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16,16-Dimethyl Prostaglandin E2derivative of prostaglandin E2

16,16-Dimethyl Prostaglandin E2

Catalog No. BCC7843
Size Price Stock
1mg $69.00 In stock
5mg $328.00 In stock
10mg $621.00 In stock
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Quality Control of 16,16-Dimethyl Prostaglandin E2

Chemical structure

16,16-Dimethyl Prostaglandin E2

Biological Activity of 16,16-Dimethyl Prostaglandin E2

Synthetic derivative of prostaglandin E2. Increases embryonic stem cell (ESC) hematopoietic colony formation in mouse bone marrow. Also induces an increase in hematopoietic stem cell (HSC) numbers and enhances Wnt activity within the HSC population in zebrafish embryos.

16,16-Dimethyl Prostaglandin E2 Dilution Calculator

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16,16-Dimethyl Prostaglandin E2 Molarity Calculator



Chemical Properties of 16,16-Dimethyl Prostaglandin E2

Cas No. 39746-25-3 SDF Download SDF
Chemical Name (5Z,11α,13E,15R)-11,15-Dihydroxy-16,16-dimethyl-9-oxo-prosta-5,13-dien-1oic acid
Standard InChI InChI=1S/C22H36O5/c1-4-5-14-22(2,3)20(25)13-12-17-16(18(23)15-19(17)24)10-8-6-7-9-11-21(26)27/h6,8,12-13,16-17,19-20,24-25H,4-5,7,9-11,14-15H2,1-3H3,(H,26,27)/b8-6+,13-12+/t16-,17?,19-,20+/m0/s1
Formula C22H36O5 M.Wt 380.52
Solubility Soluble in methyl acetate (supplied pre-dissolved -10mg/ml)
Storage Store at -80°C
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other courier with RT , or blue ice upon request.

Preparing Stock Solutions of 16,16-Dimethyl Prostaglandin E2

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 2.628 mL 13.1399 mL 26.2798 mL 52.5597 mL 65.6996 mL
5 mM 0.5256 mL 2.628 mL 5.256 mL 10.5119 mL 13.1399 mL
10 mM 0.2628 mL 1.314 mL 2.628 mL 5.256 mL 6.57 mL
50 mM 0.0526 mL 0.2628 mL 0.5256 mL 1.0512 mL 1.314 mL
100 mM 0.0263 mL 0.1314 mL 0.2628 mL 0.5256 mL 0.657 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

Background on 16,16-Dimethyl Prostaglandin E2

IC50: N/A

16,16-Dimethyl Prostaglandin E2 (dmPGE2) is the synthetic derivative ofprostaglandin E2. Since prostaglandin E has immunosuppressive effects and potentially could lessen the toxic effects of cyclosporine, prostaglandin E usage in the setting of allotransplantation has been suggested both clinically and experimentally.

In vitro: DmPGE2 was reported to cause an increase in runx11/cmyb1 HSCs, while HSCs were inhibited by indomethacin treatment in 90% of embryos. Moreover, dmPGE2 had minimal effects on the vasculature, while indomethacin altered the intersomitic vessels slightly. Imaged by confocal microscopy, red-labelled HSCs and endothelium embryos showed significantly increased HSCs following dmPGE2 exposure [1].

In vivo: In a heterotopic model of rat allograft rejection, dmPGE2 could delay the rejection onset, but all animals developed severe rejection and died subsequently. Treatment of animals with low-dose CsA in combination with dmPGE2 led to a delay in the onset as well as a reduction in the intensity of allograft rejection. In addition, a statistical relationship between procoagulant activity levels and the time of onset of rejection was observed [1].

Clinical trial: N/A

[1] North TE,Goessling W,Walkley CR,Lengerke C,Kopani KR,Lord AM,Weber GJ,Bowman TV,Jang IH,Grosser T,Fitzgerald GA,Daley GQ,Orkin SH,Zon LI.  Prostaglandin E2 regulates vertebrate haematopoietic stem cell homeostasis. Nature.2007 Jun 21;447(7147):1007-11.
[2] Koh IH,Kim PC,Chung SW,Waddell T,Wong PY,Gorczynski R,Levy GA,Cohen Z.  The effects of 16, 16 dimethyl prostaglandin E2 therapy alone and in combination with low-dose cyclosporine on rat small intestinal transplantation. Transplantation.1992 Oct;54(4):592-8.

References on 16,16-Dimethyl Prostaglandin E2

16,16-Dimethyl prostaglandin E2 efficacy on prevention and protection from bleomycin-induced lung injury and fibrosis.[Pubmed: 19059888]

In this study, we evaluated the protective effect and therapeutic potential of the prostaglandin E(2) (PGE(2)) synthetic analog 16,16-dimethyl-PGE(2) (dmPGE(2)) in the animal model of pulmonary fibrosis induced by bleomycin. Mice subjected to intratracheal administration of bleomycin (1 mg/kg) received a dmPGE(2) dose of 30 microg/kg/day by continuous subcutaneous infusion. Bronchoalveolar lavage (BAL); immunohistochemical analysis for IL-1, TNF-alpha, and nitrotyrosine; measurement of fluid content in lung; myeloperoxidase activity assay; and lung histology were performed 1 week later. Lung histology and Sircol assay for collagen deposition were performed 3 weeks after treatments. Changes of body weight and survival rate were also evaluated at 1 and 3 weeks. Compared with bleomycin-treated mice, dmPGE(2) co-treated mice exhibited a reduced degree of body weight loss and mortality rate as well as of lung damage and inflammation, as shown by the significant reduction of: (1) lung infiltration by leukocytes; (2) myeloperoxidase activity; (3) IL-1, TNF-alpha, and nitrotyrosine immunostaining; (4) lung edema; and (5) histologic evidence of lung injury and collagen deposition. In a separate set of experiments, dmPGE(2) treatment was started 3 days after bleomycin administration, and the evaluation of lung damage and inflammation was assessed 4 days later. Importantly, delayed administration of dmPGE(2) also was able to protect from inflammation and lung injury induced by bleomycin. These results, indicating that dmPGE(2) is able to prevent and to reduce bleomycin-induced lung injury through its regulatory and anti-inflammatory properties, encourage further research to find new options for the treatment of pulmonary fibrosis.

Protection against proximal tubule necrosis with 11-deoxy-16,16-dimethyl prostaglandin E2 in vitro.[Pubmed: 15522989]

11-Deoxy,16,16-dimethyl prostaglandin E2 induces specific proteins in association with its ability to protect against oxidative stress.[Pubmed: 12641431]

Prostaglandins (PGs) act locally to maintain cellular homeostasis and stimulate stress response signaling pathways. These cellular effects are diverse and are tissue-dependent. PGE(2), and the synthetic analogue, 11-deoxy,16,16-dimethyl PGE(2) (DDM-PGE(2)), protect renal proximal tubular epithelial (LLC-PK1) cells against cellular injury induced by the potent nephrotoxic and nephrocarcinogenic metabolite of hydroquinone, 2,3,5-tris-(glutathion-S-yl)hydroquinone. Although this cytoprotective response (in LLC-PK1 cells) is mediated through a thromboxane or thromboxane-like receptor coupled to AP-1 signaling pathways, the mechanism of cytoprotection is unknown. In this study, we utilized HPLC-electrospray ionization tandem mass spectrometric (ESI MS/MS) and matrix-assisted laser desorption ionization time-of-flight mass spectrometric (MALDI TOF) analysis of proteins isolated from DDM-PGE(2)-stimulated LLC-PK1 cells to identify candidate cytoprotective proteins. DDM-PGE(2) selectively stimulated the synthesis of several proteins in LLC-PK1 cells. Peptide sequencing by ESI-MS/MS of in-gel tryptic protein digests revealed the identity of eight proteins: endothelial actin binding protein, myosin, elongation factor 2 (EF-2), elongation factor 1alpha-1 (EF-1alpha), heat shock protein 90beta (HSP90beta), glucose-regulated protein 78 (GRP 78), membrane-organizing extension spike protein, and actin. Both ESI-MS/MS and MALDI-MS analysis resulted in the same protein identification. Western analysis confirmed the temporal induction of the majority of these proteins, including EF-2, EF-1alpha, HSP90beta, GRP78, and actin. The collective expression of these proteins suggests that DDM-PGE(2)-mediated cytoprotection may involve alterations in cytoskeletal organization and/or stimulation of an endoplasmic reticulum (ER) stress response. The present studies provide insights into potential downstream targets of PG signaling.

16,16-Dimethyl prostaglandin E2 inhibits indomethacin-induced small intestinal lesions through EP3 and EP4 receptors.[Pubmed: 11991626]

We evaluated the effect of various PGE analogs specific to EP receptor subtypes on indomethacin-induced small intestinal lesions in rats and investigated the relationship of EP receptor subtype with the PGE action using EP receptor knockout mice. Animals were administered indomethacin subcutaneously, and they were killed 24 hr later. 16,16-dimethyl prostaglandin E2 (dmPGE2) or various EP agonists were administered intravenously 10 min before indomethacin. Indomethacin caused hemorrhagic lesions in the rat small intestine, accompanied with an increase in intestinal motility and the number of enteric bacteria as well as iNOS and MPO activities. Prior administration of dmPGE2 dose-dependently prevented intestinal lesions, together with inhibition of those functional changes. These effects of dmPGE2 were mimicked by prostanoids (ONO-NT-012 and ONO-AE1-329), only specific to EP3 or EP4 receptors, although the intestinal motility was inhibited only by ONO-AE1-329. Intestinal mucus secretion and fluid accumulation were decreased by indomethacin but enhanced by dmPGE2, ONO-NT-012, and ONO-AE1-329 at the doses that prevented intestinal lesions. Indomethacin also caused intestinal lesions in both wild-type and knockout mice lacking EP1 or EP3 receptors, yet the protective action of dmPGE2 was observed in wild-type and EP1 receptor knockout mice but not the mice lacking EP3 receptors. These results suggest that the intestinal cytoprotective action of PGE2 against indomethacin is mediated by EP3/EP4 receptors and that this effect is functionally associated with an increase of mucus secretion and enteropooling as well as inhibition of intestinal hypermotility, the former two processes mediated by both EP3 and EP4 receptors, and the latter by EP4 receptors.


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