Eriocalyxin B induces apoptosis and cell cycle arrest in pancreatic adenocarcinoma cells through caspase- and p53-dependent pathways, should be considered a candidate for pancreatic cancer treatment; it is a specific inhibitor of STAT3, it directly targets STAT3 through a covalent linkage to inhibit the phosphorylation and activation of STAT3 and induces apoptosis of STAT3-dependent tumor cells.

在本研究中，我们证明了Eriocalyxin B在实验性自身免疫性脑炎（EAE），一种多发性硬化症的动物模型中具有有效性。Eriocalyxin B的治疗导致EAE的改善，这与脊髓炎症和脱髓鞘减少有关。Eriocalyxin B的治疗消除了采用转移EAE模型中对髓鞘少突胶质细胞糖蛋白的脑炎原性T细胞反应。Eriocalyxin B引起的效应背后的机制涉及通过Janus Kinase/Signal Transducer and Activator Of Transcription和Nuclear factor-κB信号通路以及提高活性氧种类[1]，抑制辅助性T细胞（Th）1和Th17细胞分化。