Immunosuppressants 1 Flashcards
what happens to the cell after CD4 T cell proliferates?
- may become cytotoxic (IC-2)
or
- produce antibodies via B cell/antigen specific B cells (IC-4, IC-5)
what are 2 major side effects/risks of ALL immunosuppressants?
- increased infection (ALL)
2. increased malignancies/cancer (MANY)
antithymocyte globulin
-class, mech?
inhibit T cell (non-specific antibody)
blocks all T cell function,
cytotoxic to/ decreases circulating lymphocytes
antithymocyte globulin
-Tx/ SE?
-acute renal transplant rejection
SE: may cause allergic response (due to polyclonal antibodies)
increased risk of infection and malignancy
abatacept
-class, mech?
receptor inhibitor
-CD80, CD86
inhibits initial step for binding site of MP and T cell activation affected
abatacept
-Tx, SE?
- RA arthritis
SE: increased risk of infection
belatacept
-class, mech?
receptor inhibitor
(CD80, CD86)
affect T cell activation
belatacept
-Tx, SE?
-renal transplant
SE: increased risk of infection, assc. with increased malignencies
what ends in ‘-mab’
monoclonal antibodies
what do monoclonal antibodies end in?
‘-mab’
administration route of monoclonal antibodies?
parenterally/ injection
administration route of ‘-mab’ drugs?
parenterally/ IV
do monoclonal bodies have more or less specific targets? more or less SE?
more specific targets
therefore,
less SE
monoclonal antibodies (‘mab’)- what does the middle of its name tell you?
target
what is ‘-li-‘?
immune cell (target)
what is ‘tu’?
tumor (target)
what are the three monoclonal antibody (‘-mab’) source prefixes?
xi
zu
u
what source is ‘-xi-‘?
chimeric source
-mouse antibody w/ some human pieces
what source is ‘-zu-‘?
humanized
-human ab w/ some mouse pieces
what source is ‘-u-‘?
fully human
most antigenic source?
least antigenic source?
most= chimeric source (xi) least= fully human (u)
natalizumab
-class, mech?
receptor blocker
-integrin
binds to alpha integrins on CD4 T cell and other immune cells (affects T cell activation)
natalizumab
-administration of route, target, source?
- parenterally/ IV
target: attack immune system (li); monoclonal antibody (mab)
source: humanized (zu)
natalizumab
-Tx, SE?
- Crohn’s + MS
SE: linked w/ progressive multifocal leukoencephalopathe (PML)
increased risk of infection
tocilizumab
-class, mech?
receptor blocker (IL-6)
binds IL-6 receptors (T cell activation affected)
tocilizumab
-administration route, target, source?
parenterally/ IV
target: attack immune system (li); monoclonal antibody (mab)
source: humanized (zu)
tocilizumab
-Tx, SE?
-RA
SE: increased risk of infection
ustekinumab
-class, mech?
receptor blocker
(IL-12, IL- 23)
binds to interleukins IL-12, IL-23 (T cell activation affected)
ustekinumab
-administration route, target, source?
parenterally/ IV
target: interleukin (ki); monoclonal antibody (mab)
source: fully human
ustekinumab
-Tx, SE?
-psoriasis
SE: increased risk of infection
- What is TNF (tumor necrosis factor)?
i. e. receptor, enzyme
cytokine (enzyme)
does NOT bind to receptor
what monoclonal antibody source is wanted for a little to no immune response?
fully human (u)
what does TNF do?
activator of immune system, central activator
etanercept
-class, mech?
enzyme inhibitor
-TNF
inhibits activation of T cell by TNF
etanercept
-route of administration, other?
-subcutaneously
- used in combo with other immunosupp.
- $$
etanercept
-Tx, SE?
RA
SE: increased risk of infection
infliximab
-class, mech?
enzyme inhibitor
-TNF
binds to TNF (activation of T cell affected)
infliximab
-administration route, target, source?
-IV
target: immune system; monoclonal antibody
source: chimeric
infliximab
-Tx, SE, concern?
- RA, Crohn’s
SE: can cause immune response
-infusion –> itching, hypotension, fever
concern: preexisting infection w/ fungus or TB may become worse
infliximab
-why may there be an immune response?
b/c it’s chimeric
adalimumab
-class, mech?
enzyme inhibitor
-TNF
binds TNF (T cell activation affected
adalimumab
-administration route, target, source?
-IV
target: immune system; monoclonal antibody
source: fully human
adalimumab
-Tx, SE?
-RA
SE: increased risk of infection
certolizumab
-class, mech
enzyme inhibitor
-TNF
binds TNF (T cell activation affected)
certolizumab
-administration route, target, source?
-IV
target: immune system; monoclonal antibody
source: humanized
certolizumab
-Tx, SE?
- RA, Crohn’s
SE: increased risk of infection
golimumab
-class, mech
enzyme inhibitor
-TNF
binds TNF (T cell activation affected)
golimumab
-administration route, target, source?
-IV
target: immune system; monoclonal antibody
source: fully human
golimumab
-Tx, SE?
-RA, ulcerative colitis, psoriatic arthritis
SE: increased risk of infection
what are 2 ways to block IL-1
- anakinra (receptor)
2. rilonacept (molecule)
anakinra
-class, route of administration?
receptor blocker
(IL-1)
-subQ
anakinra
-other, contraindications?
- used w/ other immunosuppressants like METHOTREXATE
- contra: should NOT be used w/ TNF inhibitors?
why should anakinra NOT be used with TNF inhibitors?
b/c almost guaranteed to get infection, suppressing imm. sys too much
rilonacept
-class
binds to IL-1 molecule
