Thomas Hunig, the German professor who founded the company which invented TGN1412, has stated he hoped his drug would one day still have a place in an almost Strangelovian interview. The man’s well of optimism is titanic in nature.
“I do hope TGN1412 can come to the market. This tragic incident does not exclude the theoretical application of TGN1412 some time in the future.
“The company knows that the strategy deserves, in the end, to prevail.
“I don’t want to hurt anybody in any way. I don’t want to come across as a crazy scientist who wants to save his baby despite the victims he has taken. Definitely not.”
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“I owe this not only to myself but also to the many excellent students and colleagues who have done fantastic science.“At the danger of sounding pathetic, I feel I owe it to the poor guys who have suffered in the TGN1412 trials.”
His last sentence, does at least show some insight. As Derek Lowe says about this story:
Let me be one of the voices informing Prof. Hunig: there is an almost overwhelming likelihood that his drug will never again come near a human being, much less near the market. Pharmaceutical companies drop compounds all the time that show far less severe side effects than this in rats – a disaster like this in man is the end of the line. That’s not to say that the whole idea of a CD28-derived drug is dead (although it’s going to be slow going after this), but TGN1412 is not going to be it. Go look for a clinical supervisory board – outside of North Korea, that is – that would allow another dosing in humans. Good luck.
[...]
I feel like the guy in the Monty Python sketch: Dr. Hunig, your drug has ceased to be.
One Comment
Has anyone seen any experimental or theoretical evidence as to the affinity of TGN1412 for mouse, monkey and human CD28 yet? There is good evidence that this is highly relevant to any pre-clinical animal dosing ( http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12707299 ) but I haven’t heard a thing about it. You’d have thought, really, that some of their animal studies should have been on transgenic animals with humanised epitopes.
Is this a case of traditional drug licensing procedures being slavishly followed despite good theoretical reasons to suspect that more specific tests were needed? It certainly reminds me of the Elan & Wyeth beta-amyloid immunisation study for Alzheimer’s disease, where, again, there were good reasons to suspect the animal testing regime was inadequate for that particular therapeutic approach.