Dr. Smith's Final Drugs

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

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

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