Anti-hRANKL-hIgG1
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Cat.code:
hrankl-mab1
- Documents
ABOUT
RANKL (TNFSF11) Inhibitor - Human IgG1 (high effector functions)
Anti-hRANKL-hIgG1 is a Denosumab-based research antibody. Denosumab (AMG-162) is a therapeutic, fully human IgG2κ monoclonal antibody (mAb) that targets the human RANKL (receptor activator of nuclear factor-κB ligand, or TNFSF11), locking the interaction of RANKL with its receptor. Denosumab is FDA-approved for the treatment of osteoporosis and bone metastasis.
Anti-hRANKL-hIgG1 comprises the variable region of Denosumab fused to a wild-type IgG1 constant region for high effector functions. For applications requiring lower Fc effector activity, InvivoGen also offers Anti-hRANKL-hIgG2, the biosimilar research antibody to Denosumab.
This antibody is suitable for effector function analysis, screening assays, and neutralization assays. It can be used together with HEK-Blue™ RANKL cells to block RANK receptor signaling induced by recombinant human RANKL (see figure).
Key features
- Each lot is functionally tested and validated
- The complete sequence of the antibody construct has been verified
- Absence of endotoxins determined by the EndotoxDetect™ assay
More isotypes of this antibody are available and can be used for comparison of biological activities such as ADCC (see below or in the 'upon request' section).
All products are for research use only, and not for human or veterinary use.
SPECIFICATIONS
Specifications
RANKL, TNFSF11
Human
Sodium phosphate buffer, glycine, saccharose, stabilizing agents
0.2 µm filtration
Neutralization assay, ELISA
Each lot is functionally tested and validated.
CONTENTS
Contents
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Product:Anti-hRANKL-hIgG1
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Cat code:hrankl-mab1
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Quantity:100 µg
Shipping & Storage
- Shipping method: Room temperature
- -20 °C
- Avoid repeated freeze-thaw cycles
Storage:
Caution:
Details
Receptor Activator of NF-κB Ligand (RANKL), also known as member 11 of the tumor necrosis factor (TNF) superfamily (TNFSF11), TNF-related activation-induced cytokine (TRANCE), or CD254, exists as a transmembrane or soluble protein produced by osteoblasts and activated T cells [1]. RANKL binds to its receptor RANK via an obligate trimer configuration [1, 2].
RANKL/RANK signaling plays a pivotal role in bone remodeling and dendritic cell survival, thereby enhancing the induction of T cell responses [1]. Upon RANKL binding, RANK trimers recruit TNF receptor-associated factor (TRAF) adaptor proteins, such as TRAF6, to TRAF-binding motifs within their cytoplasmic domains [1].
The TRAF6 signaling cascade results in the activation of NF-κB and AP-1 transcription factors. Multiple efforts have focused on the development of anti‑RANKL antibodies or small‑molecule inhibitors for blocking RANKL/RANK signaling to reduce osteoporosis, prevent skeletal-related events (SREs) from bone metastasis in cancer, or improve anti-tumor immunity [1-3].
1. Cheng ML. & Fong L., 2014. Effects of RANKL-targeted therapy in immunity and cancer. Front. Oncol. 3:329.
2. Ahern E. et al., 2018. Roles of the RANKL-RANK axis in anti-tumour immunity — implications for therapy. Nat. Rev. Clin. Oncol. 15:676-93.
3. Nakai Y. et al., 2019. Efficacy of an orally active small-molecule inhibitor of RANKL in bone metastasis. Bone Res. 7:1.
DOCUMENTS
Documents
Technical Data Sheet
Validation Data Sheet
Safety Data Sheet
Certificate of analysis
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