Anti-Human CD25 (Camidanlumab) [Clone ADCT-301] — Fc Muted™

Anti-Human CD25 (Camidanlumab) [Clone ADCT-301] — Fc Muted™

Product No.: C1055

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Product No.C1055
Clone
ADCT-301
Target
CD25
Product Type
Biosimilar Recombinant Human Monoclonal Antibody
Alternate Names
IL2RA, IL2R, p55, TAC
Isotype
Human IgG1κ
Applications
ELISA
,
FC
,
IHC
,
WB

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Antibody Details

Product Details

Reactive Species
Human
Host Species
Human
Expression Host
HEK-293 Cells
FC Effector Activity
Muted
Immunogen
Humanized antibody derived from mouse clone targeting CD25
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,
FC,
IHC,
WB
Each investigator should determine their own optimal working dilution for specific applications. See directions on lot specific datasheets, as information may periodically change.

Description

Description

Specificity
This non-therapeutic biosimilar antibody uses the same variable region sequence as the therapeutic antibody Camidanlumab but is not linked to the toxin warhead SG3199. Camidanlumab antibody activity is directed against Human CD25. This product is for research use only.
Background
CD25 is the alpha-chain of the interleukin-2 receptor1, which regulates normal immune function2, and is involved in signal transduction, cell growth and survival1. CD25 is considered an attractive target for conjugated antibody chemotherapeutic development because it is overexpressed in various hematologic malignancies and is associated with poor prognosis.

Antibody drug conjugates (ADC) use tumor-associated surface antigens to specifically target cancer cells with cytotoxic agents. Human therapeutic grade Camidanlumab is an ADC composed of a human CD25-directed antibody (HuMax-TAC) that is maleimide- conjugated at reduced interchain cysteines via a cathepsin-cleavable valine-alanine linker to a PBD toxin warhead (SG3199)3.

Camidanlumab has a strong binding affinity to CD25-positive human anaplastic large cell lymphoma derived cell lines. This research grade biosimilar has the same specificity as the original therapeutic antibody but lacks the conjugated PBD toxin warhead.
Antigen Distribution
CD25 is expressed by approximately 30% of human peripheral blood B cells, particularly those belonging to the memory B cell population. Additionally, CD25 is expressed on the cell surface of many lymphomas, including classical Hodgkin lymphoma and non-Hodgkin lymphoma.
Ligand/Receptor
IL-2
NCBI Gene Bank ID
UniProt.org
Research Area
Biomarker
.
Biosimilars
.
Immunology
.
Autoimmunity

Leinco Antibody Advisor

Powered 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 Camidanlumab biosimilars are commonly used as calibration standards or reference controls in pharmacokinetic (PK) bridging ELISA assays to quantify Camidanlumab levels in serum. In this role, they establish standard curves and quality control (QC) samples, providing a baseline for accurately measuring drug concentrations in patient samples across both biosimilar and reference formulations.

Key functions of research-grade Camidanlumab biosimilars in PK bridging ELISA:

  • Calibration Standards:
    The biosimilar is prepared at known concentrations and serially diluted to create a standard curve, which is essential for translating ELISA optical density (OD) measurements into precise serum drug concentrations. This standard curve reflects the quantitative relationship between the amount of Camidanlumab and the assay signal.

  • Reference Controls (QC Samples):
    Aliquots containing known concentrations of Camidanlumab (either biosimilar or reference) are run in parallel with test samples to monitor assay accuracy, precision, and reproducibility over time.

  • Analytical Equivalence:
    For PK bridging ELISA in biosimilar development, a single, well-characterized material (often the biosimilar) is used as the calibration standard for both the biosimilar and the original reference product. Before reaching this stage, rigorous comparability assessments are undertaken to ensure that the biosimilar and reference product behave equivalently in the ELISA (e.g., parallelism, recovery, and similar binding behavior). Once established, both the biosimilar and reference QC samples are quantified against this single standard to demonstrate consistency and minimize analytical variability.

Example: Camidanlumab Bridging ELISA Workflow

  1. Plate Coating: Microtiter wells are coated with anti-Camidanlumab antibodies.
  2. Addition of Standards and Samples:
    • Serial dilutions of the research-grade Camidanlumab biosimilar (calibrators) are added to generate the standard curve.
    • Reference controls and test serum samples are also added.
  3. Detection:
    • After incubation and washing, a conjugated (e.g., HRP-labeled) anti-Camidanlumab detection antibody is added to bind captured Camidanlumab.
    • Signal is developed with substrate and measured by absorbance.
  4. Quantification:
    • The assay's calibration curve is used to interpolate the concentration of Camidanlumab in test samples and reference controls, verifying that biosimilar and reference drug are quantified comparably.
  5. Quality and Compliance Checks:
    • QC samples ensure the assay is functioning within expected precision and accuracy criteria throughout the run.

Industry guidance and best practices recommend:

  • Using a single PK assay with one calibrator (often the biosimilar) for biosimilar/reference quantification to reduce variability and provide consistent, reliable PK data—crucial for regulatory demonstration of biosimilarity.

If Camidanlumab from different sources (biosimilar vs. reference) do not behave equivalently in the assay, these issues must be resolved through additional characterization or assay optimization before proceeding with PK studies.

Summary:
Research-grade Camidanlumab biosimilars serve as both calibration standards (standard curve generation) and reference controls (QC monitoring) in PK bridging ELISA, enabling standardized and validated quantification of drug levels in serum across biosimilar and reference preparations.

The primary in vivo models where a research-grade anti-CD25 antibody is used to study tumor growth inhibition and characterize tumor-infiltrating lymphocytes (TILs) are syngeneic mouse models and, less commonly, humanized mouse models.

Key details for each model:

  • Syngeneic mouse models are the most widely used. These involve implanting murine tumor cell lines (such as MC38, CT-26, EMT-6, Hepa1-6, A20) into immunocompetent mice of the same genetic background, then administering a research-grade anti-mouse CD25 antibody (such as clone PC61) either systemically or directly into the tumor. These models preserve a fully functional mouse immune system, allowing for:

    • Tumor growth inhibition studies following Treg depletion by anti-CD25 antibody administration.
    • Detailed phenotypic and functional characterization of TILs, including changes in CD8+ T cells, other effector lymphocytes, and regulatory T cells after treatment.
  • Humanized mouse models are less common for routine anti-CD25 studies but are essential when investigating the effects of human (rather than murine) anti-CD25 antibodies or human TIL specificity. Here, immunodeficient mice are reconstituted with human immune cells and engrafted with patient-derived or human tumor cells, then treated with anti-human CD25 antibodies.

    • While technically challenging and expensive, these models are critical for preclinical evaluation of human-specific CD25-targeting therapies.

Additional considerations:

  • Some studies have used engineered anti-CD25 antibody-loaded biomaterials (e.g., antibody-immobilized meshes) implanted near tumors in syngeneic models as a local means to capture and deplete Tregs, suppress tumor growth, and analyze local TIL populations.
  • Direct intratumoral injection of anti-CD25 immunotoxins in syngeneic models further allows dose-constrained, localized Treg depletion and TIL analysis.
  • PDX models (patient-derived xenografts) are generally not used for anti-CD25/TIL studies due to their lack of functional immune systems unless combined with human immune cell transfer (i.e., as humanized mice).

Summary Table

Model TypeTumor/Graft OriginImmune System PresentAnti-CD25 Reagents UsedTIL Characterization Possible?Typical Research Use
Syngeneic mouse modelMouse cell linesMouse (intact)Anti-mouse CD25 (e.g., PC61)Yes (mouse TILs)Most common for mechanism/TILs
Humanized mouse modelHuman tumors/cellsHuman (reconstituted)Anti-human CD25 (e.g., BA9)Yes (human TILs)Human antibody/immune targeting

Authoritative sources confirm that syngeneic models are the standard for evaluating anti-CD25 effects on tumor immunity and TILs in vivo, while humanized models are important when studying human-specific reagents or cells.

Researchers use Camidanlumab biosimilars, which target CD25 on regulatory T cells (Tregs), in combination with other checkpoint inhibitors (such as anti-CTLA-4 or anti-LAG-3 biosimilars) to study synergistic antitumor effects in immune-oncology models by exploring distinct and complementary mechanisms of T cell activation and tumor immune evasion.

Researchers typically design combination therapy studies as follows:

  • Camidanlumab biosimilars (anti-CD25 antibody-drug conjugates) are used to deplete immunosuppressive Tregs in the tumor microenvironment, potentially boosting effector T cell activity and reducing local immunosuppression.
  • Checkpoint inhibitors such as anti-CTLA-4 and anti-LAG-3 are simultaneously administered to block distinct immune checkpoints:
    • Anti-CTLA-4 primarily augments T cell induction and activation in lymph nodes.
    • Anti-LAG-3 and anti-PD-1/PD-L1 enhance effector T cell function and prevent exhaustion directly within the tumor microenvironment.

Studies often employ complex preclinical models (e.g., mouse models of melanoma or lymphoma) and clinical trials to examine:

  • Immune cell dynamics: Combination regimens activate different T cell subsets. Anti-CD25 (Camidanlumab) primarily affects Tregs and can indirectly increase CD8+ cytotoxic T cell and CD4+ helper T cell activity.
  • Synergy: Researchers assess whether depleting Tregs via Camidanlumab enhances the efficacy of checkpoint blockade by unleashing more robust antitumor responses, often quantified through objective response rates, survival metrics, and mechanistic studies that detail immune cell infiltration and activation.
  • Mechanistic differences: Combining anti-PD-1 with anti-LAG-3 requires CD4+ T cell presence for anticancer effects, while anti-PD-1/CTLA-4 acts predominantly via direct cytotoxic T cell accumulation and activation. Using Camidanlumab may further reduce Treg-mediated suppression, amplifying checkpoint inhibitor efficacy.

Key experimental steps typically include:

  • Co-administration of Camidanlumab biosimilar and checkpoint inhibitor(s), often in dose-escalation or factorial designs.
  • Immune profiling (flow cytometry, single-cell RNAseq) to track changes in Treg, CD4+, and CD8+ T cell populations.
  • Assessment of tumor growth, survival, and toxicity in animal models or early-phase human trials.
  • Statistical analyses of synergy using models such as Bliss independence and clinical synergy indexes.

In summary, Camidanlumab biosimilars are used to reduce Treg-mediated immunosuppression, and, when combined with checkpoint inhibitors targeting CTLA-4, LAG-3, or PD-1/PD-L1, enable researchers to dissect and enhance multiple axes of immune activation against tumors. This integrative approach supports the development of more effective immunotherapeutic regimens and informs personalized cancer therapy strategies.

A Camidanlumab biosimilar can be used as either the capture or detection reagent in a bridging anti-drug antibody (ADA) ELISA to monitor a patient's immune response against camidanlumab (the therapeutic drug). In a typical ADA bridging ELISA, a biosimilar to the therapeutic antibody is used because it is structurally and immunologically comparable to the reference drug, ensuring all relevant ADA subtypes are detected while facilitating assay control and supply management.

How it works:

  • Capture reagent: The Camidanlumab biosimilar is immobilized (e.g., coated or biotinylated and attached to streptavidin-coated plates) on the ELISA plate. When a patient sample (e.g., serum) is added, any ADA specific to camidanlumab will bind to the biosimilar drug fixed to the plate.

  • Detection reagent: After washing, a second, differently labeled camidanlumab biosimilar is added (such as one conjugated to horseradish peroxidase [HRP] or another detectable tag). If ADA is present (being bivalent), it forms a bridge between the capture and detection reagents—one Fab arm of ADA binds to the immobilized biosimilar, and the other to the labeled biosimilar.

  • Signal readout: The resulting complex is detected via the label (such as HRP), producing a signal proportional to the amount of ADA in the patient sample.

Rationale for using a biosimilar in this context:

  • The biosimilar antibody is functionally and immunochemically equivalent to the originator drug, so it captures all clinically relevant anti-drug antibodies that could affect therapeutic efficacy or safety.
  • Using a biosimilar as both the capture and detection reagent is standard practice in bridging ADA ELISAs for antibody therapeutics, as it ensures that both capture and detection steps reflect the drug’s full immunogenic epitope profile.

Key points:

  • The bridging format relies on the bivalency of patient-derived ADA: one arm binds the immobilized drug, the other the labeled drug, creating the “bridge”.
  • It is crucial to use high-quality and well-characterized reagents (such as the biosimilar) to avoid false positives or interference from serum components.
  • The approach is broadly applicable and validated for monoclonal antibodies and biosimilars across various immunogenicity studies.

Summary table: Application of Camidanlumab Biosimilar in Bridging ADA ELISA

Reagent RoleDescription
CaptureImmobilized Camidanlumab biosimilar captures anti-camidanlumab antibodies from patient sample
DetectionLabeled Camidanlumab biosimilar binds to captured antibodies, allowing quantitation via colorimetric or chemiluminescent detection

This approach is widely accepted for immunogenicity monitoring of therapeutic antibodies and their biosimilars.

References & Citations

1 Epperla N, Hamadani M. Curr Hematol Malig Rep. 16(1):19-24. 2021.
2 Zammarchi F, Havenith K, Bertelli F, et al. J Immunother Cancer. 8(2):e000860. 2020.
3 Flynn MJ, Zammarchi F, Tyrer PC, et al. Mol Cancer Ther. 15(11):2709-2721. 2016.
Indirect Elisa Protocol
Flow Cytometry
IHC
General Western Blot Protocol

Certificate of Analysis

Formats Available

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Disclaimer AlertProducts are for research use only. Not for use in diagnostic or therapeutic procedures.