An Acute Myocardial Infarction causes an ischemic state, in which heart tissue is starved of nutrients and oxygen and capillaries constrict.

Even after a stent is successfully deployed through Percutaneous Coronary Intervention (PCI) to restart the flow of arterial blood, the capillaries remain pathologically constricted, resulting in sustained Capillary No-Reflow.

If CNR is not resolved, it can cause long-term tissue starvation, leading to significant tissue damage and substantially increased mortality.

A majority of AMI patients experience CNR, which is a leading cause of mortality and morbidity in AMI patients.

Outcomes for Patients with CNR are worse than others, including: Larger infarct size, increased heart failure, higher incidence of repeat heart attacks and repeat hospitalizations, more renal failure, and higher incidence of MACE events overall.

There are no approved therapies for CNR – no current pharmacological treatments have been shown to have a positive effect, including current vasodilators.

There are no approved therapies for CNR – no current pharmacological treatments have been shown to have a positive effect, including current vasodilators.

¹C. M. Gibson et al. Relationship of TIMI
myocardial perfusion grade to mortality
after administration of thrombolytic
drugs. Circulation (2000) 101(2):125-30

“Pericytes” are tiny structures embedded in the capillary walls that constrict or dilate the capillaries.

CLN-2501 is a smooth-muscle myosin inhibitor; it directly targets myosin in the pericytes, relaxing their pathologically hypercontracted state and dilating the capillaries.

CLN-2501 is the first Capillary-Specific Vasodilator; it affects the capillaries but not the larger arteries, so it does not disrupt hemodynamics or vascular auto-regulation.