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