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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].

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].

CHPG sodium salt (injection; 250 nM; for 7 days) reduces significantly cerebral lesion volume[2].

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