|Source:||From Penicillium Citrinum|
|Biological Activity or Inhibitors:||1. Mevastatin inhibits the differentiation of TAO derived orbital preadipocytes by blocking PPAR-gamma mRNA expression.
2. Mevastatin triggers the phosphorylation of the EGFR and that this is because of the inhibition of farnesylated and geranylgeranylated proteins.
3.Treatment with Mevastatin alone and DAC followed by Mevastatin resulted in apoptotic response in a time- and dose-dependent manner.
4. The c-Jun N-terminal kinase pathway was required for Mevastatin-induced cell growth inhibition and apoptosis in SACC cells.
|Solvent:||Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.|
|Storage:||Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).
Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.
Need more advice on solubility, usage and handling? Please email to: email@example.com
|After receiving:||The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.|
|1 mg||5 mg||10 mg||20 mg||25 mg|
|1 mM||2.5608 mL||12.8038 mL||25.6075 mL||51.2151 mL||64.0188 mL|
|5 mM||0.5122 mL||2.5608 mL||5.1215 mL||10.243 mL||12.8038 mL|
|10 mM||0.2561 mL||1.2804 mL||2.5608 mL||5.1215 mL||6.4019 mL|
|50 mM||0.0512 mL||0.2561 mL||0.5122 mL||1.0243 mL||1.2804 mL|
|100 mM||0.0256 mL||0.128 mL||0.2561 mL||0.5122 mL||0.6402 mL|
Hum Exp Toxicol. 2014 Apr;33(4):414-23.
|The DNA methyl transferase inhibitor, 5'-aza-2-deoxycitidine, enhances the apoptotic effect of Mevastatin in human leukemia HL-60 cells.[Pubmed: 23918904]|
|We aimed to investigate possible effects of Mevastatin (Mev) alone and sequential treatment of 5'-aza-2-deoxycitidine (DAC) and Mev on HL-60 cell line using XTT (2,3-bis-(2-methoxy-4-nitro-5-sulfophenyl)-2H-tetrazolium-5-carboxanilide) assay, lactate dehydrogenase release assay, flourescence microscopy, DNA fragmentation analysis, determination of DNA synthesis rate, and active caspase-3 assay. Messenger RNA (mRNA) expression of apoptotic and antiapoptotic genes were also evaluated by semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) for BAX, BCL2, and XIAP genes and quantitative Real-time PCR for CASP3, CASP8, and CASP9 genes. We showed that treatment with Mevastatin alone and DAC followed by Mevastatin resulted in apoptotic response in a time- and dose-dependent manner. We also found that pretreatment with DAC sensitized HL-60 cells to Mevastatin and caused more apoptotic cell death than Mevastatin-alone treatment via caspase-3 activation and DNA fragmentation. Moreover, sequential addition of Mevastatin after DAC diminished DNA synthesis rate more effectively than Mevastatin-alone treatment. Furthermore, DAC pretreatment significantly increased CASP3 and CASP9 mRNA expression even with lower doses of Mevastatin. BAX, BCL2, and XIAP gene mRNA levels were also found to be changed in the presence of DAC and Mevastatin. Determination of the exact molecular effects of statins and DAC would allow us to identify new molecular targets to develop more effective treatment regimens for cancer.|
Anticancer Drugs. 2010 Aug;21(7):678-86.
|Activation of c-Jun N-terminal kinase is required for mevastatin-induced apoptosis of salivary adenoid cystic carcinoma cells.[Pubmed: 20629200]|
|This study aims to explore the proapoptotic effects and underlying mechanisms of statins on human salivary adenoid cystic carcinoma (SACC). Exposure of SACC cells to Mevastatin resulted in cell growth inhibition and apoptosis in a dose-dependent manner, accompanied by the release of cytochrome c and cleavage of caspase-3. A remarkable decrease in phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) and increase in phosphorylation of c-Jun N-terminal kinase (JNK) and p38 mitogen-activated kinase were observed. Furthermore, the JNK-specific inhibitor SP600125, but not the p38-specific inhibitor SB203580, abolished Mevastatin-induced cell growth inhibition and apoptosis in SACC cells. This was supported by results in which the JNK inhibitor efficiently blocked Mevastatin-induced JNK phosphorylation, but not p38 phosphorylation, and further decreased Mevastatin-induced phosphorylation of ERK1/2. Taken together, the results suggest that the JNK pathway was required for Mevastatin-induced cell growth inhibition and apoptosis in SACC cells. Statins could be potential anticancer agents for SACC chemotherapy.|
Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2010 May;35(5):511-7.
|Mevastatin inhibits the differentiation of thyroid-associated ophthalmopathy derived orbital preadipocytes.[Pubmed: 20543477]|
|To investigate the effect of Mevastatin (Mev) on the expression of peroxisome-proliferator-activated receptor-gamma (PPAR-gamma) mRNA and differentiation of Thyroid-associated ophthalmopathy (TAO) derived orbital preadipocytes in vitro. Mevastatin inhibits the differentiation of TAO derived orbital preadipocytes by blocking PPAR-gamma mRNA expression. The degree of inhibition is not only concentration-dependent but also associated with the stage of differentiation. The earlier the differentiation, the stronger the inhibition.|
J Neurosci Res. 2009 Jul;87(9):2138-44.
|Mevastatin-induced neurite outgrowth of neuroblastoma cells via activation of EGFR.[Pubmed: 19224573]|
|We found that Mevastatin triggered neurite outgrowth of neuroblastoma cells and examined the responsible signaling pathways. Treatment of Neuro2a cells with Mevastatin for 24 hr induced neurite outgrowth associated with up-regulation of the neuronal marker protein NeuN. Interestingly, we found that Mevastatin triggered phosphorylation of the key kinases epidermal growth factor receptor (EGFR), ERK1/2, and Akt/protein kinase B. Inhibition of EGFR, PI3K, and the mitogen-activated protein kinase cascade blocked Mevastatin-induced neurite outgrowth. Moreover, add-back experiments of cell-permeable cholesterol precursors indicated that farnesylated and geranylgeranylated proteins play a major role in statin-induced neurite outgrowth. Taken together, our results provide the first mechanistic insight into statin-triggered signaling pathways that lead to neurite outgrowth in neuroblastoma cells. Surprisingly, we revealed that Mevastatin triggered the phosphorylation of the EGFR and that this was because of the inhibition of farnesylated and geranylgeranylated proteins.|