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MF63 potently inhibited the human mPGES-1 enzyme (IC50=1.3 nM), with a high degree (>1000-fold) of selectivity over other prostanoid synthases. Microsomal prostaglandin E synthase-1 (mPGES-1) is a terminal prostaglandin E (2) (PGE (2)) synthase in the cyclooxygenase pathway. Inhibitors of mPGES-1 may block PGE (2) production and relieve inflammatory symptoms. In rodent species, MF63 strongly inhibited guinea pig mPGES-1 (IC50=0.9 nM) but not the mouse or rat enzyme. In addition, MF63 did not cause NSAID-like gastrointestinal toxic effects, such as mucosal erosions or leakage in the KI mice or nonhuman primates, although it markedly inhibited PGE2 synthesis in the KI mouse stomach.
Oncotarget. 2016 Jul 12;7(28):44350-44364.
Linking microsomal prostaglandin E Synthase-1/PGE-2 pathway with miR-15a and -186 expression: Novel mechanism of VEGF modulation in prostate cancer
MF63 purchased from AbMole
Am J Physiol Gastrointest Liver Physiol. 2016 Jun 1;310(11):G1071-80.
Microsomal prostaglandin E synthase-1 protects against Fas-induced liver injury.
MF63 purchased from AbMole
Endocr Relat Cancer. 2015 Aug;665-78.
mPGES-1 in prostate cancer controls stemness and amplifies epidermal growth factor receptor-driven oncogenicity.
MF63 purchased from AbMole
. figure 4.jpg) |
Source | Oncotarget (2016). Figure 4. MF63 (Abmole Bioscience, Houston, TX, USA) |
| Method | ||
| Cell Lines | mPGES-1+/+ cells | |
| Concentrations | 10 μM | |
| Incubation Time | 18 h | |
| Results | Moreover, MF63 increased levels of both miRs in mPGES-1+/+ cells (Figure 4C), and miR-15a and miR-186 were up-regulated with respect to mPGES-1+/+ tumors in DU145 mPGES-1-/- xenografts in vivo (Figure 4D). |
. figure 3.jpg) |
Source | Oncotarget (2016). Figure 3. MF63 (Abmole Bioscience, Houston, TX, USA) |
| Method | ||
| Cell Lines | mPGES-1+/+ cells | |
| Concentrations | 10 μM | |
| Incubation Time | ||
| Results | Consistently,MF63 (10 μM) significantly increased Dicer expression in mPGES-1+/+ cells (Figure 3B), whereas exogenous PGE-2(1 μM, 2–24 h) decreased in mPGES-1-/- cells (Figure 3C). |
. figure 1.jpg) |
Source | Oncotarget (2016). Figure 1. MF63 (Abmole Bioscience, Houston, TX, USA) |
| Method | ||
| Cell Lines | mPGES-1+/+ cells | |
| Concentrations | 10 μM | |
| Incubation Time | ||
| Results | MF63 (10 μM), a reversible mPGES-1 inhibitor, significantly decreased VEGF expression in mPGES-1+/+ cells with maximum effect at 8–18 h (Figure 1D), while exogenous PGE-2 (1 μM) increased VEGF release and expression in mPGES-1-/- cells time-dependently (Figure 1B, 1E). |
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Source | Am J Physiol Gastrointest Liver Physiol (2016) . Figure 4.mPGES-1 inhibitor MF63 (Abmole bioscience, Houston, TX) |
| Method | Western blotting analysis | |
| Cell Lines | ||
| Concentrations | 1µM | |
| Incubation Time | 6 h | |
| Results | The above effects were attenuated by pretreatment with the mPGES-1 inhibitor, MF63, in Jo2-treated mPGES-1 Tg mice (Fig. 4A). These findings indicate an important role of EGFR/Akt and associated apoptosis-regulatory molecules in mPGES-1-mediated protection against liver injury. |
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Source | Am J Physiol Gastrointest Liver Physiol (2016) . Figure 1.mPGES-1 inhibitor MF63 (Abmole bioscience, Houston, TX) |
| Method | mPGES-1 Tg mice oral gavage (twice every 12 h) | |
| Cell Lines | ||
| Concentrations | 50µg/g body weight | |
| Incubation Time | 5 h | |
| Results | Two doses of MF63 were administrated via oral gavage (every 12h) before Jo2 injection and the mice were sacrificed 5 hours after Jo2 injection (outlined in Fig. 3A). We observed that MF63 pretreatment partially reversed the resistance of mPGES-1 Tg mice to Jo2-induced liver injury (Fig. 3B-F).These findings further support the role of mPGES-1 in modulation of Fas-induced hepatocyte apoptosis and liver injury. |
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Source | Endocrinology (2015) . Figure 4. MF63 was from AbMole. |
| Method | EIA assay and western blot analysis | |
| Cell Lines | DU145, PC-3 | |
| Concentrations | 10 µ M | |
| Incubation Time | 48 h | |
| Results | MF63 (10 µmol l-1, 24-48 h) significantly inhibited PGE2 production and reversed the mesenchymal phenotype in DU145 and PC-3 cells, promoting E-cadherin and inhibiting vimentin expression (Fig. 4A, B and C). MF63 also upregulated α6-integrin and significantly reduced cell clonogenicity (Fig.4D, and E). |
| Cell Experiment | |
|---|---|
| Cell lines | A549 cells |
| Preparation method | A549 cells were seeded in 96-well dishes at a density of 25,000 cells/well and incubated for 20 h in RPMI 1640 medium supplemented with 2% fetal bovine serum (FBS). The cells were then incubated with 10 ng/ml IL-1 for 24 h in the presence of a vehicle or inhibitor from a 100-fold concentrated DMSO stock solution in a medium containing 2 or 50% FBS. Concentrations of PGE2 and PGF2 in the cell-free medium were measured by EIA (Assay Designs Inc.). IC50 values were derived from eight-point titrations. |
| Concentrations | 0.01~100 µ M |
| Incubation time | 24 h |
| Animal Experiment | |
|---|---|
| Animal models | mPGES-1 Knock-In Mice |
| Formulation | a suspension in 0.5% methylcellulose |
| Dosages | 100 mg/kg |
| Administration | oral gavage |
| Molecular Weight | 378.81 |
| Formula | C23H11ClN4 |
| CAS Number | 892549-43-8 |
| Solubility (25°C) | DMSO 42 mg/mL |
| Storage |
Powder -20°C 3 years ; 4°C 2 years In solvent -80°C 6 months ; -20°C 1 month |
| Related PGE synthase Products |
|---|
| Vipoglanstat
Vipoglanstat (BI 1029539) is an inhibitor of microsomal prostaglandin E synthase-1 (mPGES-1; IC50 = ≤0.5 nM in isolated human whole blood). Vipoglanstat reduces LPS-induced increases in the influx of neutrophils and levels of cytokines in bronchoalveolar lavage fluid (BALF), as well as the expression of PTGES, the gene encoding mPGES-1, Cox2, and Icam1 in the lung parenchyma, in a human PTGES knock-in mouse model of acute lung injury when administered at a dose of 30 mg/kg. |
| mPGES1-IN-7
mPGES-1-IN-2 is a benzimidazole-based mPGES-1 inhibitor that also inhibits adipophysin PGD synthase (I-PGDS) (5 μM, IR=60 %). |
| (E)-KME-4
(E)-KME-4 is a potent inhibitor of prostaglandin synthetase (PGS) with an IC50 of 0.28 μM; also inhibits 5-lipoxygenase with an IC50 of 1.05 μM. |
| Friluglanstat
Friluglanstat is a prostaglandin E synthase (mPGES-1) inhibitor, with anti-inflammatory activity. |
| UT-11
UT-11 is a potent and brain-permeable microsomal prostaglandin E synthase-1 (mPGES-1) inhibitor. |
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