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更新于：2026-01-27
Probucol
普罗布考
更新于：2026-01-27
概要
基本信息
最高研发阶段批准上市 |
最高研发阶段(中国)撤市 |
特殊审评- |
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结构/序列
分子式C31H48O2S2 |
InChIKeyFYPMFJGVHOHGLL-UHFFFAOYSA-N |
CAS号23288-49-5 |
关联
48
项与 普罗布考 相关的临床试验CTR20252916
普罗布考片在健康人群中的生物等效性试验
CTR20252921
普罗布考片在健康人群中的生物等效性试验
CTR20252474
普罗布考片健康人体生物等效性研究
100 项与 普罗布考 相关的临床结果
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100 项与 普罗布考 相关的转化医学
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100 项与 普罗布考 相关的专利（医药）
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1,444
项与 普罗布考 相关的文献（医药）2026-02-01EXPERIMENTAL GERONTOLOGY
Probucol attenuates bone loss in APP/PS1 mice and ameliorates Aβ42-induced osteoblast dysfunction by regulating AKT/FOXO3a signaling pathway
Article
作者: Zhou, Huadong ; Hong, Wenjuan ; Feng, Xiangqian ; Hou, Mingliang ; Li, Xiaoxiong ; Li, Jinping ; Lu, Jing ; Fu, Xiaoyan ; Yang, Hongyan ; Liu, Dong ; Liu, Yating ; Liao, Qirong ; Chen, Le ; Wang, Donglin ; Ma, Linqiu ; Zhou, Rui
BACKGROUND:
Alzheimer's disease (AD) and osteoporosis are common age-related degenerative diseases. Emerging evidence suggests that amyloid-β (Aβ) deposition may contribute to the pathogenesis of both conditions. This study investigated whether probucol could alleviate AD-associated bone loss and Aβ42-induced osteoblast dysfunction, and further explored the underlying mechanisms.
METHODS:
Female mice were divided into four groups (n = 5 per group): C57BL/6 wild-type (WT), WT treated with probucol (WT + PBC), APP/PS1 transgenic (AD) mice, and AD treated with probucol (AD+PBC). Bone mineral density (BMD) was assessed by micro-CT. Levels of pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) along with bone metabolism markers including fibroblast growth factor 23 (FGF23), sclerostin, and brain-derived neurotrophic factor (BDNF) in bone and brain tissues were measured by ELISA. FOXO3a was knocked down in the bone marrow of APP/PS1 mice via stereotactic injection of lentiviral vectors. Expression of APP and FOXO3a in bone tissue was evaluated using RT-qPCR and Western blotting (WB). Mitochondrial damage in osteoblasts and neuronal cells was assessed by transmission electron microscopy (TEM). In vitro study, osteoblast differentiation and mineralization deficits were evaluated using Alizarin Red staining. WB was used to measure the expression of AKT, FOXO3a, autophagy and apoptosis related proteins.
RESULTS:
Probucol attenuated bone loss and mitochondrial damage in both APP/PS1 and FOXO3a-knockdown APP/PS1 mice, and improved cognitive impairment and neuronal ultrastructure in APP/PS1 mice. Furthermore, probucol attenuated Aβ42-induced osteoblast differentiation and mineralization via the AKT/FOXO3a signaling pathway in vitro.
CONCLUSION:
These findings demonstrate that probucol ameliorates AD-associated bone loss and Aβ42-induced osteoblast impairments by regulating AKT/FOXO3a signaling pathway.
2025-12-01Stress biology
Dietary glycerol monolaurate mitigates heat stress-induced disruption of intestinal homeostasis and hepatic lipid metabolism in laying hens
Article
作者: Ren, Hongrui ; Zou, Cunzhi ; Ma, Wenqiang ; Gao, Jiang ; He, Bin ; Wu, Xuanfu
Abstract:
Heat stress (HS) disrupts intestinal homeostasis and hepatic lipid metabolism in poultry, yet effective interventions remain limited. We investigate the protective effects of dietary glycerol monolaurate (GML) supplementation in laying hens under HS conditions. In a 10-week trial, 504 Hy-Line Brown hens were assigned to four groups (control and GML at 65, 195, and 325 mg/kg) with six replicates per group. Hens receiving 325 mg/kg GML exhibited significantly higher egg production and egg weight (P < 0.05), alongside improved egg quality metrics, including increased shell strength and Haugh units by week 8 (P < 0.05). Histological analysis revealed that GML (325 mg/kg) improved duodenal and ileal villus height and duodenal villus-to-crypt ratios while reducing duodenal crypt depth (P < 0.05), thereby restoring gut barrier integrity. These findings were supported by reduced plasma D-lactate (D-LA) levels and upregulated expression of tight-junction proteins ZO-1 and Occludin in the ileum and jejunum (P < 0.05). In the liver, GML supplementation alleviated HS-induced steatosis, reducing lipid droplet accumulation (P < 0.05), plasma low-density lipoprotein cholesterol (LDL-C), aspartate aminotransferase (AST), and alanine aminotransferase (ALT) levels, and hepatic triglyceride content, while elevating high density lipoprotein cholesterol (HDL-C). Integrated plasma metabolomics and hepatic transcriptomics identified 36 differential metabolites (enriched in sphingolipid metabolism) and 1,176 differentially expressed genes (enriched in PPAR signaling and Fatty acid degradation), with ACSL1 as a central regulatory gene. Key genes (ACSL1, CPT1 A) and metabolites correlated positively with production performance and gut-liver health, while SCD and Probucol showed negative associations. These findings indicate that GML supplementation enhances intestinal barrier function, promotes hepatic fatty acid β-oxidation, and reinforces sphingolipid metabolism, thereby mitigating HS-induced oxidative stress and lipid dysregulation. Our results identify 325 mg/kg GML as the optimal dosage, proposing a practical strategy to enhance poultry resilience during heat stress.
2025-12-01Alzheimers & Dementia
Single‐cell digital twins identify drug targets and repurposable medicine in Alzheimer’s disease
Article
作者: Pieper, Andrew A. ; Cheng, Feixiong ; Cummings, Jeffrey L. ; Ren, Yunxiao
Abstract:
Background:
Alzheimer’s disease (AD) is a complex and poorly understood neurodegenerative disorder with a lack of effective treatments. Novel approaches for identifying FDA‐approved drugs with potential for AD treatment hold promise to address this challenge. One promising approach involves leveraging digital twins (DTs), which are virtual representations of physical entities by integrating advanced technologies such as artificial intelligence (AI), statistical modeling, network medicine, and multi‐omics analysis. DTs enable real‐time characterization of disease heterogeneities through continuous feedback and dynamic model updates, facilitating the identification of therapeutic targets.
Method:
In this study, we developed a single‐cell Digital Twin (scDT) framework to model AD progression by integrating single‐nuclei RNA‐seq (snRNA‐seq; 1,197,032 nuclei) and ATAC‐seq (snATAC‐seq; 740,875 nuclei) data from the middle temporal gyrus (MTG) of 84 donors across four stages (non‐AD, low, intermediate, and high) of AD neuropathological changes (ADNC) from the SEA‐AD cohort. This framework enabled prioritization of AD‐associated genes and identification of potential candidate drugs through a combination of gene set enrichment analysis (GSEA) and network proximity analysis.
Result:
We annotated six major cell types for snRNA‐seq and snATAC‐seq and observed distinct gene expression dynamics among these six major cell types during the early stages of ADNC, with these differences becoming more pronounced in high ADNC. By constructing cell type‐specific transcription factor (TF)‐target gene regulatory networks through leveraging peak‐to‐gene linkages and motif enrichment analyses, we identified cell type‐specific candidate
cis
‐regulatory DNA elements (cCREs). Integration of genome‐wide association study (GWAS) loci with cell type‐specific cCREs revealed 141 ADNC‐associated genes, including 36 genes targeted by FDA‐approved or clinically investigational therapies (e.g.,
ACE, ABCA1
, and
CRHR1
). Furthermore, GSEA and network proximity analyses highlighted 13 repurposable drugs (e.g., galantamine, mecamylamine, dextromethorphan, tubocurarine, gabapentin, ebselen, resveratrol, imatinib, dipyridamole, deferoxamine, gemfibrozil, lansoprazole, and probucol) associated with these ADNC‐linked genes.
Conclusion:
In summary, we demonstrated a single‐cell digital twin framework for cell type‐specific target identification and drug repurposing in AD and other AD‐related dementia if broadly applied.
100 项与 普罗布考 相关的药物交易
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 高胆固醇血症 | 美国 | 1977-02-01 | |
| 高脂血症 | 美国 | 1977-02-01 |
未上市
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 冠状动脉再狭窄 | 临床3期 | 日本 | - | |
| 冠状动脉再狭窄 | 临床3期 | 加拿大 | - | - |
| 2型糖尿病 | 临床2期 | 韩国 | 2012-10-01 | |
| 糖尿病肾病 | 临床2期 | 韩国 | 2012-10-01 |
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临床4期 | 342 | 艱廠繭網窪齋選繭觸選(製網繭簾膚獵襯蓋積壓) = 顧築膚壓膚醖醖觸遞積 鹹願壓範餘窪蓋製鬱築 (製鏇淵選網艱襯憲壓鏇 ) 更多 | - | 1997-04-01 | |||
(Control subjects) | 艱廠繭網窪齋選繭觸選(製網繭簾膚獵襯蓋積壓) = 齋蓋艱鏇觸廠遞夢繭醖 鹹願壓範餘窪蓋製鬱築 (製鏇淵選網艱襯憲壓鏇 ) 更多 |
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