Current therapeutics are designed to prevent heart attacks or to assist a damaged heart to function better. Yet, although extensively pursued, therapeutics to prevent additional post-reperfusion damage to the heart (myocardial infarct expansion) and ensuing progression to chronic heart failure have met with minimal success. Hundreds of thousands of heart attack patients in the USA and millions world-wide still endure a poor quality of life and 50%, 5-year mortality rate from chronic heart disease.
Armed with new revelations implicating hemorrhage in these poor patient outcomes, we are on track to change patient care and save lives.
Here’s how: Heart attacks are caused by a blockage of blood supply (oxygen) to support cardiac muscle cell function and viability. While removing the blockage (reperfusion) restores blood supply to save immediate death of patients, the reperfusion process causes hemorrhage in about 40% of patients. Heme and iron from red blood cells released during hemorrhage cause both additional short-term damage to the heart within days of the heart attack (acute, myocardial infarct expansion) with associated loss of heart function and long-term disease progression to chronic heart failure with associated poor quality of life and a 50% 5-year mortality rate.
Our platform of current and future products span this entire process.
While each diagnostic and therapeutic has its own independent benefits for patients, they also collectively contribute to our vision for patient care.
We have a platform of diagnostics and therapeutics to provide better patient outcomes for heart attack patients. Our knowledge of underlying mechanisms is unsurpassed and serves as the foundation for product development. Please contact us to learn more about our full product lines.
What our products do: When a patient has a heart attack, he/she is revascularized to restore blood flow, halting the initial ischemia and loss of heart muscle.
Our knowledge of why hemorrhagic heart attacks occur and the mechanisms involved with adverse patient outcomes are unsurpassed. They have led to multiple products. Our lead products (in or near human clinical trials) are presented.
Our lead drug product to suppress left ventricular remodeling, chronic heart failure, and death has shown exceptional activity in large animal models of myocardial infarction. We have further shown that the driver of disease progression in large animals also persists in humans. Importantly, our lead drug candidate does not simply treat symptoms, but instead offers a cure to disease progression.
Chronic heart failure remains the number one cause of death in the United States and abroad. Accordingly, there is a large need for our drug product with a market estimated at more than $1.5 to $3B (USD).
Therapeutics to curb the incidence of chronic heart failure have eluded the medical field and leaves chronic heart failure as the leading cause of death in the United States and abroad – UNTIL NOW. Our lead drug product to suppress chronic heart failure and death has shown unprecedented activity in large animal models of heart attack: It removes iron, suppresses fat deposition in the heart, and enables healing of the heart to suppress disease progression to chronic heart failure. We have further shown that the driver and disease process observed in large animals also persists in humans. Importantly, our lead drug candidate does not simply treat symptoms, but instead offers an actual cure to disease progression to enhance quality of life and save lives of hundreds of thousands each year. Patent awarded. Publication forthcoming in Nature, Communications.
This drug is currently in human clinical trial
Our lead drug product to suppress left ventricular remodeling, chronic heart failure, and death has shown exceptional activity in large animal models of myocardial infarction. We have further shown that the driver of disease progression in large animals also persists in humans. Importantly, our lead drug candidate does not simply treat symptoms, but instead offers a cure to disease progression.
Chronic heart failure remains the number one cause of death in the United States and abroad. Accordingly, there is a large need for our drug product with a market estimated at more than $1.5 to $3B (USD).
The more time between onset of a heart attack and reperfusion to restore blood flow, the more heart muscle cells die with loss of heart function. It has led to the adage, time = muscle. Now, a third component pioneered by the founder of Cardio-Theranostics is being realized in the field: hemorrhage = muscle. Discovery of therapeutics to prevent additional heart damage have been considered top priority for decades, but a lack of knowledge for what drove disease progression held back discovery – UNTIL NOW. We have identified a key driver of myocardial infarct expansion, and our lead drug candidate has shown unprecedented effectiveness in large animal models. Patent pending. Research publication: https://www.jacc.org/doi/abs/10.1016/j.jacc.2021.10.034. Therapeutic publication forthcoming.
This drug is currently in human clinical trials.
We have identified the key driver of myocardial infarct expansion (patent pending), we have identified several lead drug candidates with appealing safety and efficacy potential, and are preparing for evaluating these options in large animal models.
The importance of hemorrhage in additional heart damage following reperfusion and in driving chronic heart failure is becoming mainstream, with major contributions form the founder of Cardio-Theranostics. Accordingly, it is important to know who experienced a hemorrhagic heart attack and who did not so that appropriate therapeutics (such as our acute phase therapeutic) can be administered to those that can best benefit. Yet, the only means to do so currently is through use of MRI, which is counter-indicated until about 3 days after the heart attack. This is too late for effective intervention for several therapeutics. We now have a highly effective blood test for hemorrhage. Patent pending. Publication forthcoming.
This diagnostic is currently in human clinical trials.
Without preventative care, patients “at risk” are likely to have a heart attack. Accordingly, a key to prevention is identification of patients at risk – so they can receive preventative care. Current cardiac stress tests including exercise stress tests and nuclear stress tests are archaic. Both require exercise on a treadmill to make the heart work harder. By doing so, the heart requires more oxygen which, if impaired, can sometimes manifest as a change in blood pressure, heart rate, ECG, or worsening physical symptoms. Yet, each of these is just a surrogate indicator of coronary artery disease and an associated increased risk for heart attack: other indicators for high risk are not evaluated. The current treadmill test is also difficult to perform by many (if not most) people.
To attain better diagnostics, researchers have strived for decades to directly monitor oxygen in the heart (and not simply blood flow). Cardio-Theranostics research has now achieved this goal and can now monitor oxygen in a needle-free, contrast-free, and treadmill-free cardiac stress test (patent pending). The analysis reveals coronary artery disease as well as other physiological factors missed by current stress tests. By identifying more patients at risk, preventative measures can be taken to curb the incidence of heart attacks.
Our publication in Science Translational Medicine has been widely acclaimed with 73 reviews in other journals (Hsin-Jung Yang, et. al. Science Translational Medicine 29 May 2019: Vol. 11, Issue 494).
Through our research, we have implicated activation of the inflammasome in left ventricular remodeling and chronic heart failure. Our issued patent claims cover inhibitors of inflammasome activation and inflammasome signaling. The research field is now realizing the importance of the inflammasome in disease progression as evidenced by activity of cholchicine and IL-1B inhibitors on disease progression. Although in early stages, we are pursuing inflammasome inhibitors. Importantly, our data indicates that inhibitors of the inflammasome may be effective at suppressing ramifications of hemorrhage on disease progression, but likely do not represent cures: Only by removing the core driver of disease progression (see above) can disease progression be cured. Nevertheless, we anticipate anti-inflammasome drug products will likely be used in combination with our chronic heart failure therapeutics described above to delay disease progression while the chronic heart disease drug ultimately cures it over time.