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Creative Biolabs

NeuroMab™ Anti-SOD1 BBB Shuttle Antibody(NRZP-1022-ZP2567)

[CAT#: NRZP-1022-ZP2567]

Host Species:
Human
Species Reactivity:
Human
Applications:
ELISA; FC; IHC; In Vitro; In Vivo

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Product Overview

Description

Brain uptake of therapeutic antibodies is severely limited by their size. To achieve enhanced BBB crossing, Creative Biolabs developed a BBB shuttle antibody platform by utilizing the endogenous macromolecule transportation pathway, known as receptor-mediated transcytosis (RMT). The engineered antibody-based carrier is believed to significantly to increase the macromolecule brain entry to combat CNS diseases.
Notes: The BBB antibody is made-to order and available in a customized format. Please don't hesitate contact us for more details.

Species Reactivity

Human

Clonality

Monoclonal

Host Species

Human

Applications

ELISA; FC; IHC; In Vitro; In Vivo

Relevant Diseases

Amyotrophic Lateral Sclerosis
Product Properties

Storage

Store at -20°C. Do not aliquot the antibody.

Research Use Only

For research use only
Target

Target

SOD1

Official Name

SOD1

Full Name

superoxide dismutase 1

Alternative Names

SOD1; ALS; ALS1; HEL-S-44; IPOA; SOD; hSod1; homodimer; superoxide dismutase 1; soluble; superoxide dismutase 1; STAHP
Product Pictures
ELISA

Fig.1 binding specificity of the human antibodies to human recombinant SOD1.

h3D6v2 was as effective as chimeric 3D6 in inducing phagocytosis of Aβ aggregates from PDAPP mouse brain tissue. IgG was used as a negative control in this experiment because it is unable to bind Aβ and therefore cannot induce phagocytosis.

ELISA

Fig.3 The antibody binds preferentially to misfolded / aggregated human SOD1.

h3D6v2 was as effective as chimeric 3D6 in inducing phagocytosis of Aβ aggregates from PDAPP mouse brain tissue. IgG was used as a negative control in this experiment because it is unable to bind Aβ and therefore cannot induce phagocytosis.

ELISA

Fig.2 binding specificity of the human antibodies to human recombinant SOD1.

h3D6v2 was as effective as chimeric 3D6 in inducing phagocytosis of Aβ aggregates from PDAPP mouse brain tissue. IgG was used as a negative control in this experiment because it is unable to bind Aβ and therefore cannot induce phagocytosis.

IHC

Fig.4 NI-204.10D12 primarily shows SOD1 pathology as well as diffuse staining of intracellular dispersed inclusion bodies.

h3D6v2 was as effective as chimeric 3D6 in inducing phagocytosis of Aβ aggregates from PDAPP mouse brain tissue. IgG was used as a negative control in this experiment because it is unable to bind Aβ and therefore cannot induce phagocytosis.

FuncS

Fig.5 NI-204.10D12 treatment can protect against motor neuron degeneration mediated by mutant SOD-1 overexpression.

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