Bioactivity | 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]. |
Invitro | 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: |
In Vivo | CHPG sodium salt (injection; 250 nM; for 7 days) reduces significantly cerebral lesion volume[2]. Animal Model: |
Name | CHPG sodium salt |
CAS | 1303993-73-8 |
Formula | C8H7ClNNaO3 |
Molar Mass | 223.59 |
Appearance | Solid |
Transport | Room temperature in continental US; may vary elsewhere. |
Storage | 4°C, sealed storage, away from moisture *In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture) |
Reference | [1]. Qiu JL, et al. The selective mGluR5 agonist CHPG attenuates SO2-induced oxidative stress and inflammation through TSG-6/NF-κB pathway in BV2 microglial cells. Neurochem Int. 2015 Jun-Jul;85-86:46-52. [2]. Chen T, et al. The selective mGluR5 agonist CHPG protects against traumatic brain injury in vitro and in vivo via ERK and Akt pathway. Int J Mol Med. 2012 Apr;29(4):630-6. |