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Creative Biolabs

Tau Clearance Assay Service

Our innovative in vitro tau clearance assay provides researchers with a reliable and efficient method to quantify tau protein removal. This assay is designed for ease of use and high throughput, allowing for rapid screening of potential therapeutic compounds and a deeper understanding of tau clearance mechanisms. For further information regarding the products and services provided, project-specific consultation, and pricing, please submit an inquiry here.

Mechanism of Tau Protein Clearance

Tau protein is mainly cleared by the following pathways:

Alzheimer's disease-related disruption of tau degradation. (Chesser, et al., 2013)

  • Lysosomal degradation: Tau protein can enter lysosomes by endocytosis and then be degraded by hydrolases.
  • Immune-mediated clearance: Antibodies can recognize and bind to tau protein, which is then cleared by the immune system.
  • Phagocytosis by astrocytes and microglia: Astrocytes and microglia can engulf and degrade extracellular tau protein, a process that is particularly important in the pathology of Alzheimer's disease (AD).
  • Peripheral pathway: Tau protein produced in the brain can cross the blood-brain barrier (BBB) into the peripheral circulation and be cleared by the

Tau Clearance Assays at Creative Biolabs

  • Multi-dimensional Model Validation

Unlock the complexities of tau clearance with our advanced neuronal cell culture models. We offer both primary neuronal cells and human iPSC-derived neurons, providing researchers with versatile tools to investigate tau degradation pathways, screen potential therapeutics, and gain deeper insights into neurodegenerative diseases. Our rigorously characterized cell models ensure reliable and reproducible results, accelerating your research towards effective treatments.

  • Microglial Phagocytosis Mediated by Antibodies

Creative Biolabs is leading the way in tau-focused immunotherapy with our novel anti-tau antibodies. These highly specific antibodies stimulate microglial phagocytosis, effectively clearing toxic tau aggregates and opening new avenues for therapeutic intervention in AD and related tauopathies. Our commitment to rigorous testing ensures researchers have access to a reliable and innovative tool.

Fig 1: Anti-tau antibodies reduce tau levels in microglia in a concentration-dependent manner. Fig.1 In a concentration-dependent manner, anti-tau antibodies reduce P3 tau levels in microglia.2, 4

  • PROTAC Targeted Small Molecule Degradation Technology

Harness the power of targeted protein degradation with proteolysis targeting chimera (PROTAC) technology targeting tau protein. PROTACs selectively degrade tau, offering a novel therapeutic strategy for AD and other tauopathies. This cutting-edge approach allows for precise control of tau levels, enabling researchers to explore new avenues for disease intervention.

Fig 2: C004019 induces tau clearance. Fig.2 C004019 induces tau clearance by promoting its ubiquitination and proteasome-dependent proteolysis in vitro.3, 4

We provide a seamless, end-to-end solution for tau clearance research, integrating antibody engineering, PROTAC development, and precision detection technologies. This comprehensive approach, spanning from target validation to preclinical studies, eliminates the challenges of fragmented workflows and accelerates the development of effective AD treatments. To discuss pricing and scheduling for your tau research, please contact us.

References

  1. Chesser, Adrianne S., Susanne M. Pritchard, and Gail VW Johnson. "Tau clearance mechanisms and their possible role in the pathogenesis of Alzheimer disease." Frontiers in neurology 4 (2013): 122. Distributed under Open Access license CC BY 3.0, without modification.
  2. Andersson, Christian Rungsted, et al. "Antibody-mediated clearance of tau in primary mouse microglial cultures requires Fcγ-receptor binding and functional lysosomes." Scientific reports 9.1 (2019): 4658.
  3. Wang, Weijin, et al. "A novel small-molecule PROTAC selectively promotes tau clearance to improve cognitive functions in Alzheimer-like models." Theranostics 11.11 (2021): 5279.
  4. Distributed under Open Access license CC BY 4.0, without modification.
For Research Use Only. Not For Clinical Use.
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