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通过剂量依赖的方式在HeLa细胞和大鼠初级混合神经元中使HSP70B mRNA的表达增加数百倍。使用TRC051384能显著剂量依赖性地增加HSF1的转录活性，并恢复luciferase活性。在分化的THP-1细胞系中，TRC051384以6.25 μM的浓度抑制60%的LPS诱导的TNF-α表达，并以12.5 μM的浓度抑制90%[1]。

使用TRC051384处理显著减少了暂时性脑缺血大鼠模型中因中风导致的神经损伤（梗死侵犯半暗带面积减少87%，脑水肿减少25%）及残疾，即使在缺血发生后8小时进行治疗也是如此。在缺血开始后4小时启动TRC051384治疗，显著提高了生存率（第2天提高到50%，第7天达到67.3%）。TRC051384通过激活HSF1诱导HSP70的产生，从而增强了分子伴侣和抗炎活性[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].