Your "conclusion" is a total non sequitur. (in no way whatsoever follows from the statement actually made.)
You said: "Since phase II trials are the first tests of efficacy of a drug in humans, you are implying that the FDA will approve a drug on the basis of a compelling study in animals."
I made no such implication in any way, shape or form whatsoever!
It is totally dishonest to add something that was never said to a statement and the attack it on the basis of what YOU added to it. And nothing that was said or quoted in any way whatsoever implied that the FDA would approve a drug under any circumstances whatsoever (much less "a single compelling study" IN ANIMALS.
1) NO ONE has ever said nor implied that the FDA would approve a drug on the basis of a compelling study in animals"!
I provided a quote BY THE FDA that stated it had approved drugs "on the basis of a single compelling study." NO mention of ANIMALS whatsoever (that is entirely a product of your fertile imagination) The context (and the ENTIRE PAGE was posted so all the context was there) was ALL about clinical trials. Last time I checked, clinical trials were done only in humans.
Phase II's are *usually* the earliest that efficacy can be demonstrated. But IF a drug has both very low toxicity AND very high efficacy, statistical standards for efficacy could be made in Phaase I if the number of patients is sufficient.
Ask anyone knowledgeable about statitics: if, for example, something had an efficacy that was 10% or less above placebo and that only in 20% of patients, it would take tests at full therapeutic dose in many hundreds of patients to establish efficacy with a 0.05 standard (i.e.: the results have a 5% or less probability of being due to chance. The reason that clinical trials are so large is that the intent is to be able to demonstrate efficacy even if it is only slightly above placebo or untreated patients (or current standard of therapy) in only a percentage of patients.
But if, for example 9 or 10 out of a mere 10 patients had an effect much stonger than placebo/etc [for example they all rapidly recovered with no ill effects while the condition was 50% fatal or just that 50% had very serious illnesses, then efficacy would be demonstrated far above the 0.05 confidence level DESPITE the low number of patients and DESPITE that the Phase one may not have been designed to show efficacy.
Phase III's are designed to show efficacy even in drugs with very low efficacy and even when effective in only subsets of the patient population (and much of the Phase II's are aimed at identifying any subpopulations in which the drug is more effective to be able to select a subpopulation for Phase III with the best chance of success.
But when Efficacy is very high (and it does not get any higher than 100% survival of a dose that killed 100% of animals treated with the standard of care!) AND in all, or close to all patients, the statistical standard for efficacy can be met with a very small number of patients WITHOUT having selected a subpopulation most susceptible to benefits.
It is extremely unusual. But so is a drug that is close to 100% effective in close to 100% of all patients. Again IF the drug does as well in humans as in the animal studies done to date, early approval is possible.
ALSO CRITICAL TO NOTE HERE is the additional very unusual exception that the animal data are highly likely to be much more representative of the effects in humans because the drug operates without any interaction with the host*1. The notorious deviations between animal studies and humans results from differences between the way the drug is handled by human biochemmical pathways and the animals biochemical pathways. BUT THAT DOESN'T APPPLY HERE because the drug;s operative mechanism does not involve any interaction with the host's biochemical pathways at all. (and the excretion/breakdown products are either very inherently non toxic or (PEG) already extensively used in drugs and foods for many years already (GRAS).
I would submit that when you find your CONCLUSIONS and DEDUCTIONS "very, very hard to believe" it would be wise to consider the possibility that maybe the problem is that your conclusion was a non sequiter (i.e.: did NOT follow from the statement/ bad logic, etc)
*1 except for the very indirect effect of competitive inhibition which is very unlikely to be significant because there are regulatory mechanisms for ligands that would almost certainly increase the number of ligands to compenstate for the number attached to the nanoviricides (already discussed here before).
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