预约演示
更新于：2026-01-05
Acetylcysteine
乙酰半胱氨酸
更新于：2026-01-05
概要
基本信息
原研机构 |
非在研机构 |
最高研发阶段批准上市 |
最高研发阶段(中国)批准上市 |
特殊审评孤儿药 (美国)、孤儿药 (欧盟) |
登录后查看时间轴
结构/序列
分子式C5H9NO3S |
InChIKeyPWKSKIMOESPYIA-BYPYZUCNSA-N |
CAS号616-91-1 |
关联
984
项与 乙酰半胱氨酸 相关的临床试验NCT04381897
Use of N-Acetylcysteine (NAC) in the Treatment of Repetitive Behaviors (RB) and Self-Injurious Behaviors (SIB) in Cornelia de Lange Syndrome: A Randomized Double-Blind Placebo-Controlled Pilot Study
NCT07227649
NAC-REPAIR: N-Acetylcysteine-facilitated Redox-Immune Modulation for Post-surgical Analgesia and Injury Recovery
NCT07301294
Microbiological Characteristics of Biofilm on Double J Ureteral Stents After Lithotripsy: A Randomized Controlled Trial
100 项与 乙酰半胱氨酸 相关的临床结果
登录后查看更多信息
100 项与 乙酰半胱氨酸 相关的转化医学
登录后查看更多信息
100 项与 乙酰半胱氨酸 相关的专利（医药）
登录后查看更多信息
29,952
项与 乙酰半胱氨酸 相关的文献（医药）2026-12-01JOURNAL OF MOLECULAR MEDICINE-JMM
GATA1 controls metadherin transcription to promote oxidative stress-induced podocyte injury
Article
作者: Zheng, Xiaohong ; Wu, Wenting ; Peng, Fenfen ; Chen, Xiaowen ; Chen, Yihua ; Liang, Yunyi ; Zhao, Liyuan ; Tao, Danping ; Luo, Congwei ; Zheng, Zerong ; Shen, Lingyu ; Long, Haibo
Oxidative stress has been demonstrated to induce damage to podocytes, which play a pivotal role in the pathogenesis of chronic kidney disease (CKD). Metadherin (MTDH), an oncogene that has been extensively investigated in various malignancies, also contributes to podocyte injury in CKD. However, the relationship between oxidative stress and MTDH remains poorly elucidated. Here, we show that elevated oxidative stress in CKD serum induced MTDH expression and activated β-catenin signaling in podocytes, which were reversed by N-acetyl cysteine (NAC), a pharmacological antioxidant agent. Therefore, we established the oxidative stress model by administration of Advanced Oxidation Protein Products (AOPPs). As for the mechanism, oxidative stress enhanced MTDH expression both in mRNA and protein levels in podocytes. Furthermore, transcription factor prediction analysis and the Chip-qPCR assay identified that GATA1 was capable of directly binding to the MTDH promoter following AOPP stimulation. Silencing GATA1 repressed MTDH expression induced by AOPPs, while overexpressing GATA1 enhanced MTDH expression and subsequently activated β-catenin signaling. In conclusion, GATA1 induced by oxidative stress triggers MTDH transcription to activate β-catenin signaling, thereby promoting podocyte injury. Thus, targeting the GATA1/MTDH axis may present a promising therapeutic strategy for attenuating oxidative stress-induced damage in podocytes during CKD. KEY MESSAGES: Advanced Oxidative Protein Products (AOPPs) promote the accumulation of oxidative stress in circulation Metadherin is elevated in kidneys of AOPP-induced oxidative stress CKD model mice GATA1 controls transcription of MTDH in renal podocyte of CKD Silencing GATA1/MTDH axis interrupts β-catenin signaling and ameliorates podocyte injury and CKD pathology.
2026-12-01MOLECULAR BIOLOGY REPORTS
Excavatolide E triggers oxidative stress-associated apoptosis and DNA damage to inhibit bladder cancer cell proliferation
Article
作者: Yang, Che-Wei ; Chang, Hsueh-Wei ; Chang, Fang-Rong ; Yen, Chia-Hung ; Sheu, Jyh-Horng ; Chien, Tsu-Ming ; Yu, Szu-Yin
BACKGROUND:
Excavatolide E (EXCE), a biocompound extracted from the gorgonian octocoral Briareum excavatum, has received limited attention for its anticancer properties, especially in the context of bladder cancer.
METHODS:
Cell viability, flow cytometry, and Western blotting were performed to assess the antiproliferative effects and mechanisms against bladder cancer cells.
RESULTS:
In the present study, the impacts and mechanisms of EXCE's antiproliferative effects on bladder cancer cells were assessed, along with its impacts on normal cells. EXCE selectively inhibited proliferation of bladder cancer cells, as compared to normal cells, i.e., selectivity index > 2, and induced greater oxidative stress in bladder cancer cells than normal cells, regarding the induction of cellular and mitochondrial ROS, as well as the depletion of mitochondrial membrane potential. Moreover, EXCE triggered higher levels of apoptosis, both extrinsic and intrinsic caspase activation, and DNA damage in bladder cancer cells than in normal cell; these EXCE-triggered antiproliferative mechanisms were alleviated by N-acetylcysteine (NAC), a ROS inhibitor.
CONCLUSION:
Therefore, EXCE's antiproliferative activity offers a promising therapeutic approach for targeting bladder cancer cells by modulating oxidative stress, while preserving the safety of normal cells.
2026-03-01SPECTROCHIMICA ACTA PART A-MOLECULAR AND BIOMOLECULAR SPECTROSCOPY
Emission based sensing of N-acetyl cysteine via silver equipped anthraquinone derivatives
Article
作者: Yılmaz, Ülkü ; Mumcu, Taskin ; Oncuoglu, Serkan ; Mumcu, Akin ; Ertekin, Kadriye
In this work we investigated emission-based response of silver complexes of two newly synthesized anthraquinone derivatives for N-acetylcysteine (NAC) and thioglycolic acid. The interaction of the probes, DHA-dibenzonitrile and DHA-dibutanenitrile with silver nanoparticles resulted in metal chelation and following quenching of the fluorescence. To determine whether the emission intensity of the complexes was re-stored again, thiol compounds; NAC and thioglycolic acid were used. The released dyes re-emitted light, allowing the system to exhibit an intensity-based turn-on type sensor behavior for the NAC and thioglycolic acid, respectively. The re-stored fluorescence was monitored as a strong emission based analytical signal at 560 nm. The complex stoichiometries were investigated using several approaches, including Job's plot, density functional theory (DFT) and FT-IR measurements. The findings relying on HOMO-LUMO and energy gap calculations highlight that Ag coordination and following acetylcysteine adduction significantly re-shape both local nucleophilic and electrophilic regions, modulating the global electronic structure and reactivity of anthraquinone derivatives. N-acetylcysteine exhibited an exceptional spectral response at pH 9.0 in a buffered solution exhibiting 13.6 and 14.4-fold enhancement in the emission intensity, respectively. The reported linear responses for a concentration range of; 1.0 × 10-5 M -1.0 × 10-2 M, can easily be adopted to determination of the NAC levels in drugs, in vitro studies or in serum samples. Limit of detection (LOD) and limit of quantification (LOQ) values of the DHA-dibutanenitrile derivative for the NAC molecule were found to be 1.28 × 10-6 and 1.21 × 10-5 mol × L-1, respectively. Similarly, the DHA-dibenzonitrile exhibited 1.11 × 10-6 and 1.28 × 10-5 mol × L-1 of LOD and LOQ values, respectively.
100 项与 乙酰半胱氨酸 相关的药物交易
登录后查看更多信息
研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
登录
| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 支气管炎 | 中国 | 2025-05-13 | |
| 嵌甲 | 日本 | 2023-03-27 | |
| 对乙酰氨基酚过量 | 澳大利亚 | 2006-07-17 | |
| 慢性阻塞性肺疾病 | 中国 | 1985-01-01 | |
| 哮喘 | 日本 | 1965-01-05 | |
| 支气管扩张 | 日本 | 1965-01-05 | |
| 慢性支气管炎 | 日本 | 1965-01-05 | |
| 囊性纤维化 | 日本 | 1965-01-05 | |
| 喉炎 | 日本 | 1965-01-05 | |
| 咽炎 | 日本 | 1965-01-05 | |
| 肺炎 | 日本 | 1965-01-05 | |
| 肺气肿 | 日本 | 1965-01-05 | |
| 肺结核 | 日本 | 1965-01-05 | |
| 药物性肝损伤 | 美国 | 1963-09-14 | |
| 肝损伤 | 美国 | 1963-09-14 |
未上市
10 条进展最快的记录, 后查看更多信息
登录
| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 急性支气管炎 | 临床3期 | 中国 | 2019-06-21 | |
| 急性支气管炎 | 临床3期 | 中国 | 2019-06-21 | |
| 特发性肺纤维化 | 临床3期 | 比利时 | 2000-03-01 | |
| 特发性肺纤维化 | 临床3期 | 法国 | 2000-03-01 | |
| 特发性肺纤维化 | 临床3期 | 德国 | 2000-03-01 | |
| 特发性肺纤维化 | 临床3期 | 意大利 | 2000-03-01 | |
| 特发性肺纤维化 | 临床3期 | 荷兰 | 2000-03-01 | |
| 特发性肺纤维化 | 临床3期 | 西班牙 | 2000-03-01 | |
| 特发性肺纤维化 | 临床3期 | 英国 | 2000-03-01 | |
| 普通感冒 | 临床2期 | 加拿大 | 2015-01-01 |
登录后查看更多信息
临床结果
临床结果
适应症
分期
评价
查看全部结果
临床2期 | 32 | cTBS (Active Theta Burst Stimulation) | 糧築糧簾醖膚構鏇製壓(糧築壓夢網繭鹽繭醖夢) = 糧遞鏇醖範網鬱簾繭膚 觸築製獵憲鹹壓廠構衊 (築憲鹹鑰積餘蓋鹹選襯, 0.0080) 更多 | - | 2025-09-24 | ||
cTBS (Sham Theta Burst Stimulation) | 糧築糧簾醖膚構鏇製壓(糧築壓夢網繭鹽繭醖夢) = 鹹餘糧構願鹹築構餘糧 觸築製獵憲鹹壓廠構衊 (築憲鹹鑰積餘蓋鹹選襯, 0.0105) 更多 | ||||||
临床2期 | 126 | 願憲襯鑰獵觸鏇簾憲膚(網窪簾鹽積糧艱襯選鏇) = N-acetylcysteine did not significantly reduce alcohol use compared to placebo. 醖觸製衊範蓋餘鏇膚獵 (糧餘壓遞顧簾鹹襯選鏇 ) 更多 | 积极 | 2025-09-01 | |||
Placebo | |||||||
临床2期 | 急性髓性白血病 reactive oxygen species (ROS) | 30 | 鏇鑰製憲鑰鹽壓鑰齋範(觸窪網襯鬱獵醖壓顧積) = 鏇鹽餘構觸糧鏇網築艱 積觸膚衊製夢鹹廠淵鹽 (壓築窪簾網蓋餘積餘鹽 ) 更多 | 积极 | 2025-08-01 | ||
(Control Group) | 鏇鑰製憲鑰鹽壓鑰齋範(觸窪網襯鬱獵醖壓顧積) = 糧壓窪簾鑰網鹹糧鏇憲 積觸膚衊製夢鹹廠淵鹽 (壓築窪簾網蓋餘積餘鹽 ) 更多 | ||||||
临床4期 | 54 | (N-Acetylcysteine) | 選壓壓廠襯簾築選顧鑰(齋鬱願鑰夢膚鑰鹹蓋餘) = 製積餘築遞鏇鹹糧淵鑰 膚獵餘艱願製艱糧壓構 (憲鏇獵膚窪蓋願糧鑰糧, 8.1) 更多 | - | 2025-06-05 | ||
QAM+inositol+omega-3 fatty acids (Omega-3 Fatty Acids + Inositol) | 糧鏇憲獵願膚餘襯醖願(製餘鑰構糧顧醖選齋淵) = 艱膚築壓鏇顧廠構願醖 鑰壓繭繭範選衊艱夢獵 (淵製鹽觸窪網鑰積範淵, 7.7) 更多 | ||||||
临床2期 | 30 | (N-acetyl Cysteine) | 鬱築獵糧簾觸鏇廠積廠(製衊鹽餘鏇憲艱積襯鏇) = 簾顧醖製顧製選衊鹽膚 顧構窪廠蓋鬱夢蓋選醖 (鬱鬱齋鹽蓋積餘襯願構, 餘餘夢顧鑰觸窪糧築範 ~ 鬱蓋顧淵淵網獵繭遞襯) 更多 | - | 2025-04-30 | ||
(Normal Saline) | 鬱築獵糧簾觸鏇廠積廠(製衊鹽餘鏇憲艱積襯鏇) = 鏇遞願製獵構衊齋醖遞 顧構窪廠蓋鬱夢蓋選醖 (鬱鬱齋鹽蓋積餘襯願構, 糧鹹積鏇範鏇窪淵夢遞 ~ 淵鏇鹹觸觸醖範築鹹壓) 更多 | ||||||
临床3期 | 44 | (N-acetylcysteine IV Infusion at 0.5 gm Hourly) | 選艱齋醖鏇鹽製簾鏇餘(築鏇製鹽積遞鬱願襯構) = 餘構範艱鏇構膚網獵鑰 淵繭積廠構獵顧膚憲網 (鹹齋艱構壓憲餘遞選鹹, 顧願蓋壓鹽築鏇窪壓選 ~ 觸夢艱糧夢衊鏇糧顧襯) 更多 | - | 2025-04-18 | ||
Placebo+N-acetylcysteine (Placebo for N-acetylcysteine IV Infusion at 0.5 gm Hourly) | 選艱齋醖鏇鹽製簾鏇餘(築鏇製鹽積遞鬱願襯構) = 製繭膚鹹鹽艱蓋壓鏇餘 淵繭積廠構獵顧膚憲網 (鹹齋艱構壓憲餘遞選鹹, 製鹹膚獵襯網襯獵憲製 ~ 窪夢餘構夢衊壓窪憲築) 更多 | ||||||
N/A | 2,461 | (1200mg/d) | 窪範願齋觸廠顧願窪醖(鏇齋繭願範壓鏇壓膚醖) = 鑰製鹽鏇餘顧積淵顧選 衊醖選構鏇廠願積壓願 (壓鑰製蓋鹽醖廠觸艱顧 ) | 积极 | 2025-04-01 | ||
(600mg/d) | 選糧鏇構簾餘繭鏇積鹹(鏇憲鹹獵繭構窪遞壓願) = 膚範憲顧鹽蓋鹽艱築願 衊餘鬱觸鏇壓鏇築範製 (遞鹽鏇範蓋齋遞齋簾網 ) 更多 | ||||||
临床2期 | 60 | (N-acetylcysteine) | 積憲鏇夢構簾網衊醖遞(積鹹網壓膚齋齋壓淵糧) = 襯蓋鏇糧鑰簾網襯簾鏇 衊膚襯獵醖簾範範窪範 (衊夢願鬱繭淵糧鏇遞醖, 積範顧襯衊醖鏇獵顧觸 ~ 觸築衊窪鹹網鏇鏇廠鬱) 更多 | - | 2025-03-26 | ||
Placebo oral capsule (Placebo) | 積憲鏇夢構簾網衊醖遞(積鹹網壓膚齋齋壓淵糧) = 築齋齋網遞鬱願淵鏇觸 衊膚襯獵醖簾範範窪範 (衊夢願鬱繭淵糧鏇遞醖, 餘憲淵窪餘簾範簾膚範 ~ 夢醖鏇範範構憲糧齋獵) 更多 | ||||||
临床4期 | - | N-acetyl cysteine 2400 mg/day | 觸築鏇壓淵網憲餘窪遞(鬱構選簾築淵醖構願範) = 鏇鹽範製鹹積醖顧鹽觸 選觸憲齋廠鏇夢積憲鹹 (顧淵醖夢選膚鹹壓艱糧 ) 更多 | 积极 | 2025-03-04 | ||
临床2期 | 126 | (N-acetylcysteine) | 選製窪餘壓憲鑰艱鬱製(憲艱廠築鹽願網餘廠醖) = 遞願積鹽鏇醖願網夢襯 鬱壓廠顧鹹願顧鏇襯觸 (顧餘顧鬱顧窪醖積築衊, 28.3) 更多 | - | 2025-01-08 | ||
Placebo oral capsule (Placebo) | 選製窪餘壓憲鑰艱鬱製(憲艱廠築鹽願網餘廠醖) = 簾餘膚壓衊選蓋觸醖鏇 鬱壓廠顧鹹願顧鏇襯觸 (顧餘顧鬱顧窪醖積築衊, 43.1) 更多 |
登录后查看更多信息
转化医学
使用我们的转化医学数据加速您的研究。
登录
或
药物交易
使用我们的药物交易数据加速您的研究。
登录
或
核心专利
使用我们的核心专利数据促进您的研究。
登录
或
临床分析
紧跟全球注册中心的最新临床试验。
登录
或
批准
利用最新的监管批准信息加速您的研究。
登录
或
特殊审评
只需点击几下即可了解关键药物信息。
登录
或
生物医药百科问答
全新生物医药AI Agent 覆盖科研全链路，让突破性发现快人一步
立即开始免费试用!
智慧芽新药情报库是智慧芽专为生命科学人士构建的基于AI的创新药情报平台，助您全方位提升您的研发与决策效率。
立即开始数据试用!
智慧芽新药库数据也通过智慧芽数据服务平台，以API或者数据包形式对外开放，助您更加充分利用智慧芽新药情报信息。
生物序列数据库
生物药研发创新
免费使用
化学结构数据库
小分子化药研发创新
免费使用