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PHRM 845 > L 36-39 Pharm of MS drugs > Flashcards

L 36-39 Pharm of MS drugs Flashcards

1
Q

what are the 3 categories of MS treatment

A
  • treatment of acute attacks
  • disease-modifying therapies
  • symptomatic therapies
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2
Q

what are the three primary corticosteroids used for acute attacks

A

methylprednisolone and prednisone, adrenocorticotropic hormone (ACTH) is also an option but barely used becasue it is expensive

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3
Q

methylprednisolone dosage form(s) for acute attacks

A

iv and oral

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4
Q

dosage form(s) of prednisone for acute attacks

A

oral.

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5
Q

what is the likely MOA of corticosteroids in acute MS attacks? (3)

A
  • up-regulating anti-inflammatory genes
  • down-regulating pro-inflammatory genes
  • alleviating edema in demyelinated areas
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6
Q

2 interferon β1a drugs

A

avonex and rebif

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7
Q

2 interferon β1b drugs

A

betaseron and extavia

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8
Q

where do the interferon drugs act?

A

periphery and at BBB

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9
Q

2 things listed under MOA of interferon drugs

A
  • inhibition of autoreactive lymphocytes– T cells, dendritic cells
  • inhibition of BBB penetration by decreasing matrix metalloproteinase (MMP)
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10
Q

highlighted clinical feature(s) for interferon drugs

A

efficacy is reduced by neutralizing antibodies

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11
Q

MOA for glatiramer acetate (copaxone) (2 things)

A
  • synthetic polypeptide, mimics antigenic properties of myelin basic protein
  • modulation of antigen-presenting cells such as dendritic cells, leading to decreased T cell activation
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12
Q

MOA of fingolimod (3 things)

A
  • sphingosine-1-phosphate (S1P) receptor agonist
  • stimulation of oligodendrocyte survival, remyelination
  • interference with lymphocyte movement out of lymphoid organs
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13
Q

highlighted clinical feature of fingolimod

A

there was 1 side effect highlighted and it was progressive multifocal leukoencephalopathy (PML), a potentially lethal brain infection

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14
Q

where does fingolimod act?

A

CNS AND periphery to block movement of shit outside of lymphoid organs

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15
Q

3 MOA things for -zumabs (humanized monoclonal)

A
  • monoclonal antibody specific for a4 integrin
  • a4-integrin pairs with B1-integrin to produce ‘very late antigen’ (VLA-4)
  • inhibition of VLA-4 binding to its ligand (VCAM-1 on CNS vascular endothelium) and interferes with B and T cell movement into CNS
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16
Q

2 highlighted clinical features for natalizumab

A
  • a key side effect is the development of PML
  • induces the development of neutralizing antibodies -> allergic reactions
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17
Q

MOA of mitoxantrone (novantrone) (2 things)

A
  • anthracenedione with cytotoxic activity
  • reduces lymphocyte numbers by causing DNA strand breaks via intercalation, and delaying DNA repair via inhibiting topoisomerase II
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18
Q

where does mitoxantrone work

A

periphery

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19
Q

MOA of teriflunomide (Aubagio) (2 things)

A
  • cytotoxic agent that inhibits dihydroorotate dehydrogenase, an enzyme involved in de novo pyrimidine biosynthesis
  • inhibits proliferation of peripheral lymphocytes (activated B and T cells)
20
Q

3 fumarate drugs

A

-dimethyl fumarate (Tecfidera)
- diroximel fumarate (vumerity)
- monomethyl fumarate (bafiertam)

21
Q

what are fumarates metabolized by? Where does this happen?

A

esterases in GI tract, blood, tissues

22
Q

what do fumarates activate

A

Nrf2-mediated cellular antioxidant responses and anti-inflammatory pathways

23
Q

what “may” dimethyl fumarate promote?

A

remyelination

24
Q

what 2 things does dimethyl fumarate suppress?

A

activated T cells and dendritic cells in the periphery

25
Q

highligthed clinical feature for fumarates

A

“apparently PML”

26
Q

what is the dosage form for all fumarates

A

all oral and extended release

27
Q

siponimod name

A

BAF312? and Mayzent

28
Q

ozanimod name

A

zeposia

29
Q

ponesimod name

A

ponvory

30
Q

MOA of -imods

A
  • sphingosine-1-phosphate (S1P) receptor agonists
  • may stimulate oligodendrocyte survival, remyelination
  • interference with lymphocyte movement out of lymphoid organs
31
Q

what are Siponimod, Ozanimod, and. Ponesimod indicated for?

A

RRMS AND SPMS

32
Q

Cladribine name

A

mylinax

33
Q

how does cladribine (mylinax) get into cells?

A

it is taken up in cells by purine nucleoside transporters

34
Q

in what scenario is cladribine (mylinax) phosphorylated? what does it turn into?

A

when cells have high ratio of deoxycytidine kinase to deoxynucleotidase (e.g. lymphocytes and monocytes). gets phosphorylated into. triphosphate form 2-chloro-dATP

35
Q

what does 2-chloro-dATP do? (this is the thing cladribine (mylinax) turns into)?

A

damages DNA and interferes with DNA metabolism, resulting in cell death -> lymphocyte depletion

36
Q

cladribine (mylinax) dosage form

A

oral

37
Q

whats special about cladribine (mylinax)

A

it started as a chemo drug

38
Q

rituximab names

A

rituxan, mabthera, zytux

39
Q

what does Rituximab target?

A

CD20 (B cell marker) on surface of lymphocytes

40
Q

what are the two off-label indications for rituximab?

A

non-hodgkin lymphomas and rheumatoid arthritis

41
Q

what is rituximab also known as?

A

ocrelizumab.

42
Q

Rituximab stops ______ and is effective for some _______

A

RRMS, PPMS patients

43
Q

where does rituximab act>

A

periphery (on B cells)

44
Q

Drug class that is in late stage clinical trials

A

Antisense oligonucleotides

45
Q

what is ATL1102?

A

an ASO targeting VLA-4 -> predicted to have same outcome as natalizumab

PHRM 845 (34 decks)

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