EDG-7500
Targeting HCM
We are developing EDG-7500, a selective cardiac sarcomere modulator, with the aim to slow early contraction velocity and address impaired cardiac relaxation associated with symptomatic hypertrophic cardiomyopathy (HCM).
Hypertrophic Cardiomyopathy
Two major forms of HCM include obstructive (oHCM) and nonobstructive (nHCM), each leading to impaired cardiac performance. In oHCM, as the left ventricle (LV) contracts (systole) to eject oxygenated blood from the heart into systemic circulation, the mitral valve makes physical contact with the hypertrophied septal wall. This contact underlies the basis of the obstructed ejection of blood through the LV outflow tract (LVOT) creating a pressure difference, or gradient (LVOT-G) between the LV cavity and systemic circulation.
In nHCM, the hypertrophy is more symmetrically distributed in the LV walls, therefore the patient does not develop LVOT obstruction nor pressure gradient. However due to LV hypertrophy and stiffness, LV relaxation is impaired and LV filling with blood (diastole) is significantly reduced.
Healthy Heart vs. Heart with HCM
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About EDG-7500
Targeting the sarcomere
EDG-7500 is a novel oral, selective cardiac sarcomere modulator for the treatment of symptomatic HCM.
Potential to address symptomatic obstructive and nonobstructive HCM
In symptomatic obstructive and nonobstructive HCM, treatment with EDG-7500 is targeted to improve cardiac relaxation and filling without significant impairment of systolic performance.
Designed to address unmet needs in HCM
Preclinical and preliminary clinical data support EDG-7500 having the potential for significant efficacy, measured by gradient response, while preserving safety, reflected by minimal changes in ejection fraction. EDG-7500 is currently in clinical trials in symptomatic oHCM and nHCM.
EDG-7500 is an investigational therapy that has not been approved for use in HCM by any regulatory agency, as its safety and effectiveness have not been established for the treatment of this disease.
