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.
What our clients say
”Evidentic can supply different batches of reference products for precilinical research.The quick access to the on-stock batches allows for adhoc ordering, keeps costs down and makes a headstart possible!”
“Evidentic is a new source of cost-efficient therapeutic mAbs for our immonassays. And easy to order!”
“We develop innovative and biosimilar mAbs for a global market. Evidentic’s aRMPs are a great source of cost-efficient reference products for our research and development program.”
“Evidentic gives rapid access to originator biologics and different batches. For biosimilar developers and regulators, it will shorten the time to gauge the analytical acceptance range for multiple CQAs of biotherapeutics.”
Denosumab / Prolia
|API type||Denosumab 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
|Target of antibody||RANKL; Synonyms: CD254, ODF, OPGL, OPTB2, TRANCE, hRANKL2, sOdf, TNFSF11, Ly109l, OPG, Trance, cd254, odf, opgl, optb2, rankl, sodf, tnfsf11, trance
(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.
4817 ZK Breda
|Name of the manufacturer of the biological active substance||Amgen Europe B.V.
4817 ZK Breda
Amgen Technology Ireland (ADL)
|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)*
Water for injections
* Acetate buffer is fo
rmed by mixing acetic acid with sodium hydroxide