Rise in number of patients suffering from hypertrophic cardiomyopathy (HCM) worldwide has led to increased spending and focus on clinical R&D lately. With promising data attained from preclinical and phase 1 studies, it is safe to say that Cytokinetics might be an emerging player that could pioneer a treatment for HCM.
Cytokinetics Inc. is a renowned biopharmaceutical company that innovates potential treatments for patients with diseases like impaired or declining muscle function, and has recently released its data from the Phase 1 clinical trial of CK-3773274 (CK-274) in a poster session at the HFSA 23rd Annual Scientific Meeting held in Philadelphia.
Reportedly, CK-274 is a modern cardiac myosin inhibitor, built by scientists at Cytokinetics that helps improve the potential treatment of HCM caused due to increased cardiac contractility.
Earlier, the company had released the preclinical data for CK-274 at the American Heart Association’s BCVS (Basic Cardiovascular Sciences) Scientific Sessions held in Boston, showing a decrease in cardiac contractility in vivo in a mouse model of HCM and in vitro, in vivo in healthy animals.
However, the recent trial met both the secondary and primary objectives to assess the tolerability and safety of multiple and single oral doses of CK-274. Moreover, these data aid the development of CK-274 into Phase 2 studies in patients with obstructive HCM, which is likely to start in Q4 2019.
Apparently, the initial objective of this Phase 1 randomized, double-blind, multi-part, placebo-controlled, multiple and single ascending dose study was to evaluate the tolerability and safety CK-274 in medically fit candidates.
Additional objectives involved the study of PK/PD relationship in regard to cardiac function and its effects as measured by echocardiography, with no intention to find a maximum tolerated dose of CK-274.
As per in vitro studies, CK-274 inhibited cardiac myosin activity, while minimizing the cardiac myosin ATPase activity in a concentration-dependent method, with 1.3 µM’s IC50. Additionally, the drug reduced FS (fractional shortening), with very less effect on the calcium transient in adult rat cardiomyocytes.