ESCAPE Bio to Present at the 38th Annual J.P. Morgan Healthcare Conference
SAN FRANCISCO, January 8, 2020 — ESCAPE Bio, Inc., a clinical stage company developing novel, precisely targeted therapeutics for genetically defined neurodegenerative diseases, today announced that Julie Anne Smith, Chief Executive Officer, will present at the 38th Annual J.P. Morgan Healthcare Conference on Tuesday, January 14, 2020.
Date: Tuesday, January 14, 2020
Time: 1:30 p.m. PT
Location: Westin St. Francis Hotel, Elizabethan C
Ms. Smith will present clinical updates on ESCAPE’s ESB1609 program, a novel, orally-administered, brain-penetrant and highly-selective sphingosine 1-phosphate 5 (S1P5) receptor agonist, initially being developed for Niemann-Pick Disease Type C.
Additionally, Ms. Smith will present data on ESCAPE’s precisely targeted medicines for Parkinson’s disease patients with the G2019S LRRK2 mutation and Alzheimer’s disease patients with the APOE4 mutation.
About ESCAPE Bio
ESCAPE Bio is a clinical stage, privately held biopharmaceutical company developing novel precisely targeted therapeutics for genetically defined neurodegenerative diseases. ESB1609 is in a Phase 1\1b randomized, double-blind, placebo-controlled, safety, tolerability, pharmacokinetic and biomarker study of escalating multiple doses in healthy volunteers and subjects with Niemann-Pick Disease Type C. ESCAPE’s pipeline includes small molecules targeting known genetic drivers of CNS disorders including ESB1609 for the treatment of CNS lysosomal storage disorders, a small molecule kinase inhibitor for the treatment of LRRK2 Parkinson’s Disease and an Alzheimer’s disease program targeting ApoE4. For additional information, please visit www.escapebio.com.
ESB1609 is a novel, orally-administered, brain-penetrant and highly-selective sphingosine 1-phosphate 5 (S1P5) receptor agonist. S1P5 receptors are preferentially expressed within the CNS. Agonizing S1P5 receptors upregulates CNS lipid transporters and is a powerful upstream target rectifying lysosomal deficits. Results from preclinical studies have demonstrated the potential of ESB1609 to restore dysfunctional CNS lipid homeostasis and reduce downstream markers of neurodegeneration in animal models of neurodegeneration.