Dr. Smith's Final Drugs

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Can you name the Dr. Smith's Final Drugs?

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It catalyzes the conversion of arachidonic acid to prostaglandins
An anti-inflammatory drug metabolized in the colon by intestinal bacteria to produce 5-aminosalicylic acid
Binds bacterial/protozoal dihydrofolate reductase proteins 10^5 more tightly than human DHFR
Suicide inhibitor; is converted into FdUMP and forms a covalent intermediate with thymidylate synthase that cannot be reversed
Common treatment for methemoglobinemia
Anti cancer drug, can block the synthesis of thymidylate
Inhibits the electron flow from the Fe-S centers of Complex I to ubiquinone, thus blocking oxidative phosphorylation
Anticoagulant, similar to warfarin, which prevents the formation to carboxyglutamate in prothrombin.
Inhibits the production of prostaglandins;irreversible inhibitor
Large, bulky molecules;unable to bind to COX-1
Inhibits inducible nitric oxide synthase
peroxynitrite [ONOO-] scavenging compound
Anti-coagulant, binds to ant-thrombin which leads to a conformation change allowing anti-thrombin to bind to thrombin, which inactivates it, inhibiting the activation of fibrinogen
Side effects: gastrointestinal problems due to fermentation of carbohydrates in large intestines and water holding capacity of the disaccharides.
Phosphorylated by viral encoded thymidine kinase but not human thymidine kinase. Only infected cells efficiently phosphorylate the drugs, which then inhibit DNA replication
similar structure to vitamin K and competitively inhibits carboxylase.
Increases cytochrome b5 reductase
Its mechanism is to increase glutathione levels by supplying cysteine for the synthesis of glutathione
Inhibits bacterial synthesis of folate
Suicide inhibitor of xanthine oxidase
If this drug is dosed >7mg/kg, then it becomes an oxidant
Drug used to treat sickle cell disease
Relieves symptoms of gout
a prodrug of mycophenolic acid (MPA)
can also inhibit folate absorption by preventing the excess glutamates from being cleaved off
Antibiotic that directly binds to ATP synthase and inhibits both ATP synthesis and the transfer of electrons through the electron transport chain
Selective COX-2 inhibitor
converted to the deoxynucleotide, which inhibits cell division.
Associated with inflammation, cancer, colitis, and arthritis
Bind bile acids, thus decrease absorption of exogenous (dietary) cholesterol.
the committed step of its reaction is the inhibition of the conversion of PRPP into PR-amine
inhibitor of pancreatic lipase
It binds to the toxic metabolite (forming mercapturic acid) for excretion in the urine
Is converted to fluorodeoxyuridylate (has a similar structure to deoxyuridylate), which irreversibly inhibits thymidylate synthase - suicide inhibition.
Blocks electron flow from cytochrome bH to ubiquinone.
Used in treatment of inflammatory bowel disease.
used as an immunosuppressant in organ transplants and in patients with inflammatory bowel disease
non-prescription form of Orlistat
inhibits IMP dehydrogenase (IMP --> XMP [de novo pathway])
Vasodilator which releases NO
Combined antibiotic - sulfamethoxazole and trimethoprim
decrease efficiency of fat-soluble vitamin absorption due to their effect on bile acids.
An alpha-glucosidase inhibitor. It delays carbohydrate digestion in the small intestines and thus decreases blood glucose in Diabetics (type II)
Analog of uracil used to treat breast and colorectal cancer.
inhibits cell division in a similar manner as 6-mercaptopurine and is also inactivated by thiopurine methyltranserfase
Herpes treatment
Inhibits TMP production by preventing the regeneration of methylene-THF; used as an anticancer agent and in the treatment of rheumatoid arthritis
Inhibits alpha-amylase, alpha-dextrinase, maltase, and sucrase
prodrug of 6-mercaptopurine
Covalently binds to transpeptidase thus prevents synthesis of bacterial cell walls. Suicide inhibitor.
Binds at ubiquinone binding site that is close to cytochrome bH on the matrix side membrane
Used to treat acetaminophen overdose
Inhibits oxidative phosphorylation by binding to one of the ubiquinone binding sites on Complex III
Inactivated by xanthine oxidase and thiopurine methyltransferase (TPMT).
Competitively inhibits dihydrofolate reductase and prevents the regeneration of tetrahydrofolate
Works by increasing the blood concentration of fetal hemoglobin
prevents the necessary 1,3 hydride shift to reduce the CH2 to CH3 on methylenetetrahyrdofolate
Carboxylation of glutamate to carboxyglutamate in prothrombin requires the enzyme ________ and cofactor _________
Marketed by Roche as CellCept(R)
competitively inhibiting HMG CoA reductase to inhibit endogenous cholesterol synthesis
cytostatic against lymphocytes which almost entirely lack purine salvage and depend on de novo pathway for purines
Inhibits cyclooxygenase by acetylating the serine residue that lies along the path to the active site and blocks the channel
Induces hemolysis in patients with glucose 6-phosphate dehydrogenase deficiency
Inhibitor of pancreatic lipase, side effects are GI problems
Phosphorylated by human kinases but selectively interfere with viral replication. Both have modified sugars that lack 3; OH group and in effect terminates DNA synthesis
Converted to alloxanthine which binds tightly with xanthine oxidase, which decreases urate production and xanthine and hypoxanthine concentrations rise
Anticancer and rheumatoid arthritis agent that affects both DNA synthesis and de novo purine synthesis
structure similar to dihydrofolate, thus can be a competitive inhibitor of dihydrofolate reductase.
Nucleotide analog of deoxcycytidine used in treatment of pancreatic cancer
Has a modified sugar which has 2 fluorine atoms at the 2' position rather than 2 hyrdogens. Can be twice phosphorylated by deoxycytidine kinase and then dCMP kinase and acts as a s

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Created Dec 6, 2011ReportNominate
Tags:description, drug, final, smith