The biomarker data are essential for TAVO's development. When you look at the IL-12 monotherapy data, it is interesting that Natural Killer cells, the innate immune response, is more immediately responsive to intratumoral administration of EP TAVO than adaptive immunity. The adaptive immune response, I believe, takes time to reach critical density in the TME.
I would like to know more about the FOXP3 densities and proximities to CD8 observed. In case you haven't noticed, I am a firm believer that CTLA-4 on the FOXP3 Tregs are preventing T cell activation.
Would TAVO be more successful if it could be expressed more productively in the TME or TDL? Is tissue heterogeneity preventing adequate expression of IL-12? Would improvements to the plasmid construct lead to better expression, thus improvements in NK cell activation/expansion and FLT3L production? If so, then a program solely focused on improving IL-12 expression would make complete sense.
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