AGI Dermatics Presents Clinical Findings That Reveal Additional DNA Repair Benefits Of The T4 Endonuclease V (T4N5) Enzyme

FREEPORT, N.Y., Feb. 5 /PRNewswire/ -- AGI Dermatics today released new clinical data that suggests treatment of UVB-induced DNA damage with the T4 Endonuclease V (T4N5) enzyme significantly decreases MMP-1 secretion and increases repair of corresponding UVB-induced DNA damage. The research was presented in the Poster Session at the 65th Annual Meeting of the American Academy of Dermatology in Washington, D.C.

"Our previous research has demonstrated that liposome-encapsulated T4N5 is effective as a DNA repair enzyme, proven to enhance natural DNA repair in both keratinocytes and reconstructed skin," said Dan Yarosh, PhD, President, AGI Dermatics. "This new data looks at T4N5's ability to treat other effects of UVB-induced DNA damage to keratinocytes. The underlying belief was that in treating the epidermis, perhaps repair of the dermis could also be realized."

The current study examined the premise of T4N5's ability to simultaneously increase repair of cyclobutane pyrimidine dimmers (CPD) in irradiated keratinocytes (NHEK) and reduce MMP-1 secretion from fibroblasts (NHDF) exposed to irradiated NHEK media.

CPDs are the most common cause of UV-induced damage to skin DNA. NHEK were exposed to 500J/m2 UVB then treated with 1ug/mL T4N5 for 24 hours. DNA was then extracted for measurement of CPD repair. T4N5 was shown to have a significant 21% increase in repair of UVB-induced CPD.

Concurrently, media from the irradiated NHEK were transferred to NHDF for 48 hours. Production of MMP-1 was measured by ELISA. RNA was also extracted from the cells for determination of MMP-1 MRNA (Messenger Ribonucleic Acid) by RT PCR (measurement in real time). T4N5 significantly reduced MMP-1 by 96% resulting in a reduction in MMP-1 expression in the NHDF exposed to the media from irradiated NHEK.

In conclusion, the study indicates that the DNA repair enzyme T4N5 is effective in treating the MMP-1 secretions and UVB-induced DNA damage which contributes to the collagen degradation found in photodamaged and photoaged skin.

AGI Dermatics is the developer of Dimericine, a drug that is under clinical testing for treating patients with skin cancers and pre-cancers. T4N5 is the lead DNA repair enzyme in Dimericine(R). AGI also is the developer of Remergent, a doctor-dispensed skincare line based on the science of DNA repair and currently available at dermatologist and plastic surgeon offices. The DNA repair enzymes that are in the Dimericine product are similar to those found in the Remergent skin care line.

AGI Dermatics is the bio-pharmaceutical laboratory that has led the research of DNA repair of the skin for more than 20 years. Founded by Daniel B. Yarosh, PhD, AGI Dermatics specializes in skin photobiology, dedicating research and development to DNA repair, solar impact on the immune system, and cell-signaling in skin. The company's application of groundbreaking active ingredients and meticulously engineered liposome delivery systems is validated in controlled clinical studies and published in dozens of peer-reviewed scientific and medical journals. http://www.agiderm.com

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