New study identifies the role of a key growth factor in promoting formation of hair follicles and suggests a new therapeutic approach to treat baldness
BOSTON, June 3, 2013 /PRNewswire/ -- Technology exclusively licensed by Follica Inc. from the Perelman School of Medicine at the University of Pennsylvania has been used to demonstrate a new approach to regenerate hair follicles in adult mammals which could be used therapeutically in humans. The paper describing the data was published advanced online in Nature Medicine.
The paper's principal investigator, George Cotsarelis, MD, chair of Dermatology in the Perelman School of Medicine at the University of Pennsylvania, and collaborators discovered that fibroblast growth factor 9 (Fgf9), a protein produced by a population of cells of the immune system in the skin, is critical for the formation of new hair follicles after disruption of the skin. The findings illuminate a molecular mechanism to regenerate hair follicles that could enable new treatments for hair loss.
The authors first showed that Fgf9 is up-regulated in the dermis immediately before new hair follicle structures start to appear. Reducing Fgf9 expression decreased hair follicle formation, while overexpressing Fgf9 led to two to three-fold increase in the number of new hair follicles. The study supports the notion that disruption of the skin produces a window of opportunity during which the cells in the regenerating epidermis can be pushed towards becoming a hair follicle, and highlights the potential for using Fgf9 therapeutically to boost the formation of new hair follicles during this window.
"This discovery sheds light on a novel mechanism to regenerate hair follicles and opens an exciting new avenue to develop treatments for hair loss in humans," noted Dr. William Ju of Follica, Inc. "Follica has developed a technology platform that is uniquely suited to support clinical translation of these new findings. The Follica platform can be used to induce skin reepithelialization, which creates a "window of opportunity" during which the Fgf9 pathway could be modulated to potentiate hair neogenesis."
Follica has conducted preclinical testing of proprietary device configurations for skin disruption in combination with a number of known and novel drugs. The company has run a series of human clinical trials, including a Phase IIa trial, which have demonstrated follicular neogenesis in humans for the first time. These trials pave the way for the development of a breakthrough combination of a device to produce targeted skin perturbation coupled with a well-studied drug compound.
"Creating new hair follicles is essential to treating hair loss, and is something that cannot be accomplished by invasive surgical procedures such as hair transplantation or by existing drug treatments that at best simply preserve existing hair," said Dr. Bernat Olle, Follica Co-founder.
The study findings define important differences between mouse and human skin that help explain why humans tend to scar rather than regenerate. Fgf9 triggers a cascade of molecular events leading to hair follicle regeneration. Adding Fgf9 to wounds increases the regeneration of hair follicles in mice lacking gamma/delta T cells in their skin, similar to human skin.
Follica, Inc. was established around foundational discoveries in epithelial stem cell biology from Dr. Cotsarelis at the University of Pennsylvania. In 2007, Dr. Cotsarelis and colleagues reported a way to regenerate hair follicles by creating a physical disruption of the skin and then manipulating key signaling pathways involved in hair follicle formation during a limited window of time. Dr. Cotsarelis is a co-founder and scientific advisory board member of Follica.
Follica Inc. (www.follicabio.com), a privately held medical product company, was co-founded by PureTech Ventures and a group of world renowned experts in hair follicle biology and medicine. In addition to hair loss, Follica has intellectual property and development programs in various skin and follicle related indications.
SOURCE Follica Inc.
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