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ANTI-VIRAL/ANTI-ANTI-VIRAL/ANTI-FUNGAL AGENTSFUNGAL AGENTS
ANTI-VIRAL AGENTSANTI-VIRAL AGENTS
VIRUSES:Single or double stranded DNA or RNA
enclosed in a protein – CAPSIDObligate intracellular parasiteReplication depends on synthetic processes of
the host cellAnti-viral drugs must either block entry or exit
from cell or be active inside the host cell
VIRAL REPLICATIONVIRAL REPLICATION Viral attachment and entry (enfuvirtide, docosanol,
palivizumab) Adsorption and penetration into susceptible host
cells (Globulins and interferon-alfa) Un-coating of viral nucleic acid (Amantadine) Synthesis of early regulatory proteins (Fomivirsen) Synthesis of RNA or DNA (RT Inhibitors) Synthesis of late regulatory proteins (Protease Inhibitors) Packing and Assembly (maturation) of viral
particles (Rifampicin) Release from cells (Neuraminidase Inhibitors)
ANTI-VIRAL AGENTSANTI-VIRAL AGENTS
Anti-Herpes Acyclovir Famciclovir Valacyclovir
Ganciclovir Valganciclovir Lamivudine
Vidarabine Idoxuridine Trifluridine
Cidofovir Sorivudine Fomivirsen
Penciclovir
Anti-retroviral Agents Nucleoside RT inhibitorsZidovudine Zalcitabine DidanosineStavudine Lamivudine Abacavir Emtricitabine Non-nucleoside RT InhibitorsNevirapine Delavirdine Efavirenz
ANTI-Hepatitis BANTI-Hepatitis B Lamivudine Adenofovir Dipivoxil Entecavir Interferon alfa-2b Famciclovir
ANTI-Hepatitis CPegylated interferon alfa-2a and 2bRibavirin, interferon alfa 2a, 2b, alfacon
Protease InhibitorsProtease Inhibitors
Saquinavir Lopinavir/Ritonavir Indinavir Nelfinavir Amprenavir Darunavir Atazanavir Tipranavir Fosamprenavir
Anti-influenza AgentsAnti-influenza Agents
Amantadine Rimantadine
Neuraminidase Inhibitors
Oseltamivir (Tamiflu)
Zanamivir
Ribavirin Palivizumab
Interferons
MiscellaneousMiscellaneous
Immuno-modulating Agents Inosiplex Isoprinosine
Foscarnet
ANTI-HERPESANTI-HERPESANTI-VARICELLA ZOSTERANTI-VARICELLA ZOSTER
ACYCLOVIRACYCLOVIR
Acyclovir(9-[2-hydroxy methyl]-9-H-guanine)
Acyclic guanosine derivative against HSV1, HSV2, and VZV
Weaker activity against EBV, CMV
and Human Herpes Virus 6 (HHV 6)
MECHANISM OF ACTIONMECHANISM OF ACTION
REQUIRES 3 PHOSPHORYLATION STEPS:Converted to di and triphosphate
compounds by the host’s cellular enzymes
Converted to monophosphate derivative by virus-specified thymidine kinase
Acyclovir triphosphate inhibits viral DNA synthesis
Acts as a chain terminator because it lacks 3’ hydroxyl group
Competitive inhibition of deoxy-GTP for viral DNA polymerase
RESISTANCE• HSV: absence of partial production of viral
thymidine kinase, altered thymidine kinase substrate specificity, and altered viral DNA polymerase
• VZV: mutation in VZV thymidine kinase and mutations in viral DNA polymerase
PHARMACOKINETICSPHARMACOKINETICSOral bioavailability ranges from 10-30%
and decreases with increasing doseClearance thru GF and TSHalf-life: 3 hrs in normal renal function
and 20 hrs in anuriaDistributes widely in body fluids including
vesicular fluid, aqueous humor, and CSFConcentrated in breast milk, amniotic
fluid, and placentaPercutaneous absorption is low
THERAPEUTIC USESTHERAPEUTIC USES
First and recurrent genital herpes:– 200 mg 5x daily for 10 days – oral– 5 mg/kg per 8 hrs – IV
Recurrent: 400 mg 2x daily or 200 mg 3x daily
THERAPEUTIC USESTHERAPEUTIC USES
ACUTE HERPES ZOSTER (SHINGLES)SYSTEMIC ACYCLOVIR
PROPHYLAXISHSV ENCEPHALITIS ( IV form)VARICELLA ZOSTER VIRUS
INFECTIONCMV PROPHYLAXIS
SIDE EFFECTSSIDE EFFECTS
TOPICAL PREPARATIONS- mucosal irritation and transient burning to genital lesions
ORAL – nausea, diarrhea, rash, headache, renal insufficiency, and neurotoxicity
IV- renal insufficiency, CNS side effects
VALACYCLOVIRVALACYCLOVIRL- valyl ester of acyclovirRapidly converted to acyclovir after oral
administrationSerum levels are 3-5x greater than
acylcovir Treatment of primary and recurrent genital
herpes and herpes zoster infectionsPrevents CMV disease in post-transplant
patients
PharmacokineticsPharmacokinetics
Oral bioavailability is 54%s CSF fluid levels are 50%
of those in serumElimination half-life: 2.5-3.3 hoursGenerally well-tolerated
FAMCICLOVIRFAMCICLOVIR Diacetyl ester prodrug of 6 deoxy penciclovir
and rapidly converted to PENCICLOVIR by FIRST-PASS metabolism
Penciclovir does not cause chain termination Oral form is approved for managing HSV and
VZV infections First episode genital herpes
250 mg TID for 5-10 days Recurrent genital herpes – 250 mg BID for 1 year
Herpes zoster of 3 days – 500 mg TID x 10 days It is as effective as acyclovir in reducing healing time and zoster associated pain
FAMCICLOVIRFAMCICLOVIRComparable to valacyclovir in treating
zoster and reducing associated pain in older adults
500 mg TID x 10 days is comparable to high dose of acyclovir in treating zoster in immuno-compromised patients and in opthalmic zoster
Associated with dose-related reductions in Hepatitis B Virus DNA and transaminase levels in patients with chronic HBV hepatitis
PharmacokineticsPharmacokineticsOral bioavailability: 70%Intracellular half-life: 10 hours in
HSV-1 infected cells
20 hours in HSV-2 infected cells
7 hours in VZV infected cells in vitro.
Excretion: primarily in the urine
PENCICLOVIRPENCICLOVIR
Penciclovir (9-[4-hydroxy-3-hydroxymethyl but-1-yl] guanine
An acyclic guanine nucleosideActive metabolite of famciclovirSpectrum of activity and potency
against HSV & VZV is similar to acyclovir
Inhibitory activity to HSV
MECHANISM OF ACTIONMECHANISM OF ACTION
Inhibitor of viral DNA synthesis Initially phosphorylated by viral thymidine kinase
Penciclovir triphosphate has a lower affinity in competitive inhibition of viral DNA polymerase thus can not cause chain termination
100 fold less potent in inhibiting DNA polymerase than acyclovir but present in higher concentration and prolonged period in infected cells
THERAPEUTIC USESTHERAPEUTIC USES
Intravenous form- 5 mg/kg per 8-12 hrs for 7 days is comparable to acyclovir in treatment of mucocutaneous HSV infection
Topical 1% penciclovir cream applied every 2 hrs while awake for 4 days shortens healing time and symptoms by about 1 day in recurrent labial HS.
(reserved usage)
SIDE EFFECTSSIDE EFFECTS
Mutagenic at high concentrations
(IV form is not usually given)No clinically important drug
interactions have identified
TRIFLURIDINETRIFLURIDINEFluorinated pyrimidine nucleoside that
has an in vitro inhibitory activity against HSV 1 & 2 , CMV, vaccinia and certain adenoviruses
Inhibits viral DNA synthesisPhosphorylated intracellularly into its
active form by cellular enzymesIncorporation into both viral and cellular
DNA prevents its systemic use
MECHANISM OF ACTIONMECHANISM OF ACTION
Trifluridine monophosphate irreversibly inhibits thymidylate synthetase
Trifluridine triphosphate is a competitive inhibitor of thymidine triphosphate incorporation into DNA by DNA polymerases
CLINICAL USESCLINICAL USES
Primary keratoconjunctivitis and recurrent epithelial keratitis due to HSV 1 and 2
Topical trifluridine is more active than idoxuridine and comparable to vidarabine in HSV ocular infections
ADVERSE EFFECTSADVERSE EFFECTS
Discomfort upon instillation Palpebral edemaHypersensensitivity reaction,
irritations and superficial punctate or epithelial keratopathy
VIDARABINEVIDARABINEAdenosine analog with an in vitro activity
against HSV, VZV, and CMVPhosphorylated intracellularly by host
enzymes to form ara-ATP and then inhibits viral DNA polymerase
Vidarabine triphosphate is incorporated into both viral and cellular DNA
Rapidly metabolized in vivo to hypoxanthine arabinoside through removal of 6-amino group by adenosine deaminase – decrease viral activity
Therapeutic Therapeutic UsageUsage3% ointment – acute
keratoconjunctivitis, superficial keratitis, recurrent epithelial keratitis (HSV1 and 2)
IV vidarabine – HSV encephalitis, neonatal herpes, VZV infection
DOCOSANOLDOCOSANOL
Saturated 22-carbon aliphatic alcohol.Inhibits FUSION between plasma
membrane and HSV envelope resulting in prevention of viral entry into cells and subsequent viral replication.
Only for orolabial HERPES
ANTI-CMV AGENTSANTI-CMV AGENTS
GANCICLOVIRGANCICLOVIR
(9-[1,3-dihydroxy-2-prepoxymethyl]guanine)Cyclic guanosine analog that requires
triphosphorylation for activation prior to inhibiting viral DNA polymerase
Similar structure to acyclovir except in having additional hydroxymethyl group on the acyclic side chain
MECHANISM OF ACTIONMECHANISM OF ACTION Monophosphorylated intracellularly by a virus-
induced enzyme Phosphorylation is catalyzed by a viral thymidine
kinase during HSV, phosphotransferase UL97 encoded gene during CMV infection
Ganciclovir di & triphosphate formed by cellular enzymes
Triphosphate is a competitive inhibitor of deoxyguanosine triphosphate incorporation into DNA inhibiting viral rather than cellular DNA polymerase
Viral DNA incorporation causes cessation of DNA chain elongation
PHARMACOKINETICSPHARMACOKINETICS
Oral bioavailability is 6-9% following ingestion with food and less in the fasting state
CSF concentration are approximately 50 % of those in serum
CLINICAL USESCLINICAL USES
Delay progression of CMV retinitis in AIDSCMV colitis & esophagitisCMV infection in transplant patientCMV pneumonitisCMV retinitisCMV, HSV1, HSV2, EBV & HHV-8
ADVERSE REACTIONSADVERSE REACTIONSMyelosuppressionCNS toxicityVitreous hemorrhage, retinal detachmentNeutropenia (2nd wk)CNS (headache, behavioral changes,
convulsions, coma)Infusion related phlebitis, azotemia,
anemia, rash, fever, liver function test abnormalities
VALGANCICLOVIRVALGANCICLOVIR L- valyl ester prodrug of ganciclovir Hydrolyzed to active compound ganciclovir by
intestinal and hepatic enzymes Well absorbed (60%) & rapidly metabolized in
intestinal walls & liver to ganciclovir Renal excretion thru GN and TS
Usage:CMV retinitis in AIDS and for prevention of CMV in high risk kidney, heart transplant.
CIDOFOVIRCIDOFOVIR (1-[(S)-3-hydroxy-2-(phosphonomethoxy)-
propyl]cytosine dihydrate)Cytidine nucleoside analog with inhibitory
activity against human herpes, papilloma, polyoma, pox, and adenoviruses
Phosphorylation to active disphosphate is independent of viral enzymes
After phosphorylation; it acts as potent inhibitor to viral DNA polymerase
PHARMACOKINETICSPHARMACOKINETICS
Penetration into the CNS or eye have not been well characterized
Terminal half-life is 2.6 hrs, cidofovir diphosphate half-life is 17- 65 hrs
IV administration must be administered with probenecid to block active tubular secretion and decrease nephrotoxicity
CLINICAL USESCLINICAL USESCMV, HSV 1, HSV 2, VZV, EBV, HHV-6,HHV8,
adenovirus, poxvirus, poliomyxovirus, Human papilloma virus
CMV retinitisPolyoma virus associated progressive
multifocal leukoencephalopathy syndrome associated with AIDS
Topical – recurrent genital herpes, anogenital warts
FOSCARNETFOSCARNET Phosphonoformic Acid Inorganic
Pyrophosphate analog that inhibits viral DNA polymerase, RNA polymerase and HIV transcriptase directly without requiring activation by phosphorylation
Taken up slowly by cells and does not undergo significant intracellular metabolism
Reversibly blocks the pyrophosphate binding site of the viral polymerase
Inhibits cleavage of pyrophosphate from deoxynucleotide triphosphates
SIDE EFFECTSSIDE EFFECTSNephrotoxicitySymptomatic hypocalcemiaSaline loading may reduce the
risk of nephrotoxicityConcurrent administration with
pentamidine exacerbates both nephrotoxicity and hypocalcemia
CLINICAL USESCLINICAL USES
CMV retinitis, colitis, esophagitisAcyclovir- resistant HSV infection
and VZV infectionHSV, VZV, CMV, EBV, HHV-6, HHV-
8, HIV
FOMIVIRSENFOMIVIRSEN
21 mer-phosphorothioate oligonucleotideFirst FDA approved anti-sense therapy.
Binding to target mRNA results in inhibition of immediate early region 2 protein synthesis – inhibiting viral replication
Injected intravitreally in CMV retinitis in AIDS
ANTIRETROVIRAL ANTIRETROVIRAL AGENTSAGENTS
NUCLEOSIDE REVERSE NUCLEOSIDE REVERSE TRANSCRIPTASE TRANSCRIPTASE
INHIBITORS(NRTIs)INHIBITORS(NRTIs)Competitive inhibition of HIV 1 reverse
transcriptase and can be incorporated into the growing viral DNA chain to cause termination
Requires intracytoplasmic activation as a result of phosphorylation by cellular enzymes to the triphosphate form
Activity against HIV 1, HIV 2Lactic acidosis & severe hepatomegaly
with steatosis
ZIDOVUDINE ZIDOVUDINE (Azithymidine, AZT)(Azithymidine, AZT)
Deoxythymidine analogDecrease rate of clinical disease progression
and prolong survival of HIV infected individualsWell absorbed from the gut and distributed to most body tissues & fluidsEliminated by renal excretion following
glucorinadation in the liverCombination therapy with other anti-retroviral
agents enhance potency and delay resistance
CLINICAL USESCLINICAL USES
HIV – associated dementia & thrombocytopenia
Reduce rate of vertical transmission (mother-newborn) by 23%
ADVERSE EFFECTSADVERSE EFFECTS
Myelosuppression – most commonThrombocytopenia, hyperpigmentation
of nails, myopathy, anxiety, confusion and tremulousness
Fatal lactic acidosis & severe hepatomegaly w/ steatosis
DIDANOSINE (ddl)DIDANOSINE (ddl)Synthetic analog of deoxyadenosineActivity is potentiated by hydroxyurea due to
depletion of intraocular pools of d-ATPChewable, dispersable tablet, enteric coatedContains phenylalanine and NaShould be taken on an empty stomachFood, fluroquinolones and tetracycline
should be given 2 hrs before didanosine
ADVERSE EFFECTSADVERSE EFFECTS
Most major clinical toxocity:Dose –dependent pancreatitis
Painful peripheral distal neuropathyDiarrhea, hepatitis, esophageal
ulceration, cardiomyopathyCNS toxicityPrecipitate gouty attacksOptic neuritis
EMTRICITABINEEMTRICITABINE Formerly called FTC Fluorinated analogue of LAMIVUDINE with a long
intracellular half-life(>39 hrs) Oral bioavailability: 93% CSF level is LOW Mean plasma half-line: 8-9 hours Renal excretion thru GF and TS Contraindicated in children, pregnant women, and patients
with renal and hepatic failure (propylene glycol) Most common side effects-HA, diarrhea, hyper-
pigmentation in palms and soles Can not combine with LAMIVUDINE
LAMIVUDINE (3TC)LAMIVUDINE (3TC) Cytosine analog ,synergistic with other
antiretroviral nucleoside – Stavudine, Zidovudine
Oral bioavailability exceeds 80% and it is not food dependent
Elimination in urine is UNCHANGED Used in combination therapy NOTE: no combination with zalcitabine-may
inhibit intracellular phosphorylation of one another thus decreasing potency.
Approved for the treatment of chronic Hepatitis B infection
ZALCITABINE (ddC)ZALCITABINE (ddC)Cytosine analog with synergistic anti-HIV1
activity with a variety of antiretrovirals against both zidovudine sensitive and resistant strains
Associated with dose-dependent peripheral neuropathy
Oral and esophageal ulcerationsIncrease bioavailability in combination with
probenecid or cimetidineDecrease bioavailability in combination with
antacids and metoclopramide
STAVUDINE (d4T)STAVUDINE (d4T)Thymidine analogHigh oral bioavailability, not food dependentRenal excretion thru GF and TSMajor dose-limiting toxicity:
Dose-related peripheral sensory neuropathyPancreatitis, arthralgias, elevation of serum
aminotransferasesPhosphorylation is reduced by zidovudine
ABACAVIRABACAVIR Guanosine analogWell absorbed during oral administrationMetabolized by alcohol dehydrogenase and
glucuronosyl-transferase to inactive metabolites
Fatal hypersensitivity reactionsNausea, vomiting, diarrhea, headache, fatigueHyperglycemia, hypertriglyceridemia and
lactic acidosis
NUCLEOTIDE INHIBITORNUCLEOTIDE INHIBITOR
TENOFOVIRTENOFOVIR
Acyclic nucleoside phosphonate competitively inhibits HIV reverse transcriptase and cause chain termination after incorporation to DNA
Indicated for use in combination with other antiretroviral agents
PharmacokineticsPharmacokineticsOral bioavailability: 25% without food 39-40% after a high-fat meal
Serum half life: 17 hours and intracellular half-line is prolonged at more than 60 hours
Renal elimination thru GF and TS
Common Side Effects: GIT complaints
NON-NUCLEOSIDE REVERSE NON-NUCLEOSIDE REVERSE TRANSCRIPTASE TRANSCRIPTASE
INHIBITORS(NNRTIs)INHIBITORS(NNRTIs)Bind directly to a site on the HIV –1 reverse
transcriptase Blockade of RNA and DNA dependent DNA
polymerase activitiesBinding site is near but distinct from that of the
NRTI’s Neither compete with nucleoside triphosphate
nor require phosphorylation to be active
NEVIRAPINENEVIRAPINE
Oral bioavailability is > 90% Not food dependent Used as a component of a combination
antiretroviral regimen Effective in the prevention of transmission
of HIV from mother to newborn Causes severe life threatening rashes
DELAVIRDINEDELAVIRDINE
Oral bioavailability of about 85 % Metabolized to inactive metabolites by the
CYP3A & CYP2D6 P450 enzymes Plasma concentrations are reduced by
antacids, didanosine, phenytoin, phenobarbital, carbamazepine, rifabutin, rifampin, nelfinavir & saquinavir
Concentrations increased by clarithromycin, fluoxetine, & ketoconazole
EFAVIRENZEFAVIRENZ
Principally metabolized by CYP3A4 & CYP2B6 to inactive hydroxylated metabolites
Principal adverse effects: CNS (dizziness, drowsiness, insomnia, headache, confusion, amnesia, agitation, delusions, depression, nightmares, euphoria)
Pyschiatric symptoms rashes
PROTEASE INHIBITORSPROTEASE INHIBITORS
Protease--responsible for cleaving precursor molecules (immature budding particles)
PI---result in the production of immature, non-infectious viral particles
Associated w/ spontaneous bleeding in hemophilia A & B
Do not undergo process of phosphorylation
SAQUINAVIRSAQUINAVIR
Saquinavir H- hard gel capsule – poor bioavailability, should be taken within 2 hrs after a fatty meal
Saquinavir S – soft gel capsule – improved absorption 3x than hard gel capsule
Subject to first pass-metabolism by CYP3A4 Levels are increased by ritonavir, nelfinavir,
delavirdine, indinavir, ketoconazole, clarithromycin, & grapefruit juice
RITONAVIRRITONAVIR
An inhibitor of HIV 1 & HIV 2 proteasesHigh bioavailability that is increased
with foodCommon adverse effects: GIT
disturbances, paresthesias, increase aminotransferase level, altered taste, hypertriglyceridemia
INDINAVIRINDINAVIR
Specific inhibitor of HIV- 1 & HIV-2 proteasesHigher CSF penetrationMust be consumed in empty stomach for
maximal absorptionMost common adverse effects are indirect
hyperbilirubinemia & nephrolithiasis due to crystalization
NELFINAVIRNELFINAVIR
Higher absorption in the fed stateCommon adverse effects: diarrhea &
flatulence
AMPRENAVIRAMPRENAVIR
Rapidly absorbed from the GIT and
can be taken with or without foodHigh fat meals decrease absorptionCommon adverse effects: nausea, vomiting,
diarrhea, peri-oral paresthesias, rashSteven Johnson’s syndromeInhibits CYP3A4 activity
FUSION INHIBITORFUSION INHIBITOR
ENFUVIRTIDE (T-20)ENFUVIRTIDE (T-20)Newly approved antiretroviral agentBlocks entry into the cellA synthetic 36-amino acid peptide binds
to the gp41 subunit of the viral envelope glycoprotein thus preventing the conformational changes required for the fusion of the viral and cellular membranes
Administered subcutaneously in combination with other retroviral agents
ANTI-HEPATITIS ANTI-HEPATITIS AGENTSAGENTS
ADEFOVIRADEFOVIR
Phosphorylated by cellular kinases to the active diphosphate metabolite
Competitively inhibits HBV DNA polymerase
Chain termination after incorporation into viral replication
ENTECAVIRENTECAVIROral guanosine nucleoside analogCompetitively inhibits all 3 functions of HBV
DNA polymerase—base priming, reverse transcription of negative strand and synthesis of positive strand of HBV DNA.
Taken by empty stomach half life 15 hoursSignificantly HIGHER rates of HBV DNA
viral suppression than lamivudine.
INTERFERON ALFAINTERFERON ALFA
Endogenous proteins that exert complex antiviral immunomodulatory & antiproliferative activities through cellular metabolic process
Enzyme induction, suppression of cell proliferation, immunomodulatory activities & inhibition of viral replication
Inhibition of viral penetration & uncoating Treatment of both HBV & HCV
INTERFERON ALPHA 2aINTERFERON ALPHA 2a
Approved for the treatment of chronic Hepatitis C, AIDS associated Kaposi’s sarcoma, hairy cell leukemia,
chronic myelogenous leukemia
ADEFOVIRADEFOVIR
Phosphorylated by cellular kinases to the active diphosphate metabolite
Competitively inhibits HBV DNA polymerase
Chain termination after incorporation into viral replication
ENTECAVIRENTECAVIROral guanosine nucleoside analogCompetitively inhibits all 3 functions of HBV
DNA polymerase—base priming, reverse transcription of negative strand and synthesis of positive strand of HBV DNA.
Taken by empty stomach half life 15 hoursSignificantly HIGHER rates of HBV DNA
viral suppression than lamivudine.
INTERFERON ALFAINTERFERON ALFA
Endogenous proteins that exert complex antiviral immunomodulatory & antiproliferative activities through cellular metabolic process
Enzyme induction, suppression of cell proliferation, immunomodulatory activities & inhibition of viral replication
Inhibition of viral penetration & uncoating Treatment of both HBV & HCV
INTERFERON ALPHA 2aINTERFERON ALPHA 2a
Approved for the treatment of chronic Hepatitis C, AIDS associated Kaposi’s sarcoma, hairy cell leukemia,
chronic myelogenous leukemia
INTERFERON ALPHA 2bINTERFERON ALPHA 2b
Only preparation licensed for treatment of HBV & acute HCV
Leads to loss of HbeAg, normalization of aminotransferases
Administered subcutaneously or intramuscularly
Hairy cell leukemia, malignant melanoma, follicular non-Hodgkin’s lymphoma, AIDS related kaposi’s sarcoma, & chronic Hepatitis C
PEGYLATED INTERFERON PEGYLATED INTERFERON ALFAALFA
Recently introduced for treatment of chronic hepatitis C
Longer duration with slower clearance
RIBAVIRINRIBAVIRIN
Guanosine analog that is phosphorylated intracellularly by host cell enzymes
Interferes w/ the synthesis of guanosine triphosphate
Inhibit capping of viral messenger RNA Inhibit viral RNA dependent RNA polymerase of
certain viruses Influenza A, parainfluenza, RSV, paramyxoviruses,
HCV & HIV 1
ANTI-INFLUENZA ANTI-INFLUENZA AGENTSAGENTS
AMANTADINE/RIMANTADINEAMANTADINE/RIMANTADINE
(1-aminoadamantane hydrochloride) -methyl derivative - rimantadine Inhibits uncoating of viral RNA influenza A
within infected cell thus preventing replication
Effectively reduce the duration of symptoms of influenza when administered within 48 hrs of onset
Primary target is M2 proteins
OSELTAMIVIR/OSELTAMIVIR/ZanamivirZanamivir
Neuroaminidase inhibitorsInhibits replication of
both influenza A & B5 day course regimen for
both influenza A & B
NOTE: Treatment for Bird Flu
UNCLASSIFIEDUNCLASSIFIED
PALIVIZUMABPALIVIZUMABPrevention of RSV in high risk
infants—premature and those with broncho dysplasia and congenital heart disease.
Humanized monoclonal antibody
IMQUIMOD•Immune response modifier effective in topical treatment of external genitalia & perianal warts
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