CHPG is a selective mGluR5 agonist that reduces LDH release and neuronal apoptosis, activates the ERK and Akt pathways, and protects against traumatic brain injury. It also increases the number of differentiated human OPCs and alleviates LPS-induced inflammation.

Methods:
The study used BV2 microglial cells to investigate the protective effects of CHPG against SO₂ derivative-induced damage. Cells were treated with CHPG at concentrations of 10–500 μM for 24 hours to assess cell viability and LDH release. In another set of experiments, cells were treated with 0.5 mM CHPG for 30 minutes to evaluate its effects on SO₂-induced apoptosis and the expression levels of TSG-6 at both mRNA and protein levels.
Results:
CHPG significantly enhanced the viability of BV2 cells, reduced LDH release, and alleviated cellular damage caused by SO₂ derivatives. Additionally, CHPG inhibited SO₂-induced apoptosis and upregulated the expression of TSG-6 at both mRNA and protein levels, indicating its potential neuroprotective effects. [1]

Methods:
The study used adult male Sprague-Dawley rats weighing 280–320 g, which were injected with 250 nM CHPG daily for 7 consecutive days to evaluate its effect on cerebral lesion volume.
Results:
CHPG treatment significantly reduced cerebral lesion volume in rats, indicating potential neuroprotective effects. [2]

DMSO: 20 mg/mL (99.2 mM), when pH is adjusted to 2 with 1M HCL.

1M NaOH: 20 mg/mL (99.2 mM), when pH is adjusted to 11 with NaOH. Sonication is recommended.