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Biotech / Medical : IDPH--Positive preliminary results for pivotal trial of ID
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To: A.J. Mullen who wrote (1612)10/30/1998 12:33:00 AM
From: Webhead  Read Replies (2) of 1762
 
I ran a quick literature search to try and find out how Rituxan actually kills the lymphoma cells. All I found was that some cells die by complement activation (where the immune system attacks and causes the rupture of the target cell) and others by other means. In other words, not very informative! Perhaps someone more familiar with Rituxan's mode of action could chime in here. I think that Rituxan is the only monoclonal antibody that attacks cancer cells on its own (i.e. without conjugated radioactivity or toxin) so not much may be available outside of the company. Perhaps buried in the patent?

Anyway, I don't think that prior Rituxan treatment will prevent binding of the Yt labeled antibody because by the time the radioactive treatment begins, plenty of time has elapsed for new CD20 to be on the cell surface. Most receptors are removed from the cell surface within minutes to a few hours after binding to their ligand (though I don't know the specifics for cd20) so you would only end up blocking an infinitesimal number of possible binding sites. The really interesting question is WHY does Rituxan treatment fail in some people? Are there lymphoma cells that don't express cd20 or a mutated cd20 or are the cells resistant to Rituxan killing even though the antibody is bound? I am very interested in the clinical trials involving a combination of Rituxan and chemotherapy because there may be some useful synergies there that will end up helping a lot more folks.

Ed
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