plaques

Dithranol (cignoline) is an anthracene derivative that disrupts MITOCHONDRIA function and structure and is used for the treatment of DERMATOSES, especially PSORIASIS. It may cause FOLLICULITIS.

Picotamide has anticoagulant and fibrinolytic properties.

CRANAD-28 is a blood-brain barrier (BBB) penetrating two-photon imaging probe capable of visualizing amyloid plaques and labeling plaques and cerebral amyloid angiopathy.

BMS-212122 (UNII-0Z473OO6GB) is a potent inhibitor of microsomal triglyceride transfer protein (MTP) and has shown hypolipidemic effects in animal studies.BMS-212122 significantly reduced lipid content and monocyte-derived (CD68+) cells in atherosclerotic plaques.

BF-168 is a candidate probe for PET and specifically recognizes both neuritic and diffuse plaques (Ki: 6.4 nM for Aβ1-42).

TRAF-STOP inhibitor 6877002 (CD40-TRAF6 inhibitor), is a selective inhibitor of CD40-TRAF6 interaction. TRAF-STOP 6877002 reduces leukocyte recruitment, and reduces macrophage activation; reduces macrophage proliferation in atherosclerotic plaques.

Wollastonite is an industrial mineral comprised chemically of calcium, silicon, and oxygen. It has been determined to have low biopersistence in both in vivo and in vitro studies, which probably accounts for its relative lack of toxicity. There are no ple

[11C]MeS-IMPY exhibits a higher binding affinity for β-amyloid plaques extracted from Alzheimer's disease (AD) brains or AD brain homogenates than IMPY, with Ki values of 7.93 nM and 8.95 nM, respectively. [11C]MeS-IMPY is a potential radioactive ligand for positron emission tomography (PET) imaging of β-amyloid plaques.

Tau-0N4R-IN-1 (Compound 6T) is a brain-penetrant inhibitor of tau0N4R oligomerization. It effectively inhibits the fibrillization of tau 0N4R, 2N3R, and 2N4R, showcasing potent anti-seeding effects against tau in vitro, and can dose-dependently reduce α-syn oligomerization while preventing the formation of α-syn inclusions. Tau-0N4R-IN-1 demonstrates stability in mouse microsomes and reduces Aβ plaques derived from the brain tissue of AD patients. Moreover, it exhibits favorable pharmacokinetic properties in mice.

GI-Y2 is a GSDMD inhibitor that suppresses macrophage pyroptosis induced by oxidized low-density lipoprotein (ox-LDL). In vivo, GI-Y2 dose-dependently reduces atherosclerotic plaques and decreases lesion size and fibrosis in the aortic root of ApoE-/- mice. GI-Y2 holds potential for research in pyroptosis and cardiovascular diseases, such as atherosclerosis.

AZM198 is a selective, orally active, and irreversible inhibitor of MPO with an IC50 of 15.0 nM. It exhibits an IC50 of 19 μM against CYP3A4 and possesses favorable lipophilicity, membrane permeability, metabolic stability, safety, and pharmacokinetic properties. AZM198 shows efficacy in improving vascular function, atherosclerotic plaques, pulmonary hypertension, nephropathy, visceral inflammatory fat deposition, ectopic fat deposition, and liver fibrosis.

EP2 receptor antagonist-3 is a selective antagonist of the EP2 receptor, with an IC50 of 8 nM determined in the hEP2 SPA assay and an IC50 of 50 nM in the hEP2 cAMP assay. It enhances macrophage-mediated clearance of Amyloid-β plaques. In CD-1 mice, it shows moderate clearance and good exposure, and exhibits good central nervous system (CNS) exposure in both mice and rats. EP2 receptor antagonist-3 is applicable for research in Alzheimer's disease.

ODN 1826 sodium is a class B CpG ODN (oligodeoxynucleotide) and a TLR9 agonist. It induces the production of NO and iNOS and enhances apoptosis. ODN 1826 sodium boosts immune surveillance and increases the size of atherosclerotic plaques. It exhibits antitumor activity against lung cancer, glioma, and melanoma.

AV-105 is a precursor for the synthesis of florbetapir-F18 (Amyvid). Amyvid is a positron emission tomography (PET) imaging agent targeting Aβ plaques, used for the diagnosis of Alzheimer's disease.

Florbetapir F-18 is a PET agent for Abeta plaques.

ML 10 is is a [18F] positron emission tomography (PET) radiotracer that accumulates in cells presenting apoptosis-specific membrane alterations. [18F]ML-10 allows for the detection of apoptotic cells located in atherosclerotic plaques.

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]

Cholesteryl heptadecanoate is a cholesterol ester (CE) formed by the condensation of cholesterol with heptadecanoic acid, a C-17 saturated fatty acid that does not occur in any natural animal or vegetable fat at high concentrations. As such, it is commonly used as an internal standard for the quantification of cholesterol esters by GC- or LC-mass spectrometry. CEs are major constituents of lipoprotein particles carried in blood and accumulate in the fatty acid lesions of atherosclerotic plaques. CEs of various fatty acids are major constituents of murine and human adrenal glands.

Amyloid-β (1-42) (Aβ42) is a neurotoxic 42-amino acid protein fragment found in amyloid plaques in postmortem cerebral cortex from patients with Alzheimer's disease.1,2,3Aggregation of Aβ42 results in the formation of neurotoxic fibrils or globular oligomers.1Aβ42 accumulates in the brain of many transgenic mouse models of Alzheimer's disease and, in many models, the onset of amyloid deposition positively correlates with deficits in spatial learning and memory.4 1.Wolfe, M.S.Therapeutic strategies for Alzheimer's diseaseNat. Rev. Drug Discov.1(11)859-866(2002) 2.Iwatsubo, T., Odaka, A., Suzuki, N., et al.Visualization of Aβ42(43) and Aβ40 in senile plaques with end-specific Aβ monoclonals: Evidence that an initially deposited species is Aβ42(43)Neuron13(1)45-53(1994) 3.Hardy, J.A., and Higgins, G.A.Alzheimer's disease: The amyloid cascade hypothesisScience256(5054)184-185(1992) 4.Jankowsky, J.L., and Zheng, H.Practical considerations for choosing a mouse model of Alzheimer's diseaseMol. Neurodegener.12(1)89(2017)

TAMRA-Amyloid-β (1-42) peptide is a fluorescently labeled peptide. Amyloid-β (1-42) (Aβ42) is a neurotoxic 42-residue protein fragment found in amyloid plaques in postmortem cerebral cortex from patients with Alzheimer's disease. Aggregation of Aβ42 results in the formation of neurotoxic fibrils or globular oligomers. TAMRA-Amyloid-β (1-42) peptide is a labeled form of Aβ42 containing carboxytetramethyl rhodamine (TAMRA), which displays excitation/emission maxima of 543/572 nm, respectively.

The amyloid β-protein is a 39- to 43-amino acid polypeptide that is the primary constituent of senile plaques and cerebrovascular deposits in Alzheimer's disease and Down's syndrome. Additionally it acts as an inhibitor of the ubiquitin-dependent protein degradation in vitro.

β-Amyloid (1-38), derived from mice and rats, is a chemical compound comprising 38 amino acids, specifically residues 1-38 of the Aβ peptide. Notably, it serves as the primary constituent of amyloid plaques associated with Alzheimer's disease.

NBI-74330 is a high-affinity CXCR3 antagonist that inhibits the binding of CXCR3 to its ligands CXCL10 and CXCL11, reduces the formation of atherosclerotic plaques in LDL receptor-deficient mice, and decreases the migration of CD4+ T cells and macrophages to the peritoneum.

Elenbecestat,also known as E2609 is a BACE1 inhibitor. By inhibiting BACE, a key enzyme in the production of Aβ peptides, E2609 decreases the formation of these peptides which can aggregate into toxic oligomers and protofibrils and eventually form amyloid plaques in the brain. Elenbecestat has been shown to reduce Aβ levels in cerebrospinal fluid, was investigated in two global phase 3 studies in early AD.