Uses of aminosalicylic acid derivative as neuroprotective agent

A technology of aminosalicylic acid and derivatives, applied in the field of aminosalicylic acid derivatives and neuroprotective agents, to achieve strong cell damage, good neuroprotective effect, and good therapeutic activity for stroke
CN101492384AInactive Publication Date: 2009-07-29NANJING MEDICAL UNIV
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Patent Information

Authority / Receiving Office
CN · China
Current Assignee / Owner
NANJING MEDICAL UNIV
Publication Date
2009-07-29
Estimated Expiration
Not applicable · inactive patent

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Abstract

The invention relates to an aminosalicylic acid derivative. The structure of the aminosalicylic acid derivative accords with the following general formula (I). At least one of R1, R2, R3 and R5 is -OH; when R1, R2, R3 and R5 are not -OH, R1, R2, R3 and R5 are -H, -OCH3, -F, -Cl, -Br, -CF3 or -NO3; R4 is -OCH3, -F, -Cl, -Br, -CF3 or -NO3; R6 and R7 are -COOH or -OH. When R6 is -COOH, R7 is -OH; when R6 is -OH, R7 is -COOH. In the invention, target compounds have strong protection function on PC12 cell injuries caused by glutamate. And the target compounds block the coupling between PSD-95 and nNOS by specificity to develop the pharmacological action.
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Description

1. Technical field

[0001] The invention belongs to the field of pharmacy, and provides a derivative of aminosalicylic acid and the use of the derivative as a neuroprotective agent. 2. Background technology

[0002] Prior Art: Neuroprotective agents are currently a research hotspot in the treatment of ischemic stroke. So far, hundreds of neuroprotective agents have been developed for different links of the cerebral infarction cascade reaction, but except for the free radical scavenger Edaravone, almost all neuroprotective agents are effective in animal experiments, clinically ineffective or The effect is very poor, or the clinical application is limited due to serious side effects. Seeking new neuroprotective agents has become the focus of current research.

[0003] There are three main pathways for the death of neurons after cerebral ischemia injury: calcium influx caused by ischemia activates nitric oxide synthase (NOS), leading to pathological release of nitric oxide (NO...

Claims

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