atorvastatin

In vitro experiments confirmed the cytotoxicity and induction of methuosis in GBM cells by AP@CM-Ang, accompanied by the release of immune-stimulatory factors. In vivo experiments demonstrated that the nanodrug significantly enhanced tumor targeting, effectively inhibited tumor growth, and increased immune cell activation, validating its potential as a promising and safe strategy for GBM treatment.

P1, N=42, Not yet recruiting, Hangzhou Zhongmei Huadong Pharmaceutical Co., Ltd.

P4, N=15, Completed, Children's Hospital of Fudan University | Recruiting --> Completed | N=10 --> 15

P4, N=250, Recruiting, Medical University Of Vienna | Not yet recruiting --> Recruiting

P2/3, N=135, Not yet recruiting, Novartis Pharma AG | N=24 --> 135

P3, N=103, Not yet recruiting, Daiichi Sankyo Europe, GmbH, a Daiichi Sankyo Company

P2, N=150, Active, not recruiting, OHSU Knight Cancer Institute | Recruiting --> Active, not recruiting

An AS model was established in apolipoprotein E knockout(ApoE~(-/-)) mice, which were divided into a normal group, an model group, low/medium/high-dose DZTMW groups, and an atorvastatin positive control group...Its mechanism may involve the regulation of hepatic lipid metabolism by its in vivo active components to ameliorate the "phlegm-turbidity" pathology and reduce liver injury, and the inhibition of systemic inflammation to alleviate the "blood stasis" process. The study can provide a modern biological basis for the theory of "phlegm-stasis intermingling".

The rats were randomly assigned to the following groups: model group, atorvastatin calcium group(4.8 mg·kg~(-1)), low-, medium-, and high-dose Tanyu Tongzhi Optimization Decoction(TYTZD) groups(3.6, 7.2, and 14.4 g·kg~(-1)), and a normal diet control group...Western blot indicated that TYTZD reduced TLR4, p-NF-κB, and IL-1β protein expression in liver tissue. In conclusion, TYTZD may exert anti-hyperlipidemic effects through regulation of core targets such as ITGAM, TLR4, and APOC2, and by modulating the TLR4/NF-κB signaling pathway to intervene in inflammatory responses and cholesterol metabolism, thereby achieving multi-target, multi-pathway therapeutic effects against hyperlipidemia.

An atherosclerosis(AS) model was established in ApoE~(-/-) mice by feeding a high-fat diet for 14 weeks, and mice were randomly divided into a model group, MGFK high-dose group, MGFK low-dose group, and atorvastatin group...Furthermore, MGFK decreased the apoptosis rate within plaques, upregulated B-cell lymphoma-2(BCL-2) expression, downregulated BCL-2-associated X protein(BAX) and cleaved caspase-3, and promoted the phosphorylation of PI3K and AKT. These findings suggest that MGFK exerts anti-atherosclerotic effects potentially by regulating the PI3K/AKT signaling pathway, thereby reducing apoptosis within plaques, lowering levels of inflammatory cytokines and blood lipids, and attenuating plaque size, lipid content, and foam cell formation.

P4, N=100, Not yet recruiting, Menzies Institute for Medical Research