2654229
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Flashcards by lola_smily, updated more than 1 year ago
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Created by lola_smily
almost 9 years ago
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| Question | Answer |
| heparin anticoagulant parenteral mucopolysaccharide source: pig lungs, pig intestinal mucosa isolated from liver high/low (higher affinity) molecular weight acidic: carboxylic acid and sulfate groups anion: at physiological pH given as Na+ salt/poor GI absorption IV/SQ (not IM: cause hematoma) -MOA: accelerates binding of antithrombin to thrombin (inhibit it + inhibit factor 10a) -metabolism (partially): depolymerization, desulfuration --> inactive mtb (liver) -prolonged effect if: renal, hepatic dysfunction -SE: hemorrhage, alopecia (after 3-4m), thrombocytopenia if high dose (>50mg) --> heparin like effects -antidote: protamine sulfate | |
| warfarin anticoagulant oral 4-hydroxycoumarin derivative racemic mixture: S(-)>R(+) given Na+, K+ salts bioavailability: 100% onset of action: 12-48h --> slow DOA: 2-5d MOA: vitamin K antagonist (inhibit vit K epoxide reductase, vit K quinone reductase, gamma carboxylation) --> reduce factors 10,9,7,2 metabolism: S--> CYP2C9/ R--> CYP2C19 2'-hydroxywarfarin (active) caution in pregnancy: crosses placenta SE: hemorrhage, skin rash, nausea, thrombocytopenia, diarrhea, skin necrosis antidote: blood transfusion, give factors | |
| vitamin K | |
| hemiketal form of warfarin similar to hemiketal form of vit K compete for same enzyme | |
| hemiketal form of vit K share similarities with hemiketal form of warfarin | |
| (S)-7-hydroxywarfarin metabolite of warfarin by CYP2C9 | |
| (S)-6-hydroxywarfarin metabolite of warfarin by CYP2C9 | |
| 2'-hydroxywarfarin metabolite of warfarin active | |
| (R)-warfarin can be metabolized by CYP2C19 on C7 | |
| anisindione anticoagulant oral 1,3-indandione derivative onset of action: 12-48h --> slow DOA: 2-5d MOA: same as warfarin alkaline urine (red-orange color) | |
| phenindione anticoagulant oral 1,3-indandione derivative onset of action: 12-48h --> slow DOA: 2-5d MOA: same as warfarin alkaline urine (red-orange color) | |
| citric acid in vitro anticoagulant chelate Ca2+ (inhibit factor 4) | |
| EDTA in vitro anticoagulant chelate Ca2+ (inhibit factor 4) | |
| aspirin (ASA) antiplatelet inhibit COX 1 irreversibly --> inhibit PGI2 and TXA2 acidic active as such GI disturbance | |
| trifusal antiplatelet inhibit COX 1 inhibit PDE active as such metabolized to: deacetylated form (2-hydroxy-4-trifluromethylbenzoic acid HTB) --> active | |
| sulfinpyrazone antiplatelet inhibit COX 1 reversibly metabolism: inactive metabolites--> p-hydroxysulfinpyrazone, sulfone, p-hydroxysulfide, sulfide | |
| dipyridamole antiplatelet inhibit PDE (phosphodiesterase) --> increase cAMP --> inhibit release of aggregating agent inhibit adenosine reuptake --> increase cAMP | |
| cilostazole antiplatelet quinolinone derivative inhibit PDE3A inhibit adenosine reuptake orally active well absorbed increase absorption with high fat meal metabolism: CYP3A4, CYP2C19--> active: DHC, HC | |
| 3,4-dehydrocilostazol antiplatelet major active metabolite of cilostazol by CYP3A4 | |
| 4'-hydroxycilostazol antiplatelet minor active metabolite of cilostazol by CYP2C19 | |
| ticlopidine antiplatelet thienopyridine derivative prodrug orally active MOA: ADP pathway inhibitor, inhibit GP2b/3a receptor t1/2: 24-36h --> long onset of action: 48h --> slow metabolism (liver): 2-keto metabolite, thiol metabolite (active), M5 and M6 (toxic) SE: neutropenia, thrombocytopenia, skin rash, GI effects | |
| clopidogrel antiplatelet thienopyridine derivative prodrug orally active MOA: ADP pathway inhibitor t1/2= 24-36h --> long metabolism: hydrolyzation of the thiol--> active metabolite (bind to P2Y and prevent binding of ADP--> t1/2= 8h) SE: rare neutropenia, thrombocytopenia, GI effects | |
| prasugrel antiplatelet thienopyridine derivative orally active metabolism: hydrolyzed to thiolactone then thiol --> active used in combination with aspirin like clopidogrel: non competitive antagonist of P2Y12 (irreversibly)--> block ADP for the life of platelets (10days) | |
| eptifibatide antiplatelet GP2b/3a receptor antagonist cyclic heptapeptide (KGD sequence) IV t1/2= 2.5h --> short excretion: renal | |
| tirofiban antiplatelet GP2b/3a receptor antagonist non peptide (distance btw COO- and NH+ is identical to RGD sequence--> compete with fibrinogen) t1/2= 2h --> short IV excretion: renal (unchanged) | |
| epoprostenol antiplatelet prostaglandin metabolite of arachidonic acid PGI2 potent vasodilator IV t1/2= 3-6min increase in cAMP--> decrease release of aggregation mediator | |
| Abciximab | antiplatelet GP2b/3a receptor antagonist monoclonal antibody IV short t1/2= 30min |
| urokinase | fibrinolytic agent from human urine and renal cells act on plasminogen to produce plasmin nonantigenic |
| streptokinase | fibrinolytic agent from hemolytic streptococci generates more plasmin than urokinase (via 2 steps) allergic reactions (due to Ab formation) |
| anistriplase | fibrinolytic agent prodrug 2nd generation plasminogen activator acetylated-plasminogen-streptokinase-activator complex (APSAC) p-anisoyl derivative of Lys-plasminogen-streptokinase |
| alteplase | fibrinolytic agent 2nd generation plasminogen activator tissue plasminogen activator (tPA) formed by recombinant DNA techniques |
| reteplase | fibrinolytic agent 3rd generation plasminogen activator modified alteplase less affinity to fibrin clot than alteplase |
| ananase | fibrinolytic agent mixture of proteolytic enzymes from pineapple plant non selective to fibrin clot anti-inflammatory agent cheap |
| tenecteplase | fibrinolytic agent 3rd generation plasminogen activator composed of 527a.a.: 103 a.a: Thr--> Asp 117 a.a: Asp--> Glu 296-299 a.a: Lys-His-Arg-Arg--> Ala (x4) 15X higher fibrin selectivity elimination: hepatically |
| prostaglandin prostanoic acid derivative must have: 15-alpha OH 13-14 trans double bond alpha/beta chain: trans A,B,C,D,E,F,G,H,I (differ in C9-11) | |
| PGD | |
| PGE PGE1: dilation of bronchiol smooth muscle PGE2: dilation of bronchiol smooth muscle, dilation of blood vessel | |
| PGF2alpha constriction of bronchiol smooth muscle, constriction of blood vessels | |
| PGG/PGH | |
| PGI2 (prostacyclin) from PGH2 inhibit platelet aggregation dilation of blood vessels | |
| TXA2 from PGH2 aggregation of platelet constriction of blood vessels | |
| arachidonic acid cis 5,8,11,14-eicosatetraenoic acid precursor of prostaglandins by COX and leukotrienes by LOX | |
| acetanilide NSAID removed from market form: acetaminophen/ aniline --> toxic SE: methemoglobenemia, skin rash, jaundice | |
| phenacetin NSAID removed from market form: acetaminophen/ aniline --> toxic SE: nephritis, carcinogenecity in rats | |
| acetaminophen NSAID antipyretic, analgesic little antiinflammatory activity MOA: reversible inhibitor of COX3 (brain) metabolism: by CYP2E1--> N-acetylmidoquinone (reactive metabolite) by glucuronidation and sulfation | |
| N-acetylimidoquinone (NAPQI) metabolite of acetaminophen metabolism: N-acetylcysteine, glutathione (renal excretion), hepatic protein (hepatic necrosis) | |
| salicylic acid metabolite of aspirin | |
| aspirin NSAIDs MOA: irreversibly inhibits COX1 (10-100X)> COX2 enzymes by acetylating serine 530 pKa=3.49 salicylate anion essential for activity stable in dry condition -absorbtion: upper small intestine (depend on gastric pH, tablet formulation, presence of food in stomach) high pH: increase ionization--> more soluble --> less absorbed buffering agent: if high dose --> decrease absorption if low dose --> increase absorption -formulation: tablet of small particles --> absorbed faster absorption from rectal--> slow absorption after topical--> fast -metabolism: hydrolyzed to salicylic acid and acetic acid (in aqueous solution) by glucuronidation, glycine conjugation stable in: alcohol, glycerin -SE: GI disturbance, salicylism (high dose) --> tinnitis, fatal --> respiratory failure (medullary depression) at high dose, Reye's syndrome in children with viral infection :influenza, chicken pox (encephalopathy, liver damage, violent headache), GI: (PGs--> cryoprotective for the gastric mucosa) gastric distress/bleeding, acute hemorrhage (dose dependent) | |
| salicylamide NSAIDs analgesic and antipyretic (not antiinflammatory) fairly stable to heat and moisture poor water solubility for aspirin sensitive patients no gastric irritation more CNS effect than aspirin metabolism: inactive --> not hydrolyzed to salicylic acid | |
| salsalate NSAIDs dimer of salicylic acid insoluble in gastric acid juice -metabolism: partially hydrolized in intestine --> 2 salicylic acid molecules (site of absorption), forms less salicylic acid than aspirin (15%) -less gastric upset than aspirin | |
| diflunisal NSAIDs analgesic, little antipyretic insoluble in water slightly more potent than aspirin t1/2= longer than aspirin -metabolism: ether/ester glucuronide not metabolized to salicylic acid--> no gastric upset -SE: few, GI disturbances, diarrhea, skin reaction | |
| mesalamine NSAID 5-amino salicylic acid metabolite of sulfasalazine and olsalazine MOA: inhibit COX in the bowel mucosa--> decrease colonic inflammation inhibit LOX --> decrease leukotrienes | |
| sulfasalazine prodrug precursor of mesalamine metabolized by azo reductase | |
| olsalazine prodrug precursor to mesalamine in GI tract by bacterial flora act locally (not systemically) | |
| phenylbutazone NSAIDs 4-butyl-1,2-diphenyl-3,5-pyrazolidinedione not a drug of choice analgesic, antipyretic, antiinflammatory slight water soluble -to treat: painful symptoms of gout (uricosuric), rheumatoid arthritis, bursitis -metabolism: to oxyphenbutazone (active NSAID), glucuronidation, gamma-hydroxyphenylbutazone (uricosuric), gamma-ketophenylbutazone (antiinflammatory) -SE: abdominal discomfort, nausea, skin rashes, peptic ulcer, blood disorder -contraindicated: in children <14y --> due to Na+ retention | |
| oxyphenbutazone NSAIDs metabolite of phenylbutazone same potency as phenylbutazone same SE but with less GI effect | |
| indomethacin NSAIDs arylalkonic acid indole acetic acid derivative most potent (analgesic agent: more than aspirin, antipyretic agent: more than phenylbutazone, antiiflammatory agent: more than phenylbutazone) weak water soluble light sensitive rapid absorption after oral dose highly bound to plasma protein metabolized to inactive SE: GI disturbance, headache, vertigo, dizziness, severe depression, suicide attempts | |
| sulindac NSAIDs arylalkonic acid indene derivative prodrug water soluble (at alkaline pH) stable at alkaline aqueous solution, air, 100C t1/2= 8h (sulfide t1/2=16h) absorbed: as sulfoxide -metabolism: to sulfide derivative (in the cirulation) -analgesic activity: equal to indomethacin -antiinflammatory/antipyretic activity: less than indomethacin -for: rheumatoid arthritis, osteoarthritis, gouty arthritis, ankylosing spondylitis -SE: gastric irritation, headache, vertigo, dizziness, skin rash | |
| sulfide NSAID active metabolite of sulindac t1/2= 16h | |
| tolmetin sodium NSAIDs arylalkonic acid N-methylpyrrole acetic acid derivative very water soluble free acid form--> water insoluble t1/2= 1h --> short -potency: more than phenylbutazone, less than indomethacin -for: different types of arthritis -metabolism: to inactive metabolites -SE: GI disturbance (less than aspirin) | |
| diclofenac sodium NSAIDs arylalkonic acid most used NSAID in the world poor water soluble complete absorption after oral dose highly bound to plasma protein 50% bioavailabilty (first pass) analgesic, antipyretic, antiinflammatory analgesic/antipyretic agent: more potent than aspirin more potent than indomethacin -MOA: inhibit COX1 and LOX inhibit arachidonic acid release, stimulate uptake --> decrease AA availability -for: rheumatoid arthritis, osteoarthritis, ankylosing spondylitis -metabolite: 4'OH (30-40%)--> weak act. | |
| etodolac NSAIDs arylalkonic acid tetrahydropyrano acetic acid derivative rapid GI absorption highly bound to plasma protein -antiinflammatory: more potent than aspirin, sulindac less potent than indomethacin -racemate--> S(+) active -metabolized: to inactive | |
| nabumetone NSAIDs prodrug non acid derivative water insoluble analgesic: less active than aspirin -metabolism (rapid): acetic acid derivative --> 6-methoxynaphtalene-2-acetic acid (6MNA) (38%) --> active -less gastric damage (absorbed as ketone, converted to 6MNA in circulation) -for: osteoarthritis, rheumatoid arthritis | |
| 6MNA active metabolite of nabumetone in circulation | |
| ibuprofen NSAIDs arylpropionic acid 2(p-isobutylphenyl)propionic acid most used NSAID orally active -same effect as aspirin (less SE) racemic mixture--> S(+) more potent than R(-) -for: osteoarthritis, rheumatoid arthritis, antipyretic, mild to moderate pain -metabolism: to inactive metabolite give ibufenac (active)--> less potent, hepatotoxic -excretion: (+) isomer | |
| ibufenac p-isobutylphenyl acetic acid active form of ibuprofen less potent hepatotoxic | |
| fenoprofen calcium NSAIDs arylpropionic acid derivative 2(3'-phenoxyphenyl)propionic acid slightly water soluble rapid absorption after oral dose highly bound to plasma protein Na+ and Ca2+ salts (less hygroscopic): similar pharmacokinetic -antiinflammatory: less potent than ibuprofen PG synthesis inhibitor: more potent than aspirin, less potent than indomethacin metabolism: to inactive metabolites | |
| ketoprofen NSAIDs arylpropionic acid derivative) 2(3'-benzoylphenyl)propionic acid insoluble in water and many organic solvent rapidly completely absorbed after oral dose -MOA: inhibit COX, inhibit LOX, lysosomal mb stabilizer--> decrease release of lysosomal enzymes--> decrease tissue damage -for: osteoarthritis, rheumatoid arthritis, antipyretic, mild to moderate pain, dysmenorrheal -metabolism: glucuronidation, carbonyl reduction, ring hydroxylation | |
| naproxen NSAIDs arylpropionic acid derivative 2(6'-methoxy-2'-naphtyl)propionic acid both enantiomer marketed: (-)--> anaprox (naproxen Na+) complete GI absorption after oral dose 99% bound to plasma protein -PG synthesis inhibitor: more potent than aspirin, phenylbutazone, ibuprofen -antiinflammatory: less potent than indomethacin -analgesic/antipyretic: more potent than phenylbutazone, aspirin, indomethacin -ulceration: less--> than aspirin, indomethacin, ketoprofen, tolmetin more--> than sulindac -for: different types of arthritis, ankylosing spondylitis, tenditis, bursitis, mild-moderate pain -metabolism: to inactive--> glucuronidation and O-demethylation -SE: GI irritation, nausea, dizziness | |
| suprofen NSAIDs arylpropionic acid 2(4'(2'thienyl carbonyl)phenyl)propionic acid removed from market because renal failure reintroduced as mydriatic agent: for ophtalmic use --> inhibit intraoperative miosis | |
| flubiprofen NSAIDs arylpropionic acid derivative 2(2'-fluoro-4'-biphenyl)propionic acid Na+ salt: topical for ophtalmic use(ocufen)--> mydriatic agent (inhibit intraoperative miosis) free acid form: oral use (ansaid)--> top prescribed use (osteo, rheumatoid arthritis) well GI absorption after oral dose 99% bound to plasma protein antiinflammatory: more potent than aspirin, phenylbutazone antipyretic: more potent than aspirin analgesic: more potent than ibuprofen -metabolized: to inactive metabolite--> glucuronidation, sulfation, 4'OH, 3',4'OH, 3'OH, 4'-OCH3 | |
| ketorolac NSAIDs arylpropionic acid derivative 5-benzoyl-2,3-dihydro-1-pyrrolidine-1-carboxylic acid orally active highly bound to plasma protein analgesic activity: comparable to morphine for: ophtalmic use, injection, for short term management of pain | |
| oxaprozin NSAIDs arylpropionic acid derivative (not alpha methyl acetic acid derivative) complete absorption after oral dose highly bound to plasma proteins t1/2= 59h--> long onset: rapid long acting antiinflammatory: equal to aspirin -for: short, long term treatment of osteoarthritis, rheumatoid arthritis -metabolism: (in liver) p-hydroxylation --> active -SE: skin rash, mild photosensitivity | |
| fenamic acid NSAIDs arylanthranilic acid derivatives antiiflammatory/analgesic activities: little or no advantage over salicylates -MOA (like salicylates): COX inhibition -SE (like salicylates): GI disturbances, headache, dizziness, skin rash, transient hepatic and renal abnormalities | |
| mefenamic acid NSAIDs N(2',3'-xylyl)anthranilic acid Orally active water insoluble (except at high pH) Highly bound to plasma proteins analgesic (mainly), anti-inflammatory t1/2=2-4h --> short for short term pain management Metabolized: to inactive metabolites--> ester glucuronide, hydroxymethyl and dicarboxylic acid | |
| meclofenamate sodium NSAID arylanthranilic acid derivative | |
| meclofenamic acid NSAID arylanthranilic acid derivative Rapidly, completely absorbed after oral dose Highly bound to plasma proteins t1/2= 2-4h --> short -potency: 25% more than mefenamic acid -Metabolism: oxidation of methyl, ring hydroxylation and monodehalogenation | |
| meclofenamic acid metabolite active by oxidation of methyl | |
| piroxicam NSAIDs oxicam 4-hydroxy-1,2-benzothiazine carboxamides pKa=4-6 (acidic) orally active highly bound to plasma protein more potent than fenamate -potency: piroxicam> indomethacin> ibuprofen Long t ½ 38 hrs -anti-inflammatory agent: more potent than aspirin and phenylbutazone, equal to indomethacin analgesic agent: less potent than indomethacin, equal to fenoprofen, ibuprofen, naproxen and phenylbutazone -MOA: Inhibitor of COX, lysosomal enzymes release and migration of polymorphonuclear cells into inflammatory sites, inhibits collagen induced platelet aggregation -Metabolism: pyridine and aromatic benzothiazine ring hydroxylation (inactive metabolites) -SE: Same like other NSAIDs -for (most commonly used NSAIDs): osteoarthritis and rheumatoid arthritis, ankylosing spondylitis | |
| meloxicam NSAIDs oxicam 4-hydroxy-1,2-benzothiazine carboxamides pKa=4-6 (acidic) orally active highly bound to plasma protein more potent than fenamate -MOA: selectivity to COX2 -metabolism: CYP2C9 (extensively) and CYP3A4 (less) -SE: Less GI side effects | |
| celecoxib First NSAID marketed as selective COX-2 inhibitor Diarylpyrazole derivative does not contain carboxylate anion Orally active t1/2= 11h -metabolizm: into inactive metabolites -SE: Less GI disturbances than other NSAIDs, causes edema and hypertension (caution in case of CHF) | |
| valdecoxib NSAIDs selective COX2 inhibitor oxazole moiety Orally active t1/2= 7-8h -metabolizm: by CYP3A4 and CYP2D6 (substrate and inhibitor of these enzymes) | |
| parecoxib NSAIDs selective COX2 inhibitor Prodrug IV and IM (only parenterally administered coxib -metabolism: rapidly metabolized (in vivo) --> valdecoxib -analgesic: more potent than ketorolac | |
| etoricoxib NSAIDs selective COX2 inhibitor Orally active t1/2= 22h --> long -metabolism: by CYP3A4 (but is not inhibitor)--> 6'-hydroxymethyl and 1-N-oxide , glucuronides-->inactive -excretion: mainly renal elimination as metabolites | |
| prontosil antimetabolite sulfonamide prodrug ozo moiety only active in vivo metabolism: to sulfanilamide poor water soluble forms crystalluria | |
| sulfanilamide antimetabolite aniline sulfonamides White colorless bitter tasting crystals weak acids water insoluble -More soluble in alkaline solutions than acidic -available as Na+ salts --> moderately water soluble -structurally analogues of PABA --> compete with dehydropteroate synthase (get incorporated in folic acid synthesis) -do not affect mammalian cells -cross placenta -metabolism (in liver): to inactive -Activity against: gram-ve/ gram +ve, E.coli, nocardia. -SE: urinary tract disturbances, hypersensitivity, hematopoietic disturbances rare: aplastic and hemolytic anemia, agranulocytosis, thrombocytopenia kernicterus and jaundice, anorexia, nausea, vomiting and diarrhea -DDI: Potentiation of sulfonylurea oral hypoglycemics, oral anticoagulants and hydantoin (due to displacement from plasma proteins) -Drug resistance: altered enzyme (major), overproduction of PABA, reduced cellular reuptake of drug, enhanced drug inactivation | |
| sulfamethoxazole antimetabolite Sulfonamide rapidly absorbed and rapidly eliminated t1/2= 10h --> short ppb: 70% highly water soluble--> rarely produce crystalluria | |
| sulfisoxazole antimetabolite Sulfonamide rapidly absorbed and rapidly eliminated t1/2= 6h --> short ppb: 90% highly water soluble--> rarely produce crystalluria | |
| Sulfadiazine antimetabolite Sulfonamide rapidly absorbed and rapidly eliminated t1/2= 10-17h most active ppb: 45% --> low relatively water soluble --> crystalluria | |
| sulfamethizole antimetabolite Sulfonamide rapidly absorbed and rapidly eliminated t1/2= 9h -->short ppb: 90% --> highly bound | |
| sulfasalazine antimetabolite Sulfonamide poorly absorbed prodrug for: treating GI infections metabolizm: by bacteria flora | |
| sulfapyridine toxic mtb of sulfasalazine absorption: from GI excretion: in urine | |
| mesalamine 5-para-amino salycilic acid active mtb of sulfasalazine | |
| sulfadoxine antimetabolite Sulfonamide rapidly absorbed (from GI) but very slowly eliminated ppb: 98% --> highly bound t ½ 7-10 days--> extraordinary | |
| Silver sulfadiazine antimetabolite sulfonamide Topically administered their salts are very potent antimicrobial in the treatment of burns, scald & wound infection | |
| sulfacetamide antimetabolite sulfonamide Topically administered their salts are very potent antimicrobial in the treatment of burns, scald & wound infection | |
| Mafenide antimetabolite not a true sulfonamide Topically administered | |
| trimethoprim antimetabolite Not a sulfonamide Trimethoxy benzyl diaminopyridine, Bacteriostatic -MOA: Potent inhibitor of DHF reductase, Similar antibacterial spectrum to sulfonamides Higher affinity to bacterial DHF reductase than mammalian -Mostly compounded with sulfamethoxazole TMP/SMX (Cotrimoxazole) oral and IV -potency: TMP (20-50X) > SMX -absorption: TMP well absorbed from GI -ppb: 60-70% -concentrated in prostatic fluid and vaginal fluid--> most used in UTI -excretion: mainly renal, small amounts biliary -SE:- Long term use: antifolate effects, folate deficiency, megaloblastic anemia, granulocytopenia, leucopenia (reversed by folinic acid), nausea, vomiting, fever, renal damage, skin rashes, CNS disturbances | |
| polymyxin bacterial cell membrane disrupting agent Cyclic polypeptides (by Bacillus polymyxa, soil bacteria) polymyxin sulfate B (B1 and B2) Polymyxin E (E1, E2) --> colistin Bactericidal cationic detergent (5 + charges) -MOA: React with – charged phospholipids-->disrupt cell mb --> creates holes --> cell leakage -active against most Gram – (not against Gram + and anaerobics) -Pseudomonnas aeruginosa (only): elevated levels of Mg2+ and Ca2+ --> decrease activity -absorption: GI (not well), topically, IV and IM, (found in ophthalmic, otic) -for: bacterial diarrhea -poor distribution (don't enter CSF) -excretion:renal via GF -SE: topically (few), orally (high dose): nausea and vomiting ,IV: nephro and neurotoxicity (accumulates in renal tubules) Large dose: damage to mammalian cell membranes --> inhibit NMJ --> respiratory paralysis -DDI: Aminoglycosides + polymyxins--> increase risk of respiratory/renal dysfunction NMJ blockers + polymyxins--> increase effect of NMJ -Use of polymyxins--> overgrowth of non-susceptible--> superinfection | |
| daptomycin bacterial cell membrane disrupting agent Novel cyclic lipopeptide antibiotic from Streptomyces sp. Consists of 13 a.a. bactericidal (dose dependant) -MOA: on Gram + (via acyl tail--> membrane depolarization), disrupts bacterial plasma mb function without penetrating into cytoplasm -MIC (minimal inhibitory concentration): for susceptible strains is 4X< vancomycin -post-antibiotic effect (PAE) -Synergism with gentamicin against staph. and enterococci IV ppb: 90% t1/2= 6.5-32h -excretion: mainly renal (80%)--> 2/3 intact -SE: Constipation, myopathy (dose dependent), GI discomfort, nausea, diarrhea, skin rash, headache, insomnia | |
| 6-aminopenicillanic acid (6-APA) beta-lactam fermentation derived not active: very minimal activity after acylation --> active compound (penicillin) | |
| penam beta lactam antibiotic | |
| penem beta lactam antibiotic 2,3-dihydrothiazole | |
| carbapenem beta lactam antibiotic 2,3-dihydro-1H-pyrrole | |
| cefem beta lactam antibiotic 3,6-dihydro-2H-1,3-thiazine | |
| monobactam beta lactam antibiotic | |
| carbacephems beta lactam antibiotic 1,2,3,4-tetrahydropyridine | |
| oxacephems beta lactam antibiotic 3,6-dihydro-2H-1,3-oxazine | |
| Pen G benzyl penicillin beta lactam antibiotic fermentation derived must be kept dry Na and K salts are crystalline, hygroscopic and water soluble orally and parenterally stable for a long time unless in solution improved acid stability (by addition of e- withdrawing grp on side chain) -excretion: renally by tubular secretion -MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall -SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| Pen V phenoxy methyl penicillin beta lactam antibiotic must be kept dry Na and K salts are crystalline, hygroscopic and water soluble orally and parenterally stable for a long time unless in solution improved acid stability (by addition of e- withdrawing grp on side chain) -excretion: renally by tubular secretion -MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall -SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| methicillin beta lactam antibiotic semi-synthetic penicillinase resistant (bulky group on diortho) parenteral contains e-donating groups --> not acid resistant -excretion: renally by tubular secretion -MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall -SE: Nephritis / hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| nafcillin beta lactam antibiotic semi-synthetic penicillinase resistant (bulky group on diortho) parenteral contains e-donating groups --> not acid resistant -excretion: renally by tubular secretion -MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall -SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| oxacillin beta lactam antibiotic semi-synthetic penicillinase resistant improved acid stability oral -excretion: renally by tubular secretion -MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall -SE: hepatitis / hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| cloxacillin beta lactam antibiotic semi-synthetic penicillinase resistant improved acid stability oral -excretion: renally by tubular secretion -MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall -SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| dicloxacillin beta lactam antibiotic semi-synthetic penicillinase resistant improved acid stability oral -excretion: renally by tubular secretion -MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall -SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| carbenizillin beta lactam antibiotic semi-synthetic carboxypenicillin penicillinase sensitive extended spectrum : antipseudomonas parenteral -excretion: renally by tubular secretion -MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall -SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| carbenicillin phenyl beta lactam antibiotic semi-synthetic carboxypenicillin penicillinase sensitive extended spectrum : antipseudomonas parenteral -excretion: renally by tubular secretion -MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall -SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| carbenicillin indanyl beta lactam antibiotic semi-synthetic carboxypenicillin penicillinase sensitive extended spectrum : antipseudomonas parenteral -excretion: renally by tubular secretion -MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall -SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| ticarcillin beta lactam antibiotic semi-synthetic carboxypenicillin penicillinase sensitive extended spectrum : antipseudomonas parenteral -excretion: renally by tubular secretion -MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall -SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| azlocillin beta lactam antibiotic semi-synthetic ureidopenicillin penicillinase sensitive extended spectrum : antipseudomonas parenteral -excretion: renally by tubular secretion -MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall -SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| mezlocillin beta lactam antibiotic semi-synthetic ureidopenicillin penicillinase sensitive extended spectrum : antipseudomonas parenteral -excretion: renally by tubular secretion -MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall -SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| piperacillin beta lactam antibiotic semi-synthetic ureidopenicillin penicillinase sensitive extended spectrum : antipseudomonas parenteral -excretion: renally by tubular secretion -MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall -SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| Ampicillin beta lactam antibiotic alpha-aminobenzylpenicillin semi-synthetic penicillinase sensitive broad spectrum oral improved acid stability excreted renally by tubular secretion MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| amoxicillin beta lactam antibiotic alpha amino-p-hydroxybenzylpenicillin semi-synthetic penicillinase sensitive broad spectrum oral improved acid stability -excretion: renally by tubular secretion -MOA : cell wall inhibitor - inhibit PBPs, the cross linking of peptidoglycan matrix/ activate autolytic enzymes : degrade the already formed cell wall -SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| Bacampicillin beta lactam antibiotic penicillin prodrug hydrolyzed by non specific esterase --> unstable products that form active free carboxylic acid SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| Pivampicillin beta lactam antibiotic penicillin prodrug hydrolyzed by non specific esterase --> unstable products that form active free carboxylic acid SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| Talampicillin beta lactam antibiotic penicillin prodrug hydrolyzed by non specific esterase --> unstable products that form active free carboxylic acid SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| Pen G procaine beta lactam antibiotic amine salt of Pen G low water solubility given IM : local depot: slow dissolution and release --> prolong blood levels -excretion: renally by tubular secretion -SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| Pen G benzathine beta lactam antibiotic diamine salt of Pen G very water insoluble given IM : local depot: slow dissolution and release --> prolong blood levels for more than a week -excretion: renally by tubular secretion -SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| Clavulanic acid beta lactamase inhibitors weak affinity to PBPs high affinity to beta lactamase irreversible beta lactamase inhibitor (adjunct therapy) produced from streptomyces clavuligeris 1-oxopenam lack 6-amino group has 2-hydroxyethylidene moiety formulated with amoxicillin SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| Sulbactam beta lactamase inhibitor weak affinity to PBPs high affinity to beta lactamase irreversible beta lactamase inhibitor (adjunct therapy) semi-synthetic 1,1-dioxopenicillanic acid formulated with ampicillin SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| Tazobactam beta lactamase inhibitor weak affinity to PBPs high affinity to beta lactamase irreversible beta lactamase inhibitor (adjunct therapy) semi-synthetic 1,1-dioxopenicillanic acid formulated with pipericillin SE: hypersensitivity / GI disturbances / neurotoxicity (seizures) | |
| Cephalosporin C beta lactam antibiotic Isolated from C.acremonium Not potent enough to be clinically as an antibiotic Precursor to develop useful derivatives | |
| 7-ACA beta lactam antibiotic 7-aminocephalosporanic acid formed by the removal of the side chain from cephalosporin C analogous to 6-APA used to prepare semi-synthetic analogs Its 7-phenylglycine derivatives are orally active | |
| 7-ADCA beta lactam antibiotic 7-Amino-3-deacetoxy-cephalosporanic acid metabolite of pen V reduced acetoxy methyl of 7-ACA Its analogs are orally active | |
| Cephapirin beta lactam antibiotic first generation cephalosporin parenteral agent sodium salt MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefazolin beta lactam antibiotic first generation cephalosporin parenteral agent sodium salt 5 membered ring (thiadiazole) --> increase potency MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cephalexin beta lactam antibiotic first generation cephalosporin oral agent because it contains an alpha amino benzyl substituent HCl salt MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefadroxil beta lactam antibiotic first generation cephalosporin oral agent because it contains a p-hydroxybenzyl substituent MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cephradine beta lactam antibiotic first generation cephalosporin oral and parenteral agent it contains an alpha amino benzyl substituent MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefamandole nafate beta lactam antibiotic second generation cephalosporin parenteral agent contains NMTT --> bleeding problems and disulfiram side effects MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefonicid beta lactam antibiotic second generation cephalosporin parenteral agent MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefuroxime beta lactam antibiotic second generation cephalosporin parenteral agent MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefoxitin beta lactam antibiotic second generation cephalosporin parenteral agent Cephamycin : produced by Streptomyces species posses 7 alpha methoxy substituent => more resistance to beta lactamases MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefotetan beta lactam antibiotic second generation cephalosporin parenteral agent contains NMTT --> bleeding problems and disulfiram side effects Cephamycin : produced by Streptomyces species posses 7 alpha methoxy substituent => more resistance to beta lactamases MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefmetazole beta lactam antibiotic second generation cephalosporin parenteral agent contains NMTT --> bleeding problems and disulfiram side effects Cephamycin : produced by Streptomyces species posses 7 alpha methoxy substituent => more resistance to beta lactamases MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefaclor beta lactam antibiotic second generation cephalosporin oral agent because it contains an alpha amino benzyl substituent MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Loracarbef beta lactam antibiotic second generation cephalosporin oral agent because it contains an alpha amino benzyl substituent carba analogue of cefaclor : sulfur atom replaced by carbon --> less potent MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefprozil beta lactam antibiotic second generation cephalosporin oral agent because it contains a p-hydroxybenzyl substituent MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefotaxime beta lactam antibiotic third generation cephalosporin parenteral agent contains an alkoxyimino substituent => resistant to beta lactamases MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Ceftizoxime beta lactam antibiotic third generation cephalosporin parenteral agent contains an alkoxyimino substituent => resistant to beta lactamases MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Ceftriaxone beta lactam antibiotic third generation cephalosporin parenteral agent contains an alkoxyimino substituent => resistant to beta lactamases MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Biliary excretion | |
| Ceftazidime beta lactam antibiotic third generation cephalosporin parenteral agent contains an alkoxyimino substituent => resistant to beta lactamases MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefoperazone beta lactam antibiotic third generation cephalosporin parenteral agent MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Biliary excretion | |
| Cefixime beta lactam antibiotic third generation cephalosporin oral agent contains an alkoxyimino substituent => resistant to beta lactamases MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Ceftibuten beta lactam antibiotic third generation cephalosporin oral agent MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefpodoxime proxetil beta lactam antibiotic third generation cephalosporin oral agent contains an alkoxyimino substituent => resistant to beta lactamases ester prodrug MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefdinir beta lactam antibiotic third generation cephalosporin oral agent contains an alkoxyimino substituent => resistant to beta lactamases MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefditoren pivoxil beta lactam antibiotic third generation cephalosporin oral agent contains an alkoxyimino substituent => resistant to beta lactamases ester prodrug MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefepime beta lactam antibiotic fourth generation cephalosporin parenteral agent exist as zwitterion contains an alkoxyimino substituent => resistant to beta lactamases More gram -ve (against P. aeruginosa) and greater beta lactamase resistance MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefelidine beta lactam antibiotic fourth generation cephalosporin parenteral agent exist as zwitterion contains an alkoxyimino substituent => resistant to beta lactamases More gram -ve (against P. aeruginosa) and greater beta lactamase resistance MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefpirome beta lactam antibiotic fourth generation cephalosporin parenteral agent exist as zwitterion contains an alkoxyimino substituent => resistant to beta lactamases More gram -ve (against P. aeruginosa) and greater beta lactamase resistance MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefozopran beta lactam antibiotic fourth generation cephalosporin parenteral agent exist as zwitterion contains an alkoxyimino substituent => resistant to beta lactamases More gram -ve (against P. aeruginosa) and greater beta lactamase resistance MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Cefluprenam beta lactam antibiotic fourth generation cephalosporin parenteral agent exist as zwitterion contains an alkoxyimino substituent => resistant to beta lactamases More gram -ve (against P. aeruginosa) and greater beta lactamase resistance MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Ceftobiprole beta lactam antibiotic fifth generation cephalosporin parenteral agent More gram -ve (against P. aeruginosa) and greater beta lactamase resistance activity against MRSA MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Ceftaroline fosamil beta lactam antibiotic fifth generation cephalosporin parenteral agent More gram -ve (against P. aeruginosa) and greater beta lactamase resistance activity against MRSA MOA : inhibit cell wall synthesis/similar to penicillins : inhibit PBPs & activate autolytic enzymes (inhibit the last stage: stage 3) Renal excretion via tubular secretion | |
| Thienamycin beta lactam antibiotic carbapeneme Natural : streptomyces cattleya broad spectrum hydroxyethyl at C-6 --> resistant to beta lactamase chemically unstable : -undergoes beta lactam ring opening => inactive -form a dimer => inactive MOA : inhibit cell wall synthesis | |
| Imipenem beta lactam antibiotic carbapenem addition of N-formiminoyl moiety to Thienamycin --> less Nu semi-synthetic more chemically stable not orally active hydrolyzed by dehydropeptidase DHP enzyme in renal tubule => inactive and nephrotoxic metabolites formulated with cilastatin (inhibitor of DHP) MOA : inhibit cell wall synthesis | |
| Meropenem beta lactam antibiotic carbapeneme synthetic same activity as Imipenem not hydrolyzed by DHP => no need for formulation with cilastatin MOA : inhibit cell wall synthesis | |
| Ertapenem beta lactam antibiotic carbapenem synthetic same activity as Imipenem not hydrolyzed by DHP => no need for formulation with cilastatin MOA : inhibit cell wall synthesis | |
| Biapenem beta lactam antibiotic carbapenem synthetic same activity as Imipenem not hydrolyzed by DHP => no need for formulation with cilastatin MOA : inhibit cell wall synthesis | |
| Aztreonam beta lactam antibiotic monobactam synthetic chemically stable for 48h strong e-withdrawing sulfamic acid => less stable alpha methyl at C2 --> beta lactamase resistant given by injection active against gram -ve bacteria | |
| Tigemonam tigemonam beta lactam antibiotic monobactam synthetic highly resistant to beta lactamase similar spectrum to aztreonam orally active, excellent bioavailability MOA : inhibit cell wall synthesis | |
| Vancomycin non beta lactam antibiotic glycoprotein, cyclic peptide from Nocardia orientalis given parenterally MOA: inhibit cell wall synthesis through inhibition of transglycosylation step --> inhibition of elongation of peptidoglycan matrix active against MRSA SE : hypersensitivity / nephro and ototoxicity | |
| Teicoplanin non beta lactam antibiotic glycoprotein, cyclic peptide from Actinoplanes teicomyceticus given parenterally MOA: inhibit cell wall synthesis through inhibition of transglycosylation step --> inhibition of elongation of peptidoglycan matrix active against MRSA SE : hypersensitivity / nephrotoxicity | |
| Bacitracin non beta lactam antibiotic cyclic peptide produced from Bacillus subtilis inhibits dephosphorylation of the phospholipid carrier responsible for trnsporting the disaccharide across plasma membrane (late stage 1) SE: hypersensitivity / nephro and neurotoxicity ONLY topical route and IM with caution | |
| Cycloserine non beta lactam antibiotic analog of D-ala produced by streptomyces sp. MOA: competitive inhibitor of D-ala-D-ala synthetase and D-ala racemase orally active SE : - CNS effects : tremor/seizure/confusion/hallucination/psychosis - occasional hepatic damage and peripheral neuropathy | |
| naphtacene | |
| tetracycline backbone | |
| Tetracycline Tetracycline antibiotics Bacterial protein synthesis inhibitors octahydronaphtacene Natural (from streptomyces spc) or from chlortetracycline (by hydrogenolysis) Crystalline amphoteric compounds (form acid/base salts) Low water solubility (HCl salts-->water soluble) Orally active Undergoes chelation with di/trivalent cations (contraindication with dairy food and antacids) -In acidic condition: epimerization:epitetracyclin (4-beta): inactive, -H2O:anhydrotetracycline (deeper color) (double bond on C5a): inactive, formation of epianhydrotetracycline:hepatotoxic -In basic condition: lactone formation:isotetracycline: inactive Bacteriostatic (higher affinity to bacteria) -MOA: active against gram+ and gram-, aerobic and anaerobic-->broad spectrum of activity Enter by passive/active diffusion:bind to 30S subunit:inhibit protein synthesis -t1/2=6-8h-->short widely distributed (low to CSF) cross placenta excretion: renal SE: GI discomfort, discoloration of teeth, hepatotoxic at high dose, vertigo, superinfection | |
| Demeclocycline Tetracycline antibiotics Bacterial protein synthesis inhibitors octahydronaphtacene Natural (from streptomyces spc) Crystalline amphoteric compounds (form acid/base salts) Low water solubility (HCl salts:water soluble) Orally active Undergoes chelation with di/trivalent cations (contraindication with dairy food and antacids) -In acidic condition: epimerization:epitetracyclin (4-beta): inactive, -H2O:anhydrotetracycline (deeper color) (double bond on C5a): inactive, formation of epianhydrotetracycline:hepatotoxic -In basic condition: lactone formation:isotetracycline: inactive Bacteriostatic (higher affinity to bacteria) -MOA: active against gram+ and gram-, aerobic and anaerobic:broad spectrum of activity Enter by passive/active diffusion:bind to 30S subunit-->inhibit protein synthesis -t1/2=12h--> intermediate widely distributed (low to CSF) cross placenta excretion: renal SE: GI discomfort, discoloration of teeth, hepatotoxic at high dose, vertigo, superinfection, photosensitivity | |
| Minocycline Tetracycline antibiotics Bacterial protein synthesis inhibitors octahydronaphtacene Semi-synthetic Crystalline amphoteric compounds (form acid/base salts) Low water solubility (HCl salts:water soluble) Orally active Undergoes chelation with di/trivalent cations (contraindication with dairy food and antacids) Stable in acidic and basic condition More lipophilic Bacteriostatic (higher affinity to bacteria) MOA: active against gram+ and gram-, aerobic and anaerobic:broad spectrum of activity Enter by passive/active diffusion:bind to 30S subunit:inhibit protein synthesis t1/2=16h-->long completely absorbed widely distributed (to CSF:for meningitis) cross placenta excretion: biliary SE: GI discomfort, discoloration of teeth, hepatotoxic at high dose, vertigo, superinfection | |
| Sancycline Tetracycline antibiotics Bacterial protein synthesis inhibitors octahydronaphtacene Semi-synthetic Slightly more active (than tetracycline) Crystalline amphoteric compounds (form acid/base salts) Low water solubility (HCl salts:water soluble) Orally active Undergoes chelation with di/trivalent cations (contraindication with dairy food and antacids) Bacteriostatic (higher affinity to bacteria) MOA: active against gram+ and gram-, aerobic and anaerobic:broad spectrum of activity Enter by passive/active diffusion:bind to 30S subunit:inhibit protein synthesis widely distributed (low to CSF) cross placenta excretion: renal SE: GI discomfort, discoloration of teeth, hepatotoxic at high dose, vertigo, superinfection | |
| Chlortetracycline Tetracycline antibiotics Bacterial protein synthesis inhibitors octahydronaphtacene Natural (from streptomyces spc) Crystalline amphoteric compounds (form acid/base salts) Low water solubility (HCl salts:water soluble) Orally active Undergoes chelation with di/trivalent cations (contraindication with dairy food and antacids) -In acidic condition: epimerization:epitetracyclin (4-beta): inactive, -H2O:anhydrotetracycline (deeper color) (double bond on C5a): inactive, formation of epianhydrotetracycline:hepatotoxic -In basic condition: lactone formation:isotetracycline: inactive Bacteriostatic (higher affinity to bacteria) -MOA: active against gram+ and gram-, aerobic and anaerobic:broad spectrum of activity Enter by passive/active diffusion:bind to 30S subunit:inhibit protein synthesis t1/2=6-8h -->short least absorbed widely distributed (low to CSF) cross placenta excretion: renal SE: GI discomfort, discoloration of teeth, hepatotoxic at high dose, vertigo, superinfection | |
| Oxytetracycline Tetracycline antibiotics Bacterial protein synthesis inhibitors octahydronaphtacene Natural (from streptomyces spc) Crystalline amphoteric compounds (form acid/base salts) Low water solubility (HCl salts:water soluble) Orally active Undergoes chelation with di/trivalent cations (contraindication with dairy food and antacids) -In acidic condition: epimerization:epitetracyclin (4-beta): inactive, -H2O:anhydrotetracycline (deeper color) (double bond on C5a): inactive, formation of epianhydrotetracycline:hepatotoxic -In basic condition: lactone formation:isotetracycline: inactive Bacteriostatic (higher affinity to bacteria) -MOA: active against gram+ and gram-, aerobic and anaerobic:broad spectrum of activity Enter by passive/active diffusion:bind to 30S subunit:inhibit protein synthesis t1/2=6-8h--> short widely distributed (low to CSF) cross placenta excretion: renal SE: GI discomfort, discoloration of teeth, hepatotoxic at high dose, vertigo, superinfection | |
| Methacycline Tetracycline antibiotics Bacterial protein synthesis inhibitors octahydronaphtacene Semi-synthetic Crystalline amphoteric compounds (form acid/base salts) Low water solubility (HCl salts:water soluble) Orally active Undergoes chelation with di/trivalent cations (contraindication with dairy food and antacids) Exception: not stable in acidic and basic condition (undergoes hydration) Bacteriostatic (higher affinity to bacteria) -MOA: active against gram+ and gram-, aerobic and anaerobic:broad spectrum of activity Enter by passive/active diffusion:bind to 30S subunit:inhibit protein synthesis t1/2=12h--> intermediate widely distributed (low to CSF) cross placenta excretion: renal SE: GI discomfort, discoloration of teeth, hepatotoxic at high dose, vertigo, superinfection | |
| Doxycycline Tetracycline antibiotics Bacterial protein synthesis inhibitors octahydronaphtacene Semi-synthetic Crystalline amphoteric compounds (form acid/base salts) Low water solubility (HCl salts:water soluble) Orally active Undergoes chelation with di/trivalent cations (contraindication with dairy food and antacids) Stable in acidic and basic condition More lipophilic Bacteriostatic (higher affinity to bacteria) -MOA: active against gram+ and gram-, aerobic and anaerobic:broad spectrum of activity Enter by passive/active diffusion:bind to 30S subunit:inhibit protein synthesis t1/2=16h-->long completely absorbed widely distributed (low to CSF) cross placenta excretion: biliary SE: GI discomfort, discoloration of teeth, hepatotoxic at high dose, vertigo, superinfection, photosensitivity | |
| tigecycline Tetracycline antibiotics (new) Bacterial protein synthesis inhibitors 9-dimethylglycylamino substituent (DMG) Semi-synthetic Crystalline amphoteric compounds (form acid/base salts) Low water solubility (HCl salts:water soluble) Poor oral/ given IV Undergoes chelation with di/trivalent cations (contraindication with dairy food and antacids) Stable in acidic and basic condition More lipophilic Bacteriostatic (higher affinity to bacteria) -MOA: active against gram+ and gram-, aerobic and anaerobic:broad spectrum of activity Enter by passive/active diffusion:bind to 30S subunit (5X more):inhibit protein synthesis t1/2=36h--> long widely distributed (low to CSF) cross placenta/ excreted in milk excretion: biliary SE: GI discomfort (nausea, vomiting), discoloration of teeth and bone | |
| streptamine diaminoinositol moiety of aminoglycoside | |
| 2-deoxystreptamine diaminoinositol moiety of aminoglycoside | |
| spectinamine diaminoinositol moiety of aminoglycoside | |
| streptidine diaminoinositol moiety of aminoglycoside | |
| Neomycin B Aminoglycoside (amino sugar connected to aminocyclitol) From streptomyces Have a pentose lacking amino group Topically, parentarely Bactericidal (exception) MOA: active against gram- : bind irreversibly to 30S subunit: inhibit bacterial protein synthesis (mistranslation of RNA templates: insertion of wrong amino acid: holes) Most toxic Active eventhough low plasma level (post antibiotic effect) Poor GI absorption Poor distribution Poor ppb Low CSF levels (if no meningitis) Accumulation: in renal cortex and inner ear (ototoxicity) Cross placenta Excretion: renal (unchanged) SE: nephrotoxicity/ototoxicity (the higher the nb of amino group: the more toxic), NMJ blockers, teratogenic effect, rare allergic reaction | |
| gentamycin C Aminoglycoside (amino sugar connected to aminocyclitol) From micromonospora basic, polar, acid (salts) Bactericidal (exception) MOA: active against gram- : bind irreversibly to 30S subunit: inhibit bacterial protein synthesis (mistranslation of RNA templates: insertion of wrong amino acid: holes) Active eventhough low plasma level (post antibiotic effect) Poor GI absorption Poor distribution Poor ppb Low CSF levels (if no meningitis) Accumulation: in renal cortex and inner ear (ototoxicity) Cross placenta Excretion: renal (unchanged) SE: nephrotoxicity/ototoxicity (the higher the nb of amino group: the more toxic), NMJ blockers, teratogenic effect, rare allergic reaction | |
| tobramycin Aminoglycoside (amino sugar connected to aminocyclitol) From streptomyces basic, polar, acid (salts) Bactericidal (exception) MOA: active against gram- : bind irreversibly to 30S subunit: inhibit bacterial protein synthesis (mistranslation of RNA templates: insertion of wrong amino acid: holes) Active eventhough low plasma level (post antibiotic effect) Poor GI absorption Poor distribution Poor ppb Low CSF levels (if no meningitis) Accumulation: in renal cortex and inner ear (ototoxicity) Cross placenta Excretion: renal (unchanged) SE: nephrotoxicity/ototoxicity (the higher the nb of amino group: the more toxic), NMJ blockers, teratogenic effect, rare allergic reaction | |
| neltimicin Aminoglycoside (amino sugar connected to aminocyclitol) From micromonospora basic, polar, acid (salts) Bactericidal (exception) MOA: active against gram- : bind irreversibly to 30S subunit: inhibit bacterial protein synthesis (mistranslation of RNA templates: insertion of wrong amino acid: holes) Active eventhough low plasma level (post antibiotic effect) Poor GI absorption Poor distribution Poor ppb Low CSF levels (if no meningitis) Accumulation: in renal cortex and inner ear (ototoxicity) Cross placenta Excretion: renal (unchanged) SE: nephrotoxicity/ototoxicity (the higher the nb of amino group: the more toxic), NMJ blockers, teratogenic effect, rare allergic reaction | |
| amikacin Aminoglycoside (amino sugar connected to aminocyclitol) From micromonospora basic, polar, acid (salts) Bactericidal (exception) MOA: active against gram- : bind irreversibly to 30S subunit: inhibit bacterial protein synthesis (mistranslation of RNA templates: insertion of wrong amino acid: holes) Active eventhough low plasma level (post antibiotic effect) Poor GI absorption Poor distribution Poor ppb Low CSF levels (if no meningitis) Accumulation: in renal cortex and inner ear (ototoxicity) Cross placenta Excretion: renal (unchanged) SE: nephrotoxicity/ototoxicity (the higher the nb of amino group: the more toxic), NMJ blockers, teratogenic effect, rare allergic reaction | |
| kanamycin A old Aminoglycoside (amino sugar connected to aminocyclitol) From streptomyces basic, polar, acid (salts) Bactericidal (exception) MOA: active against gram- : bind irreversibly to 30S subunit: inhibit bacterial protein synthesis (mistranslation of RNA templates: insertion of wrong amino acid: holes) Active eventhough low plasma level (post antibiotic effect) Poor GI absorption Poor distribution Poor ppb Low CSF levels (if no meningitis) Accumulation: in renal cortex and inner ear (ototoxicity) Cross placenta Excretion: renal (unchanged) SE: nephrotoxicity/ototoxicity (the higher the nb of amino group: the more toxic), NMJ blockers, teratogenic effect, rare allergic reaction | |
| Macrolides Bacterial protein synthesis inhibitor large-membered lactone rings 14 or 15-membered rings attached to deoxy sugars from propionic acid units substituted amino group on sugar → weakly basic (pKa = 8) not very water soluble salt formation with glucoheptanoic and lactobionic acids increase water soluble stearate and laurylsulfate salts decrease water solubility | |
| Erythromycin macrolide natural (from Streptomyces erythreus) bacteriostatic active against gram+, aerobic well distributed (except to brain, CSF) cross placenta found in breast milk penetrates the prostatic fluid MOA: bind to 50S (reversibly): inhibit protein synthesis More effective at alkaline pH Free base form: inactivated by gastric acid, form cyclic ketal (given as enteric coated) Stearate: slightly susceptible to gastric acid inactivation ethylsuccinate preparation: absorbed first and hydrolyzed in blood to liberate free erythromycin estolate preparation (laurylsulfate propionate): more acid resistant lactobionate: suitable for IV administration t1/2= 1.2-2h enterohepatic circulation metabolism: partially excretion: biliary (95% in active form) SE: safe, GI disturbances (nausea, vomiting, anorexia, diarrhea, abdominal cramps), cholestatic hepatitis (with estolate ester), rare allergic reaction, ototoxicity (reversible at high dose) DDI: CYP3A4 inhibitor CI: with liver dysfunction patients |
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