How do your engineered cell models compare to using primary astrocytes for NMOSD research?

While primary astrocytes offer high physiological relevance, they often suffer from limited availability, donor-to-donor variability, and a finite lifespan, making reproducible, long-term studies challenging. Our engineered monoclonal cell lines provide a stable, unlimited, and highly consistent platform, ensuring your results are reproducible. For ultimate relevance, we also offer services using genetically modified primary cells.

Can you create a cell line with a specific, non-wild-type AQP4 mutation that we are studying?

Yes, absolutely. Our custom services specialize in this. We can engineer cell lines with specific point mutations, deletions, or tagged versions of AQP4 to meet your precise research needs. Please contact us to discuss your project.

Why are cell models critical for NMOSD research?

Cell models provide a controlled, human-relevant system to dissect the complex cellular and molecular events of the disease, such as complement activation and bystander cytotoxicity, which can be difficult to study in animal models alone. They are essential for screening new drugs and understanding their mechanisms of action.

Can I use my own therapeutic antibody in your models?

Absolutely. Our platforms are designed to test the efficacy of client-provided antibodies, small molecules, or other therapeutic modalities.

How do these models differ from animal models?

While animal models are crucial for studying systemic effects, our cell models offer a human-specific context, allow for higher-throughput screening, and provide a more controlled environment to dissect specific molecular pathways without confounding systemic variables.

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Neuromyelitis Optica Spectrum Disorder (NMOSD) Cell Model Products

Introduction Types Advantages Applications FAQs Related Product Sections Product List

Introduction

Neuromyelitis Optica Spectrum Disorder (NMOSD) is a severe autoimmune disease where progress in therapeutic development depends on models that accurately recapitulate its core pathology. Now understood as an "autoimmune astrocytopathy", NMOSD is primarily driven by pathogenic AQP4-IgG autoantibodies that trigger a devastating attack on astrocytes in the central nervous system.

At Creative Biolabs, we have engineered a suite of sophisticated, cell-based NMOSD models that replicate the key pathogenic events, from antibody binding and complement activation to downstream cytotoxicity and bystander neuronal injury. Reach out to our specialists to discuss your NMOSD research program and for a custom project quote.

Alternatively, specific offerings can be found by directly consulting our comprehensive Product List.

Types

We offer a portfolio of models that can be customized to your needs:

Types	Description
Astrocyte Monoculture Models	The foundational model to study direct, AQP4-IgG-mediated astrocyte injury and the efficacy of cytoprotective agents.
Astrocyte-Oligodendrocyte Co-culture Models	Specifically designed to investigate complement-mediated bystander demyelination and the efficacy of therapies aimed at protecting oligodendrocytes.
Astrocyte-Neuron Co-culture Models	The ideal platform for studying bystander neuronal loss and assessing neuroprotective therapeutic strategies.
Tri-Culture (Astrocyte-Oligodendrocyte-Neuron) Models	A comprehensive system for evaluating drug effects across multiple relevant cell types simultaneously.
Immune Cell Add-on Models	Recreate the inflammatory microenvironment by adding peripheral immune cells (e.g., NK cells, neutrophils) to model ADCC and cellular infiltration.

Advantages

Choosing our NMOSD cell models provides a distinct advantage for your drug discovery and development pipeline:

Uncover True Disease Mechanisms

Go beyond simple binding assays. Our models allow you to dissect the precise contributions of CDC, ADCC, and bystander damage in a controlled environment.

Accelerate Therapeutic Screening

Rapidly evaluate the efficacy of novel complement inhibitors, B-cell depleting agents, IL-6 receptor blockers, and other emerging therapeutic strategies.

Increase Predictive Power

Using human cell-based systems that mirror the in vivo environment reduces the risk of failure in later preclinical and clinical stages.

Ensure Data Integrity

Our highly standardized and validated models deliver reproducible results, minimizing variability and strengthening your data package.

Access Unmatched Expertise

Leverage our team's deep understanding of NMOSD pathophysiology to design the ideal experimental setup for your specific research question.

Applications

Our NMOSD models are perfectly suited for a wide range of research and preclinical applications:

Types	Description
Compound Screening	Efficacy testing for small molecules and biologics aimed at blocking key pathogenic steps.
Therapeutic Antibody Evaluation	Assess the potential of antibodies designed to inhibit AQP4-IgG binding, block complement activation (e.g., anti-C1q, anti-C5), or deplete pathogenic B cells.
Mechanism of Action (MoA) Studies	Elucidate how your lead candidate interferes with the disease process, be it through preventing MAC formation, reducing inflammatory cell recruitment, or protecting astrocytes from injury.
Neuroprotection Studies	Investigate compounds designed to protect oligodendrocytes and neurons from the toxic bystander effects prominent in NMOSD lesions.
Biomarker Discovery	Identify and validate novel biomarkers associated with astrocyte injury, inflammation, or therapeutic response in a human-centric system.

A picture that presents the NMOSD Pathophysiologic mechanisms and therapeutic targets for approved and experimental treatment options. (Carnero Contentti, et al., 2021) (OA Literature)

Fig.1 Pathophysiologic mechanisms and therapeutic targets for approved and experimental treatment options in NMOSD.¹

FAQs

How do your engineered cell models compare to using primary astrocytes for NMOSD research?
While primary astrocytes offer high physiological relevance, they often suffer from limited availability, donor-to-donor variability, and a finite lifespan, making reproducible, long-term studies challenging. Our engineered monoclonal cell lines provide a stable, unlimited, and highly consistent platform, ensuring your results are reproducible. For ultimate relevance, we also offer services using genetically modified primary cells.
Can you create a cell line with a specific, non-wild-type AQP4 mutation that we are studying?
Yes, absolutely. Our custom services specialize in this. We can engineer cell lines with specific point mutations, deletions, or tagged versions of AQP4 to meet your precise research needs. Please contact us to discuss your project.
Why are cell models critical for NMOSD research?
Cell models provide a controlled, human-relevant system to dissect the complex cellular and molecular events of the disease, such as complement activation and bystander cytotoxicity, which can be difficult to study in animal models alone. They are essential for screening new drugs and understanding their mechanisms of action.
Can I use my own therapeutic antibody in your models?
Absolutely. Our platforms are designed to test the efficacy of client-provided antibodies, small molecules, or other therapeutic modalities.
How do these models differ from animal models?
While animal models are crucial for studying systemic effects, our cell models offer a human-specific context, allow for higher-throughput screening, and provide a more controlled environment to dissect specific molecular pathways without confounding systemic variables.

Creative Biolabs offers the sophisticated platforms and profound expertise that are essential for investigating the intricate pathophysiology of NMOSD. Our validated, pathologically relevant cell models empower you to screen and characterize novel therapeutics with confidence, accelerating your journey from discovery to clinical application. Contact us for a consultation on how our state-of-the-art NMOSD cell systems can provide your research with a significant advantage and streamline your preclinical studies.