This technology is a modified statin molecule that reduces hypercholesterolemia while preventing muscle weakness, a common side effect of statin use.
Statins reduce the risk of cardiovascular disease and are the primary pharmaceutical treatment for individuals with elevated low-density lipoprotein cholesterol. Muscle-related side effects, including weakness, are among the most common adverse effects of statin therapy and can lead to decreased patient adherence and reduced tolerable doses, thereby limiting treatment effectiveness against hypercholesterolemia. Statins primarily act by inhibiting the cholesterol-synthesizing enzyme HMG-CoA reductase, but they also interact with ryanodine receptors in muscle cells, which is hypothesized to contribute to muscle weakness. Therefore, there is a need for a statin that is equally effective at inhibiting HMG-CoA reductase and does not activate ryanodine receptors.
This technology is a modified statin that reduces circulating cholesterol but binds to ryanodine receptors on muscle cells less effectively, thereby preventing the development of muscle weakness. The statin structure has been modified to prevent interaction with ryanodine receptors while maintaining interaction with HMG-CoA reductase. Preserving the conserved HMG-CoA reductase binding ability retains the molecule’s efficacy in lowering cholesterol compared to existing statin therapies.
Patent Pending
IR CU24350
Licensing Contact: Joan Martinez
