Mouse Anti-APP Recombinant Antibody (clone PFA1) (CAT#: PABW-009)

Figure 1 SPR reveals Aβ peptide binding to PFA1 via the EFRHD epitope.

(a) Kinetic analysis of Aβ(1–40) (WT) monomer at 0, 1.23, 3.70, 11.1, 33.3, 100, and 300 nM, binding to PFA1 Fab immobilized at densities of 2,720 response units (RU) (shown) and 1,280 RU (data not shown). Duplicate binding responses for each monomer concentration are overlaid with the global fit of a simple 1:1 interaction model (smooth lines), which yielded k a = (1.431 ± 0.003) × 104 M−1 s−1, k d = (5.58 ± 0.01) × 10−4 s−1, and K d = 39.0 ± 0.1 nM. (b) WT and Ala-substituted mutants of Aβ(1–40) monomers were sequentially flowed over PFA1 IgG captured on anti-IgG flow cell surfaces (SPR). Significant RU peaks show good peptide binding, whereas the absence of a peak shows no binding. Results from PFA2 were essentially identical. The D7A mutation limits but does not completely eliminate binding. The numbering scheme is Aβ(1–40)-specific.

Gardberg, A. S., Dice, L. T., Ou, S., Rich, R. L., Helmbrecht, E., Ko, J., ... & Dealwis, C. (2007). Molecular basis for passive immunotherapy of Alzheimer's disease. Proceedings of the National Academy of Sciences, 104(40), 15659-15664.

Figure 2 Plasma Aβ is decreased in 22 month old PFA1 treated female mice and increased in 22 month old PFA1 treated male mice.

A. Aβ1-40 levels were measured from plasma collected from vehicle and PFA1 treated female mice before and after 4 weeks of treatment. There was no significant change in plasma Aβ1-40 levels following treatment in vehicle treated animals. There was a significant 44% decrease (p < 0.01) in plasma Aβ1-40 levels following PFA1 treatment. B. Aβ1-42 levels were measured from plasma collected from vehicle and PFA1 treated female mice before and after treatment. There were no significant changes to Aβ1-42 in either the vehicle or PFA1 group following treatment. C. Aβ1-40 levels were measured from plasma collected from vehicle and PFA1 treated male mice before and after 4 weeks of treatment. There was no significant change in plasma Aβ1-40 levels following treatment in vehicle treated male mice. There was a significant 128% increase (p < 0.05) in Aβ1-40 levels following treatment in the PFA1 treated male mice. D. Aβ1-42 levels were measured from plasma collected from male mice before and after vehicle or PFA1 treatment. There were no significant changes to Aβ1-42 levels following treatment in either vehicle or PFA1 group.

Minami, S. S., Sidahmed, E., Aid, S., Shimoji, M., Niikura, T., Mocchetti, I., ... & Bosetti, F. (2010). Therapeutic versus neuroinflammatory effects of passive immunization is dependent on Aβ/amyloid burden in a transgenic mouse model of Alzheimer's disease. Journal of neuroinflammation, 7(1), 57.

Figure 3 The protofibril monoclonal antibody PFA1 recognizes multiple Aβ species.

5 μL of serum (S) and 10 μg of soluble protein extract from brains (B) of 22 month old AD 3 × tg mice were immunoblotted for Aβ with antibody PFA1 (left) or 6E10 (right). 1 μM synthetic Aβ40 and Aβ42 (right lanes) were loaded for comparison. Membranes were cut at 15 kDa to subject the lower panels to a longer exposure for detection purposes. PFA1 detected the 56 kDa oligomeric form of Aβ from serum with high affinity, similar to 6E10.

Minami, S. S., Sidahmed, E., Aid, S., Shimoji, M., Niikura, T., Mocchetti, I., ... & Bosetti, F. (2010). Therapeutic versus neuroinflammatory effects of passive immunization is dependent on Aβ/amyloid burden in a transgenic mouse model of Alzheimer's disease. Journal of neuroinflammation, 7(1), 57.