Therapeutic IL 17A-antibody from the original Cosentyx® commercial drug targeting the IL 17A-antigen, also referred to as Cosentyx® or secukinumab 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.
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Secukinumab / Cosentyx
Product Reference
Drug name | Cosentyx® |
INN | Secukinumab |
API type | Secukinumab is a recombinant fully human monoclonal antibody selective for interleukin-17A. Secukinumab is of the IgG1/κ-class produced in Chinese Hamster Ovary (CHO) cells |
Pharmacotherapeutic group | Immunosuppressants, interleukin inhibitors |
ATC code | L04AC10 |
Target of antibody | IL 17A; Synonyms: CTLA8, IL-17, IL-17A, IL17, Ctla-8, Ctla8, Il17, ChIL-17, IL-17F, IL17A, CTLA-8 |
General function | |
Short description | |
Pharmacodynamic properties (Mechanism of action; Source EMA document) | Secukinumab is a fully human IgG1/κ monoclonal antibody that selectively binds to and neutralises the proinflammatory cytokine interleukin-17A (IL-17A). Secukinumab works by targeting IL-17A and inhibiting its interaction with the IL-17 receptor, which is expressed on various cell types including keratinocytes. As a result, secukinumab inhibits the release of proinflammatory cytokines, chemokines and mediators of tissue damage and reduces IL-17A-mediated contributions to autoimmune and inflammatory diseases. Clinically relevant levels of secukinumab reach the skin and reduce local inflammatory markers. As a direct consequence treatment with secukinumab reduces erythema, induration and desquamation present in plaque psoriasis lesions. 9 IL-17A is a naturally occurring cytokine that is involved in normal inflammatory and immune responses. IL-17A plays a key role in the pathogenesis of plaque psoriasis, psoriatic arthritis and ankylosing spondylitis and is up-regulated in lesional skin in contrast to non-lesional skin of plaque psoriasis patients and in synovial tissue of psoriatic arthritis patients. The frequency of IL-17-producing cells was also significantly higher in the subchondral bone marrow of facet joints from patients with ankylosing spondylitis. |
Pharmacodynamic properties (Pharmacodynamic effects; Source EMA document) | Serum levels of total IL-17A (free and secukinumab-bound IL-17A) are initially increased in patients receiving secukinumab. This is followed by a slow decrease due to reduced clearance of secukinumab-bound IL-17A, indicating that secukinumab selectively captures free IL-17A, which plays a key role in the pathogenesis of plaque psoriasis. In a study with secukinumab, infiltrating epidermal neutrophils and various neutrophil-associated markers that are increased in lesional skin of plaque psoriasis patients were significantly reduced after one to two weeks of treatment. Secukinumab has been shown to lower (within 1 to 2 weeks of treatment) levels of C-reactive protein, which is a marker of inflammation. |
Original license holder | |
Marketing authorisation numbers | EU/1/14/980/001 - 007 |
Marketing authorisation holder | Novartis Europharm Limited Frimley Business Park Camberley GU16 7SR United Kingdom |
Name of the manufacturer of the biological active substance | |
Name and address of the manufacturer(s) responsible for batch release | Roche Pharma AG Emil-Barrell-Str. 1, D-79639 Grenzach-Wyhlen Germany |
Max shelf life | 36 months |
Storage conditions | 2°C – 8°C |
List of excipients | Sucrose L-histidine L-histidine hydrochloride-monohydrate Polysorbate 80 |