CAFESTOL is a ERK inhibitor for AP-1-targeted activity against PGE2 production and the mRNA expression of cyclooxygenase (COX)-2 in LPS-activated RAW264.7 cells. Cafestol has strong inhibitory activity on PGE2 production by suppressing the NF-kB activation pathway.

Cafestol抑制了脂多糖(LPS)处理的RAW264.7细胞中前列腺素E(2)(PGE(2))的产生和环氧合酶(COX)-2 mRNA的表达，揭示了其抗炎活动的分子机制。此外，Cafestol显著减少了c-Jun进入核内以及AP-1介导的荧光素酶活性。在有无Cafestol的条件下，使用纯化的外源性信号调节激酶2(ERK2)或从LPS处理的细胞中免疫沉淀的ERK进行的激酶分析中，发现Cafestol能够抑制ERK2而非ERK1和丝裂原活化蛋白激酶激酶1(MEK 1)。这些结果表明Cafestol可能是一种新型的ERK抑制剂，并且有针对LPS激活的RAW264.7细胞中PGE(2)产生的AP-1目标抑制活性[1]。

CAFESTOL在KKAy小鼠中展现了降糖性质，因此，cafestol可能有助于降低咖啡消费者发展成2型糖尿病(T2D)的风险，并可能作为一种抗糖尿病化合物发挥作用[2]。

Cafestol can postpone development of T2D in KKAy mice. Forty-seven male KKAy mice were randomized to consume chow supplemented daily with either 1.1 (high), 0.4 (low), or 0 (control) mg of cafestol for 10 weeks. Collected blood samples for fasting glucose, glucagon, and insulin as well as liver, muscle, and fat tissues for gene expression analysis. Isolated islets of Langerhans and measured insulin secretory capacity. After 10 weeks of intervention, fasting plasma glucose was 28-30% lower in cafestol groups compared with the control group (p < 0.01). Fasting glucagon was 20% lower and insulin sensitivity improved by 42% in the high-cafestol group (p < 0.05). Cafestol increased insulin secretion from isolated islets by 75-87% compared to the control group (p < 0.001)[2].