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Formula | C24H36O5 |
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Molecular Weight | 404.54 | CAS No. | 75330-75-5 | ||||
Solubility (25°C)* | In vitro | DMSO | 80 mg/mL (197.75 mM) | ||||
Ethanol | 30 mg/mL (74.15 mM) | ||||||
Water | Insoluble | ||||||
In vivo (Add solvents to the product individually and in order) |
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* <1 mg/ml means slightly soluble or insoluble. * Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations. * Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.) |
Description | Lovastatin is an inhibitor of HMG-CoA reductase with IC50 of 3.4 nM in a cell-free assay, used for lowering cholesterol (hypolipidemic agent). Lovastatin triggers autophagy. | ||
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Targets |
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In vitro | Lovastatin inhibits LPS- and cytokine-mediated production of NO and expression of iNOS in rat primary astrocytes. Lovastatin inhibits LPS-induced expression of TNF-alpha, IL-1beta, and IL-6 in rat primary astrocytes, microglia, and macrophages. [1] Lovastatin results in over 95% inhibition of DNA synthesis as measured by incorporation of [3H]thymidine into DNA. Lovastatin synchronizes cells in the G1 and not in the G0 phase of the cell cycle. Lovastatin has a similar growth-inhibitory activity against ras-dependent as well as ras-independent cell lines. [2] Lovastatin produces a profound reduction of apolipoprotein-B-containing lipoproteins, especially LDL cholesterol and, to a lesser extent, plasma triglyc- erides, and a small increase in HDL cholesterol. [3] Lovastatin arrests cells by inhibiting the proteasome, which results in the accumulation of p21 and p27, leading to G1 arrest. Lovastatin is an inhibitor of hydroxymethyl glutaryl (HMG)-CoA reductase, the rate-limiting enzyme in cholesterol synthesis. Lovastatin can be used to arrest cultured cells in the G1 phase of the cell cycle, resulting in the stabilization of the cyclin-dependent kinase inhibitors (CKIs) p21 and p27. [4] Lovastatin (2-10 mM) arrests cells in G1 and also prolonged--or arrested a minor fraction of cells in--the G2 phase of the cell cycle in human bladder carcinoma T24 cell line expressing activated p21ras. Lovastatin (50 mM) is cytotoxic in human bladder carcinoma T24 cell line expressing activated p21ras. [5] |
Cell Assay: |
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Animal Study: |
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, , Clin Cancer Res, 2016, 22(13):3310-3319
Data from [Data independently produced by , , Cell Cycle, 2018, 17(9):1138-1145]
Integration of 3D bioprinting and multi-algorithm machine learning identified glioma susceptibilities and microenvironment characteristics [ Cell Discov, 2024, 10(1):39] | PubMed: 38594259 |
Multi-omics and pharmacological characterization of patient-derived glioma cell lines [ Nat Commun, 2024, 15(1):6740] | PubMed: 39112531 |
Dysregulated Ribosome Biogenesis Is a Targetable Vulnerability in Triple-Negative Breast Cancer: MRPS27 as a Key Mediator of the Stemness-inhibitory Effect of Lovastatin [ Int J Biol Sci, 2024, 20(6):2130-2148] | PubMed: 38617541 |
Dysregulated Ribosome Biogenesis Is a Targetable Vulnerability in Triple-Negative Breast Cancer: MRPS27 as a Key Mediator of the Stemness-inhibitory Effect of Lovastatin [ Int J Biol Sci, 2024, 20(6):2130-2148] | PubMed: 38617541 |
Coordination of oxysterol binding protein 1 and VAP-A/B modulates the generation of cholesterol and viral inclusion bodies to promote grass carp reovirus replication [ Front Immunol, 2024, 15:1419321] | PubMed: 39081319 |
African swine fever virus pB318L, a trans-geranylgeranyl-diphosphate synthase, negatively regulates cGAS-STING and IFNAR-JAK-STAT signaling pathways [ PLoS Pathog, 2024, 20(4):e1012136] | PubMed: 38620034 |
Necrosulfonamide causes oxidation of PCM1 and impairs ciliogenesis and autophagy [ iScience, 2024, 27(4):109580] | PubMed: 38600973 |
NSDHL contributes to breast cancer stem-like cell maintenance and tumor-initiating capacity through TGF-β/Smad signaling pathway in MCF-7 tumor spheroid [ BMC Cancer, 2024, 24(1):1370] | PubMed: 39516821 |
Ku80 is indispensable for repairing DNA double-strand breaks at highly methylated sites in human HCT116 cells [ DNA Repair (Amst), 2024, 134:103627] | PubMed: 38219597 |
Cholesterol biosynthesis inhibition synergizes with AKT inhibitors in triple-negative breast cancer [ bioRxiv, 2024, 10.1101/2024.01.16.575899] | PubMed: none |
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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.
NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.