AQP4 (201-220) TFA can be used to induce experimental autoimmune encephalomyelitis (EAE) models [1][2][3][4]. Induction of experimental autoimmune encephalomyelitis [1][2][3][4] Background: AQP4 (201-220) TFA can break immune tolerance and activate specific T cells. AQP4 (201-220) specific T cells migrate to the AQP4 high-expression area in the central nervous system (CNS), directly killing AQP4+ astrocytes or activating glial cells, thereby inducing autoimmune inflammatory damage. Specific modeling method 1. Mice: C57BL/6J, Aqp4⁻/⁻ Mouse administration route: AQP4 (201-220) 200 μg • Subcutaneous injection (tail base of mouse) • Single administration Note: (1) AQP4 (201-220) needs to be emulsified with Freund's complete adjuvant (CFA) containing 250/500 μg of Mycobacterium tuberculosis H37Ra to form a 200 μL emulsion before administration. (2) At the same time as administration, pertussis toxin (200 ng per mouse) is injected intravenously, and the administration is repeated the next day. Clinical scoring for modeling indicators: 0 points: no disease symptoms; 1 point: loss of tail tone (tail drooping, no voluntary movement); 2 points: impaired rolling ability (unable to roll from supine to prone position); 3 points: paraplegia of both hind limbs (hind limbs unable to support weight, dragging when walking); 4 points: quadriplegia (loss of motor function in both forelimbs and hind limbs); 5 points: near-death state (no voluntary movement, weak breathing). Clinical symptoms begin to appear about 11 days after immunization (mostly 1 or 2 points), peak at about 18 days (mostly 2-3 points), and enter the recovery period at 30 days (score decreases); if the clinical score is ≥1 point, it indicates successful modeling. Histological analysis: scattered or focal inflammatory lesions are present in the gray-white matter junction; inflammatory lesions are present in the midline region of the diencephalon (near the third ventricle) and around the fourth ventricle; inflammatory infiltration is present in the inner retina, accompanied by loss of retinal ganglion cells. Cytological analysis: Significant infiltration of CD45+ immune cells and CD4+ T cells was observed in the central nervous system (brain, spinal cord, retina), with an increased number of Iba-1 and GAFP-positive cells in the lesion area. Molecular changes: Decreased AQP4 expression; increased expression of IFN-γ, IL-17, CXCL10, and CCL20.

[1]. AQP4-specific T cells determine lesion localization in the CNS in a model of NMOSD. Acta Neuropathol Commun. 2025 Feb 11;13(1):27.

[2]. Vogel A L. Adaptive immune responses to AQP4 in a murine model for neuromyelitis optica[D]. Technische Universität München, 2023.

[3]. B cells orchestrate tolerance to the neuromyelitis optica autoantigen AQP4. Nature. 2024 Mar;627(8003):407-415.

[4]. Interferon-γ controls aquaporin 4-specific Th17 and B cells in neuromyelitis optica spectrum disorder. Brain. 2024 Apr 4;147(4):1344-1361.

C97H143N27O27S.XC2HF3O2

2151.40 (free acid)

AQP4 (201-220); 2104700-59-4

His-Leu-Phe-Ala-Ile-Asn-Tyr-Thr-Gly-Ala-Ser-Met-Asn-Pro-Ala-Arg-Ser-Phe-Gly-ProHLFAINYTGASMNPARSFGP

HLFAINYTGASMNPARSFGP

White to off-white solid

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: 请将本产品存放在密封保护的环境中，避免受潮。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

DMSO : ~100 mg/mL (with sonication)
H2O : ~50 mg/mL (with sonication)

Solubility in Formulation 1: ≥ 2.5 mg/mL(saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween-80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), Clear solution.
For example, if 1 mL of working solution is to be prepared, you canAdd 100 μL of DMSO stock solution (25.0 mg/mL) to 400 μL of PEG300 and mix well; then add 50 μL of Tween-80 and mix well; finally add 450 μL of physiological saline and adjust the volume to 1 mL. Preparation of physiological saline: Dissolve 0.9 g of sodium chloride in double-distilled water and dilute to 100 mL to obtain clear physiological saline.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL(saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), Clear solution.
For example, if 1 mL of working solution is to be prepared, you canAdd 100 μL of DMSO stock solution (25.0 mg/mL) to 900 μL of 20% SBE-β-CD saline and mix well. Preparation of 20% SBE-β-CD saline (4°C, store for one week): Dissolve 2 g of SBE-β-CD powder in 10 mL of saline until completely dissolved and clear.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL(saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), Clear solution.
For example, if 1 mL of working solution is to be prepared, you canAdd 100 μL of DMSO stock solution (25.0 mg/mL) to 900 μL of corn oil and mix well.

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 (Please use freshly prepared in vivo formulations for optimal results.)