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-antiherpes agent --> DOC for HSV encephalitis -poor CNS distribution |
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-antiherpes agent -prodrug -less affinity for viral pol. than ACYCLOVIR, but can enter the cell in higher concentrations |
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-treats recurent fever blisters |
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-antiherpes agent -***can be activated by infected and host cell enzymes*** -can also be incorporated into human DNA and cause damage--> this is why it is administered LOCALLY, not systemically |
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-anti-cytomegalovirus (CMV) -can be administered via a drug releasing ocular implant--> treats RETINITIS -must be phosphorylated by the infected cell first (PHOSPHSOTRANSFERASE UL97) to be activated -prevents development of KAPOSI SARCOMA in AIDS patients ***MYELOSUPRESSION is a side effect*** |
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-anti CMV agent -Gene therapy approach to anti-viral therapy (antisense oligonucleotide) -administered intraocularly-->RETINITIS -not a first choice, but a "big gun" if other drugs don't work -can cause cataracts, or intraocular pressure |
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-treats several viruses including HIV -inhibits viral DNA and RNA polymerase or RT by inhibiting PYROPHOSPHATE binding site of the enzyme -used with Ganciclovir to treat RETINITIS, ESOPHAGITIS, and COLITIS **used when resistance to ACYCLOVIR is shown |
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-anti CMV agent along with other viruses -***given with PROBENECID*** -must be phosphorylated 2x by host cells -competitively inhibits viral DNA POLYMERASE |
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-antiretroviral (anti-HIV) -causes severe HYPERSENSITIVITY RXNS |
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-POOR ABSORPTION must be taken on empty stomach-->inactivated by gastric acids, contains buffers that can inhibit absorption of other drugs -can cause pancreatitis, hepatitis, retinal changes |
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-inhibits HEP B DNA POL and RT -hyperpigmentation of soles of hand and palms of feet |
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-inhibits HEP B and RT -can cause PANCREATITIS |
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-FLAGSHIP HIV drug -3 or more mutations necessary to acquire resistance -HIV associated dementia -prevents transfer of HIV from mother to child -can cause MYELOSUPPRESSION and HEPATOTOXICITY |
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-can cause peripheral neuropathy and ascending muscular weakness - |
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-used to prevent mother to daughter HIV transmission like Zidovudine |
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-absorption inhibited by antacids and H2 receptor antagonists -require no phosphorylation to be activated -anti-HIV 1 (not against HIV 2) -target RT -high rate of resistance development-->use several NNRTIs at once - |
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potent inhibitor in cytochrome P450 enzyme-->administered in combination with other protease inhibitor to increase clearance |
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biologic-peptide active against HIV 1 only--> bind gp41 and prevents ENTRY form occurring |
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-strong effectiveness against R5HIV1 (specific HIV strain) -alters CCR5 receptor on HOST CELL, but virus can still develop resistance |
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-inhibits viral INTEGRATION into host genome |
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-recombinant protein used to fight HEPATITIS B & C -works by eliciting immune response just like endogenous IFN alpa -can unmask autoimmune disorders, MYELOSUPPRESSION |
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-specific to HEPATITIS B -competitively inhibits HEP B DNA Polymerase |
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-Activated by host cell enzyme phosphorylation -acts against WEST NILE VIRUS, HEP C -never administered alone--> always with IFN alpha -highly CI in pregnancy including 6 months after stopping the drug |
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act against INFLUENZA A&B |
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-act against INFLUENZA A&B -CI in kids under 7 |
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-binds RSV virus -given to high risk infants and children |
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stimulates the host immune system... |
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• Activated by viral THYMIDINE KINASE (only in infected cells) • Inhibits viral DNA polymerase-->incorporates to viral DNA stoping chain elongation -poor bioavailability -resistance by mutation to thymidine kinase or DNA pol -Nephro, neuro toxicities, rashes |
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• Activated by viral thymidine kinase (only in infected cells) • Inhibits viral DNA polymerase-->incorporates to viral DNA stopping chain elongation -resistance by mutation to thymidine kinase or DNA pol -can cause MYELOSUPPRESSION, neutropenia, neurotoxicity |
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• Activated intracellularly by phosphrylation with cellular kinases •competatively inhibits RT and can get incorporated into HIV DNA • Mitochondrial toxicity (anemia, lactic acidosis) |
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• Non-competative (allosteric) inhibitors of RT -->DO NOT REQUIRE PHOSPHORYLATION FOR ACTIVATION • Active only against HIV-1 • Metabolized by Cyp-450 -cause RASHES |
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• Inhibit HIV PROTEASE which interferes with post-translational processing of precursor-->immature HIV copies -Substrates and metabolized by the Cyp-450 system ○ Ritonavir = potent inhibitor of Cyp 450, taken in combination with PIs -can cause CUSHINGOID effects |
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