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Nelfinavir Cross Resistance.
Sep 16, 1997

You have stated that first line therapy with Viracept's unique mutation pattern is an argument that has not been proven. I have read abstact I-204 for the upcoming ICAAC in Sept. Agouron will present data showing that at least 9 patients who failed Viracept, 7 of the nine (78%) were re-treated with 2 nucleosides plus Norvir and Invirase fell below detectable levels. I know you have recommended this 2 PI therapy before when resistance develops to a PI. I am more convinced than ever that my decision to start with Viracept, was the best decision, especially when I see my friends and what Crixivan has done to them. Although, I am sure w/o Crixivan they would be dead. I believe you should recommend the best treatment and answer questions about treatment w/o regard to any alliance you may have with Abbot Labs.

Response from Dr. Cohen

Let me first address the insulting implications of your last sentence. While I have participated in clinical trials and given lectures sponsored by Abbott, I have done the same with Agouron, the manufacturer of Viracept and Merck, the manufacturer of Crixivan. Although my opinions and recommendations change frequently with the accumulation of new data, they do not change based on "alliances" with drug companies.

Furthermore, I don't know why you imply that I object to using nelfinavir (Viracept) as first line therapy. I have frequently stated that my first choice for protease inhibitor therapy usually involves EITHER ritonavir/saquinavir OR nelfinavir (Viracept).

I cannot be expected to be familiar with data that have not been presented yet. I will be attending the ICAAC conference and will be paying close attention to studies that deal with drug resistance, including the one you refer to. In the meantime, let me repeat what I've said on many previous occasions regarding protease inhibitor resistance. I expect that these generalizations will still be true after the Toronto meeting:

There is extensive cross-resistance between protease inhibitors. Cross-resistance between protease inhibitors cannot be reliably predicted based on genotype information (the presence of resistance mutations). Because of #2, the utility of protease inhibitor regimens as "salvage therapy" after other protease inhibitor regimens have failed needs to be tested clinically. So far, the clinical data are sparse.

Regarding Viracept, I stand by what I've said: it has not been conclusively demonstrated that using it first will leave open more treatment options than with other agents. On the other hand it hasn't been disproved, either, and genotype evidence, imperfect as is it, would suggest that Viracept resistant virus may be easier to treat than virus resistant to some other protease inhibitors.

It is my feeling that we still don't know enough yet about cross-resistance among protease inhibitors to allow us to choose one regimen over another strictly on that basis alone. HOWEVER, there are other reasons that one might choose Viracept as the initial protease inhibitor, since it is effective and represents a nice balance in terms of convenience and tolerability.

I have no problem at all with your selection of Viracept as initial therapy, and am glad you're happy with it.

What's a "snack" with Viracept?

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