Quote:In the recent tnbc case study of one survivor.
Tecentriq was began about one month before leron.
If the combo requires pdl1 upreg to some specific level, how did a patient with liver brain and lung mets become Ned if Tecentriq prevented upreg from the beginning ?
And why would a delay before adding ici be necessary. .
Also, do you think it will eventually matter if say a tnbc patient after leron reaches a cps > 10 to be eligible for ici
In that patient 5% PD-L1 expression existed prior to administration of leronlimab which is why Tecentriq was used. Tecentriq doesn't prevent the upregulation of PD-L1 it just stops it from binding to PD-1. After leronlimab use you would see an additional rise of PD-L1 due to the increase in active M1 macrophages. The usage of a PD-L1/PD-1 inhibitor after reaching a certain level is because in trials of those ICIs it has been shown that benefit is derived at or above those levels and there is little benefit below those levels.
What I think is that all patients should start with a 700mg dose to maximize response. In almost all patients this should result in a PD-L1 cps>5, but PD-L1 inhibitors are used at levels as low as cps>1 in some cancers. I think PD-L1 inhibitors should be used when cps levels are at the standard for usage in that specific cancer with that specific inhibitor. Np delay is necessary.
In locally recurrent unresectable or metastatic TNBC, Keytruda is used when PD-L1 is cps >10, but in high-risk early-stage TNBC testing for PD-L1 doesn't even have to be done. Which is quite odd.
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