Good question, and I used to think the same. If a drug shows no toxicity in mice and small animals shouldn't it be the same in humans. If it shows efficacy in animals shouldn't it do the same in humans?
The biggest problem for the animal/human equivalence model is simply the liver. Although livers are livers whether human or animal, how the liver interacts with a drug has great variation from species to species. A drug that shows low liver toxicity in test animals may actually kill a human liver. Likewise the same for kidneys and other parts of the renal system. So, human tox studies in phase 1, dosing and tolerance, are a critical part of testing whether the anticipated reaction from animal models holds true for humans.
The second major issue is interaction with the immune system. Again, mice and humans may react differently. Immunal responses in humans may be different. A drug may cause an immunal storm in a human that is not or cannot be detected in mice. Even more, immunal reaction can manifest in ways that mice show no signs. After all, mice can't speak to tell lab workers that the drug just gave them crippling migraine-like headaches.
The third, but probably least issue, is genotoxicity. So far there have been no signs in animals, in particular in the human xenografts. But, although I don't think this will happen, if Kevetrin showed signs of genetic damage in humans that was not present in animals, it would not be one of the first hundred times.
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