Anti-Human RANKL (Denosumab)

Anti-Human RANKL (Denosumab)

Product No.: LT2800

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Product No.LT2800
Clone
AMG-162
Target
RANKL
Product Type
Biosimilar Recombinant Human Monoclonal Antibody
Alternate Names
osteoprotegerin ligand (OPGL), osteoclast differentiation factor (ODF), TNF related activation-induced cytokine (TRANCE), tumor necrosis factor ligand superfamily member 11 (TNFSF11)
Isotype
Human IgG2κ
Applications
ELISA
,
FA
,
IHC
,
WB

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Select Product Size
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Antibody Details

Product Details

Reactive Species
Human
Expression Host
HEK-293 Cells
FC Effector Activity
Active
Recommended Isotype Controls
Immunogen
Purified Recombinant Human RANKL
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.
Storage and Handling
Functional grade biosimilar 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 -80°C. Avoid Repeated Freeze Thaw Cycles.
Regulatory Status
Research Use Only (RUO). Non-Therapeutic.
Country of Origin
USA
Shipping
2-8°C Wet Ice
Additional Applications Reported In Literature ?
ELISA,
WB,
IHC,
FA
Each investigator should determine their own optimal working dilution for specific applications. See directions on lot specific datasheets, as information may periodically change.

Description

Specificity
Denosumab activity is directed against human RANKL (receptor activator of NFκB ligand).
Antigen Distribution
RANKL binds to its receptor RANK, which is located on osteoclasts and osteoclast precursors.
Background
Osteoporosis is a disease of bone microarchitecture deterioration commonly seen in postmenopausal women1. Estrogen deficiency leads to low bone mass and increased bone fragility due to bone resorption increasing more than formation. Those affected have an increased risk of fracture. RANKL (receptor activator of NFκB ligand) is a TNF family member that acts as a key bone resorption protein by mediating osteoclast formation, activation, and survival via activating its receptor RANK1,2.

Denosumab, a fully human monoclonal antibody originally generated using transgenic Xenomouse technology, selectively and with high affinity binds to and inhibits human RANKL, thus preventing interaction with and activation of its receptor RANK on the surface of osteoclasts and their precursors2. This blocking activity inhibits the formation, function, and survival of osteoclasts, resulting in reduced bone resorption and consequently reduces the risk of vertebral, nonvertebral and hip fractures. Denosumab increases bone mineral density (BMD) and trabecular and cortical bone strength, with continued antifracture and BMD benefits over 10 years of therapy. Bone resorption is inhibited in cynomolgus monkeys and humans, but not normal mice or rats.

Unlike bisphosphonates, denosumab is not incorporated into bone and its effects on bone turnover markers, BMD and histomorphometric measures are generally reversed upon its discontinuation1.

Antigen Details

Ligand/Receptor
RANK/RANKL
NCBI Gene Bank ID
UniProt.org
Research Area
Immunology
.
Osteoporosis

References & Citations

1. Deeks ED. Drugs Aging. 35(2):163-173. 2018.
2. Kostenuik PJ, Nguyen HQ, McCabe J, et al. J Bone Miner Res. 24(2):182-195. 2009.
3. Cummings SR, San Martin J, McClung MR, et al. N Engl J Med. 361(8):756-765. 2009.
4. Eastell R, Christiansen C, Grauer A, et al. J Bone Miner Res. 26(3):530-537. 2011.
5. Simon JA, Recknor C, Moffett AH Jr, et al. Menopause. 20(2):130-137. 2013.
6. Bone HG, Wagman RB, Brandi ML, et al. Lancet Diabetes Endocrinol. 5(7):513-523. 2017.
Indirect Elisa Protocol
FA
IHC
General Western Blot Protocol
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Formats Available

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