Drugs note cards.txt

inhibits COX-1 and COX-2 and therefore prostaglandin synthesis? only S-isomer is biologically active

DNA crosslinking agent, chemotherapeutic agents

topoisomerase inhibitor, induces ds DNA breaks

Anti-metabolite that inhibits enzymes involved in nucleoside production

targets activity of DNA pols (inhibits elongation), AZT commonly used in HIV therapy

Alkylating agents

binds prok RNA pol, for TB

binds DNA template and interferes is RNA pol progression (also used in tumor therapy), antibiotic

(Rett treatment)nucleoside analog that inhibits DNMTs by trapping them in a covalent complex on DNA by preventing the beta-elimination step of catalysis�resulting in the enzymes� degradation�to be active, must be incorporated into genome of cell�also toxin to bone marrow

bacterial ribosome A site

Bacterial 30S sub-unit (blocks initiation)

Bacterial 50S subunit (blocks translocation)

bacterial peptidyl transferase

Premature termination

Euk 80S ribosome

Irreversibly acetylates and inactivates COX-1 at serine residue

Monoclonal antibody designed to block integrin function and prevent leukocytes from crossing the blood brain barrier

expensive enzyme replacement therapy for Gaucher�s

a fusion protein for treatment of RA, fuse to IgG1 to allow for secretion-perturbs TNFalpha pathway, involved in inflammation

a nonpolarizing blocker of Ach

for treatment of lung, ovarian, breast, head and neck cancer. Hyperstabilizes MT by binding to B-tubulin and preventing dynamic instability

used in treatment of leukemia and lymphoma, binds to tubulin dimers to inhibit their assembly

used for treatment of gout, studied for anti-cancer drug, however extremely toxin. High affinity for tubulin and prevents polymerization

Worms

(binds to fungal MTs)

originally studied for cancer, but now used as treatment for Progeria (premature aging caused by defect in nuclear lamin, type 5 intermediate filament, causes nuclear wrinkling)

inhibits ATP binding and therefore cascade inhibited and you don�t get BCR-ABL protein, not as specific, will work against GIST (c-KIT tyrosine kinase receptor)�can develop resistance (possibly because of P loop mutation)

more specific than Imatnib and well tolerated by patients, now treatment for Ph+ CML or if pt is resistant to Imatinib

used for pts with advanced breast cancer. Targets HER2 extracellular domain. Can work by blocking dimerization, or targeting the immune system to inhibit/kill overexpressing HER2 cells, or by allosterically blocking the ligand binding site

binds to intracellular domain of HER2, helps with inflammatory breast cancer