Structure

Atorvastatin (98%)

CAS
134523-00-5
Catalog Number
ALC-FP-134523005
Category
Featured Products
Molecular Weight
558.64 g/mol
Molecular Formula
C33H35FN2O5

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Specification

Appearance
White powder
Sample Lot No.
A24Q1901

Atorvastatin for Ameliorating Age-Related Cognitive and Cortical Alterations in Rats

Atorvastatin ameliorates cerebral cortical pathological and cognitive alterations in aged rats: Histological & immunohistochemical study Elshafey M, et al. Tissue and Cell, 2026, 98, 103184.

This study investigated the experimental application of atorvastatin in aged Wistar rats (20-24 months) to assess neuroprotective effects. Rats were orally administered atorvastatin at 20 mg/kg for 30 days, with adult (3-4 months) and untreated aged rats serving as controls. Behavioral tests evaluated memory performance, while cortical tissues were analyzed for oxidative stress markers (Nrf-2, GSH, SOD, MDA), inflammatory mediators (TNF-α, IL-1β, NF-κB), and apoptosis/autophagy markers (Caspase-3, LC3, p62, SIRT1). Histopathology and immunohistochemistry assessed cortical integrity. Atorvastatin improved memory, restored oxidative-antioxidant balance, suppressed inflammation, enhanced autophagy, and mitigated apoptosis, demonstrating its experimental efficacy as a neuroprotective agent in aging-related cerebral degeneration.

Atorvastatin for the Inhibition of Fibrogenic Activation in Endocardial Fibroelastosis

Preclinical Assessment of Atorvastatin for Treatment of Endocardial Fibroelastosis Diaz-Gil D, et al. JACC: Basic to Translational Science, 2025, 10(9), 101282.

This study investigated the therapeutic potential of atorvastatin in endocardial fibroelastosis (EFE) using both in vitro and in vivo models. Neonatal rat hearts were treated with atorvastatin, and the effects on endocardial endothelial cells (EECs) were assessed via histological analysis and immunohistochemistry. Atorvastatin administration reduced EFE thickness and myocardial infiltration, inhibited fibrogenic activation of EECs, down-regulated SNAI2, and up-regulated KLF2 expression. In vitro assays further confirmed suppression of endothelial-to-mesenchymal transition. These results demonstrate the experimental application of atorvastatin in modulating fibrogenic signaling pathways, providing preclinical evidence for its potential use as a treatment strategy for EFE.

Atorvastatin for the Assessment of Male Reproductive Toxicity in Wistar Rats

Co-administration of atorvastatin with piperine induces reproductive toxicity in male Wistar rats through oxidative stress induction and downregulation of StAR, CYP11a1, 3βHSD and 17βHSD genes Ghosh S, et al. Reproductive Toxicology, 2025, 135, 108919.

This study investigated the reproductive toxicity of atorvastatin (ATR) alone and in combination with piperine (PIP) in male Wistar rats. Rats were divided into four groups (control, ATR 8 mg/kg, PIP 10 mg/kg, ATR+PIP) and orally gavaged with water suspensions daily for 28 days. Experimental evaluation included gravimetric and histomorphometric analyses, sperm motility and morphology assessment, ROS generation, lipid peroxidation (TBARS), antioxidant enzyme activities (SOD, catalase), serum testosterone quantification, qRT-PCR for steroidogenic genes (StAR, CYP11a1, 3βHSD, 17βHSD), and toluidine blue staining for sperm chromatin integrity. Co-administration of ATR+PIP induced significant oxidative stress, downregulated key steroidogenic genes, and impaired sperm parameters, demonstrating atorvastatin's potential for experimental modeling of chemically induced male reproductive toxicity.

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