Eidos Therapeutics to Present at 31st Annual ROTH Conference
SAN FRANCISCO, March 11, 2019 (GLOBE NEWSWIRE) -- Eidos Therapeutics, Inc. (Eidos) (Nasdaq: EIDX ) today announced that management is scheduled to participate in a fireside chat regarding Eidos at the 31st Annual ROTH Conference on Monday, March 18th at 8:30 a.m. PDT in Orange County, CA.
A live audio webcast at ir.eidostx.com. An archived replay of the webcast will be available on the company’s website for 90 days following the live presentation.
About Eidos Therapeutics
Eidos Therapeutics is a clinical stage biopharmaceutical company focused on addressing the large and growing unmet need in diseases caused by transthyretin (TTR) amyloidosis (ATTR). Eidos is developing AG10, a potentially disease-modifying therapy for the treatment of ATTR. AG10 is currently being studied in a pivotal global phase 3 trial (ATTRibute-CM) in ATTR cardiomyopathy patients. The innovative trial design includes two potentially registrational endpoints, change in 6-minute walk distance at 12 months and reduction in all-cause mortality and cardiovascular-related hospitalizations at 30 months. For more information, please visit www.eidostx.com.
About transthyretin amyloidosis (ATTR)
ATTR represents a significant unmet medical need with a large patient population and an inadequate current standard of care. ATTR is caused by the destabilization of TTR due to inherited mutations or aging and is commonly divided into three distinct categories: wild-type ATTR cardiomyopathy (ATTRwt-CM), mutant ATTR cardiomyopathy (ATTRm-CM), and ATTR polyneuropathy (ATTR-PN). The worldwide prevalence of each disease is approximately 400,000 patients, 40,000 patients and 10,000 patients, respectively.
All three forms of ATTR are progressive and fatal. For patients with ATTRwt-CM and ATTRm-CM, symptoms usually manifest later in life (age 50+), with median survival of three to five years from diagnosis. ATTR-PN either presents in a patient’s early 30s or later (age 50+), and results in a median life expectancy of five to ten years from diagnosis. Progression of all forms of ATTR causes significant morbidity, impacts productivity and quality of life, and creates a significant economic burden due to the costs associated with progressively greater patient needs for supportive care.
AG10 is an investigational, orally-administered small molecule designed to potently stabilize tetrameric transthyretin, or TTR, thereby halting at its outset the series of molecular events that give rise to amyloidosis, or ATTR. In a Phase 2 clinical trial in subjects with symptomatic ATTR-CM, AG10 was generally well tolerated, demonstrated >90% average TTR stabilization at day 28, and increased serum TTR concentrations, a prognostic indicator of survival in a retrospective study of ATTR-CM patients, in a dose-dependent manner. AG10 is currently being studied in an open-label extension of a Phase 2 clinical trial in patients with ATTR-CM and sites are currently being activated for a Phase 3 clinical trial of AG10 in patients with ATTR-CM (ATTRibute-CM).
AG10 was designed to mimic a naturally-occurring variant of the TTR gene (T119M) that is considered a rescue mutation because co-inheritance has been shown to prevent ATTR in individuals also inheriting a pathogenic, or disease-causing, mutation in the TTR gene. To our knowledge, AG10 is the only TTR stabilizer in development that has been observed to mimic the stabilizing structure of this rescue mutation.
Carolyn Hawley, Canale Communications, (619) 849-5382, email@example.com
Alex Gray, Burns McClellan, (212) 213-0006, firstname.lastname@example.org