ldl in 3

LDL-IN-3 belongs to synthetic compounds and is an antioxidant and anti-atherosclerotic agent with good cell permeability and cardiovascular protective properties. This compound is used for the treatment of atherosclerosis-related diseases, effectively inhibiting oxidative stress and lipid deposition, and reducing arterial plaque formation.

Subtilisin (EC 3. 4. 21. 14) is a bacterially derived serine protease that promotes hepatic LDL receptor (LDLR) degradation and can be used in the study of cardiovascular disease.

GPR109 receptor agonist-3 is an orally active GPR109 receptor agonist with an IC50 of 310 nM. It retains the antioxidant and cytoprotective properties of lipoic acid. In rats on a high-fat diet, GPR109 receptor agonist-3 reduces total cholesterol (TC), triglycerides (TG), and low-density lipoprotein cholesterol (LDL-C), while increasing high-density lipoprotein cholesterol (HDL-C). This compound is applicable for atherosclerosis research.

Isorhamnetin (3-methylquercetin) is the methylated metabolite of quercetin. Quercetin is an important dietary flavonoid with in vitro antioxidant activity. Isorhamnetin prevents endothelial cell injuries from oxidized LDL via inhibition of lectin-like ox-LDL receptor-1 upregulation, interference of ox-LDL-mediated intracellular signaling pathway (p38MAPK activation, NF-kappaB nuclear translocation, eNOS expression) and the antioxidant activity of isorhamnetin. Isorhamnetin prevents endothelial dysfunction, superoxide production, and overexpression of p47phox induced by angiotensin II. Isorhamnetin appears to be a potent drug against esophageal cancer due to it's in vitro potential to not only inhibit proliferation but also induce apoptosis of Eca-109 cells.

(±)14(15)-EET is a metabolite of arachidonic acid that is formed via epoxidation of arachidonic acid by cytochrome P450.[1],[2] It prevents increases in leukotriene B4, ICAM-1, and chemokine (C-C motif) ligand 1 (CCL2) induced by oxidized LDL in primary rat pulmonary artery endothelial cells (RPAECs) when used at a concentration of 1 μM.[3] (±)14(15)-EET induces dilation of preconstricted isolated canine coronary arterioles (EC50 = 0.2 pM).[4] It reduces myocardial infarct size as a percentage of the area at risk in a canine model of ischemia-reperfusion injury induced by left anterior descending coronary artery (LAD) occlusion when administered at a dose of 0.128 mg/kg prior to occlusion or reperfusion.[5] Reference:[1]. Chacos, N., Falck, J.R., Wixtrom, C., et al. Novel epoxides formed during the liver cytochrome P-450 oxidation of arachidonic acid. Biochem. Biophys. Res. Commun. 104(3), 916-922 (1982).[2]. Oliw, E.H., Guengerich, F.P., and Oates, J.A. Oxygenation of arachidonic acid by hepatic monooxygenases. Isolation and metabolism of four epoxide intermediates. J. Biol. Chem. 257(7), 3771-3781 (1982).[3]. Jiang, J.-X., Zhang, S.-J., Xiong, Y.-K., et al. EETs attenuate ox-LDL-induced LTB4 production and activity by inhibiting p38 MAPK phosphorylation and 5-LO/BLT1 receptor expression in rat pulmonary arterial endothelial cells. PLoS One 10(6), e0128278 (2015).[4]. Oltman, C.L., Weintraub, N.L., VanRollins, M., et al. Epoxyeicosatrienoic acids and dihydroxyeicosatrienoic acids are potent vasodilators in the canine coronary microcirculation. Circ. Res. 83(9), 932-939 (1998).[5]. Nithipatikom, K., Moore, J.M., Isbell, M.A., et al. Epoxyeicosatrienoic acids in cardioprotection: Ischemic versus reperfusion injury. Am. J. Physiol. Heart Circ. Physiol. 291(2), H537-H542 (2006).

(±)9-HODE is one of the two racemic monohydroxy fatty acids resulting from the non-enzymatic oxidation of linoleic acid. Approximately equal proportions of both isomers are found in mitochondrial and plasma membranes of rabbit reticulocytes. [1][2] Oxidized LDL contains significant amounts of esterified 9- and 13-HpODEs and HODEs. [3][4]

9(S)-HODE is produced by the lipoxygenation of linoleic acid in both plants and animals.[1],[2] It has been detected in atherosclerotic plaques, as an esterified component of membrane phospholipids and in oxidized LDL particles.[3]

Methyl protodioscin (Smilax saponin B) potentially increase HDL cholesterol while reducing LDL cholesterol and triglycerides. Methyl protodioscin has antitumor property. Methyl protodioscin induced apoptotic process in human A549 cells is closely associated with Mitochondrial membrane potential, caspase-3, and mitochondrial cytochrome c.

1. Tiliroside (Tribuloside) shows anticarcinogenic activity. 2. Tiliroside shows hepatoprotective activity. 3. Tiliroside shows antioxidant and anti-inflammatory activity, can inhibit neuroinflammation in neurodegenerative disorders. 4. Tiliroside has anti-diabetic effect, are at least partially mediated through inhibitory effects on carbohydrate digestion and glucose uptake in the gastrointestinal tract. 5. Tiliroside and gnaphaliin are antioxidants against in vitro Cu(2+)-induced LDL oxidation in the same order of magnitude compared to that of the reference drug, probucol. 6. Tiliroside enhances fatty acid oxidation via the enhancement adiponectin signaling associated with the activation of both AMP-activated protein kinase and peroxisome proliferator-activated receptor α and ameliorates obesity-induced metabolic disorders.

PCSK9 modulator-3 (Compound 13) is a potent PCSK9 modulator with an EC50 value of 2.46 nM, showing potential in hyperlipidemia research. PCSK9 is a newly established target for lowering low-density lipoprotein cholesterol (LDL-C) [1].

Pitavastatin (NK-104) is a potent inhibitor of hydroxymethylglutaryl-CoA (HMG-CoA) reductase, effectively inhibiting cholesterol synthesis from acetic acid in HepG2 cells with an IC50 of 5.8 nM. It also induces hepatocyte low-density lipoprotein-cholesterol (LDL-C) receptors and exhibits therapeutic activities such as anti-atherosclerotic, anti-asthmatic, anti-osteoarthritis, antineoplastic, neuroprotective, hepatoprotective, and reno-protective effects.

Pitavastatin-D4 Sodium Salt is a deuterated compound of Pitavastatin Sodium Salt. Pitavastatin Sodium Salt (T62598) has a CAS number of 574705-92-3. Pitavastatin (NK-104) sodium is a potent hydroxymethylglutaryl-CoA (HMG-CoA) reductase inhibitor. Pitavastatin sodium inhibits cholesterol synthesis from acetic acid with an IC 50 of 5.8 nM in HepG2 cells. Pitavastatin sodium is an efficient hepatocyte low-density lipoprotein-cholesterol (LDL-C) receptor inducer. Pitavastatin sodium also possesses anti-atherosclerotic, anti-asthmatic, anti-osteoarthritis, antineoplastic, neuroprotective, hepatoprotective and reno-protective effects [1] [2] [3] [8].

Schisanhenol (Standard) is a reference standard for research and analysis in studies involving Schisanhenol. 1. Schisanhenol (Schizanhenol) can protect against adriamycin induced heart mitochondrial toxicity. 2. Schisanhenol has antioxidative effect on human LDL oxidation, may be through scavenging free radicals. 3. Schisanhenol has anti-apoptosis effect on BACSs, may be related to its inhibition of ROS generation.

Isorhamnetin (Standard) is a reference standard for research and analysis in studies involving Isorhamnetin. Isorhamnetin (3-methylquercetin) is the methylated metabolite of quercetin. Quercetin is an important dietary flavonoid with in vitro antioxidant activity. Isorhamnetin prevents endothelial cell injuries from oxidized LDL via inhibition of lectin-like ox-LDL receptor-1 upregulation, interference of ox-LDL-mediated intracellular signaling pathway (p38MAPK activation, NF-kappaB nuclear translocation, eNOS expression) and the antioxidant activity of isorhamnetin. Isorhamnetin prevents endothelial dysfunction, superoxide production, and overexpression of p47phox induced by angiotensin II. Isorhamnetin appears to be a potent drug against esophageal cancer due to it's in vitro potential to not only inhibit proliferation but also induce apoptosis of Eca-109 cells.

Pinobanksin 3-acetate (3-O-Acetylpinobanksin), a flavonoid derivative, is a strong antioxidant found in sunflowers and honey that inhibits LDL peroxidation.

DL-3-Hydroxy-3-methylglutaryl coenzyme A disodium hydrate is the disodium salt compound of HMG coenzyme A, serving as a crucial intermediate in the synthesis of terpenes and ketone bodies. In the body, DL-3-Hydroxy-3-methylglutaryl coenzyme A disodium plays a role in lipid metabolism and acts as a precursor in cholesterol synthesis, potentially coupling with LDL receptors to regulate cholesterol production.