One of the most successful drugs ever produced is Rituximab.  Rituximab eliminates CD20 positive B-cells and treats a number of diseases, including many types of non-Hodgkin's lymphomas, CD20-positive chronic lymphocytic leukemia, rheumatoid arthritis, Wegener's Granulomatosis and Microscopic Polyangiitis. 

Despite its undeniable therapeutic value, how it works was not fully understood. Recently, Centrose discovered that CD20 interacts with an essential protein called the sodium-potassium ATPase. Centrose believes that many of the effects observed from Rituximab treatment come from this interaction.

With this discovery, Centrose designed EDC9, which targets both interacting proteins (CD20 and the sodium-potassium ATPase). To produce EDC9, Centrose took Rituximab and tethered it to a naturally produced hormone that acts on the sodium-potassium ATPase. Unlike all other drugs acting on CD20, EDC9 directly kills cells expressing high or low levels of CD20 and does this without harming other normal cells. In addition, EDC9 has depressed complement-directed cytotoxicity, which is expected to lessen the risk for certain infusion reactions (the main side effect observed with Rituximab). Studies in non-human primates show that EDC9 clears all detectable CD20 expressing cells without adverse effects. Currently EDC9 is in the manufacturing stage of development and expected to reach human testing in 2018.

Rituximab: Mechanism of Action