Recombinant mouse IL-13 protein - Bioactive cytokine

Recombinant cytokine, source: CHO cells

SPECIFICATIONS

Specifications

Source
CHO cells
Species
Mouse
Synonyms
T-cell activation protein P600
Accession sequence

P20109

Protein size
113 a.a. (A19-F131)
Molecular weight
~13 kDa
Carrier
Carrier-free
Tag
Tag-free
Purity
≥ 95% (SDS-PAGE)
Solubility

100 μg/ml in water

Formulation buffer

Glycine phosphate buffer (pH 7) containing stabilizing agents and 5% saccharose

Appearance (form)
Lyophilized
Reconstitution buffer
Endotoxin-free water (provided)
Sterility

0.22 µm filtration

Endotoxin

The absence of bacterial contamination (e.g. lipoproteins and endotoxins) has been confirmed using HEK-Blue™ TLR2 and HEK‑Blue™ TLR4 cells.

Applications

Cellular assays (tested), ELISA

Quality control

Each lot is released only after meeting predefined biological activity specifications in a cell-based assay.

CONTENTS

Contents

  • Product: 
    Recombinant mouse IL-13 (CHO)
  • Cat code: 
    rcyc-mil13
  • Quantity: 
    10 µg
Includes:

1.5 ml endotoxin-free water

Shipping & Storage

  • Shipping method:  Room temperature
  • Storage:

    • -20°C
    Stability: -20°C for up to 1 year

    Caution:

    • Avoid repeated freeze-thaw cycles

Details

Interleukin 13 background

IL-13 is a cytokine that belongs to the IL-2/γc superfamily. IL-13 is produced as a secreted monomeric molecule by activated CD4+ T cells, Natural Killer T cells (NKT cells), group 2 innate lymphoid cells (ILC2s), macrophages, mast cells, basophils, or eosinophils [1].

IL-13 binds a heterodimeric receptor composed of the IL-4Rα and IL-13Rα1 chains. This receptor is shared with IL-4, which can bind two different receptors: Type I (IL-4Rα and common γ chain) and Type II (IL-4Rα and IL-13Rα1). The binding of IL-13 to its receptor triggers a signaling cascade leading to the activation of STAT6. Subsequent gene expression drives M2 macrophage polarization, B-cell proliferation, IgE immunoglobulin class switching, and eosinophil activation and survival [1]. In non-hematopoietic cells, IL-13 is essential for mucus production, goblet cell hyperplasia, and worm expulsion [1]. Altogether, the downstream IL-13 effector functions participate in parasitic infection clearance and allergic reactions [1].

 

Relevance for therapeutics development

IL-13  is a key cytokine for controlling infections by extracellular parasites. However, along with IL-4, it also contributes to harmful allergic responses [1, 2]. As the prevalence of chronic allergic diseases such as asthma and atopic dermatitis is increasing worldwide, there has been a keen interest in the therapeutic blocking of IL-4 and IL-13 signaling.

Dupilumab is a fully human monoclonal antibody (mAb) that targets the IL-4Rα subunit [3]. It acts like a receptor antagonist and inhibits the signaling of both IL-4 and IL-13 [3]. Dupilimab was FDA-approved in 2017 for treating asthma, atopic dermatitis, and chronic sinusitis [3, 4]. Due to its favorable safety profile and established clinical use, Dupilumab holds significant promise for amending treatment options for many dermatologic conditions [5].

Tralokinumab and Lebrikizumab are fully human mAbs that target IL-13, inhibiting its receptor binding ability. Tralokinumab and Lebrikizumab were FDA-approved in 2021 and 2024, respectively, for treating moderate-to-severe atopic dermatitis [6, 7]

 

References:

1. Bernstein, Z.J., et al., 2023. Engineering the IL-4/IL-13 axis for targeted immune modulation. Immunol Rev. 320(1):29-57. 
2. Ogulur, I., et al., 2025. Type 2 immunity in allergic diseases. Cell & Mol Immunol, 22(3):211-242.
3. Harb, H. & Chatila, T.A., 2020. Mechanisms of Dupilumab. Clin Exp Allergy. 50(1):5-14.
4. https://www.accessdata.fda.gov/drugsatfda_docs/label/2022/761055s040lbl.pdf
5. Olbrich, H., et al., 2023. Dupilumab in Inflammatory Skin Diseases: A Systematic Review. Biomolecules.13(4):634.
6. https://www.accessdata.fda.gov/drugsatfda_docs/nda/2022/761180Orig1s000lbl.pdf
7. https://www.accessdata.fda.gov/drugsatfda_docs/label/2024/761306Orig1s000correctedlbl.pdf

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