Before seeing the SAE and AE data, I was above 60:40 for the m/m trial meeting its primary endpoint. Now I'm way above. It took me a lot of reading and cogitation, but I think the m/m trial is going to be easier to show an effect in than the s/c trial will be. In a nutshell, it is probably easier to prevent the cytokine storm in the first place than to reverse it.
It doesn't take disease progression in very many placebo patients to make a clear separation from the leronlimab patients. They almost did it with crude binomial counts of SAEs and AEs. Two key differences in the clinical score are 1) the quantitative measure allows greater separation than a binomial 0-1, and 2) many AEs happen early--before full CCR5 occupancy with leronlimab--and the leronlimab patients will recover from their SAEs and AEs better than the placebo patients will recover from theirs. These two extra boosts to the separation between the treatment arms will drive that p-value down quite a bit from the 0.06 and 0.08 for the SAEs and AEs (resp).
The s/c trials are binomial, so there is very little information in each data point. Sample sizes need to be large to show differences. Leronlimab will need to have about 50% reduction in mortality (depending on what the ultimate sample sizes and mortality rates are) to show significant effect. It could easily happen. I'm about 60:40.
But who knows! This is only a guess.
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