Atherosclerosis and Inflammation

Ligustrazine (Chuanxiongzine) is an orally active, blood-brain barrier-permeable alkaloid. It can be isolated from Ligusticum striatum DC. Ligustrazine reduces ROS, upregulates the levels of p-Akt/Akt and p-eNOS/eNOS, and decreases ALT and AST. It inhibits glutamate excitotoxicity, calcium overload, oxidative stress, ischemia-reperfusion injury and atherosclerotic plaque progression, enhances synaptic plasticity, and improves neurological function, cerebral infarct volume and brain water content. Ligustrazine possesses anti-inflammatory, antioxidant, lipid-lowering, endothelial protective and hepatoprotective activities. It can be used in studies related to ischemic stroke, cerebral ischemia-reperfusion injury and atherosclerosis.

DSPE-PEG2000-DBCO is a phospholipid PEG polymer that combines a hydrophobic phospholipid (DSPE), a hydrophilic polyethylene glycol spacer with a molecular weight of 1000 Da, and a reactive click chemistry terminal group (DBCO). DSPE-PEG2000-DBCO migrates to lymph nodes via the endogenous albumin transport system, implants bioorthogonal DBCO docking sites, and enables the enrichment of azide-functionalized vesicles in lymph nodes mediated by click chemistry. DSPE-PEG2000-DBCO can be used in studies related to atherosclerosis.

Cholestyramine (Cholestyramine resin) is an orally active bile acid sequestrant. Cholestyramine upregulates the expression of intestinal Apical sodium-dependent bile acid transporter and hepatic Cholesterol 7α-hydroxylase. Cholestyramine induces the expression of intestinal and hepatic cholesterol synthesis genes as well as hepatic lipogenesis genes, and promotes bile acid- and neutral sterol-mediated reverse cholesterol transport. Cholestyramine reduces intestinal cholesterol absorption and induces cholesterol efflux. Cholestyramine is applicable to research related to coronary artery disease, atherosclerotic cardiovascular disease and atherosclerosis.

PPACK TFA is a potent, peptidic inhibitor targeting thrombin and granzyme GZMK. PPACK TFA specifically blocks the activities of thrombin and GZMK, thereby inhibiting thrombin-mediated PAR-1 cleavage, as well as downstream inflammatory and procoagulant signaling pathways. Through stabilizing IκB proteins, blocking NF-κB activation and reducing systemic levels of proinflammatory/procoagulant biomarkers, PPACK TFA exerts multiple effects including anti-inflammatory, antithrombotic, barrier repair, and inhibition of atherosclerotic plaque progression. PPACK TFA binds to platelets without interference from kininogen, effectively limiting acute thrombus growth and reducing eosinophil infiltration and goblet cell hyperplasia in asthma models. PPACK TFA is an important tool molecule for investigating the mechanisms of atherosclerosis, asthma and related thromboinflammatory diseases.

Pam2CSK4 TFA is a TLR2 agonist. Pam2CSK4 TFA induces the expression of iNOS and NO in macrophage cell lines via TBK1 and MyD88 molecules. Pam2CSK4 TFA activates the NF-κB and Bruton's tyrosine kinase signaling pathways in platelets, and promotes platelet-endothelial cell interactions. TLR2 activation triggered by Pam2CSK4 TFA expands myeloid-derived suppressor cells (MDSCs) and suppresses anti-tumor immune responses in the tumor microenvironment. Pam2CSK4 TFA acts as a Th2-polarizing adjuvant in mouse vaccine models against Leishmania major and Brugia malayi. Pam2CSK4 TFA can be used in the research of various diseases, including thromboinflammatory diseases, sepsis, atherosclerosis, heart failure, influenza, lymphoma, melanoma, cutaneous leishmaniasis and lymphatic filariasis.

PXS-4728A is an orally active, selective VAP-1/SSAO inhibitor with an IC₅₀ of 5 nM and a K_i of 175 nM. PXS-4728A inhibits the expression of MMP-9. It reduces cell rolling, adhesion and migration, decreases cell infiltration levels, pro-inflammatory cytokines, chemokines and collagen deposition, and improves pulmonary function. PXS-4728A reduces the formation and progression of atherosclerotic plaques, and decreases blood lipid and blood glucose levels as well as body weight gain. PXS-4728A can be used in research related to chronic obstructive pulmonary disease, cystic fibrosis, acute pulmonary inflammation, acute lung injury, bronchiolitis obliterans syndrome, rhinovirus-exacerbated asthma, sepsis, Klebsiella pneumoniae pulmonary infection and atherosclerosis.

Avenanthramide A is an orally active phytoalexin that targets the RNA helicase DDX3 with a K_D of 8.8 μM. Avenanthramide A induces mitochondrial swelling and increased ROS production, and triggers apoptosis in CRC cells. Avenanthramide A inhibits smooth muscle cell proliferation and enhances nitric oxide production. Avenanthramide A can be used in research on colorectal cancer and atherosclerosis.

DSPE-PEG5000-DBCO is a phospholipid PEG polymer that combines a hydrophobic phospholipid (DSPE), a hydrophilic polyethylene glycol spacer with a molecular weight of 5000 Da, and a reactive click chemistry terminal group (DBCO). DSPE-PEG-DBCO migrates to lymph nodes via the endogenous albumin transport system, implants bioorthogonal DBCO docking sites, and enables the enrichment of azide-functionalized vesicles in lymph nodes mediated by click chemistry. DSPE-PEG-DBCO can be used in studies related to atherosclerosis.

D-Tagatose (D-(-)-Tagatose) is a natural low-calorie rare sugar. D-Tagatose inhibits the activities of sucrase, maltase and intestinal disaccharidases, reduces the digestion of sucrose and starch, and blocks the absorption of sucrose, maltose and glucose. D-Tagatose promotes glucokinase activity and inhibits glycogen phosphorylase activity via tagatose-1-phosphate, regulates the synthesis and decomposition of hepatic glycogen, reduces postprandial and fasting blood glucose levels, and improves hyperinsulinemia. D-Tagatose regulates lipid profiles, stimulates GLP-1 secretion, and exhibits prebiotic effects. D-Tagatose is a bulking sweetener. D-Tagatose can be used in research related to diabetes, hyperlipidemia, dental caries, atherosclerosis and type 2 diabetes.

Ziltivekimab (COR-001) is a fully human monoclonal antibody and also an IL-6 inhibitor. Ziltivekimab significantly reduces inflammatory biomarkers and Lipoprotein (a) in chronic kidney disease patients with systemic inflammation. Ziltivekimab does not increase pro-atherosclerotic lipid levels. Ziltivekimab is used in studies related to atherosclerotic thrombotic diseases and chronic kidney disease.

Gocdacimab (MEDI6570) is a fully human IgG1 monoclonal antibody inhibitor targeting the lectin-like oxidized low-density lipoprotein receptor LOX-1. By binding to LOX-1 and blocking its function, gocdacimab effectively reduces the level of free soluble LOX-1, thereby inhibiting key pathological processes such as lipid accumulation, foam cell formation, and vascular wall inflammation. Gocdacimab can interfere with atherosclerosis-related mechanisms, and it is used for research on atherosclerosis, and type 2 diabetes mellitus.

Sulfo-Cy5 azide is a near-infrared fluorescent probe with favorable click chemistry reactivity. Sulfo-Cy5 azide enables fluorescence imaging, tissue and cellular visualization of PD-L1 in tumors, and site-specific modification of anti-PD-L1 antibodies. Sulfo-Cy5 azide has been employed for RNA labeling and imaging. Sulfo-Cy5 azide can be conjugated to targeting agents for fluorescence imaging in atherosclerosis and breast cancer models (Ex/Em = 645/670 nm).

1-Palmitoyl-2-oleoyl-sn-glycero-3-PS sodium (16:0-18:1 PS (POPS)) is an anionic phosphatidylserine phospholipid with 16:0 (palmitoyl) and 18:1 (oleoyl) acyl chains. It serves as a component of biomimetic inner plasma membrane models and membrane vesicles for hemostatic response studies. 1-Palmitoyl-2-oleoyl-sn-glycero-3-PS sodium regulates membrane electrical properties by forming tethered bilayer lipid membranes. It enhances the stability of sHDL particles without altering the cholesterol efflux capacity of sHDL. 1-Palmitoyl-2-oleoyl-sn-glycero-3-PS sodium acts synergistically with phosphatidylcholine to support prothrombin activation. It serves as a component of the 4:1 POPC/POPS binary lipid bilayer model. 1-Palmitoyl-2-oleoyl-sn-glycero-3-PS sodium is applicable to research related to atherosclerosis.

Pinoresinol Diglucoside is an orally active lignan with multifunctional bioactivity. Pinoresinol Diglucoside interacts with targets including ALB, HIF1A, GSK3B, BCL2, MARK3, IL6, NF-κB p65, Nrf2, HO-1, and TLR4, and modulates pathways including PI3K-Akt, estrogen, MAPK, Rap1, AKT/mTOR/NF-κB, and TGF-β1/Smads. Pinoresinol Diglucoside regulates osteogenesis, bone resorption, oxidative stress, inflammation, apoptosis, ferroptosis, ferritinophagy, cardiac fibrosis, and vasorelaxation. Pinoresinol Diglucoside can be used for the research of osteoporosis, ischemia/reperfusion-induced brain injury, Alzheimer’s disease, myocardial ischemia-reperfusion injury, chondrodysplasia, diabetic cardiomyopathy, cardiac hypertrophy, hypertension, cisplatin-induced hearing loss, atherosclerotic cardiovascular diseases, and disuse osteoporosis.

Gypenoside XLIX is a multifunctional bioactive compound that can be isolated from Gynostemma pentaphyllum, with a K_a value of 1.58 μM for its binding to SIRT1. Gypenoside XLIX acts as a PPAR-α agonist. It inhibits the activation of TLR4-mediated NF-κB signaling pathway by activating the Sirt1/Nrf2 signaling pathway, reduces ROS accumulation, and alleviates hepatic inflammatory injury in mice with sepsis-induced liver disease. Gypenoside XLIX targets SIRT1 to block YAP-NLRP3 activation and improve sepsis-induced cardiomyopathy. Gypenoside XLIX inhibits apoptosis (Apoptosis), pyroptosis (Pyroptosis), autophagy (Autophagy), lipid peroxidation, pro-inflammatory cytokines and anti-inflammatory cytokines. Gypenoside XLIX alleviates sepsis-induced splenic injury by inhibiting inflammation and oxidative stress, and mitigates sepsis-associated encephalopathy by targeting PPAR-α. Gypenoside XLIX prevents acute kidney injury by inhibiting IGFBP7/IGF1R-mediated programmed cell death and inflammation. Gypenoside XLIX inhibits the expression and activity of vascular cell adhesion molecule-1 in cytokine-induced human endothelial cells. Gypenoside XLIX is applicable to research related to acute liver injury, lung injury, cardiomyopathy, acute splenic injury, sepsis-associated encephalopathy, acute kidney injury, atherosclerosis and chronic inflammation.

5β,6β-epoxycholestanol (Cholesterol 5β,6β-epoxide; 5β,6β-Epoxycholesterol) is an oxysterol. 5β,6β-epoxycholestanol induces cytotoxicity in bronchial epithelial cells. 5β,6β-epoxycholestanol induces lactate dehydrogenase (LDH) release and apoptosis in lymphoma cells undergoing macrophage differentiation. 5β,6β-epoxycholestanol is applicable to research related to atherosclerosis.

PPACK dihydrochloride is a potent, peptidic inhibitor targeting thrombin and granzyme GZMK. PPACK dihydrochloride specifically blocks the activities of thrombin and GZMK, thereby inhibiting thrombin-mediated PAR-1 cleavage, as well as downstream inflammatory and procoagulant signaling pathways. Through stabilizing IκB proteins, blocking NF-κB activation and reducing systemic levels of proinflammatory/procoagulant biomarkers, PPACK dihydrochloride exerts multiple effects including anti-inflammatory, antithrombotic, barrier repair, and inhibition of atherosclerotic plaque progression. PPACK dihydrochloride binds to platelets without interference from kininogen, effectively limiting acute thrombus growth and reducing eosinophil infiltration and goblet cell hyperplasia in asthma models. PPACK dihydrochloride is an important tool molecule for investigating the mechanisms of atherosclerosis, asthma and related thromboinflammatory diseases.

Bovine Factor Xa is a serine protease that plays a central role in blood coagulation, with prothrombin as its physiological substrate. Bovine Factor Xa catalyzes the conversion of prothrombin to thrombin, activates factor VIII, and hydrolyzes peptide, thioester, and amide substrates. Bovine Factor Xa cleaves protease-activated receptors 1 and 2 to activate intracellular signal transduction. Bovine Factor Xa regulates multiple cellular pathways, mediates various cellular activities, tissue remodeling and cancer cell migration, and inhibits apoptosis in some cancer cells. Bovine Factor Xa protects hippocampal neurons against glutamate-induced damage. Bovine Factor Xa participates in embryonic vascular development and regulates immune hematopoiesis; its activity is inhibited by soybean trypsin inhibitor, and cannot be enhanced by phospholipids. Bovine Factor Xa regulates immune responses and macrophage polarization, and participates in fibrosis, vascular remodeling and tumor progression through non-coagulant effects. Bovine Factor Xa can be used in research related to atherosclerosis, fibrosis, asthma, cancer, thromboinflammation, sepsis, etc.

Ligustrazine hydrochloride (Chuanxiongzine hydrochloride) is an orally active, blood-brain barrier-permeable alkaloid. It can be isolated from Ligusticum striatum DC. Ligustrazine hydrochloride reduces ROS, upregulates the levels of p-Akt/Akt and p-eNOS/eNOS, and decreases ALT and AST. It inhibits glutamate excitotoxicity, calcium overload, oxidative stress, ischemia-reperfusion injury and atherosclerotic plaque progression, enhances synaptic plasticity, and improves neurological function, cerebral infarct volume and brain water content. Ligustrazine hydrochloride possesses anti-inflammatory, antioxidant, lipid-lowering, endothelial protective and hepatoprotective activities. It can be used in studies related to ischemic stroke, cerebral ischemia-reperfusion injury and atherosclerosis.

Olpasiran (AMG 890, ARC-LPA) sodium is an N-acetyl galactosamine (GalNAc)-conjugated, hepatocyte-targeted siRNA. Olpasiran sodium directly inhibits LPA messenger RNA translation in hepatocytes and potently reduce Lp(a) concentration. Olpasiran sodium can be used for the research of cardiovascular disease, such as atherosclerosis.