First time available for research use

RANKL-antibody

Denosumab antibody from Prolia®

Therapeutic RANKL-antibody from the original Prolia® commercial drug targeting the RANKL-antigen, also referred to as Prolia® or denosumab antibody. Research-relevant quantities are available as licence-free consumable in aliquoted or diluted variant. Therapeutic monoclonal antibodies can be used from researchers in in vitro and in vivo experiments, biosimilar developers can order different batches at the same time.

Choose your antibody
rankl-antibody-denosumab
Easy Access

Easy Access

Easy to order as license-free research consumable
Multiple batches

Multiple batches

Up to 10 batches of original drugs for examining batch-to-batch variations
Reduce costs

Reduce costs

Up to 80% less compared to the original pharmaceutical price
Prompt delivery

Prompt delivery

Shipment within days worldwide according to GDP-standards
Documented origin

Documented origin

Information on batch, registration number, expiry date, GDP-compliant pedigree

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Denosumab / Prolia

Product Reference

Drug nameProlia®
INNDenosumab
API typeDenosumab is a human monoclonal IgG2 antibody produced in a mammalian cell line (CHO) by
recombinant DNA technology.
Pharmacotherapeutic group
Drugs for the treatment of bone diseases – Other drugs affecting bone
structure and mineralization
ATC code
M05BX04
Target of antibody
RANKL; Synonyms: CD254, ODF, OPGL, OPTB2, TRANCE, hRANKL2, sOdf, TNFSF11, Ly109l, OPG, Trance, cd254, odf, opgl, optb2, rankl, sodf, tnfsf11, trance
General function
Short description
Pharmacodynamic properties
(Mechanism of action; Source EMA document)
Denosumab is a human monoclonal antibody (IgG2) that targets and binds with high affinity and specificity to RANKL, preventing activation of its receptor, RANK, on the surface of osteoclast precursors and osteoclasts. Prevention of the RANKL/RANK interaction inhibits osteoclast formation, function and survival, thereby decreasing bone resorption in cortical and trabecular bone.
Pharmacodynamic properties (Pharmacodynamic effects; Source EMA document)Prolia treatment rapidly reduced the rate of bone turnover, reaching a nadir for the bone resorption marker serum type 1 C-telopeptides (CTX) (85% reduction) by 3 days, with reductions maintained over the dosing interval. At the end of each dosing interval, CTX reductions were partially attenuated from maximal reduction of ≥ 87% to approximately ≥ 45% (range 45-80%), reflecting the reversibility of Prolia’s effects on bone remodelling once serum levels diminish. These effects were sustained with continued treatment. Bone turnover markers generally reached pre-treatment levels within 9 months after the last dose. Upon re-initiation, reductions in CTX by denosumab were similar to those observed in patients initiating primary denosumab treatment.
Original license holder
Marketing authorisation numbers
EU/1/10/618/001 - 004
Marketing authorisation holder
Amgen Europe B.V.
Minervum 7061
4817 ZK Breda
The Netherlands
Name of the manufacturer of the biological active substance
Amgen Europe B.V.
Minervum 7061
4817 ZK Breda
The Netherlands


Amgen Technology Ireland (ADL)
Pottery Road
Dun Laoghaire
Co Dublin
Ireland
Name and address of the manufacturer(s) responsible for batch release
Max shelf life
36 months
Storage conditions
2°C – 8°C
List of excipients
Acetic acid, glacial*
Sodium hydroxide (for pH adjustment)*
Sorbitol (E420)
Polysorbate 20
Water for injections
* Acetate buffer is fo
rmed by mixing acetic acid with sodium hydroxide