2 years -20°C Powder, 2 weeks 4°C in DMSO, 6 months -80°C in DMSO
Biological activity
Description
Target:
HSP70
In Vivo
Treatment with TRC051384 significantly reduces stroke associated neuronal injury (87% reduction in area of penumbra recruited to infarct, and 25% reduction in brain edema) and disability in a rat model of transient ischemic stroke even when administered 8 hours post onset of ischemia. Significant improvement in survival (50% by day2 and 67.3% by day 7) is observed with TRC051384 treatment initiated at 4 hours after ischemia onset. Induction of HSP70 by TRC051384 involves HSF1 activation and results in elevated chaperone and anti-inflammatory activity[1].
In Vitro
TRC051384, dose dependently induces HSP70B mRNA by several hundred folds in both HeLa and rat primary mixed neurons. Treatment with TRC051384 results in significant dose-dependent increase in HSF1 transcriptional activity and recovery of luciferase activity. TRC051384 results in 60% inhibition at 6.25 μM and 90% inhibition at 12.5 μM of LPS-induced TNF-α expression in differentiated THP-1 cell line[1].
Kinase Assay
Cell Assay
HeLa cell transiently co-transfected with heat shock elements-luciferase reporter and normalization vector, β-galactosidase are treated with vehicle or TRC051384 (12.5 and 25 μM) for 4 hours. Cell lysates are then prepared and analyzed for luciferase and β-galactosidase activity[1].
Animal Administration
Rats: Injured hemispheres from vehicle treated animals and TRC051384 treated animals are collected at 10-hour post-initiation of tMCAo. Total RNA from each brain sample is extracted followed by cDNA preparation. Each sample of cDNA is analyzed[1].
References
[1]. Mohanan A, et al. Delayed intervention in experimental stroke with TRC051384--a small molecule HSP70 inducer. Neuropharmacology. 2011 May;60(6):991-9.
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