Atherosclerosis is a process of plaque or “atheroma” formation at the inside of arterial walls, below the layer of cells that is in contact with the circulating blood.

Most people develop plaques as they grow older, and cardiovascular disease is the no.1 cause of death. The importance of atherosclerosis is expected to further grow in line with the prevalence of diabetes and obesity. People with diabetes or obesity develop more plaques, earlier in life.

Currently there is no cure for atherosclerosis.

There are therapies to reduce the cardiovascular risk resulting from atherosclerosis, but there is still a long way to go.

Risk reduction is sought through several concomitant preventative approaches: cholesterol management, blood pressure control and coagulation management are pursued in addition to lifestyle changes. According to the WHO, current therapy reduces the risk of new and recurring infarctions only by about 36% - leaving a very large unmet medical need.

Increasing ApoA1 is a well validated clinical mechanism to reduce atherosclerosis and its clinical consequences. ApoA1 coils around HDL particles and supports its functionality in removing cholesterol from plaques.

It has been shown that if you inject ApoA1 in humans, atherosclerotic plaques are stabilized and reduced. Conversely, ApoA1 deficiency leads to accelerated atherosclerosis.

Dybly’s patent protected small molecules stimulate the liver to produce more ApoA1. This therapeutic approach of increasing the body’s own ApoA1 production avoids immunological complications potentially associated with injectable ApoA1 therapies.