ANX-M1 (Human IgG1)
Based on 1 Customer Validation
ANX-M1 is a blood-brain barrier-permeable anti-C1q antibody. ANX-M1 can slow down the progression of retinal degeneration following photo-oxidative damage. ANX-M1 has been incorporated into nanocarriers to evaluate its brain delivery efficacy in a mouse model of Alzheimer's disease. ANX-M1 is applicable for research on age-related macular degeneration and Alzheimer's disease [1].
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- Pureté : 99.0%
- Masse moléculaire:145.78 kDa
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Stockage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Activité biologique
Description
Isotype
Human IgG1 kappa
Recommend Isotype Controls
Species Reactivity
Human/Mouse
IC50 & Target
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C1q |
In Vivo
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6J (adult, postnatal day 60-90, equal numbers of male and female, photo-oxidative damage-induced retinal degeneration)[1]
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Dosage:7.5 μg/μL (intravitreal post-treatment); 7.5 μg/μL (intravitreal pre-treatment); 100 mg/kg (systemic)
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Administration:intravitreal (single dose on day 7 or day 0); intraperitoneal (days 0,4,8)
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Result:Significantly reduced TUNEL+ photoreceptor cell death at day 14 compared to IgG control (P < 0.05), significantly increased outer nuclear layer (ONL) thickness (P < 0.05), significantly improved rod a-wave and b-wave electroretinography (ERG) responses (P < 0.05, most pronounced at 1.9 log cd.s/m²), and significantly improved cone ERG responses (P < 0.05) with intravitreal post-treatment; showed no significant differences in TUNEL+ cell count, ONL thickness, IBA1+ cell count, or ERG responses compared to IgG control (P > 0.05) with intravitreal pre-treatment; reduced serum complement hemolytic activity by >50% at day 12 (P < 0.05) but showed no significant differences in TUNEL+ cell count, ONL thickness, IBA1+ cell count, or ERG responses compared to IgG control (P > 0.05) with systemic administration
Gene ID
Accession
Conjugated
Unconjugated
Reconsititution
The product can be reconstituted/diluted with sterile PBS or saline.
Application
ELISA, FACS, Functional assay
Verified Bioactivity
Chemical Information
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Appearance Liquid
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Masse moléculaire 145.78 kDa
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Color Colorless to light yellow
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SMILES
[ANX-M1 (Human IgG1)]
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Livraison
Shipping with dry ice.
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Formulation
Please refer to the lot-specific COA for specific buffer information.
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Stockage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocole
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ROS/oxidative-stress fluorescent staining
ROS/oxidative-stress fluorescent staining uses cell-permeant fluorogenic probes that become fluorescent after oxidation inside cells or tissues; commonly used examples include DCFH-DA/DCFDA for broad cellular oxidant detection, DHE for superoxide-related signal detection, MitoSOX for mitochondrial superoxide-related signal detection, and CellROX probes for oxidative-stress-associated fluorescence readouts. The assay detects probe oxidation rather than a single ROS species unless the probe and analysis method have been chemically validated for that species. DCFH-DA enters cells, is deacetylated by intracellular esterases to DCFH, and produces fluorescent DCF after oxidation, so the readout is used as an operational measure of total cellular oxidative stress rather than a species-specific ROS measurement. DHE and MitoSOX can report superoxide-related oxidation, but red fluorescence alone can include non-specific ethidium-like oxidation products; HPLC or optimized spectral approaches are
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How to Choose the Right Model Animal
Choosing the right model animal is a validity-driven decision in which the species, strain, sex, age, genetic background, disease-induction method, outcome measures, and welfare burden must match the scientific question rather than laboratory tradition or convenience. A model should be selected by judging face validity, construct validity, and predictive validity: whether it resembles the human phenotype, whether it reproduces relevant mechanisms, and whether results are likely to predict human biology or treatment response. Animal studies often fail to translate because of species differences, weak disease resemblance, poor experimental design, inadequate reporting, publication bias, and underuse of randomization, blinding, and sample-size justification. Unresolved questions include how to rank competing models objectively, how much human-disease complexity must be reproduced for a given objective, and when non-animal systems such as organoids, ex vivo tissue, or computational models
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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.
Pureté et documentation
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Fiche technique (273 KB)
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SDS (251 KB)
- English - EN (251 KB)
- Français - FR (251 KB)
- Deutsch - DE (251 KB)
- Norwegian - NO (251 KB)
- Español - ES (251 KB)
- Swedish - SV (251 KB)
- Italian - IT (251 KB)
- Korean - KR (251 KB)
- Portuguese - PT (251 KB)
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Inhibitory Antibodies User Guide (603 KB)
Références
[1]. Jiao H, et al. Subretinal macrophages produce classical complement activator C1q leading to the progression of focal retinal degeneration. Mol Neurodegener. 2018;13(1):45. Published 2018 Aug 20. [Content Brief]
[2]. Gagnon M, et al. Evaluation of Novel B1R/B2R Agonists Containing TRIOZAN™ Nanoparticles for Targeted Brain Delivery of Antibodies in a Mouse Model of Alzheimer Disease. Molecules. 2023;28(13):5206. Published 2023 Jul 4. [Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Keywords
- ANX-M1 (Human IgG1)
- Complement System
- TUNEL+ photoreceptor cell death
- C57BL/6J mice
- C1q inhibitor
- age-related macular degeneration
- intravitreally
- classical complement pathway activation
- blood-brain barrier
- ERG responses
- B6C3-Tg (APPswe/PSEN1dE9) mice
- retinal degeneration
- serum complement hemolytic activity
- B1R/B2R agonist-functionalized TRIOZAN? nanoparticles
- ONL thickness
- Alzheimer’s disease
- C1q
- Alzheimer disease
- mouse
- photo-oxidative damage
- TRIOZAN? NPs
- anti-C1q monoclonal antibody
- Inhibitor
- inhibitor
- inhibit