The heart is a voracious consumer of energy, more than any other organ. Like every other cell and organ in the body, the heart’s energy currency is adenosine triphosphate, or ATP. The heart runs through approximately six kilograms of ATP every day, which is 20 to 30 times its own weight. The heart must generate all of the ATP it needs in real time.
Under normal circumstances, both glucose (sugars) and free fatty acids (fats) are fuels for metabolism in the heart. In heart disease, oxygen levels available to cells may be lower than usual, and as a result the heart may rely to a greater extent on fatty acids to make energy. However, ATP generation is less efficient because 10% to 15% more oxygen is required to generate the same amount of ATP from fatty acids as compared to glucose.
IMB-101 is a novel pFOX (partial fatty acid oxidation) inhibitor designed to optimize the use of fuels in the heart by partially shifting from using fat to using glucose, thereby resulting in a more efficient production of energy per molecule of oxygen consumed. This approach has been validated by trimetazidine (TMZ), a pFOX inhibitor used to treat angina in Europe since the 1970s. TMZ is indicated for use in refractory angina in both the European Society of Cardiology (ESC) 2019 Guidelines for the Diagnosis and Management of Chronic Coronary Syndromes, and the ESC 2016 Guidelines for the Diagnosis and Treatment of Acute and Chronic Heart Failure.
IMB-101 is designed to have greater efficacy and a better benefit risk profile than TMZ. In pre-clinical models, IMB-101 demonstrated both greater efficacy than TMZ as well as less off target binding.
IMB-101 is a small molecule currently in development for the treatment of refractory angina.
In a Phase 1 clinical trial to study the safety, tolerability, and pharmacokinetics of IMB-101, IMB-101 was well tolerated with no drug-related serious adverse events.
We plan to initiate a Phase 2b clinical trial in refractory angina patients in the first half of 2020.
IMB-101 is a small molecule which we plan to develop for the treatment of heart failure.
In preclinical studies in heart failure, treatment with IMB-101 resulted in significantly improved ejection fraction as well as substantial reductions in the levels of cardiac fibrosis.
In a Phase 1 clinical trial to study the safety, tolerability, and pharmacokinetics of IMB-101, IMB-101 was well tolerated with no drug-related serious adverse events.