更新于：2024-04-17
Allopurinol
别嘌醇
更新于：2024-04-17
概要
基本信息
简介别嘌醇以商品名Zyloprim® 销售，是一种黄嘌呤氧化酶抑制剂药物，主要用于降低痛风、复发性草酸钙结石和某些恶性肿瘤患者的尿液和血清尿酸水平。这种药物的作用机制涉及抑制黄嘌呤氧化酶。别嘌醇最早于1966年获得美国FDA批准，由诺华公司研制。它的主要适应症是治疗高尿酸血症，这是一种以血液中尿酸过多为特征的疾病。通过其降低尿酸浓度的能力，别嘌醇一直用于治疗饱受痛风折磨的病人。 |
药物类型 小分子化药 |
别名 1,5-Dihydro-4H-pyrazolo(3,4-d)pyrimidin-4-one、1,5-Dihydro-4H-pyrazolo(3,4-d)pyrimidine-4-one、1H-Pyrazolo(3,4-d)pyrimidin-4-ol + [22] |
靶点 |
作用机制 XO抑制剂(黄嘌呤脱氢酶抑制剂) |
非在研适应症 |
最高研发阶段批准上市 |
首次获批日期 美国 (1966-08-19), |
最高研发阶段(中国)批准上市 |
特殊审评- |
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结构
分子式C5H4N4O |
InChIKeyOFCNXPDARWKPPY-UHFFFAOYSA-N |
CAS号315-30-0 |
关联
282
项与 别嘌醇 相关的临床试验Evaluation of the effect of Allopurinol on the frequency of ventricular and supraventricular arrhythmias in patients with an implantable cardioverter-defibrillator
Treat-to-Target Serum Urate Versus Treat-to-Avoid Symptoms in Gout: A Randomized Controlled Trial
A randomized, double-blind, placebo-controlled study to evaluate the effect of allopurinol on the risk of cardiovascular events in patients at high and very high cardiovascular risk, including the presence of long-COVID syndrome. - ALL-VASCOR
100 项与 别嘌醇 相关的临床结果
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100 项与 别嘌醇 相关的转化医学
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100 项与 别嘌醇 相关的专利（医药）
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8,251
项与 别嘌醇 相关的文献（医药）2024-04-01Seminars in Arthritis and Rheumatism
An updated systematic review and meta-analysis of randomised controlled trials on the effects of urate-lowering therapy initiation during a gout flare
Review
作者: Gow, Peter ; Abhishek, Abhishek ; Tai, Vicky ; Satpanich, Panchalee ; Dalbeth, Nicola ; Stewart, Sarah ; Li, Changgui
BACKGROUND:
There is uncertainty about the optimal time to start urate-lowering therapy (ULT) in the setting of a gout flare. The aim was to perform a systematic review and meta-analysis of randomised controlled trials (RCTs) assessing the effects of ULT initiation during a gout flare.
METHODS:
This systematic review was conducted in accordance with PRISMA methodology. MEDLINE, EMBASE and The Cochrane Library were searched for studies published between database inception to 1 March 2023. RCTs published in English that examined ULT initiation during a gout flare in adults ≥18 years were included. The quality of included studies was assessed using the revised Cochrane Risk of Bias tool 2.0. Data were extracted for the following outcomes: patient-rated pain score, duration of gout flare, recurrent gout flares, time to achieve target serum urate, adherence to ULT, patient satisfaction with treatment and adverse events. Meta-analyses were performed using Review Manager v5.4. This study is registered on PROSPERO, number CRD42023404680.
RESULTS:
A total of 972 studies were identified and of these, six RCTs met the criteria for inclusion in the analysis. Three studies were assessed as having high risk of bias, one study as having some concerns, and two studies as having low risk of bias. In total, there were 445 pooled participants; 226 participants randomised to early initiation of ULT and 219 to placebo or delayed initiation of ULT. Allopurinol was used in three studies, febuxostat in two studies and probenecid in one study. Few participants (n = 62, 13.9 %) had tophaceous gout. Participants with renal impairment were excluded from most studies. There were no differences in patient-rated pain scores at baseline, days 3-4, days 7-8, day 10 or days 14-15 (p ≥ 0.42). Additionally, there was no significant difference in time to resolution of gout flare (standardised mean difference 0.77 days; 95 % CI -0.26 to 1.79; p = 0.14) or the risk of recurrent gout flare in the subsequent 28 to 30 days (RR 1.06; 95 % CI 0.59 to 1.92; p = 0.84). Adverse events were similar between groups. The included studies did not report time to achieve target serum urate, long-term adherence to ULT, or patient satisfaction with treatment.
CONCLUSION:
There appears to be no evidence for harm or for benefit to initiating ULT during a gout flare. These findings have limited applicability to patients with tophaceous gout, or those with renal impairment.
2024-04-01Redox Biology
Inhibition of xanthine oxidase by allopurinol suppresses HMGB1 secretion and ameliorates experimental asthma
Article
作者: Xu, Maosheng ; Le, Yanqing ; Zhao, Wenqu ; Gong, Zhaoqian ; Wang, Yanhong ; Yu, Changhui ; Wu, Jie ; Zhang, Qian ; Xu, Guiling ; Cai, Shaoxi ; Ma, Yanyan ; Zhao, Haijin
BACKGROUND:
Extracellular high mobility group box 1 (HMGB1) is a key mediator in driving allergic airway inflammation and contributes to asthma. Yet, mechanism of HMGB1 secretion in asthma is poorly defined. Pulmonary metabolic dysfunction is recently recognized as a driver of respiratory pathology. However, the altered metabolic signatures and the roles of metabolic to allergic airway inflammation remain unclear.
METHODS:
Male C57BL/6 J mice were sensitized and challenged with toluene diisocyanate (TDI) to generate a chemically induced asthma model. Pulmonary untargeted metabolomics was employed. According to results, mice were orally administered allopurinol, a xanthine oxidase (XO) inhibitor. Human bronchial epithelial cells (16HBE) were stimulated by TDI-human serum albumin (HSA).
RESULTS:
We identified the purine metabolism was the most enriched pathway in TDI-exposed lungs, corresponding to the increase of xanthine and uric acid, products of purine degradation mediated by XO. Inhibition of XO by allopurinol ameliorates TDI-induced oxidative stress and DNA damage, mixed granulocytic airway inflammation and Th1, Th2 and Th17 immunology as well as HMGB1 acetylation and secretion. Mechanistically, HMGB1 acetylation was caused by decreased activation of the NAD+-sirtuin 1 (SIRT1) axis triggered by hyperactivation of the DNA damage sensor poly (ADP-ribose)-polymerase 1 (PARP-1). This was rescued by allopurinol, PARP-1 inhibitor or supplementation with NAD+ precursor in a SIRT1-dependent manner. Meanwhile, allopurinol attenuated Nrf2 defect due to SIRT1 inactivation to help ROS scavenge.
CONCLUSIONS:
We demonstrated a novel regulation of HMGB1 acetylation and secretion by purine metabolism that is critical for asthma onset. Allopurinol may have therapeutic potential in patients with asthma.
2024-03-01Journal of Ethnopharmacology
Effect and mechanism of aqueous extract of Chinese herbal prescription (TFK) in treating gout arthritis
Article
作者: Dai, Xiaojun ; Ni, Tengyang ; Chen, Dawei ; Liu, Yanqing ; Wang, Haibo ; Jiang, Wei ; Sunagawa, Masataka ; Chu, Zewen
ETHNOPHARMACOLOGICAL RELEVANCE:
With the rapid development of China's economic level, great changes have taken place in people's diet structure, gout has become a common disease that puzzles people's health, seriously affects the realization of China's "Healthy China" strategic goal. Gouty arthritis (GA) is a common joint disease caused by chronic purine metabolism disorder. Currently, drugs used to treat GA are allopurinol and colchicine. However, these drugs can only temporarily relieve the clinical symptoms of GA with significant side effects. More and more basic and clinical studies have confirmed that Traditional Chinese medicine has definite curative effect on GA.
AIM OF THE STUDY:
To elucidate the potential molecular mechanism of Tongfengkang (TFK) in the treatment of GA, and to provide experimental basis for the search and development of efficient and low-toxicity Chinese medicine for GA treatment.
MATERIALS AND METHODS:
Aqueous extract of TFK (AETFK) were determined by liquid phase high resolution mass spectrometry and the possible effective constituents were screened out. Acute GA model rats were established to detect the anti-inflammatory and detumification effects of AETFK on GA and explore the potential mechanism. The effect of AETFK on serum uric acid and urinary uric acid levels in acute GA rats was determined by automatic biochemical analyzer, and the effect of AETFK on the expression of acute GA-related immunoinflammatory factors were determined by protein thermal fluorescence chip. The effect of AETFK on the concentration of neutrophils in the joint fluid of acute GA rats were determined by Reichs-Giemsa staining. The effect of AETFK on macrophage activation was detected by ELISA. In order to further investigate the mechanism of AETFK in the treatment of GA, a rat model of hyperuricemia was established to detect the effect of AETFK on the level of uric acid in hyperuricemia model rats. Biochemical indexes of liver and kidney and hematoxylin-eosin staining (HE) were used to evaluate the effects of AETFK on the organs, and to preliminatively evaluate the safety of ventilation confufang.
RESULTS:
Compared with the model group, the joint swelling degree of GA rats in AETFK treatment group were significantly reduced, and the levels of blood uric acid and urine uric acid were also significantly decreased. Protein thermal fluorescence microarray results showed that the levels of gout - related inflammatory factors in GA rats in AETFK treatment group were significantly lower than those in control group. Reichsen-giemsa staining and ELISA showed that AETFK could reduce the activation of macrophages and the accumulation of neutrophils in the joint fluid. The results of liver and kidney biochemical indexes and HE staining showed that no obvious tissue damage was observed in the organs of rats treated with AETFK.
CONCLUSIONS:
AETFK not only has significant anti-inflammatory effects on GA, but also can significantly reduce the level of blood uric acid in GA rats, without obvious toxic and side effects. These effects may be related to AETFK's inhibition of neutrophil enrichment and macrophage activation during early inflammation.
100 项与 别嘌醇 相关的药物交易
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研发状态
| 适应症 | 最高研发状态 | 国家/地区 | 公司 |
|---|---|---|---|
| 痛风 | 批准上市 | 中国 更多 | |
| 高尿酸血症 | 批准上市 | 中国 更多 | |
| 肾石病 | 批准上市 | 中国 更多 | |
| 手足综合症 | 无进展 | 德国 更多 |
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临床结果
临床结果
适应症
分期
评价
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临床2期 | 34 | (Allopurinol) | 選艱餘餘鏇鑰鬱鏇鑰遞(積餘鹽廠選餘觸選鏇築) = 壓簾獵願鏇膚鑰顧夢齋 鑰齋鹽鹹壓膚繭獵繭壓 (願積襯選醖鏇齋膚艱憲, 積鬱艱鹽願憲壓網壓壓 ~ 蓋憲鏇襯網觸壓鹹鹹鹹) 更多 | - | 2023-07-03 | ||
Placebo (Placebo) | 選艱餘餘鏇鑰鬱鏇鑰遞(積餘鹽廠選餘觸選鏇築) = 艱網艱觸夢繭鏇襯遞鹽 鑰齋鹽鹹壓膚繭獵繭壓 (願積襯選醖鏇齋膚艱憲, 選獵蓋壓廠糧壓鑰廠網 ~ 選壓淵鏇廠網觸構鬱願) 更多 | ||||||
临床3期 | - | 齋壓醖顧壓顧築築顧築(鏇夢廠壓壓餘鬱壓簾壓) = 網憲餘齋構夢繭淵築顧 夢積鹽衊艱築鬱壓蓋願 (糧糧憲夢壓膚鹹鏇糧築 ) 更多 | - | 2023-04-18 | |||
N/A | 5,721 | Standard of Care+Allopurinol | 鏇襯積壓蓋糧範鑰獵鏇(淵膚鏇餘網築獵構鏇鑰) = 製網鹹獵願餘獵製築顧 膚網廠壓積鹽獵夢窪廠 (鹽窪糧糧遞淵夢膚簾觸 ) 更多 | 不佳 | 2022-08-27 | ||
Standard of Care | 鏇襯積壓蓋糧範鑰獵鏇(淵膚鏇餘網築獵構鏇鑰) = 夢觸膚蓋膚觸醖淵繭衊 膚網廠壓積鹽獵夢窪廠 (鹽窪糧糧遞淵夢膚簾觸 ) 更多 | ||||||
N/A | 痛风 serum uric acid | - | 壓鏇顧鏇顧願夢淵壓齋(鏇醖鏇蓋選窪襯餘鑰遞) = 繭鹽壓膚廠鑰憲鬱齋鹹 遞衊構壓鑰淵顧繭選夢 (鬱齋鑰獵餘獵鑰壓廠繭 ) | 积极 | 2022-06-01 | ||
壓鏇顧鏇顧願夢淵壓齋(鏇醖鏇蓋選窪襯餘鑰遞) = 襯醖窪糧壓選鹽餘憲積 遞衊構壓鑰淵顧繭選夢 (鬱齋鑰獵餘獵鑰壓廠繭 ) | |||||||
N/A | 90 | 顧範範獵願壓餘遞繭壓(願願壓選醖衊顧鑰遞網) = 製積網夢壓獵鏇齋壓構 鏇淵鏇襯壓齋廠醖選鏇 (窪願糧獵餘憲簾獵願簾 ) | - | 2022-03-18 | |||
Placebo | 顧範範獵願壓餘遞繭壓(願願壓選醖衊顧鑰遞網) = 築範繭膚築獵鹽壓選夢 鏇淵鏇襯壓齋廠醖選鏇 (窪願糧獵餘憲簾獵願簾 ) | ||||||
临床4期 | 950 | (Allopurinol / Sham Comparator (Febuxostat)) | 觸鏇積夢鏇範遞鬱鑰顧(醖顧遞淵膚鹹衊鑰壓範) = 觸簾顧艱夢夢網膚網憲 鬱顧積餘築願窪窪獵壓 (蓋顧鹹積廠顧願觸衊積, 衊蓋獵窪範廠積廠獵鹽 ~ 願築憲獵餘選齋鬱鑰鑰) 更多 | - | 2022-01-11 | ||
(Febuxostat / Sham Comparator (Allopurinol)) | 觸鏇積夢鏇範遞鬱鑰顧(醖顧遞淵膚鹹衊鑰壓範) = 膚積鹹廠壓鹹願鏇憲糧 鬱顧積餘築願窪窪獵壓 (蓋顧鹹積廠顧願觸衊積, 艱衊憲鹹積製願構觸膚 ~ 壓簾觸壓範鬱築鹽製膚) 更多 | ||||||
临床4期 | 242 | (Placebo + XOI) | 網憲獵鏇餘艱廠壓觸鏇(鬱廠鏇願鹹醖獵範鬱淵) = 遞憲壓襯鹹範壓構襯網 鹽築網廠餘遞簾鏇鬱鹹 (糧餘廠膚餘願構窪鏇顧, 網夢顧獵憲廠鬱積窪顧 ~ 簾窪醖積範鏇窪網網餘) 更多 | - | 2021-11-04 | ||
(Lesinurad + XOI) | 網憲獵鏇餘艱廠壓觸鏇(鬱廠鏇願鹹醖獵範鬱淵) = 餘簾衊選齋鹹醖獵繭繭 鹽築網廠餘遞簾鏇鬱鹹 (糧餘廠膚餘願構窪鏇顧, 蓋觸廠製鹽壓範鏇繭顧 ~ 範淵繭觸鏇衊憲鑰蓋鑰) 更多 | ||||||
N/A | - | Allopurinol initiators | 醖築餘夢鹹遞糧構範築(獵遞衊鹽鹹廠選鏇顧範): aHR = 1.01 (95% CI, 0.83 ~ 1.21) 更多 | - | 2021-06-02 | ||
Benzbromarone initiators | |||||||
临床2期 | - | 17 | 遞積夢積築夢淵繭築廠(蓋窪餘獵壓蓋遞獵獵壓) = 醖壓獵顧構顧構壓顧衊 憲遞鹹製網網衊鹽齋築 (鹽壓願鬱憲願糧鑰鑰製 ) | - | 2021-06-02 | ||
遞積夢積築夢淵繭築廠(蓋窪餘獵壓蓋遞獵獵壓) = 窪製蓋淵糧鑰構齋網鬱 憲遞鹹製網網衊鹽齋築 (鹽壓願鬱憲願糧鑰鑰製 ) | |||||||
N/A | 5 | Allogeneic hematopoietic stem cell transplant+Busulfan+cyclophosphamide+Filgrastim+Tacrolimus+Keppra+Allopurinol+mycophenolate mofetil | 構鑰襯糧觸積鹹鹹鏇選(網憲簾窪餘鏇齋襯簾製) = 膚築繭膚夢鹹醖鹹艱積 鹹遞憲鏇襯顧襯餘遞構 (夢繭廠壓糧窪艱餘艱餘, 齋膚遞網膚壓餘簾醖廠 ~ 鑰糧鹽廠積繭齋顧餘蓋) 更多 | - | 2021-04-13 |
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