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Anti Viral
 

Anti Viral

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    Anti Viral Anti Viral Presentation Transcript

    • ANTI-VIRAL/ANTI-FUNGAL AGENTS
    • ANTI-VIRAL AGENTS
      • VIRUSES :
      • Single or double stranded DNA or RNA enclosed in a protein – CAPSID
      • Obligate intracellular parasite
      • Replication depends on synthetic processes of the host cell
      • Anti-viral drugs must either block entry or exit from cell or be active inside the host cell
    • VIRAL REPLICATION
      • Viral attachment and entry ( enfuvirtide, docosanol, palivizumab )
      • Adsorption and penetration into susceptible host
      • cells ( G lobulins 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 AGENTS
      • Anti-Herpes
      • Acyclovir Famciclovir Valacyclovir
      • Ganciclovir Valganciclovir Lamivudine
      • Vidarabine Idoxuridine Trifluridine
      • Cidofovir Sorivudine Fomivirsen
      • Penciclovir
      • Anti-retroviral Agents
      • Nucleoside RT inhibitors
      • Zidovudine Zalcitabine Didanosine
      • Stavudine Lamivudine Abacavir
      • Emtricitabine
      • Non-nucleoside RT Inhibitors
      • Nevirapine Delavirdine Efavirenz
    • ANTI-Hepatitis B
      • Lamivudine
      • Adenofovir Dipivoxil
      • Entecavir
      • Interferon alfa-2b
      • Famciclovir
      • ANTI-Hepatitis C
      • Pegylated interferon alfa-2a and 2b
      • Ribavirin, interferon alfa 2a, 2b, alfacon
    • Protease Inhibitors
      • Saquinavir Lopinavir/Ritonavir Indinavir Nelfinavir Amprenavir Darunavir Atazanavir Tipranavir Fosamprenavir
    • Anti-influenza Agents
      • Amantadine Rimantadine
      • Neuraminidase Inhibitors
      • Oseltamivir (Tamiflu)
      • Zanamivir
      • Ribavirin Palivizumab
      • Interferons
    • Miscellaneous
      • Immuno-modulating Agents
      • Inosiplex Isoprinosine
      • Foscarnet
    • ANTI-HERPES ANTI-VARICELLA ZOSTER
    • ACYCLOVIR
      • 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 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
    • PHARMACOKINETICS
      • Oral bioavailability ranges from 10-30% and decreases with increasing dose
      • Clearance thru GF and TS
      • Half-life: 3 hrs in normal renal function and 20 hrs in anuria
      • Distributes widely in body fluids including vesicular fluid, aqueous humor, and CSF
      • Concentrated in breast milk, amniotic fluid, and placenta
      • Percutaneous absorption is low
    • THERAPEUTIC 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 USES
      • ACUTE HERPES ZOSTER (SHINGLES)
      • SYSTEMIC ACYCLOVIR PROPHYLAXIS
      • HSV ENCEPHALITIS ( IV form)
      • VARICELLA ZOSTER VIRUS INFECTION
      • CMV PROPHYLAXIS
    • SIDE 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
    • VALACYCLOVIR
      • L- valyl ester of acyclovir
      • Rapidly converted to acyclovir after oral administration
      • Serum levels are 3-5x greater than acylcovir
      • Treatment of primary and recurrent genital herpes and herpes zoster infections
      • Prevents CMV disease in post-transplant patients
    • Pharmacokinetics
      • Oral bioavailability is 54%s
      • CSF fluid levels are 50% of those in serum
      • Elimination half-life: 2.5-3.3 hours
      • Generally well-tolerated
    • FAMCICLOVIR
      • 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
    • FAMCICLOVIR
      • Comparable 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
    • Pharmacokinetics
      • Oral 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
    • PENCICLOVIR
      • Penciclovir (9- [4-hydroxy-3-hydroxymethyl but-1-yl] guanine
      • An acyclic guanine nucleoside
      • Active metabolite of famciclovir
      • Spectrum of activity and potency against HSV & VZV is similar to acyclovir
      • Inhibitory activity to HSV
    • MECHANISM 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 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 EFFECTS
      • Mutagenic at high concentrations
      • (IV form is not usually given)
      • No clinically important drug interactions have identified
    • TRIFLURIDINE
      • Fluorinated pyrimidine nucleoside that has an in vitro inhibitory activity against HSV 1 & 2 , CMV, vaccinia and certain adenoviruses
      • Inhibits viral DNA synthesis
      • Phosphorylated intracellularly into its active form by cellular enzymes
      • Incorporation into both viral and cellular DNA prevents its systemic use
    • MECHANISM OF ACTION
      • Trifluridine monophosphate irreversibly inhibits thymidylate synthetase
      • Trifluridine triphosphate is a competitive inhibitor of thymidine triphosphate incorporation into DNA by DNA polymerases
    • CLINICAL 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 EFFECTS
      • Discomfort upon instillation
      • Palpebral edema
      • Hypersensensitivity reaction, irritations and superficial punctate or epithelial keratopathy
    • VIDARABINE
      • Adenosine analog with an in vitro activity against HSV, VZV, and CMV
      • Phosphorylated 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 Usage
      • 3% ointment – acute keratoconjunctivitis, superficial keratitis, recurrent epithelial keratitis (HSV1 and 2)
      • IV vidarabine – HSV encephalitis, neonatal herpes, VZV infection
    • DOCOSANOL
      • 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 AGENTS
    • GANCICLOVIR
      • (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 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
    • PHARMACOKINETICS
      • 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 USES
      • Delay progression of CMV retinitis in AIDS
      • CMV colitis & esophagitis
      • CMV infection in transplant patient
      • CMV pneumonitis
      • CMV retinitis
      • CMV, HSV1, HSV2, EBV & HHV-8
    • ADVERSE REACTIONS
      • Myelosuppression
      • CNS toxicity
      • Vitreous hemorrhage, retinal detachment
      • Neutropenia (2 nd wk)
      • CNS (headache, behavioral changes, convulsions, coma)
      • Infusion related phlebitis, azotemia, anemia, rash, fever, liver function test abnormalities
    • VALGANCICLOVIR
      • 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.
    • CIDOFOVIR
      • (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
    • PHARMACOKINETICS
      • 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 USES
      • CMV, HSV 1, HSV 2, VZV, EBV, HHV-6,HHV8, adenovirus, poxvirus, poliomyxovirus, Human papilloma virus
      • CMV retinitis
      • Polyoma virus associated progressive multifocal leukoencephalopathy syndrome associated with AIDS
      • Topical – recurrent genital herpes, anogenital warts
    • FOSCARNET
      • 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 EFFECTS
      • Nephrotoxicity
      • Symptomatic hypocalcemia
      • Saline loading may reduce the risk of nephrotoxicity
      • Concurrent administration with pentamidine exacerbates both nephrotoxicity and hypocalcemia
    • CLINICAL USES
      • CMV retinitis, colitis, esophagitis
      • Acyclovir- resistant HSV infection and VZV infection
      • HSV, VZV, CMV, EBV, HHV-6, HHV-8, HIV
    • FOMIVIRSEN
      • 21 mer-phosphorothioate oligonucleotide
      • First 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 AGENTS
    • NUCLEOSIDE REVERSE TRANSCRIPTASE 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 2
      • Lactic acidosis & severe hepatomegaly with steatosis
    • ZIDOVUDINE (Azithymidine, AZT)
      • Deoxythymidine analog
      • Decrease rate of clinical disease progression and prolong survival of HIV infected individuals
      • Well absorbed from the gut and distributed
      • to most body tissues & fluids
      • Eliminated by renal excretion following glucorinadation in the liver
      • Combination therapy with other anti-retroviral agents enhance potency and delay resistance
    • CLINICAL USES
      • HIV – associated dementia & thrombocytopenia
      • Reduce rate of vertical transmission (mother-newborn) by 23%
    • ADVERSE EFFECTS
      • Myelosuppression – most common
      • Thrombocytopenia, hyperpigmentation of nails, myopathy, anxiety, confusion and tremulousness
      • Fatal lactic acidosis & severe hepatomegaly w/ steatosis
    • DIDANOSINE (ddl)
      • Synthetic analog of deoxyadenosine
      • Activity is potentiated by hydroxyurea due to depletion of intraocular pools of d-ATP
      • Chewable, dispersable tablet, enteric coated
      • Contains phenylalanine and Na
      • Should be taken on an empty stomach
      • Food, fluroquinolones and tetracycline
      • should be given 2 hrs before didanosine
    • ADVERSE EFFECTS
      • Most major clinical toxocity: Dose –dependent pancreatitis
      • Painful peripheral distal neuropathy
      • Diarrhea, hepatitis, esophageal ulceration, cardiomyopathy
      • CNS toxicity
      • Precipitate gouty attacks
      • Optic neuritis
    • EMTRICITABINE
      • 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)
      • 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)
      • 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 ulcerations
      • Increase bioavailability in combination with probenecid or cimetidine
      • Decrease bioavailability in combination with antacids and metoclopramide
    • STAVUDINE (d4T)
      • Thymidine analog
      • High oral bioavailability, not food dependent
      • Renal excretion thru GF and TS
      • Major dose-limiting toxicity:
      • Dose-related peripheral sensory neuropathy
      • Pancreatitis, arthralgias, elevation of serum aminotransferases
      • Phosphorylation is reduced by zidovudine
    • ABACAVIR
      • Guanosine analog
      • Well absorbed during oral administration
      • Metabolized by alcohol dehydrogenase and glucuronosyl-transferase to inactive metabolites
      • Fatal hypersensitivity reactions
      • Nausea, vomiting, diarrhea, headache, fatigue
      • Hyperglycemia, hypertriglyceridemia and lactic acidosis
    • NUCLEOTIDE INHIBITOR
    • TENOFOVIR
      • 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
    • Pharmacokinetics
      • Oral 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 TRANSCRIPTASE INHIBITORS(NNRTIs)
      • Bind directly to a site on the HIV –1 reverse transcriptase
      • Blockade of RNA and DNA dependent DNA polymerase activities
      • Binding site is near but distinct from that of the NRTI’s
      • Neither compete with nucleoside triphosphate nor require phosphorylation to be active
    • NEVIRAPINE
      • 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
    • DELAVIRDINE
      • 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
    • EFAVIRENZ
      • 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 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
    • SAQUINAVIR
      • 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
    • RITONAVIR
      • An inhibitor of HIV 1 & HIV 2 proteases
      • High bioavailability that is increased with food
      • Common adverse effects: GIT disturbances, paresthesias, increase aminotransferase level, altered taste, hypertriglyceridemia
    • INDINAVIR
      • Specific inhibitor of HIV- 1 & HIV-2 proteases
      • Higher CSF penetration
      • Must be consumed in empty stomach for maximal absorption
      • Most common adverse effects are indirect hyperbilirubinemia & nephrolithiasis due to crystalization
    • NELFINAVIR
      • Higher absorption in the fed state
      • Common adverse effects: diarrhea & flatulence
    • AMPRENAVIR
      • Rapidly absorbed from the GIT and
      • can be taken with or without food
      • High fat meals decrease absorption
      • Common adverse effects: nausea, vomiting, diarrhea, peri-oral paresthesias, rash
      • Steven Johnson’s syndrome
      • Inhibits CYP3A4 activity
    • FUSION INHIBITOR
    • ENFUVIRTIDE (T-20)
      • Newly approved antiretroviral agent
      • Blocks entry into the cell
      • A 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 AGENTS
    • ADEFOVIR
      • Phosphorylated by cellular kinases to the active diphosphate metabolite
      • Competitively inhibits HBV DNA polymerase
      • Chain termination after incorporation into viral replication
    • ENTECAVIR
      • Oral guanosine nucleoside analog
      • Competitively 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 hours
      • Significantly HIGHER rates of HBV DNA viral suppression than lamivudine.
    • INTERFERON 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 2a
      • Approved for the treatment of chronic Hepatitis C, AIDS associated Kaposi’s sarcoma, hairy cell leukemia,
      • chronic myelogenous leukemia
    • ADEFOVIR
      • Phosphorylated by cellular kinases to the active diphosphate metabolite
      • Competitively inhibits HBV DNA polymerase
      • Chain termination after incorporation into viral replication
    • ENTECAVIR
      • Oral guanosine nucleoside analog
      • Competitively 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 hours
      • Significantly HIGHER rates of HBV DNA viral suppression than lamivudine.
    • INTERFERON 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 2a
      • Approved for the treatment of chronic Hepatitis C, AIDS associated Kaposi’s sarcoma, hairy cell leukemia,
      • chronic myelogenous leukemia
    • INTERFERON 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 ALFA
      • Recently introduced for treatment of chronic hepatitis C
      • Longer duration with slower clearance
    • RIBAVIRIN
      • 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 AGENTS
    • AMANTADINE/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/Zanamivir
      • Neuroaminidase inhibitors
      • Inhibits replication of
      • both influenza A & B
      • 5 day course regimen for
      • both influenza A & B
      • NOTE: Treatment for Bird Flu
    • UNCLASSIFIED
    • PALIVIZUMAB
      • Prevention 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