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Find Clinical Drug Pipeline Developments & Deals for Aficamten
The company will use the proceeds for commercial launch readiness activities and for development program of CK-3773274 (aficamten) for symptomatic obstructive hypertrophic cardiomyopathy.
The company intends to use the net proceeds of this offering for commercial launch readiness activities and continuing the development program for CK-3773274 (aficamten) for the treatment of symptomatic obstructive hypertrophic cardiomyopathy.
The collaboration providing capital to support the commercialization of CK-3773274 (aficamten) for the treatment of symptomatic obstructive hypertrophic cardiomyopathy.
CK-3773274 (aficamten) is an investigational selective, small molecule cardiac myosin inhibitor. It is under clinical development for the treatment of obstructive hypertrophic cardiomyopathy in pediatric population.
The financing will enable the company to support Ji Xing Pharmaceuticals in the commercialization of JIXING’s pipeline assets in the areas of cardiovascular diseases and ophthalmology.
CK-3773274 (aficamten) is an investigational selective, small molecule cardiac myosin inhibitor. It is under phase 3 clinical development fot the treatment of obstructive hypertrophic cardiomyopathy.
CK-274 (aficamten), is small molecule cardiac myosin inhibitor discovered following an extensive chemical optimization program, which is investigated for Symptomatic Obstructive Hypertrophic Cardiomyopathy.
CK-274 (aficamten), is small molecule cardiac myosin inhibitor discovered following an extensive chemical optimization program, which is investigated for Symptomatic Obstructive Hypertrophic Cardiomyopathy.
Data from REDWOOD-HCM showed that treatment with CK-274 (aficamten), investigational selective, small molecule cardiac myosin inhibitor was associated with significant and sustained reduction in LVOT-G improvement in NYHA Functional Class and improvement in cardiac biomarker.
CK-274 (aficamten) is a novel, oral, small molecule cardiac myosin inhibitor. CK-274 is designed to reduce the number of active actin-myosin cross bridges during each cardiac cycle and consequently reduce myocardial contractility.