The press is abuzz with speculation that bapineuzumab might yet have a shot at resurrection, based on subset analyses that showed a slight (9%) difference in amyloid plaque levels in bapi patients, whose levels had appeared to level off, compared to rising levels in placebo patients. There were also decreases in CSF levels of phosphorylated tau. Somewhat puzzling is the report that the researchers have not yet parsed out mild vs. moderate AD patients, critical to their premise that bapi had an effect on the biology of the disease, albeit too late. One would assume that JNJ/Pfizer had these analyses in hand before terminating the IV bapineuzumab program–after all, would a major pharma company make such a major decision based on incomplete data? Never mind, that’s already been established. But still, while these findings leave the door open for mAb approaches administered much earlier in the disease process, a door that had been widened even further by solanezumab, they do not point to a future for bapineuzumab itself. Setting aside the fact that these very modest plaque differences were not accompanied by any changes in cognitive function or brain atrophy, thus providing no hint of meaningful efficacy at this stage of the disease, the safety profile is not going to cut it. Fifteen percent of patients developed vasogenic edema, the rate of seizures was higher in the drug group, and while the incidence of cancer was apparently not flagged in a wider bapi population review, the six cases reported do not portend regulatory relaxation. The problem is that, the earlier one must intervene in a disease like AD, the wider the net must be cast in terms of patient inclusion, at least given the current state of prodromal diagnostics. This means throwing many millions of patients into the pool, and the rates of vasogenic edema or epileptogenesis then add up to some big numbers.
Saturday Night Live used to announce “Generalissimo Francisco Franco is Still Dead.” So is bapineuzumab.