Withanolide B
(Synonyms: 睡茄素B) 目录号 : GC45158
A withanolide
Cas No.:56973-41-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Withanolide B is a withanolide that has been found in W. somnifera. Unlike withanolide A, it does not increase glucose uptake in L6 myotubes. In in silico docking studies, withanolide B was identified as a neuronal nitric oxide synthase (nNOS) inhibitor (Ki = 5.15 nM), that also inhibited inducible NOS (iNOS) and endothelial NOS (eNOS; Kis = 15.48 and 66.59 nM, respectively), and as a ligand for the PARP1 catalytic domain with an estimated Ki value of 7.54 nM.
| Cas No. | 56973-41-2 | SDF | |
| 别名 | 睡茄素B | ||
| Canonical SMILES | O=C1[C@@]2(C)[C@]([C@@H](O3)[C@@H]3[C@]4([H])[C@]2([H])CC[C@@]5(C)[C@@]4([H])CC[C@@H]5[C@H](C)[C@@]6(OC(C(C)=C(C)C6)=O)[H])(O)CC=C1 | ||
| 分子式 | C28H38O5 | 分子量 | 454.6 |
| 溶解度 | Acetonitrile: 0.1 mg/ml,Methanol: 0.5 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 | 2.1997 mL | 10.9987 mL | 21.9974 mL |
| 5 mM | 0.4399 mL | 2.1997 mL | 4.3995 mL |
| 10 mM | 0.22 mL | 1.0999 mL | 2.1997 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。
Ashwagandha in brain disorders: A review of recent developments
J Ethnopharmacol 2020 Jul 15;257:112876.PMID:32305638DOI:10.1016/j.jep.2020.112876.
Ethnopharmacological relevance: Withania somnifera (Family: Solanaceae), commonly known as Ashwagandha or Indian ginseng is distributed widely in India, Nepal, China and Yemen. The roots of plant consist of active phytoconstituents mainly withanolides, alkaloids and sitoindosides and are conventionally used for the treatment of multiple brain disorders. Aim of the review: This review aims to critically assess and summarize the current state and implication of Ashwagandha in brain disorders. We have mainly focussed on the reported neuroactive phytoconstituents, available marketed products, pharmacological studies, mechanism of action and recent patents published related to neuroprotective effects of Ashwagandha in brain disorders. Materials and methods: All the information and data was collected on Ashwagandha using keywords "Ashwagandha" along with "Phytoconstituents", "Ayurvedic, Unani and Homeopathy marketed formulation", "Brain disorders", "Mechanism" and "Patents". Following sources were searched for data collection: electronic scientific databases such as Science Direct, Google Scholar, Elsevier, PubMed, Wiley On-line Library, Taylor and Francis, Springer; books such as AYUSH Pharmacopoeia; authentic textbooks and formularies. Results: Identified neuroprotective phytoconstituents of Ashwagandha are sitoindosides VII-X, withaferin A, withanosides IV, withanols, withanolide A, Withanolide B, anaferine, beta-sitosterol, withanolide D with key pharmacological effects in brain disorders mainly anxiety, Alzheimer's, Parkinson's, Schizophrenia, Huntington's disease, dyslexia, depression, autism, addiction, amyotrophic lateral sclerosis, attention deficit hyperactivity disorder and bipolar disorders. The literature survey does not highlight any toxic effects of Ashwagandha. Further, multiple available marketed products and patents recognized its beneficial role in various brain disorders; however, very few data is available on mechanistic pathway and clinical studies of Ashwagandha for various brain disorders is scarce and not promising. Conclusion: The review concludes the results of recent studies on Ashwagandha suggesting its extensive potential as neuroprotective in various brain disorders as supported by preclinical studies, clinical trials and published patents. However vague understanding of the mechanistic pathways involved in imparting the neuroprotective effect of Ashwagandha warrants further study to promote it as a promising drug candidate.
Withanolide B promotes osteogenic differentiation of human bone marrow mesenchymal stem cells via ERK1/2 and Wnt/β-catenin signaling pathways
Int Immunopharmacol 2020 Nov;88:106960.PMID:32919219DOI:10.1016/j.intimp.2020.106960.
Background: The treatment of bone defects has always been a problem for clinicians. In recent years, research on human bone mesenchymal stem cells (hBMSCs) has found that promoting their osteogenic differentiation could be a useful therapeutic strategy for bone healing. Previous studies have been reported that Withania somnifera Dunal inhibits osteoclastogenesis by inhibiting the NF-κB signaling pathway. Withanolide B is an active component of W. somnifera Dunal, but its role in osteogenic differentiation of hBMSCs remains unknown. Here, we performed a preliminary study on the role of Withanolide B in promoting osteogenic differentiation and its possible mechanism. Methods: We investigated the effect of Withanolide B on osteogenic differentiation of hBMSCs in vitro and in vivo. The effect of Withanolide B on the activity of hBMSCs was verified by CCK-8 assay and quantitative Real-time polymerase chain reaction (qPCR) and Western blotting analysis were used to verify the effect of Withanolide B on osteogenic differentiation-specific genes and proteins. The effect of Withanolide B on ALP activity and mineral deposition was verified by ALP and ARS staining. We then used a rat tibial osteotomy model to observe the effect of Withanolide B on bone healing. Results: Withanolide B is noncytotoxic to hBMSCs and can effectively promote their osteogenic differentiation. Moreover, we found that Withanolide B can regulate the osteogenic differentiation of hBMSCs through the ERK1/2 and Wnt/β-catenin signaling pathways. When inhibitors of the ERK1/2 and Wnt/β-catenin signaling pathways were used, the enhancement of osteogenic differentiation induced by Withanolide B was attenuated. Withanolide B also effectively promoted bone healing in the rat tibial osteotomy model. Conclusions: Our results suggest that Withanolide B can promote the osteogenic differentiation of hBMSCs through the ERK1/2 and Wnt/β-catenin signaling pathways and can effectively promote bone defect healing.
Comparisons of the pharmacokinetic and tissue distribution profiles of Withanolide B after intragastric administration of the effective part of Datura metel L. in normal and psoriasis guinea pigs
J Chromatogr B Analyt Technol Biomed Life Sci 2018 Apr 15;1083:284-288.PMID:29574380DOI:10.1016/j.jchromb.2018.02.022.
A simple, highly sensitive ultra-performance liquid chromatography- electrospray ionization-mass spectrometry (LC-ESI-MS) method has been developed to quantify of Withanolide B and obakunone (IS) in guinea pig plasma and tissues, and to compare the pharmacokinetics and tissue distribution of Withanolide B in normal and psoriasis guinea pigs. After mixing with IS, plasma and tissues were pretreated by protein precipitation with methanol. Chromatographic separation was performed on a C18 column using aqueous (0.1% formic acid) and acetonitrile (0.1% formic acid) solutions at 0.4 mL/min as the mobile phase. The gradient program was selected (0-4.0 min, 2-98% B; 4.0-4.5 min, 98-2% B; and 4.5-5 min, 2% B). Detection was performed on a 4000 QTRAP UPLC-ESI-MS/MS system from AB Sciex in the multiple reaction monitoring (MRM) mode. Withanolide B and obakunone (IS) were monitored under positive ionization conditions. The optimized mass transition ion-pairs (m/z) for quantitation were 455.1/109.4 for Withanolide B and 455.1/161.1 for obakunone.
Withanolide Z, a new chlorinated withanolide from Withania somnifera
Planta Med 2008 Nov;74(14):1745-8.PMID:18988152DOI:10.1055/s-2008-1081357.
Reverse-phase preparative HPLC analysis of the n-butanol fraction of the methanolic extract of Withania somnifera Dunal (leaves) afforded a novel chlorinated withanolide, namely withanolide Z (1), along with four known withanolides, Withanolide B (2), withanolide A (3), 27-hydroxywithanolide B (4) and withaferin A (5). Their structures were elucidated by IR, MS, CD and a combination of 1 D and 2 D NMR spectral analyses. The Leishmania donovani DNA topoisomerase I inhibitory activities of the isolated compounds were determined.
Improving the inhibition of β-amyloid aggregation by withanolide and withanoside derivatives
Int J Biol Macromol 2021 Mar 15;173:56-65.PMID:33465364DOI:10.1016/j.ijbiomac.2021.01.094.
Here, we have studied the ameliorative effects of Withania somnifera derivatives (Withanolide A, Withanolide B, Withanoside IV, and Withanoside V) on the fibril formation of amyloid-β 42 for Alzheimer's disease. We analyzed reduction in the aggregation of β amyloid protein with these Ashwagandha derivatives by Thioflavin T assay in the oligomeric and fibrillar state. We have tested the cytotoxic activity of these compounds against human SK-N-SH cell line for 48 h, and the IC 50 value found to be 28.61 ± 2.91, 14.84 ± 1.45, 18.76 ± 0.76 and 30.14 ± 2.59 μM, respectively. After the treatment of the cells with half the concentration of IC 50 value, there was a remarkable decrease in the number of apoptotic cells stained by TUNEL assay indicating the DNA damage and also observed significant decrease of reactive oxygen species. Also, the binding and molecular stability of these derivatives with amyloid β was also studied using bioinformatics tools where these molecules were interacted at LVFFA region which is inhibition site of amyloid-β1 42. These studies revealed that the Withanolides and Withanosides interact with the hydrophobic core of amyloid-β 1-42 in the oligomeric stage, preventing further interaction with the monomers and diminishing aggregation.