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level: Biologic Therapies in RA

Questions and Answers List

level questions: Biologic Therapies in RA

Question	Answer
pro-inflammatory cytokines involved in the pathogenesis of RHEUMATOID ARTHRITIS secreted by synovial macrophages that stimulates synovial cells to proliferate and synthesize collagenase (degrades cartilage, stimulates bone resorption & inhibits proteoglycan synthesis)	IL-1 (Interleukin) and TNF-α (Tumor Necrosis Factor)
TNF-α inhibitors	• Adalimumab • Certolizumab • Etanercept • Golimumab • Infliximab GI ACE
Non-TNF Therapy	• Abatacept • Rituximab • Tocilizumab • Tofacitinib ART
• MOA: a recombinant monoclonal antibody that BINDS to TNF-α, thereby interfering with endogenous TNF- α activity by BLOCKING ITS INTERACTION WITH CELL SURFACE RECEPTORS • CA: RHEUMATOID ARHTRITIS, PSORIATIC ARTHRITIS, ANKYLOSING SPONDYLITIS, CROHN DISEASE (SQ weekly or every other week)	ADALIMUMAB
•A unique TNF-α blocker that contains a Fab fragment of a humanized antibody and is a POTENT NEUTRALIZER OF TNF- Α BIOLOGICAL ACTIONS (COMBINED WITH PEG) • Given every 2 weeks SQ	CERTOLIZUMAB PEGOL
•A GENETICALLY ENGINEERED, soluble, recombinant, fully human receptor fusion protein that binds to TNF- α thereby blocking its interaction with cell surface TNF- α receptors	ETANERCEPT
•MOA: neutralizes the biological activity of TNF- α by binding to it and blocking its interaction with cell surface receptors	GOLIMUMAB
• A CHIMERIC monoclonal antibody composed of human and MURINE REGIONS • MOA: binds specifically to human TNF- α and inhibits binding with its receptors	INFLIXIMAB
•Inhibit T-cell activation •MOA: COMPETES with CD28 for binding on CD80/CD86 protein, thereby PREVENTING FULL T-CELL ACTIVATION (given IV EVERY 4 WEEKS)	ABATACEPT
Activation of T-lymphocytes:	• Antigen-presenting cell (macrophages or B cells) must interact with the receptor on the T cell; • The CD80/CD86 protein on the antigen presenting cell must interact with CD28 protein on the T cell
• INHIBIT B CELL • MOA: interact against the CD20 antigen found on the surface of normal and malignant B lymphocytes, resulting in B CELL DEPLETION (GIVEN IV EVERY 16 TO 24 WEEKS; METHYLPREDNISOLONE is administered 30 mins prior to infusion to reduce severity of infusion reactions)	RITUXIMAB
•Activating T lymphocytes • Producing AUTOANTIBODIES AND RHEUMATOID FACTOR • Producing PROINFLAMMATORY CYTOKINES (TNFα and IL-1)	B cells in RHEUMATOID ARTHRITIS:
•A monoclonal antibody that INHIBITS THE ACTIONS OF IL-6 by blocking the IL-6 receptor (given as IV infusion every 4 weeks for MODERATE OR SEVERE RHEUMATOID ARTHRITIS)	TOCILIZUMAB
•An ORAL INHIBITOR OF JANUS KINASES (intracellular enzymes that modulate immune cell activity in response to the binding of inflammatory mediators to the cellular membrane)	TOFACITINIB
• MOA: INHIBITS IL-1 RECEPTOR (induced by inflammatory stimuli and mediates variety of immunologic responses, including degradation of cartilage and STIMULATION OF BONE RESORPTION) • A/E: NEUTROPENIA	ANAKINRA