Catalog #SIM0013

InVivoSIM anti-human IL-17A (Secukinumab Biosimilar)

Clone Secukinumab
Reactivities Human
Product Citations 1
Isotype Human IgG1

$235.00 - $8,140.00

$235.00 - $8.00

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  • 100 mg - $8,140.00
  • 50 mg - $4,574.00
  • 25 mg - $3,182.00
  • 5 mg - $911.00
  • 1 mg - $235.00
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Product Description

This non-therapeutic biosimilar antibody uses the same variable regions from the therapeutic antibody Secukinumab making it ideal for research use. This Secukinumab biosimilar reacts with human IL-17A, a 15-20 kDa cytokine expressed by Th17 cells, γδ T cells, iNKT cells, NK cells, LTi cells, neutrophils, and intestinal Paneth cells. IL-17A has pleiotropic effects in immunoregulation and inflammation. It plays an important role in anti-microbial and chronic inflammation by inducing cytokine and chemokine production, neutrophil influx, and the production of antibacterial peptides but it is also an inflammatory mediator in the development of autoimmune diseases including rheumatoid arthritis, asthma, multiple sclerosis, and psoriasis. Secukinumab neutralizes IL-17A.

Specifications

Isotype Human IgG1
Recommended Isotype Control(s) RecombiMAb human IgG1 isotype control, anti-hen egg lysozyme
Recommended Dilution Buffer InVivoPure pH 7.0 Dilution Buffer
Conjugation This product is unconjugated. Conjugation is available via our Antibody Conjugation Services.
Immunogen Human IL-17A
Reported Applications in vitro IL-17A neutralization
Functional assays
Immunofluorescence
Immunohistochemistry
Flow Cytometry
ELISA
Formulation PBS, pH 7.0
Contains no stabilizers or preservatives
Endotoxin ≤0.5EU/mg (≤0.0005EU/μg)
Determined by LAL gel clotting assay
Purity ≥95%
Determined by SDS-PAGE
Sterility 0.2 µm filtration
Production Purified from cell culture supernatant in an animal-free facility
Purification Protein A
RRID AB_2894734
Molecular Weight 150 kDa
Storage The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.
Need a Custom Formulation? See All Antibody Customization Options

Application References

in vitro IL-17A neutralization
Wang F, Li Y, Yang Z, Cao W, Liu Y, Zhao L, Zhang T, Zhao C, Yu J, Yu J, Zhou J, Zhang X, Li PP, Han M, Feng S, Ng BW, Hu ZW, Jiang E, Li K, Cui B. (Nat Commun). "Targeting IL-17A enhances imatinib efficacy in Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia" Nat Commun 15(1):203.
PubMed

Dysregulated hematopoietic niches remodeled by leukemia cells lead to imbalances in immunological mediators that support leukemogenesis and drug resistance. Targeting immune niches may ameliorate disease progression and tyrosine kinase inhibitor (TKI) resistance in Philadelphia chromosome-positive B-ALL (Ph<sup>+</sup> B-ALL). Here, we show that T helper type 17 (Th17) cells and IL-17A expression are distinctively elevated in Ph<sup>+</sup> B-ALL patients. IL-17A promotes the progression of Ph<sup>+</sup> B-ALL. Mechanistically, IL-17A activates BCR-ABL, IL6/JAK/STAT3, and NF-kB signalling pathways in Ph<sup>+</sup> B-ALL cells, resulting in robust cell proliferation and survival. In addition, IL-17A-activated Ph<sup>+</sup> B-ALL cells secrete the chemokine CXCL16, which in turn promotes Th17 differentiation, attracts Th17 cells and forms a positive feedback loop supporting leukemia progression. These data demonstrate an involvement of Th17 cells in Ph<sup>+</sup> B-ALL progression and suggest potential therapeutic options for Ph<sup>+</sup> B-ALL with Th17-enriched niches.

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Product Citations

  • Targeting IL-17A enhances imatinib efficacy in Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia.

    In Nat Commun on 3 January 2024 by Wang, F., Li, Y., et al.

    PubMed

    Dysregulated hematopoietic niches remodeled by leukemia cells lead to imbalances in immunological mediators that support leukemogenesis and drug resistance. Targeting immune niches may ameliorate disease progression and tyrosine kinase inhibitor (TKI) resistance in Philadelphia chromosome-positive B-ALL (Ph+ B-ALL). Here, we show that T helper type 17 (Th17) cells and IL-17A expression are distinctively elevated in Ph+ B-ALL patients. IL-17A promotes the progression of Ph+ B-ALL. Mechanistically, IL-17A activates BCR-ABL, IL6/JAK/STAT3, and NF-kB signalling pathways in Ph+ B-ALL cells, resulting in robust cell proliferation and survival. In addition, IL-17A-activated Ph+ B-ALL cells secrete the chemokine CXCL16, which in turn promotes Th17 differentiation, attracts Th17 cells and forms a positive feedback loop supporting leukemia progression. These data demonstrate an involvement of Th17 cells in Ph+ B-ALL progression and suggest potential therapeutic options for Ph+ B-ALL with Th17-enriched niches.

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