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Volumn 12, Issue 4, 2009, Pages 243-251

CK-1827452, a sarcomere-directed cardiac myosin activator for acute and chronic heart disease

Author keywords

[No Author keywords available]

Indexed keywords

CALCIUM ION; CARDIAC MYOSIN; CK 1827452; CYCLIC AMP; INOTROPIC AGENT; PLACEBO; UNCLASSIFIED DRUG;

EID: 64349116900     PISSN: 13697056     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Review
Times cited : (17)

References (59)
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    • The cardiac myosin activator, CK-1827452, accelerates the enzymatic step gating entry of myosin into its force generating state. Rodriguez HM, Kawas R, Hartman JJ, Malik F, Sakowicz R BIOPHYS J 2007 Suppl S 481A · Presents in vitro data demonstrating that CK-1827452 had an inhibitory effect on myosin-free inorganic phosphate release in the absence of actin and a stimulatory effect in the presence of actin. These results suggested that CK-1827452 increased entry of the myosin cross-bridges into the force-generating state, indicating a prolongation of the duty cycle.
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    • The selective cardiac myosin activator, CK-1827452, increases systolic function in a concentration-dependent manner in patients with stable heart failure (10/8/08). Cleland JGF, Nifontov EM, McMurray JJV, Senior R, Lang CC, Clarke CP, Francis D, Greenberg B, Mayer J, Monaghan M, Neyses L et al J CARD FAIL 2008 14 9 797-798 ·· Presents data from a phase IIa, multicenter, double-blind, randomized, placebo-controlled clinical trial with escalating doses of CK-1827452 in patients with stable heart failure (n = 40). At CK-1827452 plasma concentrations > 100 ng/ml, statistically significant placebo-corrected increases from baseline were observed in systolic ejection time (24 to 98 ms; p < 0.0001) and fractional shortening (2 to 4%; p < 0.05). Statistically significant placebo-corrected increases from baseline were observed in stroke volume (6 to 14 ml; p < 0.01) at CK-1827452 plasma concentrations > 200 ng/ml.
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    • Presents important in vitro data demonstrating that CK-1827452 did not affect diastolic length or diastolic Ca2+ levels of field-stimulated rat ventricular myocytes, ··
    • In vitro and in vivo characterization of CK-1827452, a selective cardiac myosin activator. Anderson RL, Sueoka SH, Lee KH, Rodriguez HM, Kawas RF, Godinez G, Morgan BP, Sakowicz R, Morgans DJ, Malik F, Elias KA J CARD FAIL 2006 12 6 S86 ·· Presents important in vitro data demonstrating that CK-1827452 did not affect diastolic length or diastolic Ca2+ levels of field-stimulated rat ventricular myocytes.
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    • Systolic ejection time is a sensitive indicator of left ventricular systolic function during treatment with the selective cardiac myosin activator, CK-1827452. Malik FI, Saikali KG, Clarke CP, Teerlink JR, Wolff AA J CARD FAIL 2007 13 6 S145-S146
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    • The selective cardiac myosin activator, CK-1827452, increases left ventricular systolic function by increasing ejection time: Results of a first-in-human study of a unique and novel mechanism. Teerlink JR, Malik FI, Clarke CP, Saikali KG, Escandon RD, Lee JH, Wolff AA J CARD FAIL 2006 12 9 763 ·· Presents data from a phase I, first-in-human, double-blind, randomized, placebo-controlled, dose-escalation clinical trial of CK-1827452 (0.005 to 1.0 mg/kg/h, 6 h iv infusion once weekly for 4 weeks) administered to healthy male volunteers (n, 34, CK-1827452 treatment was associated with linear dose-dependent increases in left ventricular systolic ejection fraction and fractional shortening. CK-1827452 was generally well tolerated, with an MTD determined of 0.5 mg/kg/h, at which the mean systolic blood pressure decreased by 13 mmHg (p < 0.0001) and 7.4 mmHg (p < 0.05) in standing and supine volunteers, respectively
    • The selective cardiac myosin activator, CK-1827452, increases left ventricular systolic function by increasing ejection time: Results of a first-in-human study of a unique and novel mechanism. Teerlink JR, Malik FI, Clarke CP, Saikali KG, Escandon RD, Lee JH, Wolff AA J CARD FAIL 2006 12 9 763 ·· Presents data from a phase I, first-in-human, double-blind, randomized, placebo-controlled, dose-escalation clinical trial of CK-1827452 (0.005 to 1.0 mg/kg/h, 6 h iv infusion once weekly for 4 weeks) administered to healthy male volunteers (n = 34). CK-1827452 treatment was associated with linear dose-dependent increases in left ventricular systolic ejection fraction and fractional shortening. CK-1827452 was generally well tolerated, with an MTD determined of 0.5 mg/kg/h, at which the mean systolic blood pressure decreased by 13 mmHg (p < 0.0001) and 7.4 mmHg (p < 0.05) in standing and supine volunteers, respectively.
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    • Direct activation of cardiac myosin by CK-1827452 improves cardiac function in a dog heart failure model. Malik F, Elias KA, Finer JT, Morgan BP, Sakowicz R, Anderson R, Baliga R, Conn L, Cox D, Garard M, Hartman J et al J CARD FAIL 2005 11 6 Suppl 1 Abs 017 · Presents in vitro data from field-stimulated rat ventricular myocytes. CK-1827452 did not affect the peak amplitude or dynamics of the Ca2+ transient, but increased the extent of myocyte shortening. Furthermore, CK-1827452 had no effect on PDE3 activity and was unaffected by concurrent β-blockers. In vivo data from dog models of heart failure suggested increased fractional shortening, cardiac output and stroke with no apparent effects on diastolic function or on waste of oxygen consumption, indicating an increased cardiac contractile function
    • Direct activation of cardiac myosin by CK-1827452 improves cardiac function in a dog heart failure model. Malik F, Elias KA, Finer JT, Morgan BP, Sakowicz R, Anderson R, Baliga R, Conn L, Cox D, Garard M, Hartman J et al J CARD FAIL 2005 11 6 Suppl 1 Abs 017 · Presents in vitro data from field-stimulated rat ventricular myocytes. CK-1827452 did not affect the peak amplitude or dynamics of the Ca2+ transient, but increased the extent of myocyte shortening. Furthermore, CK-1827452 had no effect on PDE3 activity and was unaffected by concurrent β-blockers. In vivo data from dog models of heart failure suggested increased fractional shortening, cardiac output and stroke volume, with no apparent effects on diastolic function or on waste of oxygen consumption, indicating an increased cardiac contractile function.
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