NS101
NS101 is an anti-FAM19A5 antibody with an IC50 of 0.2 nM and a Kd of 111 pM, as well as blood-brain barrier permeability. NS101 binds to key amino acid residues of FAM19A5, thereby blocking the interaction of LRRC4B and disrupting the FAM19A5-LRRC4B complex. NS101 increases the dendritic spine density in hippocampal neurons and the prefrontal cortex, normalizes the dendritic spine elimination rate, elevates the frequencies of mEPSC and fEPSP, and promotes the transport of brain-derived FAM19A5 into the peripheral circulation. NS101 improves cognitive function in mouse models of Alzheimer's disease. NS101 can be used for research on Alzheimer's disease. The recommended isotype control is human IgG1 kappa (HY-P99001).
For research use only. We do not sell to patients.
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
To place orders, for customer services and technical support, please contact: MedChemExpress USA
Tel: 609-228-6898 E-mail: [email protected] [email protected]
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Biological Activity
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Chemical Information
- Protocols
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Description
Isotype
Human IgG1 kappa
Recommend Isotype Controls
Species Reactivity
Human
In Vitro
NS101 potently inhibits the binding of FAM19A5 to LRRC4B in a cell-free ELISA assay with an IC50 of 205.0 pM[1].
NS101 (50 nM) blocks FAM19A5-induced reductions in spine density and increases the density of functional, SYP-positive spines in cultured mouse primary hippocampal neurons[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
NS101 (10-30 mg/kg; i.v.; weekly; 4 weeks) restores synaptic activity (mEPSC frequency, fEPSP slope) and improves short-term memory in APP/PS1 amyloidopathy mice, independent of Aβ reduction[1].
NS101 (10-50 mg/kg; i.v.; single dose) crosses the blood-brain barrier in rats, engages with FAM19A5, and facilitates transport of brain-derived FAM19A5 to the peripheral circulation in a dose-dependent manner[1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:P301S [B6.C3-Tg (Prnp-MAPT*P301S) PS19Vle/J] (male, female, 6-7 months old, tauopathy model); wild-type littermates[1]
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Dosage:10 mg/kg (prefrontal cortex spine density; cognitive testing); 30 mg/kg (dendritic spine dynamics)
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Administration:i.v.; weekly; 4 weeks (prefrontal cortex spine density; cognitive testing); i.p.; weekly; 2 doses (dendritic spine dynamics)
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Result:Restored mushroom spine density in the prefrontal cortex of P301S mice to wild-type levels, while thin and stubby spine densities remained unchanged.
Normalized the spine elimination rate in P301S mice, restoring the net spine change to wild-type levels.
Reduced latency to locate the platform, increased number of platform crossings, and increased target quadrant occupancy in Morris water maze, matching wild-type performance.
Reduced pTau levels in the cerebral cortex (but not hippocampus) of P301S mice.
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Animal Model:APP/PS1 [B6.Cg-Tg (APPswe, PSEN1dE9) 85Dbo/J] (male, 13 months old, amyloidopathy model); wild-type littermates[1]
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Dosage:10-30 mg/kg
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Administration:i.v.; weekly; 4 weeks
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Result:Restored mEPSC frequency in APP/PS1 mice to wild-type levels, with a slight increase in mEPSC amplitude.
Enhanced fEPSP slopes and fiber volley amplitudes in hippocampal CA1 neurons.
Improved the spontaneous alternation rate of APP/PS1 mice to wild-type levels, while total arm entries remained unchanged across groups.
Did not alter Aβ levels in the cerebral cortex or hippocampus of APP/PS1 mice.
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Animal Model:Sprague-Dawley[1]
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Dosage:10 mg/kg; 50 mg/kg
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Administration:i.v.; single dose
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Result:Was detected in plasma with a half-life of 7.5 days (10 mg/kg) and 11.7 days (50 mg/kg), and showed dose-dependent systemic exposure (AUC 10,336.3 h·µg/mL for 10 mg/kg; 54,415.0 h·µg/mL for 50 mg/kg).
Crossed the blood-brain barrier, peaking in the brain at 6 hours post-injection with a half-life of 11.0 days (10 mg/kg) and 8.3 days (50 mg/kg), and peaking in CSF at 36 hours with dose-dependent levels.
Increased plasma FAM19A5 levels sharply post-administration then gradually decreased over 28 days in a dose-dependent manner, while brain and CSF FAM19A5 levels decreased after an initial short-term increase.
Gene ID
Accession
NP_056196
Target
TAFA5/FAM19A5
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Format
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Product Image
Application
ELISA, FACS, Functional assay
Chemical Information
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Protocol for Water Maze
The Morris Water Maze is a rodent spatial learning and memory assay in which a mouse or rat swims in opaque water to find an escape platform; in the hidden-platform version, the animal cannot see the platform and must use distal extra-maze cues to learn its fixed spatial location. The assay primarily measures hippocampus-dependent spatial learning during acquisition trials and spatial reference memory during probe trials after platform removal; readouts include escape latency, swim path length, swim speed, quadrant occupancy, platform-site crossings, and proximity to the former platform location.
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Transepithelial/transendothelial electrical resistance assay
TEER measures electrical resistance across epithelial or endothelial monolayers cultured on permeable supports, and the readout reflects ionic conductance through the cell barrier, especially the paracellular pathway regulated by junctional integrity. TEER can be measured without destroying the monolayer and is commonly used before or during transport, permeability, barrier-disruption, and barrier-maturation experiments. TEER values are influenced by biological maturation and technical conditions; reported factors include temperature, medium formulation, passage number, electrode geometry, membrane properties, and junctional length during early monolayer maturation. Therefore, TEER should be interpreted with blank-insert subtraction, area normalization, repeated readings, and, when possible, orthogonal barrier readouts such as FITC-dextran flux or tight-junction staining.
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Primary Embryonic Hippocampal Neuron Culture
Primary embryonic hippocampal neuron culture is an in vitro method in which hippocampi from embryonic rodents are dissected, enzymatically or mechanically dissociated, plated on adhesive substrates, and maintained in defined neuronal medium or in low-density sandwich/co-culture formats to support neuronal attachment, neurite extension, polarity formation, dendritic arborization, and synapse formation. The main readouts are cell survival, neuronal purity, neurite outgrowth, axon-dendrite polarization, synaptic marker development, and functional neuronal activity, assessed by phase-contrast microscopy, immunocytochemistry for neuronal/glial markers, live imaging, or electrophysiology depending on the downstream experiment.
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Alzheimer’s Disease Modeling
Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by a progressive decline in cognitive functions and loss of specific types of neurons and synapses. Alzheimer's symptoms can be simulated in mice by injecting drugs (such as Aβ) or genetically modified.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
NS101 Related Classifications
HY-P992426 Related Classifications
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