(R)-Butaprost
(Synonyms: 丁环前列素) 目录号 : GC40716
The less active epimer of a PGE2 analog
Cas No.:69648-38-0
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
Butaprost is a structural analog of prostaglandin E2 (PGE2) with good selectivity for the EP2 receptor subtype. Butaprost has frequently been used to pharmacologically define the EP receptor expression profile of various human and animal tissues and cells. Serious confusion as to the structure of butaprost was generated by Gardiner in 1986, when he reported that the epimer of butaprost showing this selective activity was the C-16 (R)-epimer (See reference and Note). Butaprost binds with about 1/10 the affinity of PGE2 to the recombinant murine EP2 receptor, and does not bind appreciably to any of the other murine EP receptors or DP, FP, IP, or TP receptors. The pharmacology of (R)-butaprost has not been carefully studied, but it is generally considered to be the less active epimer. (NOTE: In the Gardiner paper in the 1986 British Journal of Pharmacology, butaprost appears on page 46 where it is given the name TR 4979. The structure as drawn is incorrect, in that the author was using and referring to the more active C-16 epimer, which is actually 16(S). The structure on page 46 shows the structure as 16(R). It was not until the late 1990's that careful studies both in the US and Japan correctly identified the actual configuration of C-16 in the compound called butaprost is 16(S).)
| Cas No. | 69648-38-0 | SDF | |
| 别名 | 丁环前列素 | ||
| Canonical SMILES | CCCC1(CCC1)C(O)C/C=C/[C@H]1C(O)CC(=O)C1CCCCCCC(=O)OC | ||
| 分子式 | C24H40O5 | 分子量 | 408.6 |
| 溶解度 | DMF: 25 mg/ml,DMSO: 30 mg/ml,Ethanol: 50 mg/ml,PBS (pH 7.2): 150 µ g/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 | 2.4474 mL | 12.2369 mL | 24.4738 mL |
| 5 mM | 0.4895 mL | 2.4474 mL | 4.8948 mL |
| 10 mM | 0.2447 mL | 1.2237 mL | 2.4474 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。
Modulation of carbachol-induced Ca2+ oscillations in airway smooth muscle cells by PGE2
Cell Calcium 2022 May;103:102547.PMID:35134593DOI:10.1016/j.ceca.2022.102547.
PGE2 is a potent bronchodilator, but the mechanisms underlying this effect have not been fully elucidated. Acetylcholine-induced contractions of airway smooth muscle (ASM) are associated with the generation of repetitive Ca2+ oscillations in airway smooth muscle cells (ASMC) and the force of contraction is positively correlated with the frequency of the underlying Ca2+ oscillations. The purpose of the present study was to examine if carbachol-evoked Ca2+ oscillations in isolated ASMC were inhibited by PGE2. Isolated murine ASMC loaded with fluo4-AM were imaged with a Nipkow spinning disk confocal microscope. Cells responded to application of CCh (1 μM) by generating an initial Ca2+ transient followed by a series of Ca2+ oscillations. This activity was abolished by PGE2 (300 nM) and the EP2R agonist (R)-Butaprost (3 μM) and the inhibitory effects of PGE2 were reversed by application of the EP2R antagonist PF-04418948 (100 nM). Activation of adenylate cyclase using forskolin (1 μM) mimicked the effects of PGE2. The PKA activator, 6-MB-cAMP (300 μM) reduced the frequency of CCh-induced Ca2+ oscillations by 33% and the PKA inhibitor Rp-8-CPT-cAMPs partially reversed the inhibitory effects of PGE2. The EPAC activator 007-AM (10 μM) reduced the frequency of the oscillations by 60% and joint application of 007-AM and 6-MB-cAMP reduced oscillation frequency by ∼85%. CCh-induced Ca2+ oscillations were inhibited by 2-APB and tetracaine, but caffeine-evoked Ca2+ transients were resistant to PGE2. These data suggest that PGE2 inhibits CCh-induced Ca2+ oscillations in murine ASMC via stimulation of EP2Rs and a mechanism involving activation of PKA and EPAC.
Significance of cyclooxygenase-2 induced via p38 mitogen-activated protein kinase in mechanical stimulus-induced peritoneal adhesion in mice
J Pharmacol Exp Ther 2005 Apr;313(1):286-92.PMID:15576468DOI:10.1124/jpet.104.078717.
Postoperative peritoneal adhesion represents a major complication of surgery, but the molecular mechanism underlying pathogenesis of adhesion is not fully understood. The present study investigated the roles of cyclooxygenase (COX)-1 and COX-2 in peritoneal adhesion induced by scraping the surface of the cecum and abdominal wall in mice. Slight, but macroscopically observable, peritoneal adhesion was induced even on day 1, and the extent of adhesion reached a maximum on day 7 and beyond. COX-1 mRNA was constitutively expressed in the intact cecum, and its expression level was not altered after the mechanical stimulus. In contrast, expression of the COX-2 gene was markedly increased after the stimulus, and maximum expression was observed on days 3 to 7. Mofezolac, a specific COX-1 inhibitor, had no effect on peritoneal adhesion at 30 mg/kg and had only marginal effects on prostaglandin (PG)E2 levels in the cecum or peritoneal fluid. On the other hand, two highly selective inhibitors for COX-2, NS-398 (N-[2-(cyclohexyloxy)-4-nitrophenyl]-methanesulfonamide) and CAY10404 [3-(4-methylsulphonylphenyl)-4-phenyl-5-trifluoromethylisoxazole], dose-dependently inhibited both adhesion formation and the increase in PGE2 levels (3-30 mg/kg). The effects of NS-398 were eliminated when PGE2 or (R)-Butaprost was administered exogenously. A COX-2 antisense oligonucleotide also attenuated adhesion formation. Activation of p38 mitogen-activated protein (MAP) kinase was observed in the traumatized cecum, and an MAP kinase inhibitor, SB202190 [4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)-1H-imidazole], inhibited adhesion formation (54% inhibition at 15 microM) and also reduced the COX-2 mRNA level and PGE2 levels. In conclusion, COX-2, but not COX-1, plays a significant role in mechanical stimulus-induced peritoneal formation in the mouse cecum.