Prostaglandin E2 methyl ester
(Synonyms: Dinoprostone methyl ester, PGE2 methyl ester) 目录号 : GC41171
A lipid soluble PGE2 analog
Cas No.:31753-17-0
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
Prostaglandin E2 methyl ester (PGE2 methyl ester) is an analog of PGE2 with enhanced lipid solubility. PGE2 is one of the primary cyclooxygenase products of arachidonic acid and one of the most widely investigated PGs. Its activity influences inflammation, fertility and parturition, gastric mucosal integrity, and immune modulation. The effects of PGE2 are transduced by at least four distinct receptors designated EP1, EP2, EP3, and EP4. Affinity constants (Kd) values of PGE2 for these receptors range from 1-10 nM depending on the receptor subtype and tissue.
| Cas No. | 31753-17-0 | SDF | |
| 别名 | Dinoprostone methyl ester, PGE2 methyl ester | ||
| Canonical SMILES | O=C1[C@H](C/C=C\CCCC(OC)=O)[C@@H](/C=C/[C@@H](O)CCCCC)[C@H](O)C1 | ||
| 分子式 | C21H34O5 | 分子量 | 366.5 |
| 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。 |
||
| 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 | 2.7285 mL | 13.6426 mL | 27.2851 mL |
| 5 mM | 0.5457 mL | 2.7285 mL | 5.457 mL |
| 10 mM | 0.2729 mL | 1.3643 mL | 2.7285 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。
Detection of the 15-acetate of Prostaglandin E2 methyl ester as a prominent component of the prostaglandins in the gorgonian coral Plexaura homomalla
Lipids 2002 Feb;37(2):217-21.PMID:11908914DOI:10.1007/s11745-002-0883-5.
15R-Prostaglandin E2 (PGE2) methyl ester 15-acetate (1) was isolated from the R-variety of the Caribbean sea whip coral Plexaura homomalla collected in the Florida Keys. It was present in coral samples from separate collections in 2-10% of the abundance of the major prostaglandin component, PGA2 methyl ester 15-acetate. The structure of 1 was assigned based on one- and two-dimensional 1H NMR, HPLC, and LC-MS analyses. A sample of the S-variety of P. homomalla was found to contain a similar abundance of the corresponding 15S product, Prostaglandin E2 methyl ester 15-acetate. The significance of PGE acetylation is discussed in relation to the proposed mechanism of PGA synthesis in the coral.
Effects of 15(S)-15-methyl Prostaglandin E2 methyl ester on phospholipid metabolism in rat gastric mucosa
Biochem Pharmacol 1989 Mar 15;38(6):955-60.PMID:2930596DOI:10.1016/0006-2952(89)90286-4.
The effects of 15(S)-15-methyl prostaglandin E2 (PGE2) methyl ester on gastric mucosal metabolism of phospholipids in intact rats and rats injured by intragastric instillation of acidified taurocholic acid were examined by using radioisotope-labeled precursors. The incorporation of palmitic, oleic and arachidonic acids into phosphatidylcholine (PC) and phosphatidylethanolamine (PE) was reduced by treatment with 15(S)-15-methyl PGE2 methyl ester in the intact rats, but the incorporation of glycerol was unaffected or affected only slightly. Instillation of acidified taurocholic acid resulted in decreased incorporation of palmitic acid and glycerol into PC and PE, whereas pretreatment with 15(S)-15-methyl PGE2 methyl ester caused the incorporations of these precursors to be maintained after acidified taurocholic acid treatment. These results suggest that 15(S)-15-methyl PGE2 methyl ester may reduce the incorporation of fatty acids into PC and PE by inhibition of the deacylation-reacylation cycle either directly or indirectly, whereas acidified taurocholic acid decreases de novo synthesis of PC and PE, and probably also the reacylation of fatty acid into phospholipids. Pretreatment with 15(S)-15-methyl PGE2 methyl ester protected the PC- and PE-synthesizing activity against the injury induced by acidified taurocholic acid, and this effect may be involved in the prevention of mucosal damage.
Effects of 16, 16-dimethyl Prostaglandin E2 methyl ester on aspirin-and indomethacin-induced gastrointestinal lesions in dogs
Dig Dis Sci 1980 Jun;25(6):439-48.PMID:7379677DOI:10.1007/BF01395508.
The pathogenesis of aspirin- or indomethacin-induced gastric and/or intestinal lesions was studied in dogs. 16,16-Dimethyl PGE2 methyl ester (16-DMPGE2) at 2 or 10 microgram/kg in two divided doses given intramuscularly markedly inhibited gastric lesions produced by orally ingested aspirin at 200 mg/kg/day given twice daily for 1 or 5 days. While 16-DMPGE2 at the same dose also inhibited gastric lesions induced by a single oral administration of indomethacin at 20 mg/kg, gastric lesions including deep antral ulcers, produced by repeated administration of indomethacin, were not affected. Intestinal lesions produced by indomethacin given once, or for 5 or 10 days, were not affected. These results suggest that the lack of engoenous prostaglandins may be involved in the pathogenesis of gastric lesions produced by aspirin and indomethacin given once but may not be involved in the pathogenesis of indomethacin-induced deep lesions in the stomach and intestine.
Multicomponent Strategy for the Synthesis of Prostaglandin E2 methyl ester under Anion Relay Chelation Control
J Org Chem 2016 Feb 19;81(4):1571-84.PMID:26811990DOI:10.1021/acs.joc.5b02735.
Starting with four components, the enantioselective synthesis of Prostaglandin E2 methyl ester has been achieved through a highly stereoselective heteroatom-directed conjugate addition reaction and cyclopentanone ring cyclization as the key steps. This asymmetric strategy includes (i) an asymmetric Reformatsky reaction; (ii) conjugate addition of a chiral vinyllithium reagent; (iii) cyclization to form a sulfonylated cyclopentanone in one-pot; followed by (iv) allylation of the side chain. Four carbon-carbon bond-forming processes and three stereogenic centers were established, with the steps from (ii) to (iii) being achieved in a one-pot process.
Effect of 16,16-dimethyl Prostaglandin E2 methyl ester on weanling rat skeleton: daily and systemic administration
Anat Rec 1986 Jul;215(3):305-16.PMID:3740468DOI:10.1002/ar.1092150313.
The effects of 0, 0.3, 1.0, and 3.0 mg of 16,16-dimethyl Prostaglandin E2 methyl ester (Di-M-PGE2) per kilogram per day administered subcutaneously for 21 days to fluorescent-labeled weanling rats were studied, by single-photon absorptiometric and static and dynamic histomorphometric techniques, to determine possible alterations in growth and mineralized tissue mass and their mechanisms of response. Specimens of femurs, proximal tibia, and tibial shaft were analyzed. Di-M-PGE2 caused a reduction in bone elongation and a dramatic accumulation in metaphyseal trabecular hard tissue mass. At high doses, the growth cartilage exhibited reduced thickness and degenerative cell size and cell production rate. The increased metaphyseal trabecular hard tissue mass was restricted to the secondary spongiosa region and was observed at all dose levels. The metaphysis was further characterized by an increase in bone and calcified cartilage cores, a marked elevation in osteoblast and osteoclast numbers, in osteoblast-to-osteoclast ratios, and in ratios of differentiated cells to osteoprogenitor cells. These findings were consistent with the interpretations that Di-M-PGE2 depressed bone elongation by delaying the division and maturation of growth plate chondrocytes; stimulated the differentiation of osteoblasts and osteoclasts, thus generating more differentiated bone cells but suppressing their activities; and increased metaphyseal trabecular hard tissue by creating an imbalance in osteoblasts over osteoclasts and suppressing hard tissue resorption.