Atorvastatin |
Catalog No.GC35419
One-Click Copy Product Info
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Atorvastatin is a potent synthetic HMG-CoA reductase inhibitor with IC₅₀ values of 7.6nM against the rat liver enzyme and 14.3nM against the human enzyme prepared from HepG2 cells.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 134523-00-5
Sample solution is provided at 25 µL, 10mM.
Atorvastatin is a potent synthetic HMG-CoA reductase inhibitor with IC₅₀ values of 7.6nM against the rat liver enzyme and 14.3nM against the human enzyme prepared from HepG2 cells[1]. Atorvastatin competitively inhibits HMG-CoA reductase, suppresses the mevalonate-cholesterol biosynthetic pathway, and thereby modulates downstream lipid, inflammatory, and cell-survival signaling[1][3][4]. Atorvastatin is used in research on lipid metabolism, inflammatory responses, intervertebral-disc degeneration, and neuroprotection[2][3][4][5][6][7].
In vitro, HepG2 cells treated with Atorvastatin (0.5μM; 24h) showed a 42% reduction in apolipoprotein B secretion, associated with enhanced intracellular apolipoprotein B degradation[2]. In PMA-differentiated THP-1 cells, Atorvastatin pretreatment (0-100μM; 24h), followed by lipopolysaccharide stimulation (0-100μg/mL; 24h), reduced interleukin-1β and tumor necrosis factor-α release and attenuated prostaglandin E₂, reactive oxygen species, and nitric oxide production; at 100μM, however, prostaglandin E₂ increased relative to lower-concentration responses[3]. In primary rat nucleus pulposus cells, Atorvastatin (10 and 20μM; 1h pretreatment) followed by tumor necrosis factor-α (50ng/mL; 24h) reduced matrix-catabolic and inflammatory proteins, while Atorvastatin (20μM; 1h pretreatment) decreased NLRP3, cleaved caspase-1, and GSDMD-NT by 52%, 65%, and 48%, respectively, and increased autophagic flux[4].
In vivo, rats received Atorvastatin (10mg/kg/day; oral administration once daily for 7 days) before intranasal MPTP exposure; Atorvastatin prevented short-term-memory impairment and depressive-like behavior and reduced motor deficits and substantia-nigra dopaminergic-neuron loss assessed on day21[5]. In mice, Atorvastatin (0.1mg/kg; single oral administration; behavioral assessment 1h later) produced an antidepressant-like response that was abolished by serotonin depletion or blockade of 5-HT₁A or 5-HT₂A/₂C receptors[6]. In a lipopolysaccharide-induced depressive-like behavior model, mice received Atorvastatin (1 and 10mg/kg/day; oral administration once daily for 7 days), followed by lipopolysaccharide (0.5mg/kg; single intraperitoneal injection; assessment 24h later). Atorvastatin prevented increased immobility without altering locomotor activity and prevented tumor necrosis factor-α elevation, brain-derived neurotrophic factor reduction, lipid peroxidation, and glutathione depletion in the hippocampus and prefrontal cortex[7].
References:
[1] Bergstrom JD, Bostedor RG, Rew DJ, Geissler WM, Wright SD, Chao YS. Hepatic responses to inhibition of 3-hydroxy-3-methylglutaryl-CoA reductase: a comparison of atorvastatin and simvastatin. Biochim Biophys Acta. 1998;1389(3):213-221. doi:10.1016/S0005-2760(97)00182-3.
[2] Wilcox LJ, Barrett PHR, Huff MW. Differential regulation of apolipoprotein B secretion from HepG2 cells by two HMG-CoA reductase inhibitors, atorvastatin and simvastatin. J Lipid Res. 1999;40(6):1078-1089. PMID:10357840.
[3] McFarland AJ, Davey AK, McDermott CM, Grant GD, Lewohl J, Anoopkumar-Dukie S. Statins reduce lipopolysaccharide-induced cytokine and inflammatory mediator release in an in vitro model of microglial-like cells. Mediators Inflamm. 2017;2017:2582745. doi:10.1155/2017/2582745.
[4] Chen J, Yan J, Li S, Zhu J, Zhou J, Li J, et al. Atorvastatin inhibited TNF-α induced matrix degradation in rat nucleus pulposus cells by suppressing NLRP3 inflammasome activity and inducing autophagy through NF-κB signaling. Cell Cycle. 2021;20(20):2160-2173. doi:10.1080/15384101.2021.1973707.
[5] Castro AA, Wiemes BP, Matheus FC, Lapa FR, Viola GG, Santos AR, et al. Atorvastatin improves cognitive, emotional and motor impairments induced by intranasal 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine administration in rats, an experimental model of Parkinson's disease. Brain Res. 2013;1513:103-116. doi:10.1016/j.brainres.2013.03.029.
[6] Ludka FK, Constantino LC, Dal-Cim T, Binder LB, Zomkowski A, Rodrigues AL, Tasca CI. Atorvastatin evokes a serotonergic system-dependent antidepressant-like effect in mice. Pharmacol Biochem Behav. 2014;122:253-260. doi:10.1016/j.pbb.2014.04.005.
[7] Taniguti EH, Ferreira YS, Stupp IJV, Fraga-Junior EB, Mendonça CB, Rossi FL, et al. Atorvastatin prevents lipopolysaccharide-induced depressive-like behaviour in mice. Brain Res Bull. 2019;146:279-286. doi:10.1016/j.brainresbull.2019.01.018.
| Cell experiment [1]: | |
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Cell lines |
Primary rat nucleus pulposus cells |
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Preparation Method |
Primary rat nucleus pulposus cells were isolated and cultured, and cell viability after exposure to different concentrations was measured using CCK-8. For subsequent experiments, cells were pretreated with Atorvastatin before tumor necrosis factor-α stimulation. Extracellular-matrix metabolism, NLRP3-inflammasome, and NF-κB-related markers were analyzed using quantitative PCR, western blotting, and immunofluorescence, while autophagic flux was evaluated using mRFP-GFP-LC3 and transmission electron microscopy. |
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Reaction Conditions |
10 and 20μM; 1h pretreatment |
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Applications |
Atorvastatin at 20μM attenuated tumor necrosis factor-α-induced MMP3, MMP13, ADAMTS4, and Cox-2 expression and restored collagen II and aggrecan expression. NLRP3, cleaved caspase-1, and GSDMD-NT decreased by 52%, 65%, and 48%, respectively, while the LC3-II/LC3-I ratio and autophagic flux increased. |
| Animal experiment [2]: | |
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Animal models |
Mouse model of lipopolysaccharide-induced depressive-like behavior |
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Preparation Method |
Mice received oral Atorvastatin or vehicle once daily for 7 days and were then given a single intraperitoneal lipopolysaccharide injection. Forced-swim, tail-suspension, and open-field tests were performed 24h later; tumor necrosis factor-α, brain-derived neurotrophic factor, glutathione, and malondialdehyde were then measured in the hippocampus and prefrontal cortex. |
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Dosage form |
1 and 10mg/kg/day; p.o.; 7 days |
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Applications |
Atorvastatin at 1 and 10mg/kg/day prevented the lipopolysaccharide-induced increase in immobility in the forced-swim and tail-suspension tests without altering open-field locomotion. It also prevented tumor necrosis factor-α elevation, brain-derived neurotrophic factor reduction, enhanced lipid peroxidation, and glutathione loss in the hippocampus and prefrontal cortex. |
References: [1] Chen J, Yan J, Li S, Zhu J, Zhou J, Li J, et al. Atorvastatin inhibited TNF-α induced matrix degradation in rat nucleus pulposus cells by suppressing NLRP3 inflammasome activity and inducing autophagy through NF-κB signaling. Cell Cycle. 2021;20(20):2160-2173. doi:10.1080/15384101.2021.1973707. [2] Taniguti EH, Ferreira YS, Stupp IJV, Fraga-Junior EB, Mendonça CB, Rossi FL, et al. Atorvastatin prevents lipopolysaccharide-induced depressive-like behaviour in mice. Brain Res Bull. 2019;146:279-286. doi:10.1016/j.brainresbull.2019.01.018. | |
| Cas No. | 134523-00-5 | SDF | |
| Canonical SMILES | O=C(C(C(C1=CC=CC=C1)=C(C2=CC=C(F)C=C2)N3CC[C@@H](O)C[C@@H](O)CC(O)=O)=C3C(C)C)NC4=CC=CC=C4 | ||
| Formula | C33H35FN2O5 | M.Wt | 558.64 |
| Solubility | DMSO: 100 mg/mL (179.01 mM) | Storage | Store at -20°C |
| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 1.7901 mL | 8.9503 mL | 17.9006 mL |
| 5 mM | 358 μL | 1.7901 mL | 3.5801 mL |
| 10 mM | 179 μL | 895 μL | 1.7901 mL |
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- Purity: >99.50% Appearance: A solid
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Average Rating: 5 (Based on Reviews and 25 reference(s) in Google Scholar.)