ANX-M1 (Mouse IgG1)
ANX-M1 Mouse IgG1 is a brain-penetrant C1q inhibitor. ANX-M1 Mouse IgG1 blocks classical complement pathway activation, reduces C1q concentrations in brain and plasma, and inhibits microglia-mediated synapse engulfment. ANX-M1 Mouse IgG1 can be used for the research of Huntington's disease, Alzheimer's disease, retinopathy and neuropathic pain.
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.
Biological Activity
Mouse IgG1 kappa
Human/Mouse
ANX-M1 Mouse IgG1 (7.5 μg/μL; intravitreal; single dose) reduces photoreceptor cell death, preserves retinal structure, and improves retinal function in a mouse model of photo-oxidative retinal degeneration[4].
ANX-M1 Mouse IgG1 (7.5 μg/μL; intravitreal; single dose) does not protect against photo-oxidative retinal degeneration in mice[4].
ANX-M1 Mouse IgG1 (100 mg/kg; intraperitoneal; 3 doses) inhibits serum complement activity but does not protect against photo-oxidative retinal degeneration in mice[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:C57BL/6 J (adult, postnatal day 60-90, equal numbers of male and female, photo-oxidative damage-induced retinal degeneration)[4]
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Dosage:7.5 μg/μL (1 μl volume per eye)
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Administration:intravitreal; single dose
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Result:Significantly reduced the number of TUNEL+ photoreceptor cells in the outer nuclear layer at day 14.
Significantly increased outer nuclear layer thickness (measured as rows of photoreceptor nuclei).
Significantly improved rod a-wave and b-wave electroretinography amplitudes, with the most pronounced differences at the highest flash intensity (1.9 log cd.s/m2).
Significantly increased cone electroretinography amplitudes.
Showed no significant difference in the number of IBA1+ microglia/macrophages in the outer retina and outer nuclear layer compared to control.\nShowed no significant differences in the number of TUNEL+ photoreceptor cells, outer nuclear layer thickness, number of IBA1+ microglia/macrophages in the outer retina, rod a-wave and b-wave electroretinography amplitudes, or cone electroretinography amplitudes at day 14 compared to control.
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Animal Model:C57BL/6 J (adult, postnatal day 60-90, equal numbers of male and female, photo-oxidative damage-induced retinal degeneration)[4]
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Dosage:100 mg/kg
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Administration:intraperitoneal; 3 doses (day 0, day 4, day 8)
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Result:Reduced serum complement activity by >50% compared to IgG isotype control at day 12.
Showed no significant differences in the number of TUNEL+ photoreceptor cells, outer nuclear layer thickness, number of IBA1+ microglia/macrophages in the outer retina, rod a-wave and b-wave electroretinography amplitudes, or cone electroretinography amplitudes at day 12 compared to control.
C1q
Unconjugated
The product can be reconstituted/diluted with sterile PBS or saline.
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Product Image
ELISA, FACS, Functional assay
Chemical Information
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SMILES
[ANX-M1 (Mouse IgG1)]
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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.
Purity & Documentation
References
[2]. Hong S, et al. Complement and microglia mediate early synapse loss in Alzheimer mouse models. Science. 2016;352(6286):712-716. [Content Brief]
[3]. Yousefpour N, et al. Targeting C1q prevents microglia-mediated synaptic removal in neuropathic pain. Nat Commun. 2025;16(1):4590. Published 2025 May 17. [Content Brief]
[4]. 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]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)