ldl-c

Ibrolipim (NO-1886) attenuates high glucose-induced endothelial dysfunction in cultured human umbilical vein endothelial cells via PI3K/Akt pathway.

GW590735 is an effective and selective PPARα agonist with an EC50 of 4 nM on PPARα and at least 500-fold selectivity versus PPARδ and PPARγ. GW590735 can be used in dyslipidemia studies.

Bococizumab(PF-04950615) is a humanized mAb against PCSK9 and an inhibitor of the synthesis of PCSK9 in the liver that reduces the amount of low-density lipoprotein cholesterol (LDL-C) in the blood.Bococizumab is used to treat hypercholesterolemia.

Alirocumab is a human monoclonal antibody that inhibits PCSK9. It is produced by recombinant DNA technology in Chinese hamster ovary cell suspension culture.

Polydatin (Piceid), the glycoside of Resveratrol, is originally isolated from the Chinese herb Polygonum cuspidatum. The compound can inhibit platelet aggregation and elevate the ratios of LDL-C/HDL-C and TC/HDL-C. In the myocardial cell, white blood cell, vascular smooth muscle cell, and endothelial cell, Polydatin can inhibit ICAM-1 expression, elevate Ca2+, weaken white blood cell-endothelial cell adhesion, and activate KATP channels.

Bempedoic acid (ETC1002) is an orally available, once-daily LDL-C lowering small molecule designed to lower elevated levels of LDL-C and to avoid side effects associated with existing LDL-C lowering therapies. Bempedoic acid(ETC1002) is absorbed rapidly in the small intestine and enters the liver through cell surface receptors different from those transporters that selectively take up statins. Bempedoic acid(ETC1002) is a regulator of lipid and carbohydrate metabolism.

20-HC-Me-Pyrrolidine is a potent Aster protein inhibitor with IC50=0.06~0.71 μm for Aster-A, Aster-B, and Aster-C that blocks the ability of Aster proteins to bind and transfer cholesterol, including inhibiting the movement of LDL cholesterol to the endoplasmic reticulum.

Gemcabene calcium , a first-in-class lipid-lowering agent, lowers low-density lipoprotein cholesterol (LDL-C), decreases triglycerides, and raises high-density lipoprotein cholesterol (HDL-C) andexerting anti-inflammatory activity, lowers pro-inflammatory acute-phase protein, C-reactive protein (CRP).

PCSK9-IN-29 serves as a lipid-lowering agent that enhances the expression of low-density lipoprotein receptor (LDLR) protein and reduces PCSK9 protein expression in hepG2 cells. Additionally, in crab-eating macaques on a high-fat diet, it lowers serum LDL-C, TC, and liver enzyme ALT levels, reduces body weight and fat, and boosts bone mineral content. PCSK9-IN-29 is useful for studies involving non-alcoholic fatty liver disease and obesity.

PCSK9-IN-27 (Compound 108) is a PCSK9 inhibitor with an IC50 value of 3.4 nM. It reduces the degradation of LDLR and enhances the uptake of LDL-C.

CVI-LM001 is an inhibitor of PCSK9 that regulates blood levels of low-density lipoprotein cholesterol (LDL-C) by preventing the interaction between PCSK9 and low-density lipoprotein receptors (LDLR), thereby exerting a lipid-lowering effect.

(±)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).

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.

R-IMPP is an inhibitor of PCSK9 translation. R-IMPP stimulates uptake of LDL-C in hepatoma cells by increasing LDL-R levels, without altering levels of secreted transferrin.

PCSK9 modulator-2 (Compound 1) is a potent PCSK9 modulator (EC 50 = 202 nM) with potential applications in hyperlipidemia research. Proprotein convertase subtilisin/kexin type 9 (PCSK9) is a recently validated therapeutic target for lowering low-density lipoprotein cholesterol (LDL-C) [1].

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].

PCSK9 modulator-4 (Compound 21) is a potent PCSK9 modulator (EC50 = 0.15 nM) utilized in hyperlipidemia research, targeting the recently validated low-density lipoprotein cholesterol (LDL-C) lowering mechanism [1].

AMPK activator 6 (Compound GC) activates the AMPK pathway and reduces lipid content in HepG2 and 3T3-L1 cells. It significantly suppresses increases in total cholesterol (TC), low-density lipoprotein-C (LDL-C), triglyceride (TG), and other biochemical indices in blood serum, holding research value in non-alcoholic fatty liver disease (NAFLD) and metabolic syndrome.

Pitavastatin (NK-104) sodium is a potent inhibitor of hydroxymethylglutaryl-CoA (HMG-CoA) reductase and an inducer of the hepatocyte low-density lipoprotein cholesterol (LDL-C) receptor. It inhibits acetate synthesis of cholesterol in HepG2 cells and exhibits anti-atherogenic, anti-osteoarthritic, anti-asthmatic, anti-tumour, neuroprotective, hepatoprotective, and nephroprotective effects.

Rosuvastatin Sodium is a competitive HMG-CoA reductase (HMGCR) inhibitor (IC50: 11 nM) that effectively blocks hERG currents (IC50: 195 nM), reduces the expression of mature hERG, and inhibits the interaction of heat shock protein 70 (Hsp70) with hERG protein.

Bambuterol is a prodrug of β2-agonist commonly used for the treatment of asthma and chronic obstructive pulmonary disease (COPD) with the advantage of once daily dosing and favorable side effect profile. Administration of a single-dose of R-bambuterol resulted in dose-dependent reductions in the levels of plasma LDL-C, high-density lipoprotein cholesterol (HDL-C), total cholesterol (TC), apolipoprotein B (ApoB) and apolipoprotein A1 (ApoA1) at Tmax. R-bambuterol can lower the plasma levels of LDL-C, and marginally raise the ratio of ApoA1 ApoB (indicator of HDL-C LDL-C) with both a single dose and multiple doses. R-bambuterol was more potent in LDL-C lowering than rac-bambutero

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.

Gemfibrozil-d6 is intended for use as an internal standard for the quantification of gemfibrozil by GC- or LC-MS. Gemfibrozil is a peroxisome proliferator-activated reporter α and PPARγ agonist. In vivo, gemfibrozil reduces serum total cholesterol, triglyceride, and LDL levels in a rat model of high-cholesterol diet-induced hyperlipidemia. Gemfibrozil reduces atherosclerotic plaque area, superoxide production, and expression of the genes encoding the NF-κB subunit p65 and chemokine (C-C) motif ligand 2 (CCL2) in ApoE-/- mice. Formulations containing gemfibrozil have been used in the treatment of high cholesterol.

Tafolecimab (IBI-306), a human IgG2 monoclonal antibody, specifically targets and binds to PCSK-9, thus inhibiting PCSK-9-mediated endocytosis of the LDL receptor. This action enhances the clearance of LDL-C, resulting in a decrease in LDL-C levels. Tafolecimab has potential applications in hypercholesterolemia research [1].