Since compound C or the EtOAc extract were able to inhibit P. acnes at very low concentrations and also were able to downregulate TNF-induced ICAM-1 upregulation in human endothelial cells via the NF-κB pathway, we used further in vitro models of inflammation to characterise whether these compounds might prove to be therapeutically interesting for the treatment of acne. The gene discussed is TNF; the disease is acne.