Home Metabolism HMG-CoA Reductase inhibitor - Autophagy activator Atorvastatin For research use only.

Atorvastatin

Atorvastatin is a lipid lowering agent. It is a competitive inhibitor of hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase, the rate-determining enzyme in cholesterol biosynthesis via the mevalonate pathway. Atorvastatin activates autophagy.

Atorvastatin Chemical Structure

Atorvastatin Chemical Structure

CAS: 134523-00-5

Selleck's Atorvastatin has been cited by 23 publications

Purity & Quality Control

Batch: Purity: 99.51%
99.51

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Cell Data

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HEK293 Function assay TP_TRANSPORTER: uptake in OATP1B1-expressing HEK293 cells, Km=12.4μM 15970799
L6 Function assay Inhibition of cholesterol synthesis in rat L6 cells assessed as incorporation of [14C]acetate into cholesterol, IC50=0.078μM 18412317
C2C12 Function assay 1 uM Induction of cell differentiation in mouse C2C12 cells assessed as myosin heavy chain expression at 1 uM 20081855
HepG2 Function assay 1 uM Upregulation of LDL receptor expression in human HepG2 cells at 1 uM in presence of ARH-specific siRNA 20356098
HEK293 Function assay Activity at human liver OATP1B3 expressed in HEK293 Flp-In cells, Km=0.73μM 22541068
HEK293 Function assay Activity at human liver OATP1B1 expressed in HEK293 Flp-In cells, Km=0.77μM 22541068
HEK293 Function assay Activity at human liver OATP2B1 expressed in HEK293 Flp-In cells, Km=2.84μM 22541068
HEK293 Function assay Inhibition of OATP1B1 (unknown origin) expressed in HEK293 cells using estradiol-17beta-glucuronide substrate, IC50=0.6μM 22587986
HEK293 Function assay Inhibition of OATP1B1 (unknown origin) expressed in HEK293 cells using pitavastatin substrate, IC50=0.8μM 22587986
HEK293 Function assay Inhibition of OATP1B1 (unknown origin) expressed in HEK293 cells using estrone-3-sulfate substrate, IC50=1.6μM 22587986
hepatocytes Function assay 0.1 to 10 uM up to 90 mins Drug metabolism in Sprague-Dawley rat hepatocytes assessed per 10'6 cells at 0.1 to 10 uM up to 90 mins by media-loss method, Km=0.43μM 22593038
hepatocytes Function assay 0.1 to 10 uM up to 90 mins Drug metabolism in Sprague-Dawley rat hepatocytes assessed per 10'6 cells at 0.1 to 10 uM up to 90 mins by conventional assay, Km=1.3μM 22593038
A549 Cytotoxicity assay 72 hrs Cytotoxicity against human A549 cells after 72 hrs by MTT assay, IC50=8.7μM 23570542
HS68 Cytotoxicity assay 72 hrs Cytotoxicity against human HS68 cells after 72 hrs by MTT assay, IC50=22.7μM 23570542
MEF Cytotoxicity assay 72 hrs Cytotoxicity against mouse MEF cells after 72 hrs by MTT assay, IC50=30.7μM 23570542
HepG2 Function assay 10 uM Induction of SREBP2 maturation in human HepG2 cells at 10 uM after overnight incubation by immunoblot analysis 26784936
human red blood cells Antiplasmodial assay 48 hrs Antiplasmodial activity against chloroquine-resistant Plasmodium falciparum W2 infected in human red blood cells after 48 hrs by SYBR test, IC50=10.3μM 26988303
Hep3G Function assay 25 uM 48 hrs Inhibition of HMG CoA reductase in human Hep3G cells assessed as increase in LDL receptor expression at 25 uM incubated for 48 hrs by immunofluorescence method 31005367
A549 Function assay Reductase Activity Assay: The HMGR activity was performed using HMG-CoA reductase assay kit from Sigma-Aldrich with the human recombinant protein or 100 μg total cell lysates from A549 cells. Lovastatin was used as a positive control, and SAHA as a negati, IC50=0.0116μM ChEMBL
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Biological Activity

Description Atorvastatin is a lipid lowering agent. It is a competitive inhibitor of hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase, the rate-determining enzyme in cholesterol biosynthesis via the mevalonate pathway. Atorvastatin activates autophagy.
In vitro
In vitro

Atorvastatin, one of the statins, inhibits the c-Myc pathway in chronic myeloid leukemia (CML) cells, demonstrating that c-Myc is a target of statins.[1]
Cell Research Cell lines murine CML-KLS+ cells, OP-9 stromal cells
Concentrations 2 μM
Incubation Time 3 days
Method

CML cKit+Lineage Sca1+ (KLS) cells are isolated from CML mice. Thereafter, the effect of statins on the colony-forming capacity of CML-KLS cells is determined. Freshly isolated CML-KLS cells are co-cultured with OP-9 stromal cells in the presence of IM (1 M), DA (0.5 M), and rosuvastatin (2 M) or atorvastatin (2 M) for 72 h. Thereafter, the cells are washed with PBS and transferred to semi-solid medium. The number of colonies is counted under the microscope.
Experimental Result Images Methods Biomarkers Images PMID
Growth inhibition assay Cell viability 24815071
Western blot PDX-1 / BETA2 / NeuroD 30863781
In Vivo
In vivo

ATV-Exos activates AKT/eNOS signaling pathway to augment the angiogenesis of endothelial cells via upregulating miR-211-3p, thereby resulting in accelerated wound regeneration of the diabetic rats.[2]
Animal Research Animal Models Sprague-Dawley rats ofdiabetes models
Dosages 50 μg/mL
Administration s.c
NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT04915183 Not yet recruiting Hearing Loss|Head and Neck Cancer National Institute on Deafness and Other Communication Disorders (NIDCD)|National Institutes of Health Clinical Center (CC) January 12 2024 Phase 3
NCT06191991 Active not recruiting Healthy Volunteers Aligos Therapeutics November 3 2023 Phase 1

Chemical lnformation & Solubility

Molecular Weight 558.64 Formula

C33H35FN2O5
CAS No. 134523-00-5 SDF --
Smiles CC(C)C1=C(C(=C(N1CCC(CC(CC(=O)O)O)O)C2=CC=C(C=C2)F)C3=CC=CC=C3)C(=O)NC4=CC=CC=C4
Storage (From the date of receipt) 3 years -20°C powder

In vitro
Batch:

DMSO : 100 mg/mL ( (179.0 mM)； Moisture-absorbing DMSO reduces solubility. Please use fresh DMSO.)

Ethanol : 17 mg/mL

Water : Insoluble


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