ViCardia Therapeutics, Inc.

ViCardia Therapeutics, Inc.

ViCardia Therapeutics, Inc.

ViCardia Therapeutics, Inc., a Delaware corporation, founded in 2017, is a clinical-stage biopharmaceutical company focused on the discovery, development and commercialization of novel therapies for treating heart failure (HF) involving mitochondrial dysfunction.

Company details

930 Montgomery Street, Suite 600 , San Francisco , California 94133 USA
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Business Type:
Manufacturer
Industry Type:
Pharmaceuticals
Market Focus:
Nationally (across the country)
Year Founded:
2017

ViCardia is led by a highly experienced management team, board of directors and board of scientific advisors with extensive experience treating chronic and acute heart failure and conducting cardiovascular research.

Addressing the Underlying Cause of Heart Failure
Our mission: to be the leader in heart failure research and treatment focused on mitochondrial dysfunction and AMPK activation.

Our goal is to improve the healthspan of the acute heart failure patient and to improve their healthy lifespan – living a long and healthy life

Heart Failure (HF) is a complex, progressive clinical syndrome in which there is dyspnea or exertional limitation due to impairment of ventricular filling or ejection of blood, or a combination of both.

Once developed, HF results in significant morbidity and mortality, with a 1-year mortality rate of 7.2% and a 1-year hospitalization rate of 31.9% in patients with chronic HF.

In patients hospitalized for Acute Decompensated Heart Failure, these rates increase to 17.4% and 43.9%.

HF has traditionally been broadly subclassified according to the left ventricular ejection fraction (LVEF) into 3 categories:
  • heart failure with preserved ejection fraction (HFpEF) - LVEF ≥50%
  • heart failure with midrange ejection fraction (HFmEF) - LVEF 41%-49%
  • HF with reduced ejection fraction (HFrEF), in which the LVEF is ≤40%

Hospitalization due to Acute Decompensated Heart Failure marks a critical stage in the progression of chronic heart failure resulting in an acute event, worsening the prognosis for early mortality after repeat hospitalizations.

Currently, there is no acute therapy that reduces mortality risk in patients with Acute Decompensated Heart Failure. GP531 provides the clear pathway to a life-saving therapy for millions of patients worldwide in a cost effective manner.

Failure to produce an adequate amount of energy causes mechanical failure of the heart.
When heart muscle cells are put under stress, for example by high blood pressure or by oxygen deprivation (such as occurs during a heart attack), they switch from using fatty acids as their source of energy to using glucose.

The well-oxygenated heart consumes several different substrates and converts them to a common form of chemical energy that fuels myocardial contraction and is required for viability.

The mechanisms underlying the development of HF are multiple, complex, and not well understood, primarily because HF is not a disease, but a manifestation of diverse cardiac and noncardiac abnormalities.

Adequate amounts of ATP must be generated to support the heart’s contractile demands and maintain viability for the other cells in the body. Abnormalities in cardiac metabolism, such as a lack of ATP-ADP metabolism, cause mechanical failure of the heart.

Dysfunctional mitochondria produce less cellular energy (ATP) and produce increased levels of reactive oxygen species (ROS), both of which lead to oxidative stress and ultimately to HF.

Mitochondrial dysfunction is the most important event in the development of Heart Failure.
Dysfunctional mitochondria produce less cellular energy (ATP) and produce increased unhealthy levels of reactive oxygen species (ROS), both of which lead to oxidative stress and ultimately to heart failure.