Superoxide Dismutase 1 (SOD1, Cu/Zn-SOD) is a cytoplasmic metalloenzyme that catalyzes the dismutation of superoxide radicals (O₂⁻) into oxygen and hydrogen peroxide — a critical first step in cellular antioxidant defense. SOD1 mutations are the most well-characterized genetic cause of familial amyotrophic lateral sclerosis (fALS), with over 200 disease-associated variants identified. Misfolded SOD1 aggregates are a pathological hallmark of ALS, making SOD1 a major therapeutic target.
abinScience offers a diverse SOD1 reagent panel — broad-reactivity polyclonal antibodies for human and mouse/rat, a VHH nanobody for enhanced epitope access, an InVivoMAb-grade antibody for in vivo neutralization studies, and recombinant SOD1 proteins.
Why abinScience?
✓ InVivoMAb grade — AP-101 clone — in vivo-ready for ALS preclinical studies (low endotoxin, azide-free)
✓ VHH nanobody — SAA1203 — small-format antibody for detecting intracellular SOD1 aggregates with superior penetration
✓ Broad reactivity polyclonal — Rabbit polyclonal reactive to human + multiple mammalian species
✓ Mouse/rat-specific option — Dedicated mouse/rat-reactive polyclonal for rodent ALS models
Available Products
Anti-SOD1 Antibodies
Multiple antibody formats — polyclonal, nanobody, and InVivoMAb — for diverse SOD1 research applications.
SOD1 Recombinant Proteins
Purified recombinant SOD1 proteins for enzyme activity assays, western blot positive controls, and immunization.
About the Target
Gene: SOD1 (also: Cu/Zn-SOD, ALS1, hSOD1)
UniProt: P00441 (Human)
Molecular weight: ~16 kDa (monomer); functions as a ~32 kDa homodimer
Enzymatic activity: 2 O₂⁻ + 2 H⁺ → O₂ + H₂O₂
SOD1 is one of three superoxide dismutase isoforms (SOD1 cytoplasmic, SOD2 mitochondrial, SOD3 extracellular). Each SOD1 subunit binds one copper and one zinc ion essential for catalytic activity. In ALS pathology, mutant SOD1 acquires a toxic gain-of-function independent of its enzymatic activity — misfolded SOD1 forms oligomers and aggregates that disrupt proteostasis, mitochondrial function, and axonal transport in motor neurons. The SOD1-G93A transgenic mouse is the most widely used ALS preclinical model.
Frequently Asked Questions
What is SOD1 and why is it important in ALS research?
SOD1 is a cytoplasmic antioxidant enzyme. Mutations in SOD1 cause approximately 20% of familial ALS cases and 1–2% of all ALS cases. Mutant SOD1 protein misfolds and aggregates in motor neurons, triggering neurodegeneration through mechanisms including ER stress, mitochondrial dysfunction, and impaired autophagy. Anti-SOD1 therapies (antisense oligonucleotides, antibodies) are active areas of clinical development.
What is the InVivoMAb anti-SOD1 antibody used for?
The AP-101 InVivoMAb is designed for systemic administration in animal studies to evaluate whether antibody-mediated clearance of misfolded SOD1 can slow disease progression in ALS mouse models (e.g., SOD1-G93A). The formulation is endotoxin-controlled and azide-free to minimize injection site reactions and confounding immune effects.
Why choose a nanobody for SOD1 detection?
SOD1 aggregates form dense intracellular inclusions that can be difficult for conventional 150 kDa IgG antibodies to fully penetrate. The ~15 kDa nanobody (SAA1203) can access epitopes within these compact structures more effectively, which is particularly valuable for immunohistochemical staining of motor neuron inclusions in ALS tissue sections.
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All products are for research use only (RUO). Not intended for diagnostic or therapeutic use. Product availability and specifications are subject to change. Visit individual product pages for the most current information.
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