更新于：2024-11-01

COX x DAAO

更新于：2024-11-01

基本信息

关联

项与 COX x DAAO 相关的药物

Salicylic acid/Benzoic Acid/Boric Acid/Lactic acid

水杨酸/苯甲酸/硼酸/乳酸

靶点

COX x DAAO

作用机制

COX抑制剂 [+2]

在研机构-

原研机构-

在研适应症

皮肤真菌病

非在研适应症-

最高研发阶段批准上市

首次获批国家/地区-

首次获批日期1800-01-20

Bifonazole/Benzoic Acid/Salicylic acid

联苯苄唑/苯甲酸/水杨酸

靶点

COX x CYP51A1 x DAAO

作用机制

COX抑制剂 [+2]

在研机构-

原研机构-

在研适应症

皮肤真菌病

非在研适应症-

最高研发阶段批准上市

首次获批国家/地区-

首次获批日期1800-01-20

Salicylic acid/Benzoic Acid

水杨酸/苯甲酸

靶点

COX x DAAO

作用机制

COX抑制剂 [+1]

在研机构-

原研机构-

在研适应症

真菌病

非在研适应症-

最高研发阶段批准上市

首次获批国家/地区-

首次获批日期1800-01-20

项与 COX x DAAO 相关的临床试验

IRCT20220516054874N8 / Recruiting临床2期IIT

Evaluation of the effects of Ellagic acid on the hs-CRP level in patients with myocardial infarction

开始日期2023-06-22

申办/合作机构

Mashhad University of Medical Sciences

IRCT20180103038199N16 / Recruiting临床2期IIT

Evaluation of the effectiveness of ellagic acid on liver steatosis in patients with non-alcoholic fatty liver disease

开始日期2023-04-21

申办/合作机构

Mashhad University of Medical Sciences

ChiCTR2300067756 / Suspended临床1期IIT

Nutritional intervention of dietary protocatechuic acid in people with hypercholesterolemia

开始日期2023-01-31

申办/合作机构

中山大学

100 项与 COX x DAAO 相关的临床结果

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100 项与 COX x DAAO 相关的转化医学

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0 项与 COX x DAAO 相关的专利（医药）

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项与 COX x DAAO 相关的文献（医药）

2015-02-01·Journal of Pharmacology and Experimental Therapeutics3区 · 医学

Glutamate-Mediated Upregulation of the Multidrug Resistance Protein 2 in Porcine and Human Brain Capillaries

3区 · 医学

Article

作者: Potschka, Heidrun ; Kluger, Gerhard ; Salvamoser, Josephine D ; Kudernatsch, Manfred ; Pascher, Bettina ; Luna-Munguia, Hiram ; Getzinger, Thekla ; Pieper, Tom

As a member of the multidrug-resistance associated protein (MRP) family, MRP2 affects the brain entry of different endogenous and exogenous compounds. Considering the role of this transporter at the blood-brain barrier, the regulation is of particular interest. However, there is limited knowledge regarding the factors that regulate MRP2 in neurologic disease states. Thus, we addressed the hypothesis that MRP2 might be affected by a glutamate-induced signaling pathway that we previously identified as one key mechanism in the regulation of P-glycoprotein. Studies in isolated porcine brain capillaries confirmed that glutamate and N-methyl-d-aspartic acid (NMDA) exposure upregulates expression and function of MPR2. The involvement of the NMDA receptor was further suggested by the fact that the NMDA receptor antagonist MK-801 [(5S,10R)-(+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine], as well as the NMDA receptor glycine binding site antagonist L-701,324 [7-chloro-4-hydroxy-3-(3-phenoxy)phenyl-2(1H)-quinolinone], prevented the impact of glutamate. A role of cyclooxygenase-2 was indicated by coincubation with the cyclooxygenase-2 inhibitor celecoxib and the cyclooxygenase-1/-2 inhibitor indomethacin, which both efficaciously abolished a glutamate-induced upregulation of MRP2. Translational studies in human capillaries from surgical specimen demonstrated a relevant MRP2 efflux function and indicated an effect of glutamate exposure as well as its prevention by cyclooxygenase-2 inhibition. Taken together the findings provide first evidence for a role of a glutamate-induced NMDA receptor/cyclooxygenase-2 signaling pathway in the regulation of MRP2 expression and function. The response to excessive glutamate concentrations might contribute to overexpression of MRP2, which has been reported in neurologic diseases including epilepsy. The overexpression might have implications for brain access of various compounds including therapeutic drugs.