Compound 36, a potent dual PDE4/7 inhibitor and TRPA1 antagonist, exerted strong anti-TNF-α activity in vivo in lipopolysaccharide (LPS)-induced endotoxemia, which was manifested by a significant reduction in the maximum plasma concentration of TNF-α by 90.2% [21]. Here, TNF is linked to serum lipopolysaccharide activity.