Anti-Human IL-17A (Secukinumab) [Clone AIN457] — Fc Muted™
Anti-Human IL-17A (Secukinumab) [Clone AIN457] — Fc Muted™
Product No.: I-1215
Product No.I-1215 Clone AIN457 Target IL-17A Product Type Biosimilar Recombinant Human Monoclonal Antibody Alternate Names CTLA8, interleukin 17A Isotype Human IgG1κ Applications ELISA , FA , FC , IF , IHC |
Antibody DetailsProduct DetailsReactive Species Human Host Species Human Expression Host HEK-293 Cells FC Effector Activity Muted Immunogen Humanized antibody derived from mouse clone 2321 Product Concentration ≥ 5.0 mg/ml Endotoxin Level < 1.0 EU/mg as determined by the LAL method Purity ≥95% by SDS Page ⋅ ≥95% monomer by analytical SEC Formulation This biosimilar antibody is aseptically packaged and formulated in 0.01 M phosphate buffered saline (150 mM NaCl) PBS pH 7.2 - 7.4 with no carrier protein, potassium, calcium or preservatives added. Due to inherent biochemical properties of antibodies, certain products may be prone to precipitation over time. Precipitation may be removed by aseptic centrifugation and/or filtration. State of Matter Liquid Product Preparation Recombinant biosimilar antibodies are manufactured in an animal free facility using only in vitro protein free cell culture techniques and are purified by a multi-step process including the use of protein A or G to assure extremely low levels of endotoxins, leachable protein A or aggregates. Pathogen Testing To protect mouse colonies from infection by pathogens and to assure that experimental preclinical data is not affected by such pathogens, all of Leinco’s recombinant biosimilar antibodies are tested and guaranteed to be negative for all pathogens in the IDEXX IMPACT I Mouse Profile. Storage and Handling Functional grade preclinical antibodies may be stored sterile as received at 2-8°C for up to one month. For longer term storage, aseptically aliquot in working volumes without diluting and store at ≤ -70°C. Avoid Repeated Freeze Thaw Cycles. Regulatory Status Research Use Only Country of Origin USA Shipping 2-8°C Wet Ice Additional Applications Reported In Literature ? ELISA, FA, IF, IHC, FC Each investigator should determine their own optimal working dilution for specific applications. See directions on lot specific datasheets, as information may periodically change. DescriptionDescriptionSpecificity This non-therapeutic biosimilar antibody uses the same variable region sequence as the therapeutic antibody Secukinumab. This product is for research use only. Secukinumab activity is directed against IL-17A. Background IL-17 is a group of proinflammatory cytokines (IL-17A to IL-17F) released by T helper 17
(Th17) cells1. IL-17A is the key effector cytokine of the group1 and is involved in normal inflammatory and immune responses2. Additionally, increased IL-17A plays an important role in the pathogenesis of ankylosing spondylitis (AS), a chronic autoimmune inflammatory disease that primarily affects the axial skeleton2, and in the progression of psoriatic arthritis1. Secukinumab is a fully humanized monoclonal antibody that binds selectively to IL-17A and inhibits its interaction with the IL-17 receptor, thereby inhibiting the release of proinflammatory cytokines and chemokines2. Secukinumab was developed as an IL-17A inhibitor for the treatment of AS and has been approved for the treatment of AS, plaque psoriasis, and psoriatic arthritis. In AS, the levels of a variety of biomarkers (CRP, S100A8, and S100A9) decrease with secukinumab treatment along with symptoms. Secukinumab was generated in transgenic mice engineered to express the human IgG/κ repertoire in lieu of the murine immunoglobulin repertoire using recombinant human IL-17 as immunogen3. Murine hybridoma cells were obtained that secrete the human IgG/κ antibody and selection for activity against IL-17A was performed. Secukinumab may have significant cross-reactivity with IL-17F, depending on the chosen experimental conditions5. Antigen Distribution IL-17A is expressed by Th17 cells, mast cells, and neutrophils. Ligand/Receptor Il-17R NCBI Gene Bank ID UniProt.org Research Area Autoimmune . Biosimilars . Cancer . Immunology . Inflammatory Disease Leinco Antibody AdvisorPowered by AI: AI is experimental and still learning how to provide the best assistance. It may occasionally generate incorrect or incomplete responses. Please do not rely solely on its recommendations when making purchasing decisions or designing experiments. Research-grade Secukinumab biosimilars are used as calibration standards or reference controls in pharmacokinetic (PK) bridging ELISAs to establish accurate, quantitative measurement of drug concentration in serum samples, typically by serving as the analytical standard curve against which test samples—including reference and biosimilar products—are measured. This process supports the bioanalytical comparability assessments that underpin PK bridging studies in biosimilar development. Key details on use:
Workflow summary:
This process ensures consistent, reproducible, and comparable quantitation of Secukinumab (biosimilar and reference) in PK studies, meeting regulatory expectations for demonstrating biosimilar pharmacokinetic similarity. The primary mouse models used to study anti-IL-17A antibody effects on tumor growth inhibition and tumor-infiltrating lymphocytes (TILs) are predominantly syngeneic models, with some studies utilizing xenograft approaches. Syngeneic ModelsEO771 Breast Cancer Model represents one of the most extensively characterized syngeneic systems for anti-IL-17A research. In this model, mice are challenged with 1 × 10⁶ syngeneic EO771 tumor cells, followed by anti-IL-17A antibody treatment at doses ranging from 200-400 mg/mouse administered four times at weekly intervals. This model demonstrated that anti-IL-17A treatment significantly reduced tumor burden and, when combined with anti-PD-L1 antibodies, substantially improved survival rates by approximately 70%. MT/ret-derived Primary Cutaneous Melanoma (CM) Model utilizes mice carrying the human ret transgene with wild-type BRAF status. This syngeneic model specifically examines the interaction between IL-17A signaling and dual immune checkpoint inhibition (CTLA-4 and PD-1). The model employs both IL-17A-neutralizing antibodies and recombinant mouse IL-17A to demonstrate that IL-17 signaling creates a favorable tumor microenvironment with increased immune infiltration, particularly neutrophils. B16-F10 Melanoma Models have been employed in multiple configurations. One approach uses standard B16F10 cells in syngeneic settings, while another utilizes B16F10 cells in Foxp3 DTR (diphtheria toxin receptor) mice to study the relationship between IL-17A and CD8+ T cell exhaustion. Additionally, xenograft studies using B16-F10 cells in IL-17⁻/⁻ mice have been conducted to examine IL-17A's role in melanoma progression. Characterization of Tumor-Infiltrating LymphocytesThe syngeneic models are particularly valuable for TIL characterization because they maintain fully intact and functional immune systems. Anti-IL-17A treatment in these models has revealed several key immunological changes: Enhanced CD8+ T Cell Response: Anti-IL-17A treatment promotes stronger CD8+ T cell responses within the tumor microenvironment, contributing to improved antitumor immunity. The treatment appears to reverse IL-17A-mediated promotion of CD8+ T cell terminal exhaustion. Neutrophil Modulation: IL-17 signaling significantly influences neutrophil infiltration patterns, with IL-17A creating conditions that favor increased neutrophil presence in tumors. This neutrophil recruitment appears to support the clinical benefit observed with dual checkpoint inhibition. Regulatory T Cell Reduction: Anti-IL-17A treatment decreases the percentage of regulatory T cells (Tregs) in tumor tissues, contributing to a more immunologically active tumor microenvironment. Model-Specific ConsiderationsSyngeneic tumor models present unique advantages for anti-IL-17A research because they recapitulate the complex interactions between the immune system and tumors. However, these models require cross-reactive therapeutics that can recognize murine targets, which can be addressed through transgenic syngeneic mice expressing human targets, syngeneic tumor models overexpressing human antigens, or chimeric antibody-based agents. The research demonstrates that anti-IL-17A treatment works synergistically with other immunotherapies, particularly PD-L1 blockade, by reducing PD-L1 expression in tumor tissues and enhancing tumor-specific immune responses. This combination approach has proven more effective than single-agent therapy in extending survival in these preclinical models. Researchers investigating combinations of Secukinumab biosimilars (targeting IL-17A) with checkpoint inhibitors such as anti-CTLA-4 or anti-LAG-3 biosimilars in complex immune-oncology models primarily aim to evaluate synergistic antitumor effects and immune modulation, though clinical data remains limited and such combinations are generally considered experimental. Key points based on available evidence:
Experimental models typically involve:
Cautions and limitations:
Summary Table — Combination Use in Research:
In summary, while checkpoint inhibitor combinations are established in some cancer types, use of Secukinumab biosimilar with other checkpoint inhibitors remains primarily an experimental research approach reserved for complex immune-oncology models or for addressing immune toxicity, with clinical application largely unproven and limited to case reports or ongoing trials. A Secukinumab biosimilar can be used as both the capture and detection reagent in a bridging ADA ELISA to monitor a patient’s immune response (ADA formation) against Secukinumab therapy by taking advantage of its structural similarity to the reference drug. This format relies on the ability of bivalent anti-drug antibodies in patient samples to “bridge” between Secukinumab biosimilar molecules immobilized on the plate and those labeled with a detection tag, such as biotin or HRP. Essential context:
Supporting details:
Summary of technique:
This use of the Secukinumab biosimilar as both capture and detection reagent allows robust and clinically relevant monitoring of ADA formation during Secukinumab therapy. References & Citations1 Aboobacker S, Kurn H, Al Aboud AM. Secukinumab. [Updated 2023 Jun 20]. In: StatPearls
[Internet]. Treasure Island (FL): StatPearls Publishing; 2023 Jan-. Available from:
https://www.ncbi.nlm.nih.gov/books/NBK537091/ 2 Blair HA. Drugs. 79(4):433-443. 2019. 3 Patent US7807155B2. https://patents.google.com/patent/US7807155B2/en 4 Elain G, Jeanneau K, Rutkowska A, et al. Glia. 62(5):725-735. 2014. 5 Beerli RR, Bauer M, Fritzer A, et al. MAbs. 6(6):1608-1620. 2014. Technical ProtocolsCertificate of Analysis |
Formats Available
Prod No. | Description |
---|---|
I-1210 | |
I-1215 |
