Beta-Eudesmol
(Synonyms: β-桉叶醇) 目录号 : GC35501
A sesquiterpene with diverse biological activities
Cas No.:473-15-4
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
β-Eudesmol is a sesquiterpene that has been found in a variety of plants, including Cannabis, and has diverse biological activities.1,2 It is a noncompetitive antagonist of nicotinic acetylcholine receptors (nAChRs) that decreases the open time and opening frequency of nAChR channels when used at concentrations of 40 and 80 ?M and increases the decay phase of depolarization when used at a concentration of 100 ?M in isolated mouse diaphragm muscle.3 β-Eudesmol (50-100 ?M) inhibits VEGF- and bFGF-induced proliferation in human umbilical vein endothelial cells (HUVECs).4 It also inhibits proliferation of HeLa, SGC-7901, and BEL-7402 cells when used at concentrations ranging from 10 to 100 ?M and reduces tumor growth in H22 and S-180 mouse tumor models when administered at doses ranging from 2.5 to 5 mg/kg. β-Eudesmol is an agonist of the transient receptor potential (TRP) receptor subtypes TRPA1, TRPV3, and TRPM8 and increases food intake and plasma levels of ghrelin in rats.5,6
1.Elzinga, S., Fischedick, J., Podkolinski, R., et al.Cannabinoids and terpenes as chemotaxonomic markers in CannabisNat. Prod. Chem. Res.3(4)181(2015) 2.Kimura, I.Medical benefits of using natural compounds and their derivatives having multiple pharmacological actionsYakugaku Zasshi126(3)133-143(2006) 3.Kimura, M., Nojima, H., Muroi, M., et al.Mechanism of the blocking action of β-eudesmol on the nicotinic acetylcholine receptor channel in mouse skeletal musclesNeuropharmacology30(8)835-841(1991) 4.Ma, E.L., Li, Y.C., Tsuneki, H., et al.β-Eudesmol suppresses tumour growth through inhibition of tumour neovascularisation and tumour cell proliferationJ. Asian Nat. Prod. Res.10(1-2)159-167(2008) 5.Ohara, K., Fukada, T., Okada, H., et al.Identification of significant amino acids in multiple transmembrane domains of human transient receptor potential ankyrin 1 (TRPA1) for activation by eudesmol, an oxygenized sesquiterpene in hop essential oilJ. Biol. Chem.290(5)3161-3171(2015) 6.Ohara, K., Fukuda, T., Ishida, Y., et al.β-Eudesmol, an oxygenized sesquiterpene, stimulates appetite via TRPA1 and the autonomic nervous systemSci. Rep.7(1)15785(2017)
| Cas No. | 473-15-4 | SDF | |
| 别名 | β-桉叶醇 | ||
| Canonical SMILES | C[C@]12[C@@](C(CCC2)=C)([H])C[C@H](C(C)(O)C)CC1 | ||
| 分子式 | C15H26O | 分子量 | 222.37 |
| 溶解度 | DMSO : 100 mg/mL (449.70 mM; Need ultrasonic); H2O : < 0.1 mg/mL (insoluble) | 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。 |
||
| 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 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 4.497 mL | 22.485 mL | 44.9701 mL |
| 5 mM | 0.8994 mL | 4.497 mL | 8.994 mL |
| 10 mM | 0.4497 mL | 2.2485 mL | 4.497 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。
Anti-angiogenic effects of Beta-Eudesmol and atractylodin in developing zebrafish embryos
Comp Biochem Physiol C Toxicol Pharmacol 2021 May;243:108980.PMID:33493664DOI:10.1016/j.cbpc.2021.108980.
Angiogenesis is the process of formation of new blood vessels which plays an essential role in the normal physiological development of the organs and systems. Several factors contribute to and regulate this process. Unregulated angiogenesis, however, is harmful and is usually found in tumors and cancerous cells. β-Eudesmol and atractylodin are sesquiterpenoid contents extracted from the rhizome of Atractylodes lancea (AL). Reports suggest potential anti-angiogenic activities of both compounds. In this study, the anti-angiogenic activities of both compounds were investigated using the well-established zebrafish in vivo model. Zebrafish embryos were treated with a series of concentrations (6.3, 12.5, 25, and 50 μM) of β-eudesmol and (6.3, 12.5, and 25 μM) of atractylodin up to 72 h post-fertilization. Assessment of the effects on phenotypic blood vessel development (sub-intestinal vessel intersection count) revealed that both the compounds inhibited vessel development, particularly at higher concentrations. At the genetic levels, only β-eudesmol significantly downregulated the expression of the Vegfaa gene and also its receptor Vegfr2. β-Eudesmol also affected the expression of Vegfaa protein in a concentration-dependent manner. Results indicate that β-eudesmol exerts anti-angiogenic property through inhibition of Vegfaa at both the gene and protein levels. However, atractylodin does not possess this property.
Beta-Eudesmol suppresses tumour growth through inhibition of tumour neovascularisation and tumour cell proliferation
J Asian Nat Prod Res 2008 Jan-Feb;10(1-2):159-67.PMID:18253884DOI:10.1080/10286020701394332.
In the present study, we investigated the potential anti-angiogenic mechanism and anti-tumour activity of Beta-Eudesmol using in vitro and in vivo experimental models. Proliferation of human umbilical vein endothelial cells (HUVEC) stimulated with vascular endothelial growth factor (VEGF, 30 ng/ml) and basic fibroblast growth factor (bFGF, 30 ng/ml) was significantly inhibited by Beta-Eudesmol (50-100 microM). Beta-Eudesmol (100 microM) also blocked the phosphorylation of cAMP response element binding protein (CREB) induced by VEGF (30 ng/ml) in HUVEC. Beta-Eudesmol (10-100 microM) inhibited proliferation of HeLa, SGC-7901, and BEL-7402 tumour cells in a time- and dose-dependent manner. Moreover, Beta-Eudesmol treatment (2.5-5 mg/kg) significantly inhibited growth of H(22) and S(180) mouse tumour in vivo. These results indicated that Beta-Eudesmol inhibited angiogenesis by suppressing CREB activation in growth factor signalling pathway. This is the first study to demonstrate that Beta-Eudesmol is an inhibitor of tumour growth.
Beta-Eudesmol induces neurite outgrowth in rat pheochromocytoma cells accompanied by an activation of mitogen-activated protein kinase
J Pharmacol Exp Ther 2002 Jun;301(3):803-11.PMID:12023507DOI:10.1124/jpet.301.3.803.
Beta-Eudesmol, a sesquiterpenoid isolated from "So-jutsu" (Atractylodis lanceae rhizomas), is known to have various unique effects on the nervous system. We examined in detail the mechanism by which Beta-Eudesmol modified neuronal function using rat pheochromocytoma cells (PC-12). Beta-Eudesmol at concentrations of 100 and 150 microM significantly induced neurite extension in PC-12 cells, which was accompanied, at the highest concentration, by suppression of [(3)H]thymidine incorporation. Beta-Eudesmol at concentrations of 100 and 150 microM also evoked a significant increase in intracellular Ca(2+) concentration ([Ca(2+)](i)) in these cells, as determined by the fura 2 assay. Much of this increase remained even after the extracellular Ca(2+) was chelated by EGTA. The [Ca(2+)](i) increase induced by Beta-Eudesmol was partially inhibited by the phosphoinositide-specific phospholipase C (PI-PLC) inhibitor 1-[6-[[17beta-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione (U-73122) (2 microM) under extracellular Ca(2+)-free conditions. Furthermore, Beta-Eudesmol, in a concentration-dependent fashion, caused an accumulation of inositol phosphates. Beta-Eudesmol (150 microM) promoted phosphorylation of both mitogen-activated protein kinase (MAPK) and cAMP-responsive element binding protein in a time-dependent manner. These phosphorylations were suppressed by the MAPK kinase inhibitor 2-(2'-amino-3'-methoxyphenol)-oxanaphthalen-4-one (PD98059) (50 microM), U-73122 (2 microM), the calmodulin inhibitor N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide hydrochloride (W7) (1-10 microM), and the protein kinase A inhibitor N-[2-(4-bromocinnamylamino)ethyl]-5-isoquinoline (H89) (1-10 microM). Beta-eudesmol-induced neurite extension was significantly inhibited by both U-73122 (2 microM) and PD98059 (30 microM), suggesting the involvement of PI-PLC and MAPK in neurite outgrowth. Beta-Eudesmol, being a small molecule, may therefore be a promising lead compound for potentiating neuronal function. Furthermore, the drug may be useful in helping to clarify the mechanisms underlying neuronal differentiation.
Antiangiogenic activity of Beta-Eudesmol in vitro and in vivo
Eur J Pharmacol 2005 Apr 11;512(2-3):105-15.PMID:15840394DOI:10.1016/j.ejphar.2005.02.035.
Abnormal angiogenesis is implicated in various diseases including cancer and diabetic retinopathy. In this study, we examined the effect of Beta-Eudesmol, a sesquiterpenoid alcohol isolated from Atractylodes lancea rhizome, on angiogenesis in vitro and in vivo. Proliferation of porcine brain microvascular endothelial cells and human umbilical vein endothelial cells (HUVEC) was inhibited by Beta-Eudesmol (50-100 microM). It also inhibited the HUVEC migration stimulated by basic fibroblast growth factor (bFGF) and the tube formation by HUVEC in Matrigel. Beta-Eudesmol (100 microM) blocked the phosphorylation of extracellular signal-regulated kinase (ERK) 1/2 induced by bFGF or vascular endothelial growth factor. Furthermore, Beta-Eudesmol significantly inhibited angiogenesis in subcutaneously implanted Matrigel plugs in mice and in adjuvant-induced granuloma in mice. These results indicate that Beta-Eudesmol inhibits angiogenesis, at least in part, through the blockade of the ERK signaling pathway. We considered that Beta-Eudesmol may aid the development of drugs to treat angiogenic diseases.
Mechanism of the blocking action of Beta-Eudesmol on the nicotinic acetylcholine receptor channel in mouse skeletal muscles
Neuropharmacology 1991 Aug;30(8):835-41.PMID:1780041DOI:10.1016/0028-3908(91)90117-t.
Beta-Eudesmol, an uncharged alcohol contained in Atractylodes lancea, blocks the neuromuscular junction. Atractylodes lancea is prescribed in a traditional Chinese medicine and plays a main role for "alleviation of pain in skeletal muscle". By using the cell-attached patch-clamp or conventional intracellular technique, the site of action of Beta-Eudesmol on the nicotinic acetylcholine (ACh) receptor (nAChR) channel in skeletal muscle of the adult mouse, was investigated and compared with that of different types of blockers of the nicotinic ACh receptor channel (bupivacaine, chlorpromazine and phencyclidine). Beta-Eudesmol (200 microM) depressed completely the nerve-evoked twitch tension and reduced the amplitude and quantal size of endplate potentials but did not alter either the quantal content, resting membrane potential or action potential. Beta-Eudesmol (100-200 microM) decreased the amplitude of ACh potentials and accelerated the slow decay of depolarization, induced by the continuous application of ACh. Beta-Eudesmol (40 microM) and phencyclidine (10 microM) decreased both the open time and opening frequency, without affecting the single channel conductance. Bupivacaine (10 microM) decreased only the open time. Chlorpromazine (10 microM) decreased only the opening frequency. These results indicate that the blocking effect of Beta-Eudesmol on nerve-evoked contraction, was due to blockade of nicotinic ACh receptor channels at the neuromuscular junction. Like phencyclidine, Beta-Eudesmol blocked the nicotinic ACh receptor channel in both the open and closed conformations, and accelerated the desensitization of the nicotinic ACh receptor.