更新于：2024-07-01
Deferiprone
去铁酮
更新于：2024-07-01
概要
基本信息
原研机构 |
最高研发阶段批准上市 |
最高研发阶段(中国)- |
特殊审评快速通道 (美国)、加速批准 (美国)、孤儿药 (美国)、孤儿药 (欧盟) |
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结构
分子式C7H9NO2 |
InChIKeyTZXKOCQBRNJULO-UHFFFAOYSA-N |
CAS号30652-11-0 |
关联
75
项与 去铁酮 相关的临床试验A randomised, double-blind, placebo-controlled trial examining the safety and efficacy of deferiprone in patients with neuroferritinopathy
Cardiac MRI-guided Deferiprone Therapy for Acute Myocardial Infarction Patients
Long-term Iron Chelation in the Prevention of Secondary Remote Degeneration After Stroke
100 项与 去铁酮 相关的临床结果
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100 项与 去铁酮 相关的转化医学
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100 项与 去铁酮 相关的专利（医药）
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1,602
项与 去铁酮 相关的文献（医药）2024-03-01Journal of environmental sciences (China)
Chronic administration of triclosan leads to liver fibrosis through hepcidin-ferroportin axis-mediated iron overload
Article
作者: Zhang, Lecong ; Song, Yang ; Zhang, Ping ; Liu, Jing ; Xu, Fang
Triclosan (TCS) has been manufactured as an antibacterial compound for half a century. Currently, it is widely used in various personal care products; however, its potential adverse effects raise a lot of attention. Here, we create a long-term oral administration mouse model and identify the corresponding hepatotoxicity of TCS. We discover that daily intragastric administration of 10 mg/kg TCS to mice for 12 weeks results in severe hepatic fibrosis. Further study displays that hepatic iron increased 18%, 23% and 29% upon oral TCS treatment for 4, 8 and 12 weeks, respectively. Accompanied by hepatic iron variation, splenic and duodenal iron are increased, which indicates systemic iron disorder. Not only excessive iron accumulated in the liver, abnormal hepatic malondialdehyde, prostaglandin synthase 2 and glutathione peroxidase 4 are pointed to ferroptosis. Additional study uncovers that hepcidin expression increases 7%, 10%, 4% in serum and 2.4-, 4.8-, and 2.3-fold on transcriptional levels upon TCS exposure for 4, 8 and 12 weeks, individually. Taken together, the mice in the TCS-treated group show disordered systemic iron homeostasis via the upregulated hepatic hepcidin-ferroportin axis. Meanwhile, both hepatic iron overload (systemic level) and hepatocyte ferroptosis (cellular level) are accused of TCS-induced liver fibrosis. Ferriprox®, an iron scavenger, significantly ameliorates TCS-induced liver fibrosis. In summary, this study confirms the impact of TCS on liver fibrosis; a critical signal pathway is also displayed. The significance of the current study is to prompt us to reevaluate the "pros and cons" of TCS applications.
2024-03-01Neural regeneration research
Single-neuron neurodegeneration as a degenerative model for Parkinson's disease.
Review
作者: Huenchuguala, Sandro ; Segura-Aguilar, Juan
The positive effect of levodopa in the treatment of Parkinson's disease, although it is limited in time and has severe side effects, has encouraged the scientific community to look for new drugs that can stop the neurodegenerative process or even regenerate the neuromelanin-containing dopaminergic nigrostriatal neurons. Successful preclinical studies with coenzyme Q10, mitoquinone, isradipine, nilotinib, TCH346, neurturin, zonisamide, deferiprone, prasinezumab, and cinpanemab prompted clinical trials. However, these failed and after more than 50 years levodopa continues to be the key drug in the treatment of the disease, despite its severe side effects after 4-6 years of chronic treatment. The lack of translated successful results obtained in preclinical investigations based on the use of neurotoxins that do not exist in the human body as new drugs for Parkinson's disease treatment is a big problem. In our opinion, the cause of these failures lies in the experimental animal models involving neurotoxins that do not exist in the human body, such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and 6-hydroxydopamine, that induce a very fast, massive and expansive neurodegenerative process, which contrasts with the extremely slow one of neuromelanin-containing dopaminergic neurons. The exceedingly slow progress of the neurodegenerative process of the nigrostriatal neurons in idiopathic Parkinson's patients is due to (i) a degenerative model in which the neurotoxic effect of an endogenous neurotoxin affects a single neuron, (ii) a neurotoxic event that is not expansive and (iii) the fact that the neurotoxin that triggers the neurodegenerative process is produced inside the neuromelanin-containing dopaminergic neurons. The endogenous neurotoxin that fits this degenerative model involving one single neuron at a time is aminochrome, since it (i) is generated within neuromelanin-containing dopaminergic neurons, (ii) does not cause an expansive neurotoxic effect and (iii) triggers all the mechanisms involved in the neurodegenerative process of the nigrostriatal neurons in idiopathic Parkinson's disease. In conclusion, based on the hypothesis that the neurodegenerative process of idiopathic Parkinson's disease corresponds to a single-neuron neurodegeneration model, we must search for molecules that increase the expression of the neuroprotective enzymes DT-diaphorase and glutathione transferase M2-2. It has been observed that the activation of the Kelch-like ECH-associated protein 1/nuclear factor (erythroid-derived 2)-like 2 pathway is associated with the transcriptional activation of the DT-diaphorase and glutathione transferase genes.
2024-03-01Neuropharmacology
Phosphoproteomics implicates glutamatergic and dopaminergic signalling in the antidepressant-like properties of the iron chelator deferiprone
Article
作者: Li, Shanshan ; Mees, Isaline ; Luza, Sandra ; Renoir, Thibault ; Uzungil, Volkan ; Ang, Ching-Seng ; Hannan, Anthony J ; Opazo, Carlos M ; Williamson, Nicholas A ; Bush, Ashley I
BACKGROUND:
Current antidepressants have limitations due to insufficient efficacy and delay before improvement in symptoms. Polymorphisms of the serotonin transporter (5-HTT) gene have been linked to depression (when combined with stressful life events) and altered response to selective serotonergic reuptake inhibitors. We have previously revealed the antidepressant-like properties of the iron chelator deferiprone in the 5-HTT knock-out (KO) mouse model of depression. Furthermore, deferiprone was found to alter neural activity in the prefrontal cortex of both wild-type (WT) and 5-HTT KO mice.
METHODS:
In the current study, we examined the molecular effects of acute deferiprone treatment in the prefrontal cortex of both genotypes via phosphoproteomics analysis.
RESULTS:
In WT mice treated with deferiprone, there were 22 differentially expressed phosphosites, with gene ontology analysis implicating cytoskeletal proteins. In 5-HTT KO mice treated with deferiprone, we found 33 differentially expressed phosphosites. Gene ontology analyses revealed phosphoproteins that were predominantly involved in synaptic and glutamatergic signalling. In a drug-naïve cohort (without deferiprone administration), the analysis revealed 21 differentially expressed phosphosites in 5-HTT KO compared to WT mice. We confirmed the deferiprone-induced increase in tyrosine hydroxylase serine 40 residue phosphorylation (pTH-Ser40) (initially revealed in our phosphoproteomics study) by Western blot analysis, with deferiprone increasing pTH-Ser40 expression in WT and 5-HTT KO mice.
CONCLUSION:
As glutamatergic and synaptic signalling are dysfunctional in 5-HTT KO mice (and are the target of fast-acting antidepressant drugs such as ketamine), these molecular effects may underpin deferiprone's antidepressant-like properties. Furthermore, dopaminergic signalling may also be involved in deferiprone's antidepressant-like properties.
37
项与 去铁酮 相关的新闻（医药）2024-06-26
·医药地理
临床研究上市批准临床结果
2024-06-20
·恒瑞医药
ASCO会议抗体药物偶联物临床结果临床2期临床1期
2024-05-31
·恒瑞医药
ASCO会议抗体药物偶联物临床结果申请上市临床1期
100 项与 去铁酮 相关的药物交易
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研发状态
批准上市
10 条最早获批的记录, 后查看更多信息
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| 适应症 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|
| 镰状细胞血症 | 美国 | 2021-04-30 | |
| 铁过剩 | 欧盟 | 1999-08-25 | |
| 铁过剩 | 冰岛 | 1999-08-25 | |
| 铁过剩 | 列支敦士登 | 1999-08-25 | |
| 铁过剩 | 挪威 | 1999-08-25 | |
| 地中海贫血 | 欧盟 | 1999-08-25 | |
| 地中海贫血 | 冰岛 | 1999-08-25 | |
| 地中海贫血 | 列支敦士登 | 1999-08-25 | |
| 地中海贫血 | 挪威 | 1999-08-25 |
未上市
10 条进展最快的记录, 后查看更多信息
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| 适应症 | 最高研发状态 | 国家/地区 | 公司 | 日期 |
|---|---|---|---|---|
| 泛酸激酶相关神经变性 | 临床3期 | 美国 | 2012-12-13 | |
| 泛酸激酶相关神经变性 | 临床3期 | 德国 | 2012-12-13 | |
| 泛酸激酶相关神经变性 | 临床3期 | 意大利 | 2012-12-13 | |
| 泛酸激酶相关神经变性 | 临床3期 | 英国 | 2012-12-13 | |
| 急性肾损伤 | 临床3期 | - | 2012-01-01 | |
| 慢性肾病 | 临床3期 | - | 2012-01-01 | |
| 输血依赖性贫血 | 临床3期 | 埃及 | 2007-08-01 | |
| 输血依赖性贫血 | 临床3期 | 印尼 | 2007-08-01 | |
| 输血依赖性贫血 | 临床3期 | 马来西亚 | 2007-08-01 | |
| 帕金森病（青年型、早发型） | 临床2期 | 加拿大 | 2016-10-12 |
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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 | 140 | Placebo (Placebo) | 網鬱膚選鹽膚衊窪積艱(壓鏇鏇襯繭蓋餘蓋壓遞) = 積製憲鬱壓構鹽遞獵簾 築鑰糧選選廠觸顧繭製 (簾積廠築構網醖鏇襯獵, 築構構壓窪衊範繭齋齋 ~ 繭顧構顧範淵憲夢獵壓) 更多 | - | 2024-04-10 | ||
(Deferiprone 300 mg) | 網鬱膚選鹽膚衊窪積艱(壓鏇鏇襯繭蓋餘蓋壓遞) = 憲顧襯淵膚觸鬱觸鏇憲 築鑰糧選選廠觸顧繭製 (簾積廠築構網醖鏇襯獵, 鏇衊顧夢觸鬱築選獵簾 ~ 願艱窪廠遞蓋製鹹選顧) 更多 | ||||||
临床4期 | 64 | (Deferiprone) | 製醖築積網遞鏇構繭願(選繭衊廠範顧繭憲餘糧) = 簾鏇齋餘糧鏇願艱壓遞 衊醖願壓築膚觸願願選 (廠構襯餘獵築艱積網鹽, 壓鑰醖簾蓋鹽積衊蓋鑰 ~ 鏇積獵簾構願齋醖廠構) 更多 | - | 2024-03-15 | ||
Placebo (Placebo) | 製醖築積網遞鏇構繭願(選繭衊廠範顧繭憲餘糧) = 襯鏇淵蓋艱鏇夢廠積製 衊醖願壓築膚觸願願選 (廠構襯餘獵築艱積網鹽, 選襯鏇淵鏇艱顧憲淵鏇 ~ 顧積顧糧鏇繭構築選艱) 更多 | ||||||
N/A | - | (Group A (ANC ≥0.2 to <0.5)) | 蓋壓範構願積願獵衊鬱(範遞廠鑰網鏇製鏇夢齋) = 獵鏇衊齋餘艱衊鑰艱顧 餘鑰積願淵襯構艱網構 (鹽鬱餘遞鏇願膚遞膚淵 ) 更多 | - | 2023-12-10 | ||
(Group B (ANC ≥0.1 to <0.2)) | 蓋壓範構願積願獵衊鬱(範遞廠鑰網鏇製鏇夢齋) = 齋壓衊築醖簾壓顧鹹糧 餘鑰積願淵襯構艱網構 (鹽鬱餘遞鏇願膚遞膚淵 ) 更多 | ||||||
临床2期 | 372 | 範壓糧範淵糧餘齋鹽窪(淵範範築廠憲窪築鬱簾) = 2 participants 鹹窪遞夢壓簾蓋憲製範 (壓餘鬱鬱構艱鑰鹹鬱襯 ) 更多 | 不佳 | 2022-12-01 | |||
Placebo | |||||||
临床4期 | 134 | 觸衊製繭願壓襯膚製衊(蓋蓋襯廠蓋鹽淵窪鑰範) = neutropenia 9.0% and abdominal pain 7.5% 憲醖膚齋壓範鹹膚窪鏇 (積膚淵廠夢鑰選餘糧鹹 ) 更多 | 积极 | 2022-08-26 | |||
临床4期 | 64 | 廠餘壓襯獵獵襯網繭膚(鹽鹹衊築憲窪製網鹽製) = 膚膚壓築構夢壓淵範淵 鬱願範膚繭艱遞簾鑰衊 (夢膚糧築築蓋顧憲網構 ) 更多 | 积极 | 2022-05-12 | |||
placebo | 廠餘壓襯獵獵襯網繭膚(鹽鹹衊築憲窪製網鹽製) = 鬱夢鏇製艱鹽餘觸築網 鬱願範膚繭艱遞簾鑰衊 (夢膚糧築築蓋顧憲網構 ) 更多 | ||||||
临床4期 | 228 | 觸醖襯衊簾簾蓋衊齋鑰(構蓋簾簾選顧積構願淵) = 夢膚獵積齋觸遞蓋製鹹 積廠鑰網廠獵遞願積選 (製鏇構鏇簾觸憲鬱蓋積 ) | 积极 | 2021-11-30 | |||
觸醖襯衊簾簾蓋衊齋鑰(構蓋簾簾選顧積構願淵) = 遞製膚選製鏇觸醖網糧 積廠鑰網廠獵遞願積選 (製鏇構鏇簾觸憲鬱蓋積 ) | |||||||
临床4期 | 230 | (Deferiprone) | 蓋簾糧糧襯窪製鹽襯範(蓋艱醖醖顧餘繭齋遞鏇) = 觸淵憲範衊顧餘憲獵願 齋襯齋簾構網糧願鑰築 (製鬱範獵網糧選簾憲壓, 鏇範夢膚觸鑰鬱網網艱 ~ 鏇構製夢築積願築餘窪) 更多 | - | 2021-08-10 | ||
(Deferoxamine) | 蓋簾糧糧襯窪製鹽襯範(蓋艱醖醖顧餘繭齋遞鏇) = 衊願醖製鹹膚衊夢鹽製 齋襯齋簾構網糧願鑰築 (製鬱範獵網糧選簾憲壓, 積廠製製鏇膚積壓構蓋 ~ 壓簾艱齋窪鹹製願餘鹹) 更多 | ||||||
临床2期 | 30 | (Low Dosage) | 製齋襯壓襯製艱鏇淵築(構繭膚糧艱醖網醖餘蓋) = 積願繭醖壓憲鏇餘網窪 顧鬱艱齋窪窪網願憲獵 (鹹鹹廠夢鏇鑰齋築鏇蓋, 簾簾膚鹽製糧鏇選鏇夢 ~ 衊遞鬱鏇蓋繭遞夢糧繭) 更多 | - | 2021-06-18 | ||
(High Dosage) | 製齋襯壓襯製艱鏇淵築(構繭膚糧艱醖網醖餘蓋) = 衊網蓋鏇廠鹽艱遞艱鏇 顧鬱艱齋窪窪網願憲獵 (鹹鹹廠夢鏇鑰齋築鏇蓋, 觸鏇醖窪繭顧淵襯齋壓 ~ 製蓋顧觸衊鏇選積齋築) 更多 |
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