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tetranor-PGDM Sale

(Synonyms: tetranorPGD Metabolite, tetranor-Prosatglandin D Metabolite) 目录号 : GC45025

The major urinary metabolite of PGD2

tetranor-PGDM Chemical Structure

Cas No.:70803-91-7

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25μg
¥2,262.00
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50μg
¥4,300.00
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100μg
¥8,137.00
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产品描述

Prostaglandin D2 is synthesized by hematopoietic-type PGD-synthase (H-PGDS) in mast cells and is released in large quantities during allergic and asthmatic anaphylaxis. PGD2 is also produced in the brain by lipocalin-PGD-synthase also known as β-trace. In the brain, PGD2 produces normal physiological sleep and lowering of body temperature. Further pharmacological actions include inhibition of platelet aggregation and relaxation of vascular smooth muscle. tetranor-PGDM is a major metabolite of PGD2 that is detectable in human and mouse urine. The levels of tetranor-PGDM and 2,3-dinor-11β-PGF2α , a related PGD2 metabolite, in human urine were found to be 1.5 ± 0.3 and 0.6 ± ng/mg creatinine, respectively. tetranor-PGDM was detected in murine urine at a level of 8.1 ± 1.3 ng/mg creatinine.

Chemical Properties

Cas No. 70803-91-7 SDF
别名 tetranorPGD Metabolite, tetranor-Prosatglandin D Metabolite
Canonical SMILES O[C@@H]1[C@H](CCC(O)=O)[C@@H](CCC(CCCCC(O)=O)=O)C(C1)=O
分子式 C16H24O7 分子量 328.4
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1 mg 5 mg 10 mg
1 mM 3.0451 mL 15.2253 mL 30.4507 mL
5 mM 0.609 mL 3.0451 mL 6.0901 mL
10 mM 0.3045 mL 1.5225 mL 3.0451 mL
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Research Update

Extraction and measurement of urinary tetranor-PGDM in disposable diapers

J Pharmacol Sci 2021 Oct;147(2):208-210.PMID:34384569DOI:10.1016/j.jphs.2021.06.011.

Urinary tetranor-PGDM is a useful diagnostic biomarker for food allergy which often affects infants. We attempted to extract and measure urinary tetranor-PGDM absorbed in polymer of diapers. We applied CaCl2 to the collected polymer, determined the adequate time length of shaking the polymer to release urine, and measured tetranor-PGDM in the extracted urine. This procedure provided high linearity and recovery rate in tetranor-PGDM measurement. We also found that urinary tetranor-PGDM was stable for 24 h at 4°C in diapers. This method can be useful to monitor the food allergic condition of non-toilet trained children.

Development of Monoclonal Antibody-Based EIA for tetranor-PGDM which Reflects PGD2 Production in the Body

J Immunol Res 2021 Apr 26;2021:5591115.PMID:33997056DOI:10.1155/2021/5591115.

tetranor-PGDM is a metabolite of PGD2. Urinary tetranor-PGDM levels were reported to be increased in some diseases, including food allergy, Duchenne muscular dystrophy, and aspirin-intolerant asthma. In this study, we developed a monoclonal antibody (MAb) and a competitive enzyme immunoassay (EIA) for measuring tetranor-PGDM. Spleen cells isolated from mice immunized with tetranor-PGDM were utilized to generate Ab-producing hybridomas. We chose hybridomas and purified MAb against tetranor-PGDM to develop competitive EIA. The assay evaluated the optimal ionic strength, pH, precision, and reliability. Specificity was determined by cross-reactivity to tetranor-PGEM, tetranor-PGFM, and tetranor-PGAM. Recovery was determined by spiking experiments on artificial urine. Optimal ionic strength was 150 mM NaCl, and optimal pH was pH 7.5. Metabolites other than tetranor-PGDM did not show any significant cross-reactivity in the EIA. The assay exhibited a half-maximal inhibition concentration (IC50) of 1.79 ng/mL, limit of detection (LOD) of 0.0498 ng/mL, and range of quantitation (ROQ) value of 0.252 to 20.2 ng/mL. The intra- and inter-assay variation for tetranor-PGDM was 3.9-6.0% and 5.7-10.4%, respectively. The linearity-dilution effect showed excellent linearity under dilution when artificial urine samples were applied to solid-phase extraction (SPE). After SPE, recovery of tetranor-PGDM in artificial urine averaged from 82.3% to 113.5% and was within acceptable limits (80%-120%). We successfully generated one monoclonal antibody and developed a sensitive competitive EIA. The established EIA would be useful for routine detection and monitoring of tetranor-PGDM in research or diagnostic body fluids.

Prostaglandin D2 metabolite in urine is an index of food allergy

Sci Rep 2017 Dec 15;7(1):17687.PMID:29247205DOI:10.1038/s41598-017-17798-w.

Food allergy is immediate hypersensitive reactions to ingested foods. Since early diagnosis is effective for disease control, development of an objective diagnostic index is required. Using mediator-lipidomics, we found that levels of the urinary prostaglandin D2 (PGD2) metabolite, tetranor-PGDM, reflected the severity of the allergic symptoms and intestinal mast cell hyperplasia in mice. Repeated oral challenges with ovalbumin promoted allergic symptoms in sensitized mice. Particularly, the allergic mice presented with increased numbers of intestinal mast cells, which strongly expressed hematopoietic PGD synthase (H-PGDS). The levels of urinary tetranor-PGDM increased as the disease progressed. Treatment with a mast cell inactivator or an anti-inflammatory steroid attenuated these symptoms and decreased the tetranor-PGDM urinary levels. The levels of urinary tetranor-PGDM did not correlate with the disease severity in murine models of colitis, asthma, or allergic dermatitis. Furthermore, we have shown that urinary levels of tetranor-PGDM were significantly higher in patients with food allergy than those in healthy volunteers and patients with other types of allergic diseases such as asthma, allergic rhinitis, and atopic dermatitis. These findings suggest that urinary tetranor-PGDM is a useful diagnostic index of food allergy in both mice and humans.

Urinary prostaglandin metabolites as Duchenne muscular dystrophy progression markers

Brain Dev 2018 Nov;40(10):918-925.PMID:30006121DOI:10.1016/j.braindev.2018.06.012.

Background: Patients with Duchenne muscular dystrophy (DMD) exhibit increased prostaglandin D2 (PGD2) expression in necrotic muscle and increased PGD2 metabolites in their urine. In mouse models, inhibiting PGD2 production suppresses muscle necrosis, suggesting a possible intervention through PGD2-mediated activities. Objective: We investigated the involvement of PGD2 and its potential use as a marker of pathological progression in DMD. Methods: Sixty-one male children with DMD and thirty-five age-matched controls were enrolled in the study. DMD patients were divided into "ambulant" and "non-ambulant" groups, which were further subdivided into "steroid" and "non-steroid" therapy groups. Levels of the PGD2 metabolite tetranor-PGDM (t-PGDM) and creatinine were measured in both spot and 24-hour urine samples, with comparisons between groups made according to geometric mean values. Results: DMD patients had significantly higher levels of creatinine-corrected t-PGDM in spot urine samples as compared with the control group. Additionally, both ambulant and non-ambulant DMD groups had significantly higher levels of t-PGDM as compared with controls, with no significant difference in t-PGDM levels observed between steroid and non-steroid groups. Moreover, total creatinine excretion in 24-hour urine samples was significantly lower in DMD patients as compared with controls, and although DMD patients had lower muscle mass than controls, their overall levels of t-PGDM did not differ significantly from those in the non-ambulant and control groups. Conclusion: PGD2 might help explain the progression and symptomatic presentations (e.g., ambulatory difficulty) associated with DMD, suggesting it as a useful pathological marker and use of a selective PGD2 inhibitor as a potential treatment modality.

Aspirin-intolerant asthma (AIA) assessment using the urinary biomarkers, leukotriene E4 (LTE4) and prostaglandin D2 (PGD2) metabolites

Allergol Int 2012 Sep;61(3):393-403.PMID:22627848DOI:10.2332/allergolint.11-RA-0403.

The clinical syndrome of aspirin-intolerant asthma (AIA) is characterized by aspirin/nonsteroidal anti-inflammatory drug intolerance, bronchial asthma, and chronic rhinosinusitis with nasal polyposis. AIA reactions are evidently triggered by pharmacological effect of cyclooxygenase-1 inhibitors. Urine sampling is a non-invasive research tool for time-course measurements in clinical investigations. The urinary stable metabolite concentration of arachidonic acid products provides a time-integrated estimate of the production of the parent compounds in vivo. AIA patients exhibits significantly higher urinary concentrations of leukotriene E(4) (LTE(4)) and 1,15-dioxo-9α-hydroxy-2,3,4,5-tetranorprostan-1,20-dioic acid (tetranor-PGDM), a newly identified metabolite of PGD(2), at baseline. This finding suggests the possibility that increased mast cell activation is involved in the pathophysiology of AIA even in a clinically stable condition. In addition, lower urinary concentrations of primary prostaglandin E(2) and 15-epimer of lipoxin A(4) at baseline in the AIA patients suggest that the impaired anti-inflammatory elements may also contribute to the severe clinical outcome of AIA. During the AIA reaction, the urinary concentrations of LTE(4) and PGD(2) metabolites, including tetranor-PGDM significantly and correlatively increase. It is considered that mast cell activation probably is a pathophysiologic hallmark of AIA. However, despite the fact that cyclooxygenease-1 is the dominant in vivo PGD(2) biosynthetic pathway, the precise mechanism underlying the PGD(2) overproduction resulting from the pharmacological effect of cyclooxygenease-1 inhibitors in AIA remains unknown. A comprehensive analysis of the urinary concentration of inflammatory mediators may afford a new research target in elucidating the pathophysiology of AIA.