drug names: final Flashcards
Cyclosporin A, Tacrolimus
Binding to specific protein co-factors. (CpN and FKBP respectively) then inhibits calcineurin (phosphatase that activates NF-AT which activate Tc cells)
Chimeric Antigen Receptor T-Cell Therapy
Engineered cytotoxic T cells to target cancer
Antimicrobial Peptides (AMP) and Pore-forming toxins
Cathelicidins and Defensins
Daptomycin
Melittin
Disrupt membranes by charge-charge interactions. AMPs are positive and bacterial membranes are negative. This helps bind them together.
A(dapt) to amp up for the defenses of the Catholic church ; we can use bees (they’re lit)
Protein A
Binds IgG Fc domains to inhibit opsonization and phagocytosis, used by Staph
Lymes Disease:
recruits protein H and CD59 mimic (lyme sounds like lie)
HIV
incorporates CD59 into viral envelope, inhibiting MAC-mediated lysis
Hereditary Angioedema
Defect in C1 inhibitor. Caused by upregulation of C4a and C2a
angie is the chinese 1 (c1)
Systemic Lupus Erythematosus
Classical pathway defect. Usually clears immune complexes and apoptotic cells. Leads to autoantibody formation.
Infliximab, Adalimumab
Monoclonal antibodies that inhibit TNF- alpha.
Etanercept
Fusion protein with Fc domain that has TNF receptor.
Needs low-dose Methotrexate and adjunct.
ppl who are tanner like fusion food
Reperfusion Injury:
Once deprived of oxygen, necrotic cells induce complement response that leads to runaway immune response.
Complement-Focused Therapies:
Eculizumab (soliris) and Compstatin
compliments excludes (ecul) compton
Eculizumab (soliris)
Anti-C5 antibody for post-MI.
Compstatin
C3 Inhibitor, proposed for macular degeneration and psoriasis