PeptideDB

CHPG sodium salt

CAS: 1303993-73-8 F: C8H7ClNNaO3 W: 223.59

CHPG sodium salt is a selective mGluR5 agonist, and attenuates SO2-induced oxidative stress and inflammation through TSG
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This product is for research use only, not for human use. We do not sell to patients.

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.