| | | I’ve never figured out how or why the company decided to go after TROP-2 as a target, it was a commonly known antigen. It is so common on solid tumors that I wonder if most researchers simply thought it would be expressed on a lot of normal tissue and cause side effects. The early pre-clinical testing showed very good responses. Dr. Tom was especially impressed with what they were seeing and was the earliest “cheerleader” on this board on that target and the results.
There was a lot of information on TROP-2 way back then, but I couldn’t find any antibodies or clinical trials or significant patents, that kind of amazed me. I think when clinical trials started, the company itself may have been surprised at the lack of side effects. The efficacy really shouldn’t be much of a surprise since the antibody doesn’t have to have any real therapeutic value, it’s the payloads job to do that, it just has to keep that warhead away from normal tissue that would cause problems.
So to some degree, they got lucky with hRS7, much like IDEC did with CD20, but as Mr. Fitzhugh posted,they did develop a great linker to go with it and at least up to this point, the payload is doing a good job. That is not to suggest it can’t be improved, there is little doubt in my mind that it can be. It’s highly doubtful they found the best toxin on the first try, and there’s been little investigation, if any, into combinations or other toxins added to the linker.
There should be way more of the hRS7 story ahead of us than behind us. |
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