Atorvastatin

Research use only, not for human use.

A competitive inhibitor of HMG-CoA reductase that acts as a lipid-lowering agent for prevention of events associated with cardiovascular disease.

A competitive inhibitor of HMG-CoA reductase that acts as a lipid-lowering agent for prevention of events associated with cardiovascular disease.Dyslipidemia Approved(In Vitro):Atorvastatin treatment decreases apoptosis of myocardial cells by down-regulating GRP78, caspase-12 and CHOP expression in myocardial cells after myocardial infarction, and the endoplasmic reticulum (ER) stress is activated in response to heart failure and angiotensin II (Ang II) stimulation.(In Vivo):Atorvastatin (20-30 mg/kg; oral gavage; once a day; for 28 days; ApoE / mice) treatment significantly reduces endoplasmic reticulum (ER) stress signaling proteins, the number of apoptotic cells, and the activation of Caspase12 and Bax in the Ang II-induced ApoE-/- mice. Proinflammatory cytokines such as IL-6, IL-8, IL-1β are all remarkably inhibited after Atorvastatin treatment.

Atorvastatin treatment decreases apoptosis of myocardial cells by down-regulating GRP78, caspase-12 and CHOP expression in myocardial cells after myocardial infarction, and the endoplasmic reticulum (ER) stress is activated in response to heart failure and angiotensin II (Ang II) stimulation.

Atorvastatin (20-30 mg/kg; oral gavage; once a day; for 28 days; ApoE?/? mice) treatment significantly reduces endoplasmic reticulum (ER) stress signaling proteins, the number of apoptotic cells, and the activation of Caspase12 and Bax in the Ang II-induced ApoE-/- mice. Proinflammatory cytokines such as IL-6, IL-8, IL-1β are all remarkably inhibited after Atorvastatin treatment. Animal Model:Forty 8-week-old ApoE?/? mice induced with angiotensin II (Ang II) Dosage:20 mg/kg, 30 mg/kg Administration:Oral gavage; once a day; for 28 days Result:Significantly reduced ER stress signaling proteins, the number of apoptotic cells, and the activation of Caspase12 and Bax in the Ang II-induced ApoE?/? mice. Proinflammatory cytokines such as IL-6, IL-8, IL-1β were all remarkably inhibited.

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Metabolic Enzyme/Protease

HMGCR

HMGCR

Cardiovascular Disease

Dyslipidemia

134523-00-5

558.6398

C33H35FN2O5

>98% (HPLC)

10 mM in DMSO

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

1H-Pyrrole-1-heptanoic acid, 2-(4-fluorophenyl)-β,δ-dihydroxy-5-(1-methylethyl)-3-phenyl-4-[(phenylamino)carbonyl]-, (βR,δR)-

(-20℃)

With Ice Pack

≥ 2 years