AGI Dermatics Clinical Data Indicate Bicyclic Monoterpene Diols Suppress MMP1 and Stimulate Collagen Through TNF-a...( Clinical Data Presented at the 66th ...),Health

Clinical Data Presented at the 66th Annual Meeting of the American Academy

of Dermatology

FREEPORT, N.Y., Feb. 11 /PRNewswire/ -- AGI Dermatics clinical research indicates that the ability of bicyclic monoterpene diols (BMTds) to reduce collagenese MMP-1 secretion and increase collagen production is dependent on the TNF-a signaling in the fibroblasts. The data was presented at the Poster Session at the 66th Annual Meeting of the American Academy of Dermatology in San Antonio.

"Our prior research showed that BMTds increase collagen gene expression and protein production while decreasing MMP-1 secretion," said Daniel Yarosh, PhD, President, AGI Dermatics. "This study gives us insight into the cellular communication that allows BMTds to work so effectively and efficiently in treating photodamaged skin."

BMTds, a class of compounds known to increase nitric oxide levels, were recently reported to play a major role in collagen synthesis. AGI scientists questioned whether the transmission of BMTd factors were influenced by the role of Interleukin-6 (IL-6) and TNF-A in regulating collagen 1 and MMP-1 secretions.

In earlier studies of BMTds, AGI scientists observed a linear increase in BMTd concentrations and secretion of interleukin-6 (IL-6), a multi-functional cytokine that mediates a wide variety of functions in cells, promotes cell proliferation and regulates gene expression. By blocking the IL-6 signaling with a neutralizing IL-6 antibody, studies showed a concomitant increase in MMP-1 and a reduction in collagen 1. The effect of the neutralizing antibody, however, was gradually overcome by increasing BMTd concentrations, indicating that IL-6 is not involved in the transmission of the BMTd effect. Results indicated a linear decrease in MMP-1 secretion and an increase in collagen production, two key components in treatment of photoaged skin.

Similarly, blocking TNF-a signaling in the fibroblasts with
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