GemfibrozilCAS# 25812-30-0 |
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Quality Control & MSDS
Number of papers citing our products
Chemical structure
3D structure
| Cas No. | 25812-30-0 | SDF | Download SDF |
| PubChem ID | 3463 | Appearance | Powder |
| Formula | C15H22O3 | M.Wt | 250.33 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | CI-719 | ||
| Solubility | DMSO : 100 mg/mL (399.47 mM; Need ultrasonic) | ||
| Chemical Name | 5-(2,5-dimethylphenoxy)-2,2-dimethylpentanoic acid | ||
| SMILES | CC1=CC(=C(C=C1)C)OCCCC(C)(C)C(=O)O | ||
| Standard InChIKey | HEMJJKBWTPKOJG-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C15H22O3/c1-11-6-7-12(2)13(10-11)18-9-5-8-15(3,4)14(16)17/h6-7,10H,5,8-9H2,1-4H3,(H,16,17) | ||
| 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. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Gemfibrozil is an activator of PPAR-α, used as a lipid-lowering drug; Gemfibrozil is also a nonselective inhibitor of several P450 isoforms, with Ki values for CYP2C9, 2C19, 2C8, and 1A2 of 5.8, 24, 69, and 82 μM, respectively.In Vitro:Gemfibrozil is an activator of PPAR-α, used as a lipid-lowering drug[1]; also a nonselective inhibitor of several P450 isoforms, with Ki values for CYP2C9, 2C19, 2C8, and 1A2 of 5.8, 24, 69, and 82 μM, respectively[3]. Gemfibrozil (100, 150, 200 μM) inhibits the cytokine-induced NO production in a concentration dependent manner in human U373MG astroglial cells, and such effects are not due to any change of the stability of iNOS mRNA. Gemfibrozil (50, 100, 200 μM) inhibits human iNOS promoter-derived luciferase activity in cytokine-stimulated human U373MG astroglial cells. Furthermore, Gemfibrozil (50, 100, 150, and 200 μM) shows no effects on the viability of the cells[1]. Gemfibrozil considerably inhibits both M-23 and M-1 formation (catalyzed by CYP2C8 and CYP3A4), with Ki (IC50) values of 69 μM (95 μM) and 273 μM (>250 μM), respectively, in human liver microsomes. Gemfibrozil (0-250 μM) dose dependently inhibits the formation of M-23 (IC50, 68 μM) and M-1 (IC50, 78 μM) in recombinant CYP2C8, but shows no appreciable effect on the formation of these metabolites in recombinant CYP3A4[3].In Vivo:Gemfibrozil (62 mg/kg/day, p.o.) treatment initiated 3 days before spinal cord injury (SCI) causes decreased locomotor function, and induces a trend for decreased white matter sparing after injury in mice. Gemfibrozil (62 mg/kg/day, p.o.) decreases macrophage immunoreactivity but increases T cell infiltration into spared tissue[2]. References: | |||||
Gemfibrozil Dilution Calculator
Gemfibrozil Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 3.9947 mL | 19.9736 mL | 39.9473 mL | 79.8945 mL | 99.8682 mL |
| 5 mM | 0.7989 mL | 3.9947 mL | 7.9895 mL | 15.9789 mL | 19.9736 mL |
| 10 mM | 0.3995 mL | 1.9974 mL | 3.9947 mL | 7.9895 mL | 9.9868 mL |
| 50 mM | 0.0799 mL | 0.3995 mL | 0.7989 mL | 1.5979 mL | 1.9974 mL |
| 100 mM | 0.0399 mL | 0.1997 mL | 0.3995 mL | 0.7989 mL | 0.9987 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. | |||||
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Gemfibrozil (Lopid) is a compound used to lower lipid levels.
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Peroxisome Proliferator-Activated Receptor alpha Activation Suppresses Cytochrome P450 Induction Potential in Mice Treated with Gemfibrozil.[Pubmed:28374976]
Basic Clin Pharmacol Toxicol. 2017 Sep;121(3):169-174.
Gemfibrozil, a peroxisome proliferator-activated receptor alpha (PPARalpha) agonist, is widely used for hypertriglyceridaemia and mixed hyperlipidaemia. Drug-drug interaction of Gemfibrozil and other PPARalpha agonists has been reported. However, the role of PPARalpha in cytochrome P450 (CYP) induction by fibrates is not well known. In this study, wild-type mice were first fed Gemfibrozil-containing diets (0.375%, 0.75% and 1.5%) for 14 days to establish a dose-response relationship for CYP induction. Then, wild-type mice and Pparalpha-null mice were treated with a 0.75% Gemfibrozil-containing diet for 7 days. CYP3a, CYP2b and CYP2c were induced in a dose-dependent manner by Gemfibrozil. In Pparalpha-null mice, their mRNA level, protein level and activity were induced more than those in wild-type mice. So, Gemfibrozil induced CYP, and this action was inhibited by activated PPARalpha. These data suggested that the induction potential of CYPs was suppressed by activated PPARalpha, showing a potential role of this receptor in drug-drug interactions and metabolic diseases treated with fibrates.
Modelling the photochemical attenuation pathways of the fibrate drug gemfibrozil in surface waters.[Pubmed:27987461]
Chemosphere. 2017 Mar;170:124-133.
Gemfibrozil (GFZ) is a relatively persistent pollutant in surface-water environments and it is rather recalcitrant to biological degradation. The GFZ photochemical lifetimes are relatively short in shallow waters with low levels of dissolved organic carbon (DOC), but they can reach the month-year range in deep and high-DOC waters. The main reason is that GFZ undergoes negligible reaction with singlet oxygen or degradation sensitised by the triplet states of chromophoric dissolved organic matter, which are the usually prevalent photochemical pathways in deep and high-DOC sunlit waters. Nitrate and nitrite scarcely affect the overall GFZ lifetimes, but they can shift photodegradation from direct photolysis to the OH process. These two pathways are the main GFZ phototransformation routes, with the direct photolysis prevailing in shallow environments during summer. Under these conditions the GFZ photochemical lifetimes are also shorter and the environmental significance of photodegradation correspondingly higher. The direct photolysis of GFZ under UVB irradiation yielded several transformation intermediates deriving from oxidation or cleavage of the aliphatic lateral chain. A quinone derivative (2,5-dimethyl-1,4-benzoquinone), a likely oxidation product of the transformation intermediate 2,5-dimethylphenol, is expected to be the most acutely and chronically toxic compound arising from GFZ direct photolysis. Interestingly, literature evidence suggests that the same toxic intermediate would be formed upon OH reaction.
Gemfibrozil, food and drug administration-approved lipid-lowering drug, increases longevity in mouse model of late infantile neuronal ceroid lipofuscinosis.[Pubmed:28199020]
J Neurochem. 2017 May;141(3):423-435.
Late Infantile Neuronal Ceroid Lipofuscinosis (LINCL) is a rare neurodegenerative disease caused by mutations in the Cln2 gene that leads to deficiency or loss of function of the tripeptidyl peptidase 1 (TPP1) enzyme. TPP1 deficiency is known to cause the accumulation of autofluoroscent lipid-protein pigments in brain. Similar to other neurodegenerative disorders, LINCL is also associated with neuroinflammation and neuronal damage. Despite investigations, no effective therapy is currently available for LINCL. Therefore, we administered Gemfibrozil (gem), an food and drug administration (FDA)-approved lipid-lowering drug, which has been shown to stimulate lysosomal biogenesis and induce anti-inflammation, orally, at a dose of 7.5 mg/kg body wt/day to Cln2((-/-)) mice. We observed that gem-fed Cln2((-/-)) mice lived longer by more than 10 weeks and had better motor activity compared to vehicle (0.1% Methyl cellulose) treatment. Gem treatment lowered the burden of storage materials, increased anti-inflammatory factors like SOCS3 and IL-1Ra, up-regulated anti-apoptotic molecule like phospho-Bad, and reduced neuronal apoptosis in the brain of Cln2((-/-)) mice. Collectively, this study reinforces a neuroprotective role of gem that may be of therapeutic interest in improving the quality of life in LINCL patients.
Transport behavior of the pharmaceutical compounds carbamazepine, sulfamethoxazole, gemfibrozil, ibuprofen, and naproxen, and the lifestyle drug caffeine, in saturated laboratory columns.[Pubmed:28284639]
Sci Total Environ. 2017 Jul 15;590-591:708-719.
Despite the large number of pharmaceutically active compounds found in natural environments little is known about their transport behavior in groundwater, which is complicated by their wide range of physical and chemical properties. The transport behavior of five widely used and often detected pharmaceutical compounds and one lifestyle drug has therefore been investigated, using a set of three column experiments. The investigated compounds were the anticonvulsant carbamazepine, the lifestyle drug caffeine, the antibiotic sulfamethoxazole, the lipid regulator Gemfibrozil, and the nonsteroidal anti-inflammatories ibuprofen and naproxen. The columns were filled with three different types of sand. The substrates consisted of artificially prepared iron-coated sand, artificially prepared organic carbon sand (with 5% leaf compost), and natural aquifer sand from Long Point, Ontario (Canada). The experiments were conducted simultaneously under the same hydraulic conditions and with the same input solution of about 1mug.L(-1) of each compound. The transport behavior of the organic compounds differed significantly between both the different columns and the different compounds. A strong correlation was observed between the retardation factors for carbamazepine, Gemfibrozil, and ibuprofen and the organic carbon content of the substrate. While the retardation increased with increasing organic carbon content, no direct relationship was observed between the organic carbon content and the removal of these compounds. In contrast, the retardation factors for sulfamethoxazole and naproxen showed no correlation with the organic carbon content but these compounds were significantly removed in the presence of organic matter. The influence of the Fe(3+) surfaces in the iron-coated sand was less significant than expected, with all compounds except for sulfamethoxazole having retardation factors <1.8. Caffeine was so strongly removed during transport through those substrates containing organic carbon that no reliable retardation factor could be determined.
