Secukinumab

Therapeutic Secukinumab antibody from the original Cosentyx® commercial drug

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IL 17A
Monoclonal Antibody
Cosentyx®
150 mg/mL
40 µL
6 mg
-80°C
12/2017
409,00 
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IL 17A
Monoclonal Antibody
Cosentyx®
150 mg/mL
40 µL
6 mg
-80°C
02/2019
409,00 
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Max: 10
Min: 1
Step: 1
IL 17A
Monoclonal Antibody
Cosentyx®
150 mg/mL
40 µL
6 mg
-80°C
03/2018
409,00 
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Max: 10
Min: 1
Step: 1
IL 17A
Monoclonal Antibody
Cosentyx®
150 mg/mL
40 µL
6 mg
-80°C
09/2019
409,00 
view product
Max: 10
Min: 1
Step: 1
IL 17A
Monoclonal Antibody
Cosentyx®
150 mg/mL
40 µL
6 mg
-80°C
06/2018
409,00 
view product
Max: 10
Min: 1
Step: 1
IL 17A
Monoclonal Antibody
Cosentyx®
150 mg/mL
40 µL
6 mg
-80°C
12/2018
409,00 
view product
Max: 10
Min: 1
Step: 1

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Cosentyx® / Secukinumab Reference Product

Drug nameCosentyx®
INNSecukinumab
API typeSecukinumab 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 releaseRoche 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
Evidentic Support
+49 (0) 30 959 99 8831

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