Targeting Talk: Antagonists vs. Targeted Toxins

Recently, I attended a talk where the speaker said that a targeted toxin was able to work when an antagonist did not. Can you explain how your technology is different?

Certainly. It is a very interesting question and one that helps explain the Targeting Technology quite well. An antagonist is used to block a receptor on a cell to keep it from binding a target molecule and activating the cell. For example, a substance P antagonist binds to the substance P (NK-1) receptor. The hypothesis was that if the antagonist binds to the receptor, substance P cannot bind and the cell will not be activated. The reality is that there are other receptors besides the substance P receptor on that cell. If any of these other receptors bind to their target molecules, then the cell will still be activated.

It sometimes is not enough to block one particular receptor. The ATS targeting technology (molecular surgery) can use any of these cell surface receptors to target and completely eliminate the cell. That way, there are no receptors left to bind; no cell left to be activated. Importantly, molecular surgery cleanly removes one particular cell type and does not damage bystander cells. Once the debris from the targeted cell is cleared away, there is nothing remaining to interfere or affect the normal action/interaction of other cells.