Table 1.

Shows a summary of the design and main findings of included studies

Study ID	Study Design	Population	Sample size in each group		Finding
			Bapineuzumab	Placebo
Salloway et al., 2009 [13]	- Phase II, randomized in a ratio of 8:7, double- blinded. - Patients received 6 infusions of bapineuzumab or placebo, 13 weeks apart. Final assessment occurred at 78 weeks.	• Patients aged from 50 to 85 years. • Met criteria for AD and had MRI findings, consistent with AD. • Mini-Mental State Examination (MMSE) score of 16 to 26. • Rosen Modified Hachinski Ischemic score < 4. • Participants were excluded from the study if they had a clinically significant neurological (other than AD) or systemic disease.	124 patients were allocated in 1 of 4 sequential dose cohorts (0.15, 0.5, 1.0, or 2.0 mg/kg).	110 patients were allocated to Placebo group.	No significant treatment differences were found in the primary efficacy analysis. However, exploratory analyses showed potential differences on cognitive and functional outcomes in study completers and APOE- 4 non-carriers.
Salloway et al., 2014 (Carriers) [16]	- Phase IIIa, randomized in a ratio of 3:2, double blinded. - Patients received 6 infusions of bapineuzumab or placebo, 13 weeks apart. Final assessment occurred at 78 weeks.	• Patients aged from 50 to 88 years. • Met criteria for AD and had MRI findings, consistent with AD. • Carriers of the apolipoprotein E (APOE) ε4 allele • Mini–Mental State Examination (MMSE) of 16 to 26. • Score on the Hachinski Ischemic scale of 4 or lower. • Participants were excluded from the study if they had a clinically significant neurological (other than AD) or systemic disease.	658 patients were allocated to bapineuzumab 0.5 mg per kg group.	432 patients were allocated to placebo group.	No differences between bapineuzumab and placebo in terms of change from baseline in the ADAS-cog11 and DAD scores (P = 0.80 and 0.34 respectively). Therefore, Bapineuzumab did not improve the clinical outcomes in AD patients.
Salloway et al., 2014 (Non-carriers) [16]	- Phase IIIb, randomized 3:3:4, double blinded. - Patients received 6 infusions of bapineuzumab or placebo, 13 weeks apart. Final assessment occurred at 78 weeks.	• Patients aged from 50 to 88 years. • Met criteria for AD and had MRI findings, consistent with AD. • Non-Carriers of the apolipoprotein E (APOE) ε4 allele • Mini–Mental State Examination (MMSE) of 16 to 26. • Score on the Hachinski Ischemic scale of 4 or lower. • Participants were excluded from the study if they had a clinically significant neurological (other than AD) or systemic disease.	621 patients were allocated to bapineuzumab groups. - Bapineuzumab 0.5 mg per kg: 337 - Bapineuzumab 1.0 mg per kg: 307	524 patients were allocated to placebo group.	No differences were found between bapineuzumab (Both doses) and placebo groups in terms of change from baseline in the ADAS-cog11 and DAD scores (P = 0.64 and 0.07 respectively). Therefore, bapineuzumab did not improve the clinical outcomes in patients with AD.
Black et al., 2010 [15]	- Phase II, randomized, third-party unblinded. - Patients received bapineuzumab or placebo with dose escalation every 10 weeks. Final assessment occurred at 52 weeks.	• Patients aged from 50 to 88 years. • Met criteria for AD and had MRI findings, consistent with AD. • Mini-Mental State Examination (MMSE) score of 14 to 26. • Rosen Modified Hachinski Ischemic score ≤ 4. • Participants were excluded from the study if they had a clinically significant neurological (other than AD) or systemic disease.	22 patients were allocated to bapineuzumab groups. - Bapineuzumab 0.5 mg/kg: 6 - Bapineuzumab 1.5 mg/kg: 6 - Bapineuzumab 5 mg/kg: 10	8 patients were allocated to placebo group.	MMSE scores improved at lower doses of bapineuzumab (0.5 and 1.5 mg/kg) compared to placebo, but not with the highest dose (5 mg/kg). Moreover, The 5 mg/kg dose was significantly associated with MRI amyloid abnormalities that resolved over time.
Arai et al., 2015 [17]	- Phase I, randomized, double- blinded. - Patients received one infusion of the study drug or placebo. Final assessment occurred at 52 weeks.	• Patients aged from 50 to 85 years. • Met criteria for AD and had MRI findings, consistent with AD. • Mini-Mental State Examination (MMSE) score of 14 to 26. • Rosen Modified Hachinski Ischemic score ≤ 4. • Participants were excluded from the study if they had a clinically significant neurological (other than AD) or systemic disease.	24 patients were equally allocated to 4 dose cohorts (0.15, 0.5, 1, or 2 mg/kg).	8 patients were allocated to placebo group.	Plasma β-amyloid levels increased with increasing doses of bapineuzumab. Bapineuzumab was well tolerated at all doses in Japanese patients with mild to moderate AD.
Rinne et al., 2010 [14]	- Phase II, randomized, double- blinded. - Patients received 6 infusions of bapineuzumab or placebo, 13 weeks apart. Final assessment occurred at 78 weeks.	• Patients aged from 50 to 85 years. • Met criteria for AD and had MRI findings, consistent with AD. • Mini-Mental State Examination (MMSE) score of 18 to 26. • Rosen Modified Hachinski Ischemic score ≤ 4. • Participants had amyloid-B loads in the range expected for patients with Alzheimer’s disease, defined as 11C–PiB PET retention ratios relative to the cerebellum of 1 to 5 or more in at least three brain regions among the anterior cingulate, posterior cingulate, frontal, temporal, and parietal cortices. • Participants were excluded from the study if they had a clinically significant neurological (other than AD) or systemic disease.	19 patients were allocated to 1 of 3 sequential dose cohorts (0.5, 1.0, 2.0 mg/kg).	7 patients were allocated to placebo group.	Treatment with bapineuzumab for 78 weeks reduced cortical carbon-11-labelled Pittsburgh compound B (C-PiB) retention, compared to placebo. Adverse events were typically mild to moderate in severity and transient in duration.