ATC Group: L04AC Interleukin inhibitors

The World Health Organization's ATC classification organizes medical drugs based on therapeutic properties, chemical composition, and anatomy. It helps make essential medicines readily available globally and is widely used in the pharmaceutical industry.

Position of L04AC in the ATC hierarchy

Level Code Title
1 L Antineoplastic and immunomodulating agents
2 L04 Immunosuppressants
3 L04A Immunosuppressants
4 L04AC Interleukin inhibitors

Group L04AC contents

Code Title
L04AC01 Daclizumab
L04AC02 Basiliximab
L04AC03 Anakinra
L04AC04 Rilonacept
L04AC05 Ustekinumab
L04AC07 Tocilizumab
L04AC08 Canacinumab
L04AC09 Briakinumab
L04AC10 Secukinumab
L04AC11
L04AC12
L04AC13
L04AC14
L04AC15
L04AC16
L04AC17
L04AC18
L04AC19
L04AC20
L04AC21
L04AC22
L04AC23
L04AC24
L04AC25

Active ingredients in L04AC

Active Ingredient Description
Anakinra

Anakinra neutralises the biologic activity of interleukin-1α (IL-1α) and interleukin-1β (IL-1β) by competitively inhibiting their binding to interleukin-1 type I receptor (IL-1RI). Interleukin-1 (IL-1) is a pivotal pro-inflammatory cytokine mediating many cellular responses including those important in synovial inflammation.

Basiliximab

Basiliximab is a murine/human chimeric monoclonal antibody (IgG1κ) that is directed against the interleukin-2 receptor α-chain (CD25 antigen), which is expressed on the surface of T-lymphocytes in response to antigenic challenge. Basiliximab specifically binds with high affinity (KD-value 0.1 nM) to the CD25 antigen on activated T-lymphocytes expressing the high affinity interleukin-2 receptor (IL-2R) and thereby prevents binding of interleukin-2, a critical signal for T-cell proliferation in the cellular immune response involved in allograft rejection.

Brodalumab

Brodalumab is a recombinant fully human monoclonal immunoglobulin IgG2 antibody that binds with high affinity to human IL-17RA and blocks the biological activities of the pro-inflammatory cytokines IL-17A, IL-17F, IL-17A/F heterodimer and IL-25, resulting in inhibition of the inflammation and clinical symptoms associated with psoriasis.

Canacinumab

Canacinumab is a human monoclonal anti-human interleukin-1 beta (IL-1 beta) antibody of the IgG1/κ isotype. Canacinumab binds with high affinity specifically to human IL-1 beta and neutralises the biological activity of human IL-1 beta by blocking its interaction with IL-1 receptors, thereby preventing IL-1 beta-induced gene activation and the production of inflammatory mediators.

Daclizumab

Daclizumab beta is a humanised IgG1 monoclonal antibody that binds to CD25 (IL-2Rα), and prevents IL-2 binding to CD25, resulting in higher levels of IL-2 available for signalling through the intermediate-affinity IL-2 receptor. Key effects of this IL-2 pathway modulation potentially related to the therapeutic effects of daclizumab beta in MS include selective antagonism of activated T-cell responses, and expansion of immunoregulatory CD56bright natural killer (NK) cells, which have been shown to selectively decrease activated T-cells.

Guselkumab

Guselkumab is a human IgG1λ monoclonal antibody (mAb) that binds selectively to the interleukin 23 (IL-23) protein with high specificity and affinity. IL-23, a regulatory cytokine, affects the differentiation, expansion, and survival of T cell subsets, (e.g., Th17 cells and Tc17 cells) and innate immune cell subsets, which represent sources of effector cytokines, including IL-17A, IL-17F and IL-22 that drive inflammatory disease. In humans, selective blockade of IL-23 was shown to normalize production of these cytokines.

Ixekizumab

Ixekizumab is an IgG4 monoclonal antibody that binds with high affinity (<3 pM) and specificity to interleukin 17A (both IL-17A and IL-17A/F). Elevated concentrations of IL-17A have been implicated in the pathogenesis of psoriasis by promoting keratinocyte proliferation and activation, as well as in the pathogenesis of psoriatic arthritis. Neutralisation of IL-17A by ixekizumab inhibits these actions.

Mirikizumab

Mirikizumab is a humanised IgG4 monoclonal, anti-interleukin-23 (anti-IL-23) antibody that selectively binds to the p19 subunit of human IL-23 cytokine and inhibits its interaction with the IL-23 receptor. In humans, selective blockade of IL-23 was shown to normalise production of effector cytokines, including IL-17A, IL-17F and IL-22 that drive inflammatory disease.

Rilonacept

Rilonacept is a dimeric fusion protein which binds to and blocks the activity of the cytokine IL-1 and binds both IL-1β and IL-1α. Rilonacept is indicated for the treatment of Cryopyrin-Associated Periodic Syndromes (CAPS) with severe symptoms.

Risankizumab

Risankizumab is a humanised immunoglobulin G1 (IgG1) monoclonal antibody that selectively binds with high affinity to the p19 subunit of human interleukin 23 (IL-23) cytokine and inhibits IL-23-dependent cell signalling and release of proinflammatory cytokines. Risankizumab is indicated for the treatment of moderate to severe plaque psoriasis.

Sarilumab

Sarilumab is a human monoclonal antibody (IgG1 subtype) that specifically binds to both soluble and membrane-bound IL-6 receptors (IL-6Rα), and inhibits IL-6-mediated signalling which involves ubiquitous signal-transducing glycoprotein 130 (gp130) and the Signal Transducer and Activator of Transcription-3 (STAT-3). In functional human cell-based assays, sarilumab was able to block the IL-6 signalling pathway, measured as STAT-3 inhibition, only in the presence of IL-6.

Satralizumab

Satralizumab is a recombinant humanised immunoglobuline G2 (IgG2) monoclonal antibody (mAb) that binds to soluble and membrane-bound human IL-6 receptor (IL-6R) and thereby prevents IL-6 downstream signalling through these receptors.

Secukinumab

Secukinumab is a fully human IgG1/κ monoclonal antibody that selectively binds to and neutralises the proinflammatory cytokine interleukin-17A (IL-17A). Treatment with secukinumab reduces erythema, induration and desquamation present in plaque psoriasis lesions.

Siltuximab

Siltuximab is a monoclonal antibody that forms high affinity, stable complexes with soluble bioactive forms of human IL-6. Siltuximab prevents the binding of human IL-6 to both soluble and membrane-bound IL-6 receptors (IL-6R), thus inhibiting the formation of the hexameric signaling complex with gp130 on the cell surface.

Spesolimab

Spesolimab is a humanised antagonistic monoclonal immunoglobulin G1 (IgG1) antibody blocking human IL36R signalling. Binding of spesolimab to IL36R prevents the subsequent activation of IL36R by cognate ligands (IL36 α, β and γ) and downstream activation of pro-inflammatory pathways.

Tildrakizumab

Tildrakizumab is a humanized IgG1/k monoclonal antibody that specifically binds to the p19 protein subunit of the interleukin-23 (IL-23) cytokine without binding to IL-12 and inhibits its interaction with the IL-23 receptor. Tildrakizumab inhibits the release of proinflammatory cytokines and chemokines.

Tocilizumab

Tocilizumab binds specifically to both soluble and membrane-bound IL-6 receptors (sIL-6R and mIL-6R). IL-6 is involved in diverse physiological processes such as T-cell activation, induction of immunoglobulin secretion, induction of hepatic acute phase protein synthesis and stimulation of haemopoiesis. IL-6 has been implicated in the pathogenesis of diseases including inflammatory diseases, osteoporosis and neoplasia.

Ustekinumab

Ustekinumab is a fully human IgG1κ monoclonal antibody that binds with specificity to the shared p40 protein subunit of human cytokines interleukin (IL)-12 and IL-23. Ustekinumab inhibits the bioactivity of human IL-12 and IL-23 by preventing p40 from binding to the IL-12R1 receptor protein expressed on the surface of immune cells. Abnormal regulation of IL 12 and IL 23 has been associated with immune mediated diseases, such as psoriasis, psoriatic arthritis, Crohn’s disease and ulcerative colitis.

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