antiviral pharmacology/medchem Flashcards
immune globulin use
acute, serious infections
post exposure prophylaxis
used with nucleoside antiviral
herpes genome
dsDNA
influenza genome
(-) ssRNA
viruses that use host polymerase
DNA viruses herpes (human and simplex) varicella epstein-barr CMV
acyclovir MoA
guanosine analog prodrug
terminates DNA chain synthesis
what converts acyclovir to active drug
- viral thymidine kinase does first phosphorylation
- guanosine monophosphate kinase does rest
resistance mechanisms to acyclovir and valacyclovir
- deficient thymidine kinase
- altered thymidine kinase
- altered DNA polymerase
gancyclovir activity against
CMV
HSV
VZV
HHV
ganciclovir toxicity
high because its less specific to viral thymidine kinase
-potential for bone marrow toxicity
famciclovir features
- prodrug of penciclovir which increases bioavailability
- similar to acyclovir but longer duration
cidofovir MoA
cytosine analog that inhibits DNA synthesis
No viral TK needed
cidofovir dose limiting toxicity
nephrotoxicity
cidofovir route
IV only due to poor bioavailability
foscarnet MoA
inhibits DNA polymerase by blocking nucleotide binding, with no need of triphosphate (thus TK) like acyclovir and others
foscarnet side effects
headache tremor seizures hallucinations *all due to chelation of calcium*
foscarnet dose limiting toxicity
nephrotoxicity
hypocalcemia
foscarnet route
IV only
idoxuridine and trifluridine (thymidine analogs) MoA
is phosphorylated then inhibits DNA synthesis by inhibiting thymidylic phosphorylase
fomivirsen use
CMV retinitis
fomivirsen MoA
inhibits replication through specific and nonspecific mechanisms like virus binding
fomivirsen route
eye injection (intravitreal)
docosanol use
cold sores
imiquimod use
HPV infections
imiquimod MoA
not fully understood, does induce secretion of pro-inflammatory cytokines