Isobavachalcone significantly inhibits both oligomerization and fibrillization of Aβ42, whereas bavachinin inhibits fibrillization and leads to off-pathway aggregation. Both of the compounds attenuated Aβ42-induced toxicity in a SH-SY5Y cell model [1]. Bavachinin, has potent anti-angiogenic activity in vitro and in vivo. Bavachinin inhibited increases in HIF-1α activity in human KB carcinoma (HeLa cell derivative) and human HOS osteosarcoma cells under hypoxia in a concentration-dependent manner, probably by enhancing the interaction between von Hippel-Lindau (VHL) and HIF-1α [2].in vivo: significantly inhibited Th2 cytokine production, including IL-4, IL-5 and IL-13. Notably, this compound almost completely blocked inflammation in the ovalbumin (OVA)-sensitized animal asthma model [3].
References:
[1]. Chen X, et al. Isobavachalcone and bavachinin from Psoraleae Fructus modulate Aβ42 aggregation process through different mechanisms in vitro. FEBS Lett. 2013 Sep 17;587(18):2930-5.
[2]. Nepal M, et al. Anti-angiogenic and anti-tumor activity of Bavachinin by targeting hypoxia-inducible factor-1α. Eur J Pharmacol. 2012 Sep 15;691(1-3):28-37.
[3]. Chen X, et al. Treatment of allergic inflammation and hyperresponsiveness by a simple compound, Bavachinin, isolated from Chinese herbs. Cell Mol Immunol. 2013 Nov;10(6):497-505.
| Cas No. | 19879-30-2 | SDF | |
| 别名 | 补骨脂二氢黄酮甲醚; 7-O-Methylbavachin; Bavachinin A | ||
| Canonical SMILES | O=C1C[C@@H](C2=CC=C(O)C=C2)OC3=C1C=C(C/C=C(C)/C)C(OC)=C3 | ||
| 分子式 | C21H22O4 | 分子量 | 338.4 |
| 溶解度 | DMF: 50 mg/mL,DMF:PBS (pH 7.2)(1:3): 0.25 mg/mL,DMSO: 30 mg/mL,Ethanol: 20 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 | 2.9551 mL | 14.7754 mL | 29.5508 mL |
| 5 mM | 0.591 mL | 2.9551 mL | 5.9102 mL |
| 10 mM | 0.2955 mL | 1.4775 mL | 2.9551 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。
Bavachinin inhibits cholesterol synthesis enzyme FDFT1 expression via AKT/mTOR/SREBP-2 pathway
Int Immunopharmacol 2020 Nov;88:106865.PMID:32827918DOI:10.1016/j.intimp.2020.106865.
Non-alcoholic fatty liver disease (NAFLD) is a progressive and chronic liver disease. No effective drug is currently approved for the treatment of NAFLD. Traditionally it is thought that pathogenesis of NAFLD develops from some imbalance in lipid control, thereby leading to hepatotoxicity and disease development. Squalene synthase (SQS), encoded by FDFT1, is a key regulator in cholesterol synthesis and thus a potential target for the treatment of NAFLD. Here we could identify Bavachinin, a component from traditional Chinese medicine Fructus Psoraleae (FP), which apparently protects HepaRG cells from palmitic acid induced death, suppressing lipid accumulation and cholesterol synthesis through inhibition of FDFT1 through the AKT/mTOR/SREBP-2 pathway. Over-expression of FDFT1 abolished Bavachinin (BVC) -induced inhibition of cholesterol synthesis. The data presented here suggest that Bavachinin acts as a cholesterol synthesis enzyme inhibitor, and might serve as a drug for treating NAFLD in the future.
Induction of G2/M Cell Cycle Arrest via p38/p21Waf1/Cip1-Dependent Signaling Pathway Activation by Bavachinin in Non-Small-Cell Lung Cancer Cells
Molecules 2021 Aug 25;26(17):5161.PMID:34500594DOI:10.3390/molecules26175161.
Lung cancer is the most commonly diagnosed malignant cancer in the world. Non-small-cell lung cancer (NSCLC) is the major category of lung cancer. Although effective therapies have been administered, for improving the NSCLC patient's survival, the incident rate is still high. Therefore, searching for a good strategy for preventing NSCLC is urgent. Traditional Chinese medicine (TCM) are brilliant materials for cancer chemoprevention, because of their high biological safety and low cost. Bavachinin, which is an active flavanone of Proralea corylifolia L., possesses anti-inflammation, anti-angiogenesis, and anti-cancer activities. The present study's aim was to evaluate the anti-cancer activity of Bavachinin on NSCLC, and its regulating molecular mechanisms. The results exhibited that a dose-dependent decrease in the cell viability and colony formation capacity of three NSCLC cell lines, by Bavachinin, were through G2/M cell cycle arrest induction. Meanwhile, the expression of the G2/M cell cycle regulators, such as cyclin B, p-cdc2Y15, p-cdc2T161, and p-wee1, was suppressed. With the dramatic up-regulation of the cyclin-dependent kinase inhibitor, p21Waf1/Cip1, the expression and association of p21Waf1/Cip1 with the cyclin B/cdc2 complex was observed. Silencing the p21Waf1/Cip1 expression significantly rescued bavachinin-induced G2/M cell accumulation. Furthermore, the expression of p21Waf1/Cip1 mRNA was up-regulated in bavachinin-treated NSCLC cells. In addition, MAPK and AKT signaling were activated in bavachinin-added NSCLC cells. Interestingly, bavachinin-induced p21Waf1/Cip1 expression was repressed after restraint p38 MAPK activation. The inhibition of p38 MAPK activation reversed bavachinin-induced p21Waf1/Cip1 mRNA expression and G2/M cell cycle arrest. Collectively, bavachinin-induced G2/M cell cycle arrest was through the p38 MAPK-mediated p21Waf1/Cip1-dependent signaling pathway in the NSCLC cells.
Bavachinin mitigates DMH induced colon cancer in rats by altering p53/Bcl2/BAX signaling associated with apoptosis
Biotech Histochem 2021 Apr;96(3):179-190.PMID:32664769DOI:10.1080/10520295.2020.1778087.
Bavachinin is a flavanone obtained from the Chinese herb, Fructus Psoraleae. Flavonoids and flavanones are recognized as cancer preventive agents. We investigated the anticancer properties of Bavachinin using a model of dimethylhydrazine (DMH and dextran sodium sulfate (DSS) induced rat colon cancer. We investigated aberrant crypt foci (ACF), hyperplastic lesions, catalase (CAT), superoxide dismutase (SOD) and glutathione (GST) levels in Wistar rats. Expression of cancer biomarkers including IL-6, p53, Bcl2 and BAX was investigated. We found that Bavachinin administered to rats re-established the colonic crypts that were damaged by DMH and prevented progression of the cancer.
Bavachinin Induces G2/M Cell Cycle Arrest and Apoptosis via the ATM/ATR Signaling Pathway in Human Small Cell Lung Cancer and Shows an Antitumor Effect in the Xenograft Model
J Agric Food Chem 2021 Jun 9;69(22):6260-6270.PMID:34043345DOI:10.1021/acs.jafc.1c01657.
Lung cancer is grouped into small cell lung cancer (SCLC) and non-SCLC (NSCLC). SCLC exhibits a poor prognosis, and the current anticancer treatment remains unsatisfactory. Bavachinin, present in the seed of Psoralea corylifolia, shows anti-inflammatory effects, immune modulation, and anticancer potency. This study aims to investigate the antitumor effect of Bavachinin on SCLC and its underlying mechanism. The SCLC cell line H1688 was treated with different concentrations of Bavachinin and showed decreased viability with arrested G2/M and sub-G1 phase cell accumulation at a concentration as low as 25 μM. Expression levels of caspase-3, -8, and -9, as well as Fas, FasL, and Bax, increased with the concentration of Bavachinin. The accumulated sub-G1 cells and annexin V confirmed increasing apoptotic cancer cells after treatment. The accumulated G2/M phase cells with increasing levels of phosphorylated CDC25C, CDC2, ATM/ATR, and CHK2/CHK1 confirmed the arrested cell cycle caused by Bavachinin via a dose-dependent manner. This phenomenon can be reversed by an ATM/ATR inhibitor, caffeine. Following the administration of Bavachinin to xenograft mice with SCLC, the tumor burden decreased without impairing hematologic or hepatorenal functions. Bavachinin induces SCLC apoptosis via intrinsic and extrinsic pathways and causes cancer cell cycle arrest via the ATM/ATR signaling pathway.
A Bavachinin analog, D36, induces cell death by targeting both autophagy and apoptosis pathway in acute myeloid leukemia cells
Cancer Chemother Pharmacol 2022 Sep;90(3):251-265.PMID:35960342DOI:10.1007/s00280-022-04462-y.
Purpose: Acute myeloid leukemia (AML) is an aggressive hematologic malignancy with high mortality, and it is urgent to find new and optimized treatment strategies for AML. In this study, Bavachinin, isolated from Psoralea corylifolia L. exhibiting extensive anti-tumor activity in many solid tumors and a series of its synthesized analogs, were screened for their anti-cancer activity on AML cell lines. Methods: The cell viability of AML cells was measured using CCK-8 assays. Cell apoptosis and cell cycle were detected by flow cytometry. The expression of apoptosis-related protein and autophagy-related protein/gene was detected by western blot, immunofluorescence or RT-PCR. Subcutaneous mice tumor model was used to evaluate the anti-cancer activity of D36 in vivo. Results: D36 robustly induced AML cells death in a dose-dependent manner with the IC50 value of 1.0 μM for HL-60 cells and 0.81 μM for MV4-11 cells at 24 h. D36 activated autophagy by inducing the accumulation of LC3B and promoting the autophagy flux. In addition, D36 triggered the extrinsic apoptosis by upregulating the protein level of FAS, cleaved-caspase 8, cleaved-caspase 3 and cleaved-PARP. D36 also blocked the cell cycle at S phase or G2/M phase in AML cells. In addition, we find that activation of caspase cascade induced apoptosis and meanwhile activated autophagy, autophagy activation in turns contributes to apoptosis. Furthermore, D36 suppressed the tumor growth in HL-60 AML-bearing mice without obvious side effects. Conclusion: This study suggests that D36 is a promising small-molecule for the treatment of acute myeloid leukemia.