Cardiovascular disease (CVD) is the leading cause of death globally. Verve is committed to developing gene editing medicines that disrupt the current chronic care model to improve outcomes for patients.
Disrupting the Chronic Care Model
Despite advances in treatment over the last 50 years, CVD remains a global epidemic. The current paradigm of chronic care is fragile – requiring rigorous patient adherence, extensive healthcare infrastructure and regular healthcare access – and leaves many patients without adequate care. CVD is a leading contributor to reductions in life expectancy and is one of the most expensive health conditions in the U.S., costing the national healthcare system more than $350 billion per year in costs and lost productivity.
Boldly Tackling ASCVD
CVD collectively refers to diseases of the heart and blood vessels, which are diagnosed as atherosclerotic cardiovascular disease (ASCVD) or cardiomyopathy, among others. In ASCVD, which is a large subset of CVD, cholesterol drives the development of atherosclerotic plaque, a mixture of cholesterol, cells and cellular debris in the wall of a blood vessel that results in hardening of the arteries, and can lead to fatal outcomes such as heart attack and stroke.
Only 39% of individuals in a third-party clinical trial reported adherence to statin therapy in the year following a heart attack, even when the medicine was provided free of charge.
Current therapies – including daily pills or intermittent injections – are prescribed over decades with costs that can be prohibitively expensive.
Existing therapeutics carry side effects for a subset of the population.
The current treatment approach starts too late, often after significant and irreparable damage has been done to the body.
Ongoing access to oral medications and specialist physicians is limited in low- and middle-income countries where rate of ASCVD is rising.
Human genetic studies have shown that certain individuals have gene variants that cause elevated blood levels of low-density lipoprotein cholesterol (LDL-C), leading to increased risk for ASCVD and ASCVD-related outcomes such as heart attack. Conversely, studies have found that certain gene variants are associated with natural disease resistance and reduce the risk for ASCVD. For instance, a subset of the population carries a naturally protective variant of a gene known as PCSK9. People born with this variant have extremely low LDL-C levels and are heart-healthy and resistant to heart attack.
Our gene editing medicines are designed to mimic the protective effects of naturally occurring resistance mutations. By potently and durably lowering cumulative LDL-C exposure throughout a patient’s lifetime, our gene editing medicines could fundamentally disrupt the chronic care model for treating patients with or at risk for ASCVD and relieve the significant burden placed on patients, providers and the healthcare system.