Name | Sodium amino(2-chloro-5-hydroxyphenyl)acetate |
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Synonyms |
Sodium amino(2-chloro-5-hydroxyphenyl)acetate
Benzeneacetic acid, α-amino-2-chloro-5-hydroxy-, sodium salt (1:1) |
Description | CHPG sodium salt is a selective mGluR5 agonist, and attenuates SO2-induced oxidative stress and inflammation through TSG-6/NF-κB pathway in BV2 microglial cells[1]. CHPG sodium salt protects against traumatic brain injury (TBI) in vitro and in vivo by activation of the ERK and Akt signaling pathways.[2]. |
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Related Catalog | |
Target |
mGluR5 NF-κB ERK Akt |
In Vitro | CHPG sodium salt (10-500 µM; 24 hours) significantly increases the cell viability and decreases the LDH release after SO2 derivatives treatment[1]. CHPG sodium salt (0.5 mM; 30 mins ) protects BV2 cells against SO2-induced apoptosis[1]. CHPG sodium salt (0.5 mM; 30 mins) treatment alone increases the expression of TSG-6 in both mRNA and protein levels[1]. Cell Viability Assay[1] Cell Line: BV2 microglial cells Concentration: 10, 50, 100 and 500 µM Incubation Time: 24 hours Result: Increased the cell viability. Apoptosis Analysis[1] Cell Line: BV2 microglial cells Concentration: 0.5 mM Incubation Time: 30 mins Result: Protected BV2 cells against SO2-induced apoptosis. Western Blot Analysis[1] Cell Line: BV2 microglial cells Concentration: 0.5 mM Incubation Time: 30 mins Result: Increased the expression of TSG-6 in both mRNA and protein levels. |
In Vivo | CHPG sodium salt (injection; 250 nM; for 7 days) reduces significantly cerebral lesion volume[2]. Animal Model: Adult Sprague-Dawley male rats weighing 280-320 g[2] Dosage: 250 nM Administration: Injection; for 7 days Result: Reduced significantly cerebral lesion volume. |
References |
Molecular Formula | C8H7ClNNaO3 |
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Molecular Weight | 223.589 |
Exact Mass | 223.001221 |