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Monoclonal antibody targeting TNF.

Monoclonal antibody targeting TNF.

Monoclonal antibody targeting IL-6R.

Monoclonal antibody targeting IL-17A.

Monoclonal antibody targeting the shared p40 subunit of IL-12 and IL-23.

Monoclonal antibody blocking IL-4/IL-13 receptor signalling.

Soluble TNF receptor fusion protein.

Monoclonal antibody targeting PD-1.

Monoclonal antibody targeting PD-1.

Drug class that suppresses multiple inflammatory gene programmes.

Chimeric IgG1 (human Fc + murine variable region) anti-CD20 mAb: ADCC (FcγRIIIa on NK cells), CDC (C1q → MAC), and direct apoptosis signalling. Depletes CD20+ B cells (naive, GC, memory) but NOT plasma cells (CD20-negative). RA, ANCA vasculitis, DLBCL, FL, CLL, MS (off-label/ocrelizumab preferred), ITP, pemphigus.

Humanised IgG1 anti-CD20 mAb: lower immunogenicity than rituximab (human Fc+variable), similar ADCC mechanism. RRMS and PPMS (Ocrelizumab is the only FDA-approved PPMS therapy). SC formulation available 2023. Mechanism in MS: depletes leptomeningeal B cell aggregates that drive compartmentalised CNS inflammation in progressive MS.

Anti-CD3 Fc-silent mAb (Fc modified to prevent ADCC/CDC): binds CD3ε on T cells without Fc receptor engagement → T cell exhaustion/regulatory programme in autoreactive Th1 cells driving insulitis → shifts Th1:Treg ratio in islets. Does not globally deplete T cells.

Selective JAK1/JAK2 inhibitor (oral, once daily): blocks multiple cytokine pathways (IL-6, IFN-α/β, GM-CSF) + AAK1 inhibition (reduces viral endocytosis). Approved: RA, AD, alopecia areata, COVID-19 ARDS. A knowledge-graph screen proposed JAK1/2 plus AAK1 inhibition for COVID-19 in early 2020, before the trial programme tested it.

Human IgG1κ anti-IFNAR1 mAb: blocks ALL type I interferons (IFN-α, IFN-β, IFN-ω) simultaneously by targeting receptor subunit 1. Downstream of pDC IFN-α production. FDA approved 2021 for moderate-severe SLE (first new SLE mechanism biologic since belimumab 2011). IFN-signature-high patients respond better (75% of SLE patients).

Ciltacabtagene autoleucel: BCMA-targeting CAR-T with 4-1BB co-stimulatory domain + DUAL BCMA-binding scFv (higher avidity → kills cells with lower BCMA expression; reduces antigen escape). 4-1BB → sustained oxidative phosphorylation-biased T cell memory → superior long-term persistence vs CD28 co-stim.

Anti-CD3 × anti-CD19 BiTE (bispecific T cell engager, 55kDa tandem scFv): one arm grabs CD3 on any T cell, other arm grabs CD19 on B cell/tumour → forced T cell-tumour cell contact → CTL-mediated killing WITHOUT requiring MHC-I, antigen presentation, or prior T cell sensitisation. First BiTE approved (FDA 2014, B-ALL).

Human IgG1λ anti-BAFF/BLyS mAb: neutralises soluble BAFF → reduces B cell survival signal → autoreactive B cells more likely to undergo apoptosis. Does NOT block APRIL (which binds TACI and BCMA on plasma cells) → does NOT deplete plasma cells. IV + SC formulation.

Humanised IgG1κ anti-CD19 mAb with afucosylation (enhanced NK ADCC): targets ALL CD19+ cells including naive B cells, GC B cells, memory B cells, AND PLASMABLASTS (CD20-negative, CD19+). Reaches the plasmablast compartment that rituximab misses.

First allosteric kinase inhibitor approved in immunology: binds JH2 pseudokinase regulatory domain of TYK2 (NOT the ATP-binding active JH1 domain). JH2 of TYK2 structurally distinct from JAK1/2/3 JH2 domains → highly selective inhibition of TYK2-dependent receptors (IL-12R, IL-23R, IFN-αβR) without meaningful JAK1/2/3 activity.

Humanised IgG1κ anti-IgE mAb: binds free IgE (same epitope as FcεRI binding site on IgE) → prevents IgE loading onto mast cells/basophils → FcεRI receptor downregulates (requires IgE ligand for surface expression) → less mast cell arming → reduced degranulation response to allergens. Not allergen-specific → prevents all IgE-mediated reactions simultaneously.

Human IgG2λ anti-TSLP mAb: blocks TSLP (thymic stromal lymphopoietin) the upstream epithelial alarmin. TSLP activates ILC2 AND DCs (→Th2) AND mast cells AND basophils → blocking TSLP prevents ALL downstream type-2 inflammation simultaneously, regardless of the dominant effector cell.

Neutralises IL-1β.

Binds CD80/CD86 and blocks CD28 co-stimulation.

Blocks CTLA-4, enhancing priming and depleting intratumoural Tregs.

Recombinant IL-1Ra blocking IL-1α and IL-1β signalling.

Blocks C5 cleavage → no C5a or MAC.

Neutralises IL-5 → depletes eosinophils.

Gut-selective block of lymphocyte homing.

Disrupts microtubules → impairs neutrophil migration and NLRP3 assembly.

Blocks calcineurin → NFAT cannot enter nucleus → no IL-2.

Shared class effect of infliximab, adalimumab, etanercept and others.

Lipid-nanoparticle mRNA encoding antigen; self-adjuvanting through innate sensing

Replicating weakened pathogen; strong durable immunity, contraindicated in severe immunosuppression

Polysaccharide conjugated to carrier protein or purified antigen + adjuvant; T-dependent responses without live pathogen

Non-replicating whole pathogen or split antigen; usually needs adjuvant and boosters

Delivers antigen at mucosal inductive sites aiming for sIgA and local T-cell memory

Polyclonal T-cell-depleting antibody used for induction and rejection

Pooled donor IgG given intravenously or subcutaneously to replace missing antibody function

CD19-directed CAR-T used to reset B-cell autoimmunity