S-Adenosyl-L-methionine disulfate tosylate
(Synonyms: S-腺苷-L-甲硫氨酸; Ademetionine disulfate tosylate; S-Adenosyl methionine disulfate tosylate; AdoMet disulfate tosylate) 目录号 : GC30843
S-Adenosyl-L-methionine disulfate tosylate是一种甲基供体和辅因子，它参与多种生物过程，包括表观遗传调控、蛋白质的翻译后修饰和代谢。
Cas No.:97540-22-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Cell experiment [1]: | |
Cell lines | Cal-33 and JHU-SCC-011 cells |
Preparation Method | Cal-33 and JHU-SCC-011 cells were treated with 300 μM S-Adenosyl-L-methionine disulfate tosylate and the cells were harvested after 24 and 48 hours, respectively, for flow cytometry and western blot analysis. |
Reaction Conditions | 300μM, 24h or 48h |
Applications | S-Adenosyl-L-methionine disulfate tosylate can regulate the cell cycle progression of Cal-33 and JHU-SCC-011 cells and reduce the expression of cyclins B1, E1 and D1. |
| Animal experiment [2]: | |
Animal models | Pentylenetetrazole (PTZ)-induced kindling model in rats |
Preparation Method | Out of 48 rats, 24 rats were used for standardization of the pentylenetetrazole (PTZ) kindling model. The remaining 24 rats were divided into 4 groups with 6 rats in each group as follows: 1. disease control: 0.9% normal saline 1 ml intraperitoneally (ip) + PTZ 35 mg/kg ip; 2. positive control: sodium valproate 200 mg/kg ip + PTZ 35 mg/kg ip; 3. S-Adenosyl-L-methionine disulfate tosylate 50 mg/kg oral + PTZ 35 mg/kg ip; 4. S-Adenosyl-L-methionine disulfate tosylate 100 mg/kg oral+ PTZ 35 mg/kg ip. |
Dosage form | 50 and 100 mg/kg, oral |
Applications | A higher dose of S-Adenosyl-L-methionine disulfate tosylate (100 mg/kg) exhibited an increase in seizure latency and a decrease in seizure severity score. |
References: [1] Mosca L, Minopoli M, Pagano M, Vitiello F, Carriero MV, Cacciapuoti G, Porcelli M. Effects of S-adenosyl-L-methionine on the invasion and migration of head and neck squamous cancer cells and analysis of the underlying mechanisms. Int J Oncol. 2020 May;56(5):1212-1224. [2] Dhediya RM, Joshi SS, Gajbhiye SV, Jalgaonkar SV, Biswas M. Evaluation of antiepileptic effect of S-adenosyl methionine and its role in memory impairment in pentylenetetrazole-induced kindling model in rats. Epilepsy Behav. 2016 Aug;61:153-157. | |
S-Adenosyl-L-methionine disulfate tosylate is a methyl donor and cofactor. It is involved in a variety of biological processes, including epigenetic regulation, post-translational modification of proteins and metabolism. Preparations containing S-Adenosyl-L-methionine disulfate tosylate have been used as dietary supplements. S-Adenosyl-L-methionine disulfate tosylate also exhibits antiproliferative, pro-apoptotic and anti-metastatic effects in human cancers[1-2].
S-Adenosyl-L-methionine disulfate tosylate (300 μM) can regulate the cell cycle progression of Cal-33 and JHU-SCC-011 cells and reduce the expression of cyclins B1, E1, and D1. S-Adenosyl-L-methionine disulfate tosylate (200 μM and 300 μM) can inhibit the migration of Cal-33 and JHU-SCC-011 cells in a dose-dependent manner after 24 hours and 48 hours, respectively[2]. The combination of 5‑fluorouracil (5-FU) with 5-Adenosyl-L-methionine disulfate tosylate at 5-40 μg/ml can protect the anticancer effect of 5-FU by regulating the expression of DNA methyltransferases (DNMTs)[3].
In the elevated plus maze test, rats given S-Adenosyl-L-methionine disulfate tosylate (100 mg/kg) showed the greatest reduction in transfer latency at day 26, confirming the memory-improving effect of S-Adenosyl-L-methionine disulfate tosylate. Animals treated with 100 mg/kg S-Adenosyl-L-methionine disulfate tosylate showed decreased malondialdehyde and increased glutathione levels, suggesting that S-Adenosyl-L-methionine disulfate tosylate has antioxidant properties in the PTZ-induced rat model. The antioxidant properties of S-Adenosyl-L-methionine disulfate tosylate may improve cognitive impairment caused by oxidative stressl[4]. S-Adenosyl-L-methionine disulfate tosylate (30 mg/kg) can prevent autism spectrum disorder (ASD)-like behaviors caused by early postnatal valproic acid treatment in rat pups[5].
References:
[1] Loenen, W.A.M.S-Adenosylmethionine: Jack of all trades and master of everything?Biochem. Soc. Trans.34(2)330-333(2006).
[2] Mosca L, Minopoli M, Pagano M, Vitiello F, Carriero MV, Cacciapuoti G, Porcelli M. Effects of S-adenosyl-L-methionine on the invasion and migration of head and neck squamous cancer cells and analysis of the underlying mechanisms. Int J Oncol. 2020 May;56(5):1212-1224.
[3] Ham MS, et al. S-adenosyl methionine specifically protects the anticancer effect of 5-FU via DNMTs expression in human A549 lung cancer cells. Mol Clin Oncol. 2013 Mar;1(2):373-378.
[4] Dhediya RM, Joshi SS, Gajbhiye SV, Jalgaonkar SV, Biswas M. Evaluation of antiepileptic effect of S-adenosyl methionine and its role in memory impairment in pentylenetetrazole-induced kindling model in rats. Epilepsy Behav. 2016 Aug;61:153-157.
[5] Ornoy A, et al. S-adenosyl methionine prevents ASD like behaviors triggered by early postnatal valproic acid exposure in very young mice. Neurotoxicol Teratol. 2019 Jan-Feb;71:64-74.
S-Adenosyl-L-methionine disulfate tosylate是一种甲基供体和辅因子，它参与多种生物过程，包括表观遗传调控、蛋白质的翻译后修饰和代谢。含有S-Adenosyl-L-methionine disulfate tosylate的制剂已被用作膳食补充剂。S-Adenosyl-L-methionine disulfate tosylate还在人类癌症中表现出抗增殖、促凋亡和抗转移作用[1-2]。
S-Adenosyl-L-methionine disulfate tosylate（300μM）能够调节 Cal-33和JHU-SCC-011细胞周期进程，降低细胞周期蛋白B1、E1和D1的表达。S-Adenosyl-L-methionine disulfate tosylate（200 μM和300 μM）能够分别在24小时和48小时后以剂量依赖性方式抑制Cal-33和JHU-SCC-011细胞迁移[2]。5-40 μg/ ml的S-Adenosyl-L-methionine disulfate tosylate与5-氟尿嘧啶（5-FU）联合使用，可通过调节DNA甲基转移酶（DNMTs）的表达保护5-FU的抗癌作用[3]。
在高架十字迷宫测试中，给予S-Adenosyl-L-methionine disulfate tosylate（100 mg/kg）的大鼠在第26天时表现出最大程度的转移潜伏期缩短，证实了S-Adenosyl-L-methionine disulfate tosylate的记忆改善作用。使用100 mg/kg S-Adenosyl-L-methionine disulfate tosylate处理的动物表现出丙二醛减少和谷胱甘肽水平升高，这表明在PTZ诱导的大鼠模型中S-Adenosyl-L-methionine disulfate tosylate具有抗氧化特性，而S-Adenosyl-L-methionine disulfate tosylate的抗氧化特性可能会改善氧化应激导致的认知障碍[4]。S-Adenosyl-L-methionine disulfate tosylate（30 mg/kg）可预防幼鼠出生后早期丙戊酸处理引起的自闭症谱系障碍（ASD）样行为[5]。
| Cas No. | 97540-22-2 | SDF | |
| 别名 | S-腺苷-L-甲硫氨酸; Ademetionine disulfate tosylate; S-Adenosyl methionine disulfate tosylate; AdoMet disulfate tosylate | ||
| Canonical SMILES | N[C@@H](CC[S+](C[C@@H]1[C@H]([C@H]([C@H](N2C=NC3=C2N=CN=C3N)O1)O)O)C)C(O)=O.O=S(O)([O-])=O.O=S(O)(O)=O.OS(=O)(C4=CC=C(C)C=C4)=O | ||
| 分子式 | C22H34N6O16S4 | 分子量 | 766.8 |
| 溶解度 | DMSO : ≥ 50 mg/mL (65.21 mM);Water : 33.33 mg/mL (43.47 mM) | 储存条件 | Store at -20°C,protect from light, stored under nitrogen |
| 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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| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.3041 mL | 6.5206 mL | 13.0412 mL |
| 5 mM | 0.2608 mL | 1.3041 mL | 2.6082 mL |
| 10 mM | 0.1304 mL | 0.6521 mL | 1.3041 mL |
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动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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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，
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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。
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Protective effect of S-adenosyl-L-methionine against CCl4-induced hepatotoxicity in cultured hepatocytes
Effect of S-adenosyl-L-methionine disulfate tosylate salt (SAMe-ST) and L-methionine (L-Met) on primary cultured rat hepatocytes were studied. In cultured hepatocytes treated with CCl4, SAMe-ST and L-Met suppressed the decrease in urea-nitrogen secretion as well as the leakages of GOT and GPT. The membrane-protective action of these two compounds was verified by the histological data. Failure of SAMe-ST to counteract CCl4-induced reduction of radioactive leucine incorporation into the trichloroacetic acid-insoluble materials in hepatocytes indicates that the observed effects of SAMe-ST or L-Met do not involve acceleration of protein synthesis. The present results indicate that SAMe-ST remarkably protects hepatocytes from CCl4-induced hepatotoxicity, probably by either changing the structure or compositions of membrane phospholipids or by modifying the interaction of CCl4 with the intracellular drug-metabolizing enzyme systems.
Protective effects of S-adenosyl-L-methionine against enzyme leakage from cultured hepatocytes and hypotonic hemolysis
Effects of S-adenosyl-L-methionine disulfate tosylate salt (SAMe-ST) and L-methionine (L-Met) on rat erythrocytes and primary cultured hepatocytes were studied. SAMe-ST in concentrations of 0.2 to 5.0 mg/ml protected erythrocytes from hypotonic hemolysis. Almost an identical level of protection was provided by SAMe chloride, suggesting that this protective effect is due to the SAMe moiety itself but not its sulfate or tosylate moiety. L-Met also showed a slight protective effect, but at higher concentrations, it slightly enhanced hemolysis. When the cultured hepatocytes were treated with SAMe-ST, the leakage of enzymes from the hepatocytes were significantly decreased compared with that in the control. L-Met also showed similar protective effects, but to a lesser degree than in the case of SAMe-ST. SAMe-ST significantly increased Na+.K(+)-ATPase activity. The present results indicate that SAMe remarkably inhibits hypotonic hemolysis and enzyme leakage from cultured hepatocytes and that its mechanism is probably related to a change in the membrane property.
Pharmacokinetic properties of S-adenosylmethionine after oral and intravenous administration of its tosylate disulfate salt: a multiple-dose, open-label, parallel-group study in healthy Chinese volunteers
Background: S-adenosylmethionine (SAMe) is an endogenous molecule that plays an important role in cellular metabolism. Despite being widely used as a dietary supplement with claimed benefits for numerous conditions, there is little information about the pharmacokinetic properties of exogenous SAMe.
Objectives: One aim of this study was to characterize the pharmacokinetic properties of SAMe after administration of single and multiple doses of orally and intravenously administered SAMe tosylate disulfate (STD) in healthy male and female Chinese volunteers. Because men have higher erythrocyte levels of endogenous SAMe than do women, we also assessed the effects of sex on the disposition of SAMe.
Methods: A simple and sensitive assay for SAMe based on liquid chromatography-mass spectrometry using selected-ion monitoring of analyte and acyclovir as internal standard was developed and validated. The assay was used to study the pharmacokinetic properties of SAMe. STD was administered as single and multiple doses of enteric-coated tablets and IV infusion of STD to groups of healthy native Chinese volunteers. After an overnight fast, male and female Chinese volunteers were assigned to receive STD 1000 mg for 5 days, either in enteric-coated tablet formulation or as a 250-mL IV infusion. Blood samples were collected 24 hours after the first and last dose and used for determining plasma SAMe concentrations and pharmacokinetic parameters. For the oral formulation, SAMe concentrations were corrected for concentrations of endogenous SAMe. Pharmacokinetic parameters were calculated for men and women separately and for the total group of volunteers. Adverse events were monitored using a physician during blood collection and by spontaneous reporting.
Results: Twenty healthy volunteers were enrolled (oral formulation: 5 men, 5 women; mean [SD] age, 24.1 [4.7] years [range, 21-37 years]; mean [SD] weight, 59.9 [4.8] kg [range, 54-70 kg]; IV formulation: 5 men, 5 women; mean [SD] age, 22.6 [1.8] years [range, 21-27 years]; mean [SD] weight, 59.5 [5.4] kg [range, 53-67 kg]). None of the between-sex differences in SAMe pharmacokinetic properties were significant. The (mean [SD]) pharmacokinetic properties of singledose oral SAMe in men and women, respectively, were as follows: C(max), 2.37 (1.58) and 2.50 (1.83) micromol/L; T(max), 5.40 (1.14) and 5.20 (1.48) hours; AUC(0-24), 8.56 (5.16) and 10.3 (8.0) micromol/L/h; and t(1/2beta), 6.06 (1.80) and 6.28 (2.60) hours. Corresponding values with the single-dose IV formulation were: C(max), 127 (49) and 211 (94) micromol/L; T(max), 1.90 (0.22) and 1.60 (0.22) hours; AUC(0-24), 329 (84) and 480 (176) micromol/L/h; and t(1/2beta), 4.34 (0.57) and 3.83 (0.78) hours. The single-dose oral:IV ratios of AUC(0-24) in men and women, respectively, were 2.60% and 2.14% (degrees of fluctuation: 4.96 [1.77] and 9.49 [0.91]). The pharmacokinetic properties of multiple-dose oral and IV SAMe were not significantly different from those with single-dose administration. None of the volunteers reported any adverse events during the study.
Conclusions: In this small study in healthy Chinese volunteers, there were no significant differences in the pharmacokinetic parameters of SAMe between men and women or between single- and multiple-dose administration of STD 1000 mg administered orally or intravenously. No evidence of accumulation of SAMe in plasma was found on multiple dosing. Both enteric-coated tablets and the IV infusion were well tolerated in these volunteers.
S-adenosylmethionine protects against acetaminophen hepatotoxicity in two mouse models
Because S-adenosylmethionine promotes synthesis of hepatic glutathione in chronic liver disease and is well tolerated in man, we investigated its use as an antidote to acetaminophen hepatotoxicity in two mouse models. In C57Bl6 mice, deaths were abolished by S-adenosylmethionine given within 1 hr of 3.3 mmol/kg body wt acetaminophen (0 of 32 vs. 13 of 49, p less than 0.005) and reduced if given 2 to 5 hours after acetaminophen administration (4 of 42 vs. 13 of 49, p less than 0.01). Mixed disulfate/tosylate salt of S-adenosylmethionine abolished mortality in C3H mice given 2 mmol/kg body wt acetaminophen (0 of 24 vs. 4 of 18; p less than 0.05). In both mouse models, S-adenosylmethionine reduced depletion of plasma (median = 20.8 mumol/L vs. 14.6 mumol/L) and liver glutathione (198% vs. 100%; p less than 0.05), liver damage and release of AST after acetaminophen administration. Pretreatment with buthionine sulfoximine, which inhibits glutathione synthesis, abolished the beneficial effect of S-adenosylmethionine on survival and plasma glutathione level. S-adenosylmethionine reduces acetaminophen hepatotoxicity by metabolism of the active moiety to glutathione. This benefit may last as long as 5 hr after acetaminophen ingestion.