plaques

Dithranol (cignoline) 是蒽醌衍生物，可破坏线粒体功能和结构，用于治疗皮肤病。

Picotamide 具有抗凝和纤维蛋白溶解特性。

CRANAD-28 是一种血脑屏障（BBB）穿透型双光子成像探头，能够显示淀粉样蛋白斑块，可以标记斑块和脑淀粉样血管病。

BMS-212122 (UNII-0Z473OO6GB) 是一种有效的微粒体甘油三酯转移蛋白(MTP )抑制剂，在动物实验中显示出降血脂作用。BMS-212122 显著减少动脉粥样硬化斑块中的脂质含量和单核细胞衍生(CD68+)细胞。

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)是一种 CD40-TRAF6 相互作用的选择性抑制剂，可以抑制 RAW 细胞中 NF-κB 活化。TRAF-STOP 6877002 可阻止小鼠动脉粥样硬化的恶化，减少白细胞募集和巨噬细胞的活化，减少动脉粥样硬化斑块中的巨噬细胞增殖。

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

MeS-IMPY在与来自阿尔茨海默病（AD）患者大脑或AD脑匀浆中提取的β-amyloid plaques结合时展现出较IMPY更高的亲和力（Ki分别为7.93和8.95 nM）。[11C]MeS-IMPY作为一种潜在的放射性配体，适用于正电子发射断层扫描（PET）成像，用于探测β-淀粉样斑块。

tau-0N4R-IN-1（Compound 6T）作为一种穿透脑屏障的抑制剂，能够抑制tau 0N4R、2N3R及2N4R的纤维化。该化合物具有显著的抗播种效应，在体外能够剂量依赖地减少α-syn的寡聚，并阻止α-syn包涵体的形成。在小鼠微粒体中表现出稳定性，并能减少AD患者脑组织中的Aβ斑块。此外，tau-0N4R-IN-1在小鼠体内展示出优良的药代动力学特性。

GI-Y2是一种GSDMD抑制剂，能够抑制氧化低密度脂蛋白 (ox-LDL) 诱导的巨噬细胞焦亡 (Pyroptosis)。在体内，GI-Y2能够以剂量依赖的方式减少ApoE-/-小鼠的动脉粥样硬化斑块，降低主动脉根的病变大小和纤维化程度。GI-Y2 有望用于细胞焦亡和心血管疾病的研究，例如动脉粥样硬化。

AZM198 是一种具有选择性且具有口服活性的不可逆MPO抑制剂，IC50为15.0 nM。它对CYP3A4的IC50为19 μM。AZM198 具有良好的脂溶性、膜通透性、代谢稳定性、安全性和出色的药代动力学特性。该化合物在改善血管功能、动脉粥样硬化斑块、肺动脉高压、肾病、内脏炎性脂肪沉积、异位脂肪沉积以及肝纤维化等方面均具有活性。

EP2 receptor antagonist-3 是一种选择性的 EP2 受体拮抗剂，在 hEP2 SPA 实验中的 IC50 为 8 nM，和在 hEP2 cAMP 实验中的 IC50 为 50 nM。其可增强巨噬细胞对 Amyloid-β 斑块的清除。在 CD-1 小鼠中，该化合物表现出适中的清除率和良好的暴露，并且在小鼠和大鼠中具有良好的中枢神经系统 (CNS) 暴露。EP2 receptor antagonist-3 可用于阿尔茨海默病的研究。

ODN 1826 sodium 是一种 B 类 CpG ODN (寡脱氧核苷酸)和TLR9 激动剂，能够诱导 NO 和 iNOS 产生，同时增强凋亡 (Apoptosis)和免疫监视。该化合物还会增加主动脉粥样硬化斑块大小，对肺癌、胶质瘤和黑色素瘤显示出抗肿瘤活性。

AV-105是合成florbetapir-f18(Amyvid)的前体。Amyvid是靶向Aβ斑块的正电子发射断层(PET)显像剂，用于诊断阿尔茨海默病。

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是一种高亲和力的CXCR3拮抗剂,能够抑制CXCR3与其配体CXCL10和CXCL11的结合，减轻LDL受体缺陷小鼠动脉粥样硬化斑块的形成,减少CD4+ T细胞和巨噬细胞向腹腔的迁移。

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.