President and CEO, TearSolutions Inc.
Lacripep, A Replacement Therapy For Dry Eye
Lacripep(TM) is a peptide fragment of the 119 amino acid protein, Lacritin. Both Lacritin and its peptide fragments are present in normal tear and deficient in all forms of Dry Eye. TearSolutions has demonstrated that Lacripep(TM) has all of the Biology of Lacritin and consequently is developing Lacripep(TM) as a natural replacement therapy in the treatment of Dry Eye. Preclinical studies have established that Lacripep(TM) can heal the corneal surface epithelium, increase the production of tear's aqueous, lipid and mucin components (returning them to normal levels), restore corneal surface sensory neurons and normal control of tear production. Clinically, the restoration of the corneal epithelium as a barrier protecting the cornea is expected to reduce staining for the cornea by Fluorescein. Fluorescein corneal staining (FCS) is an FDA approvable endpoint. Lacripep(TM) is currently in a Phase 2 POC clinical study which should be completed in 2015. The design criteria of this study and an analysis of the masked interim data will be discussed.
Dr. Gadek is a medicinal chemist with a Ph.D. from UC Berkeley and 35 years of experience in the Biotechnology and Pharmaceutical industry. He has co-authored more than fifty peer review journal articles detailing the identification of novel candidates for clinical trials in cardiovascular, metabolic, inflammatory and auto-immune diseases. He has developed experience and expertise in both the biotech start-up and large pharmaceutical company space: guiding the discovery and development of novel chemical entities as both drug substances and drug products, defining clinical and regulatory strategies which position molecules for clinical and commercial success based on their mechanism of action (MOA) from concept through approval. Most recently Dr. Gadek has focused his efforts in the ocular arena with the discovery and development of Xiidra, leading to its approval by the FDA in 2016. Xiidra’s MOA targets the adhesion, migration, proliferation and inflammatory cytokine release by T-cells as the source of dry eye’s disease pathophysiology. Thus, preclinical MOA was translated into the first agent to demonstrate dose dependent inhibition of both the symptoms and signs of dry eye.