Reposting this here:
The discussion should not be "what are the odds Zan's cardioprotective properties will be replicated from the lab and in the clinic?". The discussion should be "what are the odds the complete absence of cardiotoxicity observed at Sheba 2.0 was not a result of Zan's cardioprotective properties?".
15 evaluable patients, no observed cardiotoxicity, despite 4 patients (26%) experiencing elevated troponin levels. Even a slight increase in the troponin level will often mean there has been some damage to the heart.
Coincidentally, 24-27% of Clofarabine patients experience cardiotoxicity (LV dysfunction) - https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8352330/
One might conclude that the cardiotoxic effect of Clofarabine was experienced by 26% of patients at Sheba 2.0. Fortunately, Clofarabine was also dosed with a drug that, albeit preclinically, has been shown to protect heart cells from damage by multiple anticancer agents...
Again, what are the odds the complete absence of cardiotoxicity observed at Sheba 2.0 was not a result of Zan's cardioprotective properties?
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