4 biggest reasons why bapineuzumab might fail
1) treating to late. recent literature suggest that 70% of neurons are dead by the time a patient is diagnised with mild to moderate AD. By the way, same literature also says 45% of neurons are dead by the time a patient has MCI or prodromal: Aysmptomatic (like the genentech crenenzumab trial in columbia) is the way to go.
2) ph 2 was a fluke. In the phase 2 post-hoc results, the non-carrier PBO arm did worse than any mild to moderate PBO in any of the past large ph 3 trials. the carrier active arm and non-carrier active arm performed almost the same, but the PBO in non-carrier made the difference
3) patient population selection. Also, in a slew of literature over the past 3-5 years, 30-40% of pateints diagnosed with AD , were deemed not to have AD upon autopsy. Biomarkers are needed for patient selection and they were not used in the bapi trials
4) amyloid hypothesis is false.
having said this, i think it has a better chance than solanezumab as solanezumab does not target all forms of ABETA. solanezumab also doesn't have many cases of vasogenic edema., which i think is a positive for bapineuzumab
I think bapineuzumab works and will work in asymptomatic patients with AD pathology. the question is whether JnJ and PFE will continue to invest if the current trials fail. if not, my attention would turn to gantenerumab (roche) and crenezumab (Genentech) and maybe the merck bace molecule
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