1. Metabolic Enzyme/Protease
    Anti-infection
    Autophagy
    Apoptosis
  2. HMG-CoA Reductase (HMGCR)
    Bacterial
    Autophagy
    Apoptosis
    Antibiotic
  3. Mevastatin

Mevastatin (Synonyms: Compactin; ML236B)

Cat. No.: HY-17408 Purity: 99.59%
Handling Instructions

Mevastatin (Compactin) is a first HMG-CoA reductase inhibitor that belongs to the statins class. Mevastatin is a lipid-lowering agent, and induces apoptosis, arrests cancer cells in G0/G1 phase. Mevastatin also increases endothelial nitric oxide synthase (eNOS) mRNA and protein levels. Mevastatin has antitumor activity and has the potential for cardiovascular diseases treatment.

For research use only. We do not sell to patients.

Mevastatin Chemical Structure

Mevastatin Chemical Structure

CAS No. : 73573-88-3

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10 mM * 1 mL in DMSO USD 62 In-stock
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50 mg USD 55 In-stock
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100 mg USD 90 In-stock
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500 mg USD 270 In-stock
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Based on 5 publication(s) in Google Scholar

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Description

Mevastatin (Compactin) is a first HMG-CoA reductase inhibitor that belongs to the statins class. Mevastatin is a lipid-lowering agent, and induces apoptosis, arrests cancer cells in G0/G1 phase. Mevastatin also increases endothelial nitric oxide synthase (eNOS) mRNA and protein levels. Mevastatin has antitumor activity and has the potential for cardiovascular diseases treatment[1][2][3].

IC50 & Target

HMG-CoA reductase[1][2]
Apoptosis[1]

In Vitro

Mevastatin (0-128 µM; 5 days; Caco-2 cells) treatment causes a dose-dependent decrease in cell number[1].
Mevastatin (32-128 µM; 24-72 hours; Caco-2 cells) treatment causes an early G0/G1 phase and a late G2/M phase cell cyclr arrest[1].
Mevastatin (32-128 µM; 72 hours; Caco-2 cells) treatment causes a down-regulation of cyclin-dependent kinases (cdk) 4 and cdk 6 as well as cyclin D1, while cdk 2 and cyclin E protein levels remained unchanged. Cell cycle inhibitors p21 and p27 are significantly upregulated by Mevastatin[1].
Mevastatin (16-256 µM; Caco-2 cells) treatment induces apoptosis in a dose-dependent manner[1].
Treatment of Neuro2a cells with mevastatin for 24 hours induced neurite outgrowth associated with up-regulation of the neuronal marker protein NeuN. Mevastatin triggers 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 blocks Mevastatin-induced neurite outgrowth[4].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Viability Assay[2]

Cell Line: Caco-2 cells
Concentration: 0 µM, 8 µM, 16 µM, 32 µM, 64 µM, 128 µM
Incubation Time: 5 days
Result: Caused a dose-dependent decrease in cell number.

Cell Cycle Analysis[2]

Cell Line: Caco-2 cells
Concentration: 32 µM, 64 µM, 128 µM
Incubation Time: 24 hours, 48 hours, 72 hours
Result: Caused a dose-dependent increase of cells in G0/G1 and G2/M phases of the cell cycle.

Western Blot Analysis[2]

Cell Line: Caco-2 cells
Concentration: 32 µM, 64 µM, 128 µM
Incubation Time: 72 hours
Result: Resulted in a down-regulation of cyclin-dependent kinases (cdk) 4 and cdk 6 as well as cyclin D1.
In Vivo

Mevastatin (2-20 mg/kg; delivered via ALZET miniosmotic pumps; daily; for 7, 14, or 28 days; wild-type 129-SV/eVTAcBr male mice and eNOS-deficient male mice) treatment increases levels of endothelial nitric oxide synthase (eNOS) mRNA and protein, reduces infarct size, and improves neurological deficits in a dose- and time-dependent manner[2].
The topical infusion of Mevastatin (2.5 pmol/hr) increases bone mass (MRL/MpJ mouse) of isografted bone by increasing bone turnover and, at least in part, by promoting the expression of bone morphogenetic protein-2 (BMP-2) mRNA and receptor activator of NF-κB ligand (RANKL) mRNA[3].

MCE has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Wild-type 129-SV/eVTAcBr male mice and eNOS-deficient male mice (18-22 g) with the filament model[2]
Dosage: 2 mg/kg or 20 mg/kg
Administration: Delivered via 7- or 14-day ALZET miniosmotic pumps implanted subcutaneously; daily; for 7, 14, or 28 days
Result: Increased levels of endothelial nitric oxide synthase (eNOS) mRNA and protein, reduced infarct size, and improved neurological deficits in a dose- and time-dependent manner.
Molecular Weight

390.51

Formula

C₂₃H₃₄O₅

CAS No.

73573-88-3

SMILES
Shipping

Room temperature in continental US; may vary elsewhere.

Storage

4°C, protect from light

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

Solvent & Solubility
In Vitro: 

DMSO : 25 mg/mL (64.02 mM; Need ultrasonic)

Preparing
Stock Solutions
Concentration Solvent Mass 1 mg 5 mg 10 mg
1 mM 2.5608 mL 12.8038 mL 25.6075 mL
5 mM 0.5122 mL 2.5608 mL 5.1215 mL
10 mM 0.2561 mL 1.2804 mL 2.5608 mL
*Please refer to the solubility information to select the appropriate solvent.
In Vivo:
  • 1.

    Add each solvent one by one:  10% DMSO    40% PEG300    5% Tween-80    45% saline

    Solubility: ≥ 2.5 mg/mL (6.40 mM); Clear solution

  • 2.

    Add each solvent one by one:  10% DMSO    90% (20% SBE-β-CD in saline)

    Solubility: ≥ 2.5 mg/mL (6.40 mM); Clear solution

  • 3.

    Add each solvent one by one:  10% DMSO    90% corn oil

    Solubility: ≥ 2.5 mg/mL (6.40 mM); Clear solution

*All of the co-solvents are provided by MCE.
References
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Keywords:

MevastatinCompactin ML236BHMG-CoA Reductase (HMGCR)BacterialAutophagyApoptosisAntibioticStatinsBMP-2NF-κBRANKLlipid-loweringEGFRphosphorylationeNOSneuroprotectioncardiovascularInhibitorinhibitorinhibit

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Mevastatin
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