| Bioactivity | CHPG 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 protects against traumatic brain injury (TBI) in vitro and in vivo by activation of the ERK and Akt signaling pathways[2]. | |||||||||
| Invitro | CHPG (10-500 µM; 24 hours) significantly increases the cell viability and decreases the LDH release after SO2 derivatives treatment[1]. CHPG (0.5 mM; 30 mins ) protects BV2 cells against SO2-induced apoptosis[1]. CHPG (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 (injection; 250 nM; for 7 days) reduces significantly cerebral lesion volume[2]. Animal Model: | |||||||||
| Name | CHPG | |||||||||
| CAS | 170846-74-9 | |||||||||
| Formula | C8H8ClNO3 | |||||||||
| Molar Mass | 201.61 | |||||||||
| Appearance | Solid | |||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | |||||||||
| Storage |
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| 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. |