The use of a Wnt inhibitor Wnt-C59 in the preparation of a drug for treating SCN5A mutation-induced dilated cardiomyopathy (DCM) is provided. With SCN5A genotype detection as a breakthrough point, a Wnt pathway-specific inhibitor Wnt-C59 is used to inhibit the abnormal activation of the Wntβ-Catenin pathway caused by SCN5A gene mutation, thereby improving the prognosis of cardiac function in a patient with SCN5A gene mutation-induced DCM. In experiments, aging and adriamycin-induced DCM models are constructed, and the therapeutic effect of Wnt-C59 on DCM is detected through indexes such as changes in cardiac function and activation of related signal molecules, which provides a theoretical basis for use of Wnt-C59 in the clinical treatment of DCM. A new treatment method for SCN5A mutation-induced DCM is provided to bring dawn to such patients and has promising application prospects.

The use of a Wnt inhibitor Wnt-C59 in the preparation of a drug for treating SCN5A mutation-induced dilated cardiomyopathy (DCM) is provided. With SCN5A genotype detection as a breakthrough point, a Wnt pathway-specific inhibitor Wnt-C59 is used to inhibit the abnormal activation of the Wntβ-Catenin pathway caused by SCN5A gene mutation, thereby improving the prognosis of cardiac function in a patient with SCN5A gene mutation-induced DCM. In experiments, aging and adriamycin-induced DCM models are constructed, and the therapeutic effect of Wnt-C59 on DCM is detected through indexes such as changes in cardiac function and activation of related signal molecules, which provides a theoretical basis for use of Wnt-C59 in the clinical treatment of DCM. A new treatment method for SCN5A mutation-induced DCM is provided to bring dawn to such patients and has promising application prospects.

Described herein are methods of for treating and/or preventing Major adverse cardiovascular events (MACE). by administering to a subject in need thereof, a combination of a sodium-glucose transport protein 2 (SGLT2) inhibitor and a compound of Formula I or a stereoisomer, tautomer, pharmaceutically acceptable salt, or hydrate thereof, wherein the variables of Formula I are as defined herein.

##STR00001##

Described herein are methods of for treating and/or preventing Major adverse cardiovascular events (MACE). by administering to a subject in need thereof, a combination of a sodium-glucose transport protein 2 (SGLT2) inhibitor and a compound of Formula I or a stereoisomer, tautomer, pharmaceutically acceptable salt, or hydrate thereof, wherein the variables of Formula I are as defined herein.

##STR00001##

This invention relates to methods of treating and/or preventing cardiovascular diseases and conditions and to methods of reducing the risk of cardiovascular death, reducing the risk of hospitalization for heart failure, reducing the risk of hospitalization for heart failure, reducing the risk of urgent visits for heart failure, and slowing the progression of kidney disease.

This invention relates to methods of treating and/or preventing cardiovascular diseases and conditions and to methods of reducing the risk of cardiovascular death, reducing the risk of hospitalization for heart failure, reducing the risk of hospitalization for heart failure, reducing the risk of urgent visits for heart failure, and slowing the progression of kidney disease.

The treatment of diastolic dysfunction in a subject and, in particular, compositions for use and methods in treating diastolic dysfunction are disclosed. In one aspect, the disclosure provides a composition for use comprising a therapeutically effective amount of a substance that increases the level and/or activity of a crystalline protein in cardiomyocytes of the subject. In particular, the composition for use according to the disclosure comprises a therapeutically effective amount of the alpha B crystalline protein. It was found that the composition for use is capable of treating diastolic dysfunction and diastolic heart disease in subjects with failing hearts that have a higher cardiomyocyte stiffness than controls. Particularly, addition of alpha B crystalline reduced the higher stiffness of failing cardiomyocytes to the level observed in control cardiomyocytes.

The invention relates to a method for detecting residual, undifferentiated pluripotent stem cells (PSCs) in a culture of cells differentiated from PSCs, the method comprising: culturing the cells on a substrate coated with laminin-521 and E-cadherin in a medium comprising a ROCK inhibitor; quantitating in the cultured cells expression of a marker of residual, undifferentiated PSCs; and comparing the marker expression in the cultured cells with the marker expression in a reference culture of cells comprising a known proportion of PSCs, wherein lower marker expression in the culture of cells than marker expression in the reference culture of cells indicates absence of residual, undifferentiated PSCs in the cultured cells or presence of residual, undifferentiated PSCs in the cultured cells at a proportion lower than the known proportion of PSCs in the reference culture of cells. The invention also relates to a method for manufacturing a therapeutic composition and a method for treating or preventing a condition in a subject.

The present invention relates to the protein myeloid-derived growth factor (MYDGF) or nucleic acids encoding said protein for use in treating or preventing fibrosis and hypertrophy. The present invention also relates to the protein MYDGF or nucleic acids encoding said protein for use in treating heart failure. The present invention also relates to vectors comprising the nucleic acid, host cells expressing the nucleic acid, and methods for use in treating fibrosis and hypertrophy, and for use in treating heart failure.

The present invention relates to the protein myeloid-derived growth factor (MYDGF) or nucleic acids encoding said protein for use in treating or preventing fibrosis and hypertrophy. The present invention also relates to the protein MYDGF or nucleic acids encoding said protein for use in treating heart failure. The present invention also relates to vectors comprising the nucleic acid, host cells expressing the nucleic acid, and methods for use in treating fibrosis and hypertrophy, and for use in treating heart failure.