dyslipidemia

Lycorine (Narcissine) inhibits protein synthesis and may inhibit ascorbic acid biosynthesis, although studies on the latter are controversial and inconclusive.

4-Hydroxyflavanone is a natural product, shows full vasorelaxing effects

KD-026 (SLx 4090), a microsomal triglyceride transfer protein (MTP) inhibitor(IC50 = 8.0 nM), is used in type 2 diabetes studies.

Seladelpar (MBX 8025) has been used in trials studying the treatment of Hyperlipidemia.

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.

2,2,14,14-Tetramethyl-8-oxopentadecanedioic acid (compound example II-9) is a ketone used in the research of cardiovascular diseases, dysproteinemias, dyslipidemias, and glucose metabolism disorders.

Muraglitazar (BMS-298585) is a dual agonist of PPARα/γ that exerts metabolic regulatory effects including lipid modulation, glucose reduction, improvement of insulin resistance, and weight loss. It is indicated for the treatment of type 2 diabetes and associated dyslipidemia. Muraglitazar exhibits potent in vitro activity against human PPARα (EC50 = 320 nM) and PPARγ (EC50 = 110 nM).

GS-9667, a selective and partial agonist of the A(1) adenosine receptor (AR), represents an effective therapy for Type 2 diabetes (T2DM) and dyslipidemia via lowering of free fatty acids (FFA).

GW-493838 is a potent adenosine A1A receptor agonist for the treatment of dyslipidemia and neuropathic pain, with analgesic effects on post-herpetic neuralgia or peripheral nerve damage caused by trauma or surgery.

Phanginin A, a natural product discovered in Caesalpinia sappan Linn, activates SIK1 and inhibits gluconeogenesis in mouse primary hepatocytes. Phanginin A increases PDE4 activity and suppresses the hepatic cAMP/PKA/CREB pathway, improving metabolic disorders in ob/ob mice. It may be used in studies of type 2 diabetes.

WAY-297848 is a novel glucokinase activator for the prevention or treatment of hyperglycemia, diabetes mellitus, obesity, dyslipidemia, and metabolic syndrome.

DB1976 dihydrochloride (DB1976 2HCl) , a transcription factor PU.1 inhibitor with potential anti-inflammatory activity, slowed down inflammation and fibrosis and improved glucose homeostasis and dyslipidemia in mice in in vivo experiments.DB1976 dihydrochloride promotes apoptosis and may be used in studies of metabolic dysfunction and non-alcoholic steatohepatitis.

Exicorilant is a selective and oral active glucocorticoid receptor (GR) antagonist (Ki: 7 nM) and it also has the potential to overcome adiposity, glucose intolerance, and dyslipidemia.

PPARα agonist5 is an orally active, selective partial agonist of PPARα with an EC50 of 3 nM. It reduces lipid accumulation and upregulates PPARα target genes, exhibiting anti-hepatic steatosis properties. Additionally, PPARα agonist5 demonstrates significant lipid-lowering and glucose-lowering effects through partial PPARγ agonist activity and mild inhibition of protein tyrosine phosphatase 1B (PTP1B) with an IC50 of 79.1 μM. It has favorable safety and is applicable in the study of dyslipidemia in type 2 diabetes.

AMPK activator17 (Compound 10g) is an orally bioavailable AMPK activator. It significantly inhibits lipogenesis (IC50: 3.4 μM) and improves dyslipidemia. By activating the AMPK pathway, AMPK activator17 suppresses early adipocyte differentiation (mitotic clonal expansion) and enhances mitochondrial function and fatty acid oxidation in mature adipocytes. It improves dyslipidemia through promoting cholesterol reverse transport. AMPK activator17 is applicable in research on obesity and associated metabolic disorders, such as type 2 diabetes and cardiovascular diseases.

PPARδ agonist10 (compound 7) is an orally active, selective partial agonist of PPARδ, with EC50 values of 0.053 μM for hPPARδ(LBD)-GAL4 and 0.30 µM for mPPARδ. In transactivation assays, it acts as a partial PPARδ agonist but fully stimulates muscle cell free fatty acid oxidation both in vitro and in vivo. PPARδ agonist10 can be utilized for dyslipidemia research.

MK-8245 analog is an analog of MK-8245 which is a liver-targeted Inhibitor of Stearoyl-CoA Desaturase (SCD). It is useful for the Treatment of Dyslipidemia and Diabetes.

Plozasiran, previously called ARO-APOC3, is a first-in-class investigational RNA interference (RNAi) therapeutic that is specifically designed to actively suppress hepatic production of apolipoprotein C-III (APOC3), a critical structural and functional component of triglyceride-rich lipoproteins (TRLs) and a central regulator of systemic triglyceride metabolism, thereby addressing dyslipidemia at the level of gene expression through targeted post-transcriptional silencing mechanisms.

THR-β agonist 9 is a potent and selective THR-β activator, which shows sensitivity to His435 mutations with an EC50 of 3.2 nM. It demonstrates moderate selectivity, approximately 10-fold, and effectively activates various His435 mutants (H435A, H435Y, and H435R), with EC50 values ranging from 134.2 nM to 515.5 nM. THR-β agonist 9 presents potential for research into conditions such as dyslipidemia, metabolic syndrome-associated steatohepatitis (MASH), and resistance to thyroid hormone (RTH).

GSK-1292263 (hydrochloride) is an orally active GPR119 agonist with a pEC50 of approximately 6.9 nM for human and 6.7 nM for rat GPR119. It is utilized in research related to type 2 diabetes and dyslipidemia.

PPARα agonist6 (Compound 15) is a PPARα agonist employed in dyslipidemia research.

Solbinsiran is an siRNA targeting the ANGPTL3 protein in the liver, used in research on dyslipidemia.

Solbinsiran sodium is an siRNA compound that targets the ANGPTL3 protein in the liver and is used for research in dyslipidemia.

TLC-2716 is an orally active LXRα and LXRβ inhibitor, localized to the intestines and liver, with EC50 values of 7 nM and 15 nM, respectively. It suppresses the transcriptional activity of LXRα/β, downregulates genes involved in lipogenesis, lipid absorption, and lipoprotein metabolism, while preserving peripheral cholesterol reverse transport. TLC-2716 reduces lipid accumulation, inhibits the expression of inflammatory and fibrotic genes, enhances the clearance of triglyceride-rich lipoproteins, and improves glucose homeostasis and insulin sensitivity. In animal models and humanized liver mice, TLC-2716 lowers serum and hepatic triglyceride levels, plasma cholesterol levels, and other atherosclerosis-inducing lipid markers. It is applicable in research related to dyslipidemia and associated cardiometabolic disorders.