The Arbiser lab focuses on solving clinical problems. This involves using a complete knowledge of what is already known to solve problems today, instead of waiting for a mythical silver bullet in the future - an approach he learned from renowned expert Dr. Judah Folkman (pictured with me).
Dr. Arbiser and his team also focus on developing novel small molecules that are first in class to address common skin, inflammation, and cancer needs.
Representative Canfield imaging of a patient in the study. The patient is visualized at baseline, week 4, and week 12 of treatment with ACU-D1, allowing evaluation of erythema. Red pigmentation represents hemoglobin, while purple pigmentation represents melanin. The decrease in melanin visualization may represent a clinical improvement of background melasma.
Image used with permission: Jackson JM, Coulon R, Arbiser JL. Evaluation of a First-in-Class Proteasome Inhibitor in Patients With Moderate to Severe Rosacea. J Drugs Dermatol. 2021 Jun 1;20(6):660-664. doi: 10.36849/JDD.2021.5925. PMID: 34076401.
Mechanism of action of ACU-D1. ACU-D1 blocks the activity of the 26S proteasome. By blocking the activity of the 26S proteasome, the degradation of inhibitor of NFkB (IkB) is prevented. If IkB is not degraded, then IkB prevents the activation of NFkB. As a result, NFkB target genes are decreased, such as interleukin-1 beta, interleukin-6, and interleukin-8. NFkB is activated by the two major inputs for rosacea, namely toll like receptor activation (TLR) and IL1b.
Image used with permission: Jackson JM, Coulon R, Arbiser JL. Evaluation of a First-in-Class Proteasome Inhibitor in Patients With Moderate to Severe Rosacea. J Drugs Dermatol. 2021 Jun 1;20(6):660-664. doi: 10.36849/JDD.2021.5925. PMID: 34076401.
