Storage
The kit is shipped at ambient temperature (10-30°C) and should be stored at 2-8°C for long term storage. Keep away from heat or direct sunlight. The strips of microtiter plate are stable up to the expiry date of the kit in the broken, but tightly closed bag when stored at 2-8°C.
General Description
Infliximab is a tumour necrosis factor (TNFα) blocker and a chimeric monoclonal IgG1 antibody composed of human constant (75%) and murine variable (25%) regions. Infliximab is produced by a recombinant cell line cultured by continuous perfusion. TNFα is a key proinflammatory cytokine involved in chronic inflammatory diseases. Its hyperactivity and enhanced signalling pathways can be observed in inflammatory diseases where it activates further pro-inflammatory cascades. By binding to both the soluble subunit and the membrane-bound precursor of TNFα, infliximab disrupts the interaction of TNFα with its receptors and may also cause lysis of cells that produce TNFα.
Infliximab is an IgG1κ monoclonal antibody that binds to soluble and transmembrane forms of TNFα with high affinity to disrupt the pro-inflammatory cascade signalling. Binding of the antibody to TNFα prevents TNFα from interacting with its receptors. Infliximab does not neutralize TNFα (lymphotoxin-α), a related cytokine that utilizes the same receptors as TNFα. Blocked actions of TNFα further leads to downregulation of local and systemic proinflammatory cytokines (i.e. IL-1, IL-6), reduction of lymphocyte and leukocyte migration to sites of inflammation, induction of apoptosis of TNF-producing cells (i.e. activated monocytes and T lymphocytes), increased levels of nuclear factor-κB inhibitor, and reduction of reduction of endothelial adhesion molecules and acute phase proteins. Its inhibitory actions on TNFα was demonstrated in human fibroblasts, endothelial cells, neutrophils, B and T lymphocytes and epithelial cells. Infliximab also attenuates the production of tissue degrading enzymes synthesized by synoviocytes and/or chondrocytes.
Therapeutic drug monitoring (TDM) is the clinical practice of measuring specific drugs at designated intervals to maintain a constant concentration in a patient's bloodstream, thereby optimizing individual dosage regimens. The indications for drug monitoring include efficacy, compliance, drug-drug interactions, toxicity avoidance, and therapy cessation monitoring. Additionally, TDM can help to identify problems with medication compliance among noncompliant patient cases.
Biologic medicinal products (biologics) have transformed treatment landscapes worldwide for patients with haematological or solid malignancies with the 21st century. Today, as data exclusivity periods of first wave biologics approach expiration/have expired, several biosimilar products (i.e., biologics that are considered to be similar in terms of quality, safety and efficacy to an approved 'reference' biologic) are being developed or have already been approved for human use.
Like all biologics, biosimilars are structurally complex proteins that are typically manufactured using genetically engineered animal, bacterial or plant cell culture systems. As a consequence of this molecular complexity and the proprietary nature of the manufacturing process, which will inevitably result in the use of different host cell lines and expression systems as well as related differences in manufacturing conditions, it is not possible to manufacture exact copies of a reference biologic.
When administered to patients, all therapeutic proteins have the potential to induce an unwanted immune response (i.e., to stimulate the formation of antidrug antibodies [ADAs]). The impact of immune responses can range from no apparent effect to changes in pharmacokinetics, loss of effect and serious adverse events. Furthermore, the immunogenicity profile of a biologic can be significantly altered by even small differences in its manufacturing process that are accompanied by a change in product attributes, as well as differences in dosing schedules, administration routes or patient populations.
COA
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