Sol-Gel Technologies Ltd to Host Virtual KOL Event on Gorlin Syndrome and the Upcoming Phase 3 Trial for SGT-610 - Seite 2

About Ervin Epstein, Jr., MD

Dr. Ervin Epstein, Jr., MD is a leading dermatologist in Oakland, California. He received his medical degree from University of California (San Francisco) School of Medicine and was in practice for more than 50 years. He served as the Co-Founder, Medical Advisor, and Director at PellePharm, Inc. He also served as Research Dermatologist and Clinical Professor of Dermatology at the University of California, San Francisco. His research interests have focused on the molecular biology of inherited and neoplastic skin diseases. has served as President of the Society for Investigative Dermatology. Ervin Epstein has also served on the boards of numerous dermatological organizations including The American Dermatological Association. His publications have appeared in New England Journal of Medicine, Nature, and Science.

About Alon Seri-Levy, PhD

Alon Seri-Levy, PhD co-founded Sol-Gel and has served as chief executive officer since the Company’s inception in 1997 and as a member of the board of directors until 2014. Prior to founding Sol-Gel, Dr. Seri-Levy established the computer-aided drug design department at Peptor Ltd., an Israeli research and development company that specialized in the development of peptide-based drug products. Dr. Seri-Levy holds a PhD in Chemistry (summa cum laude) from The Hebrew University of Jerusalem, Israel, and conducted his post-doctoral studies at Oxford University, United Kingdom. Dr. Seri-Levy was reappointed to our board of directors in January 2018, immediately following the pricing of the company’s initial public offering.

About Gorlin Syndrome and SGT-610

SGT-610, a hedgehog signaling pathway blocker, has the potential to be the first ever treatment for Gorlin syndrome, if approved. Gorlin syndrome, an autosomal dominant genetic disorder affecting approximately 1 in 27,000-31,000 people in the U.S., is mostly caused by inheritance of one defective copy of the tumor suppressor patched homolog 1 (PTCH1) gene. Normally, the PTCH1 gene blocks the smoothened, frizzle class receptor (SMO) gene, turning off the hedgehog signaling pathway when it is not needed. Mutations in the PTCH1 gene may cause a loss of PTCH1 function, release of SMO, and may allow basal cell carcinoma (BCC) tumor cells to divide uncontrollably. Patidegib, the active substance in SGT-610, is designed to block the SMO signal, thus, allowing cells to function normally and reducing the production of new tumors.