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MOA of Amantadine
RIBAVIRIN
MOA
PHARMACOKINETICS
THERAPEUTIC USES
1.
2.
3.
ADVERSE EFFECTS
Hepatocelluar carcinoma
Cirrhosis
Immunomodulators
INTERFERON
Condylomata acuminata
Kaposi sarcoma.
Pegylated interferon
MOA
THERAPEUTIC USES
IFN- Used in
Chronic Hepatitis B & C
Genital warts, caused by papilloma virus.
Hairy cell Leukemia.
Kaposis Sarcoma.
IFN- Used in
Relapsing remitting multiple sclerosis
IFN- used in
Chronic granulomatous disease
Pharmacokinetics
Adverse Effects
ACYCLOVIR
Guanosine derivative.
Active against HSV & VZV.
HSV causes cold sores, conjunctivitis, mouth ulcers, genital
infections and rarely encephalitis (inflammation of the brain
parenchyma) in immunocompromised (having an immune
system that has been impaired by disease or treatment) pts.
VZV causes shingles (painful localized skin rash, usually with
blisters (fluid filled sacks) on top of the reddish skin , chicken
pox.
MOA
Inhibits viral replication by inhibiting viral DNA
Polymerase.
Acyclovir is phosphorylated to monophosphate
by herpes virus-encoded enzyme, thymidine
kinase.
Host cell kinases then convert monophosphate to
Di & triphosphate compounds.
Acyclovir triphosphate act as a substrate for
viral DNA polymerase and incorporated into viral
DNA causing premature DNA chain termination.
Less effective against the host enzyme.
Pharmakokinetic.
Given orally I/V or topically.
Oral B.A 15-20%.
PPL 1-2 hrs.
T = 3 hrs.
Distribution widely distributed, diffuses
tissues and body fluids and CSF.
Partially metabolize to inactive product.
Excreted by kidney by Glomerular Filtration
and partly by tubular secretion.
Therapeutic Uses
Oral Acylovir used in: Primary genital herpes, recurrent genital herpes.
Long term chronic suppression of genital
herpes.
Recurrent herpes labialis.
Decreases total no of lesion and duration of
varicella and cutaneous zoster.
I/V Acyclovir
Prophalactically before organ transplantation,
prevents reactivation of HSV.
Herpes simplex encephalitis.
Neonatal HSV infection.
Serious HSV or HZV infections.
In immunocompromised pts with zoster I/V
acyclovir reduces incidence of cutaneous and visceral
dissemination.
ADVERSE EFFECTS
Well tolerated, minimum adverse effects.
N, D, headache.
Local inflamm, during I/V inj, if there is
extravasation of solu.
I/V infusion reversible renal dysfunction, due
to crystalline nephropathy and neurological
toxicity (delirium, seizures (A seizure is the physical
changes in behavior that occur after an episode of
abnormal electrical activity in the brain).
Ganciclovir
Cidofovir
Formivirsen
Foscarnet
Valganciclovir
GANCICLOVIR
MOA
Ph. K
Clinical Uses
I/V administration use
Ph. K
Clinical Uses
Decreases rate of disease progression and prolongs
survival in HIV infected individuals.
Adverse Effects
Most common Myelosuppression resulting in
Anemia, neutropenia
GIT intolerance, headache, insomnia
Less frequent thrombocytopenia, hyperpigmentation
of nails, myopathy.
At higher doses: - Anxiety, confusion, tremulousness.
DIDANOSINE
Dideoxyinosine (ddI)
Synthetic analog of deoxyadenosine.
Second drug approved to treat HIV infection
not recommended for initial treatment of HIV
disease.
Used for Zidovudine resistant HIV infection.
MOA
Drug is phosphorylated in the host cells to triphosphate,
dideoxyadenosine in which form it act as DNA chain
terminator and inhibitor of the viral reverse transcriptase.
Adverse Effects
Dose dependent pancreatitis.
Dose related peripheral painful distal neuropathy.
Diarrhea, hepatitis, esophageal ulceration, cardiomyophthy.
CNS toxicity headache, irritability, insomnia.
Asymptomatic hyperuricemia, may precipitate attack of gout
in susceptible individuals.
Retinal changes and optic neuritis.
MOA
PHARMACOKINETICS
Given orally
ADVERSE EFFECTS
N,V,D