Hi James, I like rumors like that (Lidakol works less well than plain vasoline). Disasters in clinical trials are a favorate of mine to look into. The reasons for the less than wonderful outcome of the phase 3 trials with lidakol seem credible to me. Assuming that there was no funny business in the trials (and I assume there was not since the trials were not what lidak would want), there is real resons to believe that the placebo was very active.
First, the natural course of the oral herpes infection was definitely shortened. In these patients, I am told that the study checked outbreaks before and after the medication or placebo. Outbreaks were the typical 7-10 days. With the drug (and placebo), outbreaks dropped to ?less than 5 days, with much less pain and severity.
Second, the placebo is very similar to the active drug. I read somewhere that the FDA was backing off insisting on very similar chemical profils for placebos because of unexpected activity (was this because of lidakol?).
Third, lidakol was much better than the placebo for pain reduction and prevention of outbreaks than the placebo. (I think prevention was around 75% or 80%......without the drug, an episode resolved spontaneously in only 13%). This is from memory, a while back I posted a long wordy post that goes into this stuff, the numbers are hopefully more accurate than these here.
I still find this an interesting speculation with a potential very high upside. I think that antisense tech. may eventually be better, but I really doubt that the FDA will allow messing with DNA and RNA for oral herpes until antisense side-effects can be assessed.
I knew that 4 partners was Tisch, but I did not know it was the rugrats. |
