HOME
Back to Projects

SET Therapeutics

SETTM (Safe Editing Therapeutics) will offer patients a simple, safe way to reduce their risk of Coronary Artery Disease. We aim to provide patients and physicians with SETTM, a safe, long-lasting treatment for reducing the risk of coronary artery disease by the sustained reduction of atherogenic LDL-cholesterol in their bloodstreams. In the twenty years since their introduction, statins have generated over $250 billion in sales as the standard of care. Because our unique gene therapy approach works in a way completely different from the widely used HMG CoA reductase inhibitors (i.e., statins), it will offer a new alternative to the millions of patients who do not benefit from statins and it can be used as a powerful complementary treatment for the additional millions of patients striving to attain very low target LDL-c levels.

SETTM has several advantages over the statins. It is long-lasting; SETTM will need to be administered only once or twice per year obviating the concern of patients and physicians about non-compliance. It uses a natural mechanism; SETTM works by a natural mechanism that is, in fact, normal in many mammals, so it is unlikely to have effects on other biochemical pathways that could lead to adverse events, especially at high doses. It is not a chemical; because SETTM is not a low molecular weight drug, the likelihood of interactions with other drugs is reduced.

FWT 's leading scientists Dr. John Daiss and Chad Galloway have partnered with Dr. Harold Smith of the University of Rochester, whom has one venture backed company based on his inventions already under a proof-of-concept development effort funded by FWT and the National Heart, Lung and Blood Institute. Despite the project being at its earliest stage, it represents a broad potential and huge market opportunity whereby we have empirically shown along 5 different measures successful treatment within accepted animal models the reduction on bad cholesterol and improvement in good cholesterol.

One such measure, shown above, shows where control hamster had about twice as much ApoB100 as ApoB48, the Group 5 hamsters had 4-5 times as much ApoB48 as ApoB100 suggesting a significant change in editing activity. The decrease in ApoB100/ApoB48 is due to both a significant reduction in the level of ApoB100 (p = 0.002) and an increase in the level of ApoB48 suggesting that intracellular ApoB48 is elevated at the expense of ApoB100 as predicted in our model.