SY-640
目录号 : GC61310
SY-640是乙酰胺衍生物，具有有效的保肝作用。SY-640可减轻痤疮丙酸杆菌和脂多糖诱导的小鼠肝损伤。
Cas No.:168705-70-2
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
SY-640 is an Acetamide derivative and has potent hepatoprotective effect. SY-640 reduces Propionibacterium acnes and Lipopolysaccharide-induced liver injury in mice[1][2].
SY-640 inhibits the number of liver-infiltrating cells and attenuates the increased expression of leukocyte function-associated antigen-1 on these cells[1].
SY-640 (Oral; 150 mg/kg; once daily for 7 days) significantly inhibits Propionibacterium acnes and Lipopolysaccharide-induced liver injury, but a single administration is without effect[1]. SY-640 (p.o.; 150 mg/kg; once daily for three days) significantly increases the liver microsomal cytochrome P-450 content and aminopyrine demethylase activity in mice. The hepatic microsomal aminopyrine demethylase activity is obviously inhibited two hours after oral administration of SY-640[2].
[1]. Y Tanaka, et al. Hepatoprotective effect of SY-640, a novel acetamide derivative, on Propionibacterium acnes and lipopolysaccharide-induced liver injury in mice. Arch Int Pharmacodyn Ther. Mar-Apr 1995;329(2):319-30. [2]. P F Li, et al. [Inhibitory effect of 2-(N-acetyl-methyl amino)-3',4'-methylenedioxyacetyl-aminophene(SY-640) on covalent binding of carcinogenic benzo(a)pyrene with mouse hepatocyte nuclear DNA]. Yao Xue Xue Bao. 1997 Sep;32(9):663-8.
| Cas No. | 168705-70-2 | SDF | |
| Canonical SMILES | CC(N(C)CC1=CC2=C(OCO2)C=C1)=O | ||
| 分子式 | C11H13NO3 | 分子量 | 207.23 |
| 溶解度 | DMSO: 100 mg/mL (482.56 mM) | 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 | 4.8256 mL | 24.1278 mL | 48.2556 mL |
| 5 mM | 0.9651 mL | 4.8256 mL | 9.6511 mL |
| 10 mM | 0.4826 mL | 2.4128 mL | 4.8256 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。
Hepatoprotective effect of SY-640, a novel acetamide derivative, on Propionibacterium acnes and lipopolysaccharide-induced liver injury in mice
Arch Int Pharmacodyn Ther 1995 Mar-Apr;329(2):319-30.PMID:8540770doi
The hepatoprotective effect of SY-640 on Propionibacterium acnes and lipopolysaccharide-induced liver injury in mice and its protective mechanism were examined. Oral administration of SY-640, 150 mg/kg once daily for 7 days, significantly inhibited Propionibacterium acnes and lipopolysaccharide-induced liver injury, but a single administration was without effect. Liver-infiltrating cells (T-lymphocytes and macrophages) play an important role in Propionibacterium and lipopolysaccharide-induced liver injury and express a higher level of leukocyte function-associated antigen-1. SY-640 inhibited the number of liver-infiltrating cells and attenuated the increased expression of leukocyte function-associated antigen-1 on these cells. Tumor necrosis factor-alpha mediated Propionibacterium acnes and lipopolysaccharide-induced liver injury, and SY-640 inhibited the elevation of the serum tumor necrosis factor-alpha concentration after injection of lipopolysaccharide in Propionibacterium acnes-primed mice. The putative effects of SY-640 are inhibitory effects on infiltration into the liver and on activation of T-lymphocytes and macrophages after Propionibacterium acnes-priming, and attenuation of expression of cell adhesion molecules such as leukocyte function-associated antigen-1. The immunological effect of SY-640 is likely to be closely related to the inhibition of Propionibacterium and lipopolysaccharide-induced liver injury.
[Inhibitory effect of 2-(N-acetyl-methyl amino)-3',4'-methylenedioxyacetyl-aminophene(SY-640) on covalent binding of carcinogenic benzo(a)pyrene with mouse hepatocyte nuclear DNA]
Yao Xue Xue Bao 1997 Sep;32(9):663-8.PMID:11596290doi
Many carcinogens must be first transformed into electrophilic ultimate carcinogens via metabolic activation in liver microsomes before covalent binding to nucleophilic center of DNA. SY-640 is a synthetic compound with hepatoprotective activity. Results of the present study indicate that the covalent binding of 3H-benzo(a)pyrine to mouse hepatocyte nuclear DNA in vitro and in vivo was markedly inhibited by SY-640. Further studies found that the liver microsomal cytochrome P-450 content and aminopyrine demethylase activity were significantly increased in mice treated with SY-640 (150 mg.kg-1 p.o.) once daily for three days, while the hepatic microsomal aminopyrine demethylase activity was obviously inhibited two hours after oral administration of SY-640 150 mg.kg-1 in mice. The aminopyrine demethylase activity of liver microsomes from normal, PB- and 3-MC-treated mice was also significantly inhibited by the addition of SY-640 in vitro. When SY-640 was incubated with NADPH-reduced mouse liver microsomes, a metabolic-intermediate(MI) complex at 457 nm was formed. The effects of SY-640 on cytochrome P-450 and its formation of MI complex with cytochrome P-450 may partially explain why SY-640 could inhibit covalent-binding of BP to mouse hepatocyte DNA in vitro.
[Studies on the role of nitric oxide and tumor necrosis factor in immunological liver injury in mice and effects of new anti-hepatitis compounds on the liver injury]
Sheng Li Ke Xue Jin Zhan 1996 Jan;27(1):47-9.PMID:8731983doi
An immunological liver injury model was established by injection of micro lipopolysaccharide (LPS) into BCG (bacilli Calmette Guéin)-primed mice. It was found that nitric oxide (NO) played dual effects in the liver damage induced by BCG+LPS. The NO coming from phagocytic cells showed toxic effects while those from the other cells displayed beneficial effects. Tumor necrosis factor (TNF) released by macrophages was also implicated to be a key factor in the liver damage induced by BCG + LPS. Kupffer cells were involved in BCG + LPS-induced liver injury by releasing NO and TNF. The mechanism(s) by which the two new hepatoprotectants (SY-801 and SY-640) reduced BCG + LPS-induced liver damage may be through enhancing mouse plasma NO levels and lowering NO production and TNF expression by macrophages.