Deslanoside
(Synonyms: 去乙酰西地兰; Deacetyllanatoside C; Desacetyllanatoside C) 目录号 : GC38903
A cardiac glycoside
Cas No.:17598-65-1
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
Deslanoside is a cardiac glycoside that has been found in D. lanata.1 It induces ventricular tachycardia in anesthetized dogs when administered intravenously at a dose of 0.18 mg/kg.2 Formulations containing deslanoside have been used in the treatment of congestive heart failure and cardiac arrythmias.
1.Koren, G., and Soldin, S.J.Cardiac glycosidesClin. Lab. Med.7(3)587-606(1987) 2.Ghani, M.F., and Smith, J.R.The effectiveness of magnesium chloride in the treatment of ventricular tachyarrhythmias due to digitalis intoxicationAm. Heart J.88(5)621-626(1974)
| Cas No. | 17598-65-1 | SDF | |
| 别名 | 去乙酰西地兰; Deacetyllanatoside C; Desacetyllanatoside C | ||
| 分子式 | C47H74O19 | 分子量 | 943.08 |
| 溶解度 | DMSO: 100 mg/mL (106.04 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 | 1.0604 mL | 5.3018 mL | 10.6036 mL |
| 5 mM | 0.2121 mL | 1.0604 mL | 2.1207 mL |
| 10 mM | 0.106 mL | 0.5302 mL | 1.0604 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。
The Cardiac Glycoside Deslanoside Exerts Anticancer Activity in Prostate Cancer Cells by Modulating Multiple Signaling Pathways
Cancers (Basel) 2021 Nov 19;13(22):5809.PMID:34830961DOI:10.3390/cancers13225809.
Prostate cancer (PCa) is a leading cause of cancer-related deaths among men worldwide, and novel therapies for advanced PCa are urgently needed. Cardiac glycosides represent an attractive group of candidates for anticancer repurposing, but the cardiac glycoside Deslanoside has not been tested for potential anticancer activity so far. We found that Deslanoside effectively inhibited colony formation in vitro and tumor growth in nude mice of PCa cell lines 22Rv1, PC-3, and DU 145. Such an anticancer activity was mediated by both the cell cycle arrest at G2/M and the induction of apoptosis, as demonstrated by different functional assays and the expression status of regulatory proteins of cell cycle and apoptosis in cultured cells. Moreover, Deslanoside suppressed the invasion and migration of PCa cell lines. Genome-wide expression profiling and bioinformatic analyses revealed that 130 genes were either upregulated or downregulated by Deslanoside in both 22Rv1 and PC-3 cell lines. These genes enriched multiple cellular processes, such as response to steroid hormones, regulation of lipid metabolism, epithelial cell proliferation and its regulation, and negative regulation of cell migration. They also enriched multiple signaling pathways, such as necroptosis, MAPK, NOD-like receptor, and focal adhesion. Survival analyses of the 130 genes in the TCGA PCa database revealed that 10 of the deslanoside-downregulated genes (ITG2B, CNIH2, FBF1, PABPC1L, MMP11, DUSP9, TMEM121, SOX18, CMPK2, and MAMDC4) inversely correlated, while one deslanoside-upregulated gene (RASD1) positively correlated, with disease-free survival in PCa patients. In addition, one deslanoside-downregulated gene (ENG) inversely correlated, while three upregulated genes (JUN, MXD1, and AQP3) positively correlated with overall survival in PCa patients. Some of the 15 genes have not been implicated in cancer before. These findings provide another candidate for repurposing cardiac glycosides for anticancer drugs. They also suggest that a diverse range of molecular events underlie Deslanoside's anticancer activity in PCa cells.
Interaction of serotonin and Deslanoside on cardiac rhythm in the cat
Eur J Pharmacol 1978 Sep 15;51(2):167-77.PMID:699982DOI:10.1016/0014-2999(78)90341-2.
The present study was performed to determine whether increases in the tissue content of serotonin creatinine SO4 in the periphery would influence the arrhythmogenic effect of Deslanoside. This was accomplished by infusing serotonin into anesthetized cats exposed to a subarrhythmic dose of Deslanoside, determining doses of Deslanoside required to produce ventricular tachycardia and ventricular fibrillation, and determining ventricular pacemaker rate (obtained during vagal-induced sinus node suppression). It was found that animals receiving serotonin creatinine SO4 plus Deslanoside exhibited a greater increase in ventricular rate during sinus node suppression than with 5-HT infusion alone. No corresponding increase in ventricular pacemaker rate during sinus node suppression was observed with creatinine SO4 plus Deslanoside. In addition, the dose of Deslanoside to produce ventricular fibrillation in these animals was significantly correlated with the increase in ventricular pacemaker rate seen during th 5-HT infusion in the presence of Deslanoside. Studies were also performed to determine whether the arrhythmogenic interaction of serotonin with Deslanoside was associated with alterations in either cardiac tissue, blood or plasma levels of serotonin and 5-hydroxyindoleacetic acid. The data revealed a significant correlation between serotonin content in the left ventricle and the dose of Deslanoside required to produce ventricular fibrillation. These results suggest that exogenous serotonin interacts with Deslanoside to enhance the arrhythmogenic action of Deslanoside.
Characteristics of deslanoside-induced modulation on jejunal contractility
World J Gastroenterol 2012 Nov 7;18(41):5889-96.PMID:23139604DOI:10.3748/wjg.v18.i41.5889.
Aim: To characterize the dual effects of Deslanoside on the contractility of jejunal smooth muscle. Methods: Eight pairs of different low and high contractile states of isolated jejunal smooth muscle fragment (JSMF) were established. Contractile amplitude of JSMF in different low and high contractile states was selected to determine the effects of Deslanoside, and Western blotting analysis was performed to measure the effects of Deslanoside on myosin phosphorylation of jejunal smooth muscle. Results: Stimulatory effects on the contractility of JSMF were induced (45.3% ± 4.0% vs 87.0% ± 7.8%, P < 0.01) by Deslanoside in 8 low contractile states, and inhibitory effects were induced (180.6% ± 17.8% vs 109.9% ± 10.8%, P < 0.01) on the contractility of JSMF in 8 high contractile states. The effect of Deslanoside on the phosphorylation of myosin light chain of JSMF in low (78.1% ± 4.1% vs 96.0% ± 8.1%, P < 0.01) and high contractile state (139.2% ± 8.5% vs 105.5 ± 7.34, P < 0.01) was also bidirectional. Bidirectional regulation (BR) was abolished in the presence of tetrodotoxin. Deslanoside did not affect jejunal contractility pretreated with the Ca(2+) channel blocker verapamil or in a Ca(2+)-free assay condition. The stimulatory effect of Deslanoside on JSMF in a low contractile state (low Ca(2+) induced) was abolished by atropine. The inhibitory effect of Deslanoside on jejunal contractility in a high contractile state (high Ca(2+) induced) was blocked by phentolamine, propranolol and L-NG-nitro-arginine, respectively. Conclusion: Deslanoside-induced BR is Ca(2+) dependent and is related to cholinergic and adrenergic systems when JSMF is in low or high contractile states.
Antagonism of deslanoside-induced cardiotoxicity by combined nicotinic and muscarinic blockade of autonomic ganglia
J Pharmacol Exp Ther 1975 Oct;195(1):126-32.PMID:241837doi
The effect of ganglionic blockade on cardiotoxicity induced by Deslanoside (25 mug/kg i.v. at 15-minute intervals) was evaluated in Dial-urethane anesthetized cats. Electrocardiogram, blood pressure and pre- and postganglionic cardiac sympathetic nerve recordings were monitored. When Deslanoside was given to control animals, 150 +/- 8.2 and 179 +/- 11.9 mug/kg produced ventricular tachycardia and ventricular fibrillation, respectively. Pretreatment of cats with either hexamethonium or atropine alone did not influence the doses of Deslanoside required to produce ventricular tachycardia or ventricular fibrillation. However, pretreatment with the combination of hexamethonium and atropine significantly increased the dose of Deslanoside needed to produce ventricular tachycardia (181 +/- 12.3 mug/kg) and ventricular fibrillation (219 +/- 12.3 mug/kg). Furthermore, administration of atropine to hexamethonium-pretreated cats intoxicated with Deslanoside decreased deslanoside-induced postganglionic nerve activity. These results indicate that blockade of both nicotinic and muscarinic ganglionic transmission is essential for a protective influence against cardiotoxicity induced by Deslanoside.
Effect of in vivo Deslanoside on the uptake of serotonin into platelets
Arch Int Pharmacodyn Ther 1979 Nov;242(1):44-9.PMID:543748doi
The purpose of our study was to determine whether Deslanoside administered in vivo results in inhibition of the active transport of [3H]-serotonin into blood platelets. Experiments were performed in cats and arterial blood samples were taken prior to initiating Deslanoside infusion and at the point when it appeared from the ECG that ventricular fibrillation was imminent. Toxic arrhythmogenic doses of Deslanoside were found to produce a significant reduction in the uptake of [3H]-serotonin into platelets. This increase in free serotonin in plasma caused by inhibition of uptake may play a role in the cardiotoxicity of Deslanoside.