13,14-dihydro-15-keto Prostaglandin D2
(Synonyms: 13,14-dihydro-15-keto PGD2) 目录号 : GC41411
CRTH2/DP2 agonist
Cas No.:59894-07-4
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: >95.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
13,14-dihydro-15-keto Prostaglandin D2 (13,14-dihydro-15-keto PGD2) is a metabolite of PGD2 which is formed through the 15-hydroxy PGDH pathway. 13,14-dihydro-15-keto PGD2 was recently identified as a selective agonist for the CRTH2/DP2 receptor.[1] It also inhibits ion flux in a canine colonic mucosa preparation. [2] In humans, 13,14-dihydro-15-keto PGD2 is further metabolized to give 11β-hydroxy compounds which have also undergone β-oxidation of one or both side chains. Virtually no 13,14-dihydro-15-keto PGD2 survives intact in the urine.[3] [4]
Reference：
[1]. Rangachari, P.K., and Betti, P.A. Biological activity of metabolites of PGD2 on canine proximal colon. Am. J. Physiol. 264(5 Pt 1), G886-G894 (1993).
[2] Hirai, H., Tanaka, K., Yoshie, O., et al. Prostaglandin D2 selectivity induces chemotaxis in T helper type 2 cells, eosinophils, and basophils via seven-transmembrane receptor CRTH2. J. Exp. Med. 193(2), 255-261 (2001).
[3]. Liston, T.E., and Roberts, L.J., II. Metabolic fate of radiolabeled prostaglandin D2 in a normal human male volunteer. J. Biol. Chem. 260(24), 13172-13180 (1985).
[4]. Morrow, J.D., Prakash, C., Awad, J.A., et al. Quantification of the major urinary metabolite of prostaglandin D2 by a stable isotope dilution mass spectrometric assay. Anal. Biochem. 193(1), 142-148 (1991).
| Cas No. | 59894-07-4 | SDF | |
| 别名 | 13,14-dihydro-15-keto PGD2 | ||
| 化学名 | 9α-hydroxy-11,15-dioxo-prost-5Z-en-1-oic acid | ||
| Canonical SMILES | CCCCCC(=O)CC[C@H]1C(=O)CC(O)C1C/C=C\CCCC(=O)O | ||
| 分子式 | C20H32O5 | 分子量 | 352.5 |
| 溶解度 | DMF: 50 mg/ml,DMSO: 30 mg/ml,Ethanol: 50 mg/ml,PBS pH 7.2: 2.5 mg/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 | 2.8369 mL | 14.1844 mL | 28.3688 mL |
| 5 mM | 0.5674 mL | 2.8369 mL | 5.6738 mL |
| 10 mM | 0.2837 mL | 1.4184 mL | 2.8369 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。
Polyunsaturated fatty acid metabolites as novel lipidomic biomarkers for noninvasive diagnosis of nonalcoholic steatohepatitis
J Lipid Res 2015 Jan;56(1):185-92.PMID:25404585DOI:10.1194/jlr.P055640.
Lipotoxicity is a key mechanism thought to be responsible for the progression of nonalcoholic fatty liver (NAFL) to nonalcoholic steatohepatitis (NASH). Noninvasive diagnosis of NASH is a major unmet clinical need, and we hypothesized that PUFA metabolites, in particular arachidonic acid (AA)-derived eicosanoids, in plasma would differentiate patients with NAFL from those with NASH. Therefore, we aimed to assess the differences in the plasma eicosanoid lipidomic profile between patients with biopsy-proven NAFL versus NASH versus normal controls without nonalcoholic fatty liver disease (NAFLD; based on MRI fat fraction <5%). We carried out a cross-sectional analysis of a prospective nested case-control study including 10 patients with biopsy-proven NAFL, 9 patients with biopsy-proven NASH, and 10 non-NAFLD MRI-phenotyped normal controls. We quantitatively compared plasma eicosanoid and other PUFA metabolite levels between NAFL versus NASH versus normal controls. Utilizing a uniquely well-characterized cohort, we demonstrated that plasma eicosanoid and other PUFA metabolite profiling can differentiate between NAFL and NASH. The top candidate as a single biomarker for differentiating NAFL from NASH was 11,12-dihydroxy-eicosatrienoic acid (11,12-diHETrE) with an area under the receiver operating characteristic curve (AUROC) of 1. In addition, we also found a panel including 13,14-dihydro-15-keto Prostaglandin D2 (dhk PGD2) and 20-carboxy arachidonic acid (20-COOH AA) that demonstrated an AUROC of 1. This proof-of-concept study provides early evidence that 11,12-diHETrE, dhk PGD2, and 20-COOH AA are the leading eicosanoid candidate biomarkers for the noninvasive diagnosis of NASH.