Catalog No.S4223 Synonyms: ML-236B
Molecular Weight(MW): 390.51
Mevastatin is a competitive inhibitor of HMG-Coenzyme A (HMG-CoA) reductase with a binding affinity 10,000 times greater than the HMG-CoA substrate itself.
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Sterol-starved HepG2 cells were treated with vehicle or mevastatin for 24 h before exposure to the indicated concentrations of MK-2206 for a further 14 h. Cells were then harvested and subjected to Western blot analysis. Upper panel shows one representative blot from six experiments. Lower panel: the immunoblots data were plotted relative to vehicle-treated cells. Error bars represent SD. One, two and three asterisks indicate p < 0.05, p < 0.01 and p < 0.001, respectively, compared with matched vehicle-treated cells.
Atherosclerosis, 2018, 276:28-38. Mevastatin purchased from Selleck.
SAHA and Statins on the proliferation of TNBC cells. TNBC or MCF-10A cells were treated with (D) Mevastatin, (E) Mevastatin + 0.5 μmol/l SAHA. Except for that a final concentration of 0.5 μmol/l SAHA was used in combination groups, serial 2-fold dilutions of each compound in a final concentration range of 32–0.03 μmol/l were used in experiments. Cell counting was assessed by using CCK8 reagent at 72 h after treatments. Dose-response curves were plotted as concentration (logarithmic scale) versus normalized response-variable slope using non-linear regression by software Prism 5.0 (Graphpad). Experiments were performed in triplicate, and data were presented as the mean±S.E.M.
Eur J Pharmacol, 2017, 813:161-171. Mevastatin purchased from Selleck.
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Choose Selective HMG-CoA Reductase Inhibitors
|Description||Mevastatin is a competitive inhibitor of HMG-Coenzyme A (HMG-CoA) reductase with a binding affinity 10,000 times greater than the HMG-CoA substrate itself.|
Mevastatin is a cholesterol-lowering agent isolated from Penicillium citinium. It reduces cholesterol synthesis to 50% of control at 0.01 pg/mL (26 nM).  It is structurally similar to the HMG, a substituent of the endogenous substrate of HMG-CoA reductase. Mevastatin is a prodrug that is activated in vivo via hydrolysis of the lactone ring. The hydrolyzed lactone ring mimics the tetrahedral intermediate produced by the reductase allowing the agent to bind with 10,000 times greater affinity than its natural substrate. The bicyclic portion of mevastatin binds to the coenzyme A portion of the active site. Mevastatin increases levels of eNOS mRNA and protein, reduces infarct size, and improves neurological deficits in a dose- and time-dependent manner.
|In vivo||At doses of 5 and 20 mg/kg, mevastatin produces reduction of serum cholesterol levels at 3 hours after oral administration. It lowers the levels of serum cholesterol by approximately 30 % at a dose of 20 mg/kg.  Mevastatin lowers hepatic production of cholesterol by competitively inhibiting HMG-CoA reductase. Cholesterol levels are reduced only after 28 days of treatment and does not correlate with infarct reduction. Baseline absolute cerebral blood flow is 30% higher after 14-day high-dose treatment. |
|In vitro||DMSO||78 mg/mL (199.73 mM)|
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