TRC051384 is a heat shock protein 70 (HSP70) inducer that reduces stroke-associated neuronal damage and increases survival in a rat model of transient ischemic stroke, activates heat shock factor-1 and leads to elevated molecular chaperone and anti-inflammatory activity, and enhances Hsp72 expression in neurons and glial cells.

TRC051384 significantly enhances HSP70B mRNA expression hundreds of times in both HeLa cells and rat primary mixed neurons in a dose-dependent fashion. Additionally, it markedly boosts HSF1 transcriptional activity and luciferase recovery upon treatment, following a dose-responsive pattern. Furthermore, TRC051384 demonstrates substantial inhibitory effects on LPS-induced TNF-α expression in the differentiated THP-1 cell line, achieving 60% inhibition at 6.25 μM and 90% inhibition at 12.5 μM [1].

Administering TRC051384 significantly diminishes stroke-related neuronal damage and disability in a rat model of transient ischemic stroke, achieving an 87% reduction in the area of the penumbra recruited to infarct and a 25% reduction in brain edema, even when treatment commences 8 hours after ischemia onset. Additionally, initiating TRC051384 treatment 4 hours post-ischemia onset notably enhances survival rates, with a 50% improvement by day 2 and a 67.3% increase by day 7. The mechanism underlying TRC051384's efficacy involves the induction of HSP70 through HSF1 activation, which amplifies chaperone and anti-inflammatory activities[1].

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].

DMSO: 16.67 mg/mL (35.81 mM), Sonication is recommended.

10% DMSO+40% PEG300+5% Tween 80+45% Saline: 2 mg/mL (4.3 mM), Sonication is recommended.