Quiz 3 Material Flashcards
Azithromycin (Zpak, Zithromax)
Macrolides/Ketolides
MOA: Binds to 50s ribosomal subunit and block peptidyltransferase center to prevent AA elongation (also inhibit 50s subunit formation)
Demeclocycline
Tetracyclines
MOA: Reversibly bind to the 30s ribosomal subunit preventing binding of tRNA = prevent protein synthesis
Neomycin
Aminoglycosides
MOA: Bind to specific 30s ribosomal proteins and interfere with the initiation of protein synthesis
Tigecycline
Tetracyclines
MOA: Reversibly bind to the 30s ribosomal subunit preventing binding of tRNA = prevent protein synthesis
Streptomycin
Aminoglycosides
MOA: Bind to specific 30s ribosomal proteins and interfere with the initiation of protein synthesis
Telithromycin
Macrolides/Ketolides
MOA: Binds to 50s ribosomal subunit and block peptidyltransferase center to prevent AA elongation (also inhibit 50s subunit formation)
Minocycline
Tetracyclines
MOA: Reversibly bind to the 30s ribosomal subunit preventing binding of tRNA = prevent protein synthesis
Gentamicin
Aminoglycosides
MOA: Bind to specific 30s ribosomal proteins and interfere with the initiation of protein synthesis
Amikacin
Aminoglycosides
MOA: Bind to specific 30s ribosomal proteins and interfere with the initiation of protein synthesis
Chloramphenicol
Other Protein Synthesis Inhibitors
MOA: Binds to the 50s subunit and inhibits peptide bond formation, Also has a high affinity to mammalian mitochondrial ribosomes
Clindamycin
Other Protein Synthesis Inhibitors
MOA: Same as erythromycin: Bind to the 50s ribosomal subunit and block the peptidyltransferase center to prevent AA chain elongation, Can also inhibit formation of the 50s subunit
Linezolid
Other Protein Synthesis Inhibitors
MOA: Inhibits formation of ribosomal complex, which binds to the 50s subunit near interface with the 30s subunit
Doxycycline
Tetracyclines
MOA: Reversibly bind to the 30s ribosomal subunit preventing binding of tRNA = prevent protein synthesis
Fidaxomicin
Macrolides/Ketolides
MOA: Binds to 50s ribosomal subunit and block peptidyltransferase center to prevent AA elongation (also inhibit 50s subunit formation)
Cotrimoxazole (Trimethoprim + Sulfamethoxazole)
Antifolate Drugs (Sulfa-Drugs)
MOA: Combination of trimethoprim and sulfamethoxazole – greater activity and broader spectrum than either drug used alone
Ciprofloxacin (Cipro)
2nd Generation Fluoroquinolones
MOA: Dual mechanism: Inhibit replication of DNA by interfering with DNA gyrase and topoisomerase IV
Ofloxacin
2nd Generation Fluoroquinolones
MOA: Dual mechanism: Inhibit replication of DNA by interfering with DNA gyrase and topoisomerase IV
Moxifloxacin
4th Generation Fluoroquinolones
MOA: Dual mechanism: Inhibit replication of DNA by interfering with DNA gyrase and topoisomerase IV
Clarithromycin
Macrolides/Ketolides
MOA: Binds to 50s ribosomal subunit and block peptidyltransferase center to prevent AA elongation (also inhibit 50s subunit formation)
Posaconazole
Azoles
MOA: Inhibits the P450 enzyme responsible for converting lanosterol to ergosterol (disrupts fungal membrane structure and function), also inhibits human and gonadal and adrenal steriod synthesis
Levofloxacin (Levaquin)
3rd Generation Fluoroquinolones
MOA: Dual mechanism: Inhibit replication of DNA by interfering with DNA gyrase and topoisomerase IV
Erythromycin
Macrolides/Ketolides
MOA: Binds to 50s ribosomal subunit and block peptidyltransferase center to prevent AA elongation (also inhibit 50s subunit formation)
Norfloxacin
2nd Generation Fluoroquinolones
MOA: Dual mechanism: Inhibit replication of DNA by interfering with DNA gyrase and topoisomerase IV
Gemifloxacin
4th Generation Fluoroquinolones
MOA: Dual mechanism: Inhibit replication of DNA by interfering with DNA gyrase and topoisomerase IV
Tobramycin
Aminoglycosides
MOA: Bind to specific 30s ribosomal proteins and interfere with the initiation of protein synthesis
Sulfacetamide
Antifolate Drugs (Sulfa-Drugs)
MOA: Compete with dihydropteroate synthetase and inhibit folate production in bacteria (thus inhibit division and growth), Structural analogues of PABA
Nitrofurantoin
Urinary Tract Antiseptics
MOA: Bacteria that are sensitive reduce the drug to a toxic intermediate (damages bacterial DNA)
Fluconazole
Azoles
MOA: Inhibits the P450 enzyme responsible for converting lanosterol to ergosterol (disrupts fungal membrane structure and function), also inhibits human and gonadal and adrenal steriod synthesis
Sulfamethoxazole
Antifolate Drugs (Sulfa-Drugs)
MOA: Compete with dihydropteroate synthetase and inhibit folate production in bacteria (thus inhibit division and growth), Structural analogues of PABA
Micafungin
Echinocandins
MOA: interfere with the synthesis of B-glucan, which disrupts cell wall and causes lysis and cell death
Trimethoprim
Antifolate Drugs (Sulfa-Drugs)
MOA: Inhibits dihydrogolate reductase – prevents conversion of dihydrofolic acid to tetrahydrofolic acid (thus interfere with folate production in bacteria), higher affinity to bacterial enzyme than mammalian
Methenamine
Urinary Tract Antiseptics
MOA: Decomposed at acidic pH of 5.5 or less, Produces formaldehyde which is toxic to bacteria
Amphotericin B
Polyene Antibiotics
MOA: Binds to ergosterol in the plasma membrane and forms a pore
Tetracycline
Tetracyclines
MOA: Reversibly bind to the 30s ribosomal subunit preventing binding of tRNA = prevent protein synthesis
Capreomycin
Second-Line Antimycobacterial Drugs
MOA: Inhibits protein synthesis
Ketoconazole
Azoles
MOA: Inhibits the P450 enzyme responsible for converting lanosterol to ergosterol (disrupts fungal membrane structure and function), also inhibits human and gonadal and adrenal steriod synthesis
Voriconazole
Azoles
MOA: Inhibits the P450 enzyme responsible for converting lanosterol to ergosterol (disrupts fungal membrane structure and function), also inhibits human and gonadal and adrenal steriod synthesis
Anidulafungin
Echinocandins
MOA: interfere with the synthesis of B-glucan, which disrupts cell wall and causes lysis and cell death
Caspofungin
Echinocandins
MOA: interfere with the synthesis of B-glucan, which disrupts cell wall and causes lysis and cell death
Nystatin
Polyene Antibiotics
MOA: Binds to ergosterol in the plasma membrane and forms a pore
Flucytosine
Other Antifungal Drugs
MOA: Enters fungal cell and disrupts DNA/protein synthesis (similar to anti-metabolites)
Griseofulvin
Other Antifungal Drugs
MOA: Inhibits fungal mitosis, deposited in newly forming skin protecting it from new infection
Terbinafin
Other Antifungal Drugs
MOA: Inhibits squalene epoxidase - Causes: block biosynthesis of ergosterol AND squalene builds up and becomes toxic
Ethambutol
First-Line Antimycobacterial Drugs
MOA: interfere with cell wall synthesis
Sulfadiazine
Antifolate Drugs (Sulfa-Drugs)
MOA: Compete with dihydropteroate synthetase and inhibit folate production in bacteria (thus inhibit division and growth), Structural analogues of PABA
Isoniazid
First-Line Antimycobacterial Drugs
MOA: Prodrug (activated by mycobacterial enzyme), active molecule targets enzymes responsible for synthesis of mycolic acid and blocks its production (mycolic acid = essential for cell wall integrity)
Pyrazinamide
First-Line Antimycobacterial Drugs
MOA: Lowers intracellular pH and inhibits growth
Rifampin
First-Line Antimycobacterial Drugs
MOA: Interacts with bacterial RNA polymerase (block transcription)
Rifabutin
First-Line Antimycobacterial Drugs
MOA: Interacts with bacterial RNA polymerase (block transcription)
Oseltamivir (Tamiflu)
Antiviral Drugs for Respiratory Virus Infections (Influenza)
MOA: Neuraminidase Inhibitors = selectively inhibits the enzyme neuraminidase (which is essential to live cycle of this virus) and prevent release of new virions (works against Type A and B)
Rifapentine
First-Line Antimycobacterial Drugs
MOA: Interacts with bacterial RNA polymerase (block transcription)
Ethionamide
Second-Line Antimycobacterial Drugs
MOA: Structurally similar to Isoniazid - Prodrug (activated by mycobacterial enzyme), active molecule targets enzymes responsible for synthesis of mycolic acid and blocks its production (mycolic acid = essential for cell wall integrity)
Cycloserine
Second-Line Antimycobacterial Drugs
MOA: Prevents cell wall synthesis
Telaprevir
Antiviral Drugs for Hepatitis
MOA: bind to active site of HCV protease
Streptomycin
Second-Line Antimycobacterial Drugs
MOA: Bind to specific 30s ribosomal proteins and interfere with the initiation of protein synthesis
Macrolides
Second-Line Antimycobacterial Drugs
MOA: Binds to 50s ribosomal subunit and block peptidyltransferase center to prevent AA elongation (also inhibit 50s subunit formation)
Dapsone
Drugs Used in Leprosy
MOA: Similar to sulfonamides, inhibits folate synthesis
Amantadine
Antiviral Drugs for Respiratory Virus Infections (Influenza)
MOA: Inhibitors of Viral Uncoating = block viral membrane matrix protein MA (which functions as a channel for H+ ions, required for fusion of viral membrane with host cell membrane)
Fluoroquinolones
Second-Line Antimycobacterial Drugs
MOA: Dual mechanism: Inhibit replication of DNA by interfering with DNA gyrase and topoisomerase IV
Rimantadine
Antiviral Drugs for Respiratory Virus Infections (Influenza)
MOA: Inhibitors of Viral Uncoating = block viral membrane matrix protein MA (which functions as a channel for H+ ions, required for fusion of viral membrane with host cell membrane)
Zanamivir
Antiviral Drugs for Respiratory Virus Infections (Influenza)
MOA: Neuraminidase Inhibitors = selectively inhibits the enzyme neuraminidase (which is essential to live cycle of this virus) and prevent release of new virions (works against Type A and B)
Boceprevir
Antiviral Drugs for Hepatitis
MOA: bind to active site of HCV protease
Interferon
Antiviral Drugs for Hepatitis
MOA: Induce host cell enzymes to inhibit viral RNA translation
Lamivudine
Antiviral Drugs for Hepatitis
MOA: Inhibits hepatitis B DNA polymerase and HIV reverse transcriptase
Tenofovir
Antiviral Drugs for Hepatitis
MOA: Inhibits viral reverse transcriptase
Acyclovir
Antiviral Drugs for Herpesvirus Infections
MOA: Converted to active form by viral enzyme (thymidine kinase), competes as a substrate for viral DNA polymerase and is incorporated into the viral DNA
Famciclovir
Antiviral Drugs for Herpesvirus Infections
MOA: Converted to active form by viral enzyme (thymidine kinase), competes as a substrate for viral DNA polymerase and is incorporated into the viral DNA
Valacyclovir
Antiviral Drugs for Herpesvirus Infections
MOA: Converted to active form by viral enzyme (thymidine kinase), competes as a substrate for viral DNA polymerase and is incorporated into the viral DNA
Ganciclovir
Antiviral Drugs for Cytomegalovirus Infections
MOA: must be activated by viral enzyme, inhibits viral DNA polymerase and can be Incorporated into viral DNA
Ribavirin
Antiviral Drugs for Hepatitis
MOA: activated by kinases that phosphorylate the drug, active metabolites inhibit purine metabolism (block synthesis of viral DNA and RNA)
Itraconazole
Azoles
MOA: Inhibits the P450 enzyme responsible for converting lanosterol to ergosterol (disrupts fungal membrane structure and function), also inhibits human and gonadal and adrenal steriod synthesis
Clofazimine
Drugs Used in Leprosy
MOA: Binds to DNA and prevents it from serving as a template for replication
Cidofovir
Antiviral Drugs for Cytomegalovirus Infections
MOA: inhibits viral DNA synthesis, does NOT depend on vial enzymes
Trifluridine
Antiviral Drugs for Herpesvirus Infections
MOA: inhibits the incorporation of thymidine triphosphate into viral DNA, can incorporate into viral DNA (and cellular DNA)