drugs Flashcards by Julie Ment

fluoroquinolone target

termination of bacterial DNA replication

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fluoroquinolone MOA

inhibits gyrase and topo IV so it inhibits both gram pos/neg bacteria

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topoisomerase poisons target

Eukaryote DNA

replication

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topoisomerase poisons MOA

Trap topo:DNA
complex -> cause single
and double-strand DNA breaks
topo trap

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topoisomerase uses

cancer therapy

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Alkylating agents target

Modification of DNA

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Alkylating agents MOA

Interstrand cross-link to DNA

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Crosslinking agents target

Modification of DNA

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Crosslinking agents MOA

Intrastrand cross-link DNA

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Rifampicin target

prokaryotic RNAP

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Rifampicin MOA

binds to beta subunit>prevent movement of sigma factor>RNAP cannot interact w/promoter>prevent transcription at early stage

prevent interaction with beta sigma fam

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alpha-amantitin target

eukaryotic RNAP 2

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alpha-amantitin MOA

inhibit RNAP>inhibit elongation phase of transcription

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Rifampicin uses

tuberculosis

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Rifampicin resistance

2 ways:

1) bacteria acquires mutations at particular positions around the binding site
2) expressing Arr: ADP-ribosylates Rifampicin

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RNAi therapy target

deleterious genes (mRNA)

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RNAi therapy MOA

forms RISC, binds miRNA and mediates formation of duplex btwn guide strand and mRNA, prevents translation by stim degradation of polyA tail

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RNAi therapy uses

treatment of hereditary transthyretin-mediated amyloidosis

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Tetracycline MOA

delivery of activated tRNA to A site by elongation factor EF-Tu inhibited

cycling=delivery

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streptomycin MOA

inhibits GTP-powered proofreading by EF-Tu

“streps” away ability to read

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chloramphenicol MOA

blocks A-site and peptidyl transfer

“ram” into A site

erythromycin MOA

bind just outside the P-site, inhibit translocation

erythro=red
blush at “P” site

puromycin MOA

binds to A site (mimics 3’ end of aa-tRNA)> prevents subsequent peptidyl transfer> triggers premature termination

“pur”= mimicking cat

SW02

allosteric agonist of Hsp70,
enhancing its ability to inhibit protein aggregation

“SWeet you’re gonna help me”

Gusperimus

Hsp70 inhibitor approved as an immunosuppressant in Europe and Japan "Gusto"= large, covers both countries

Tanespimycin

Hsp90 inhibitors, developed as anti-cancer drugs "Tanes"=tails, nine(90) tales

bortezomib MOA

inhibit proteasome a(bort) proteasome

bortezomib use

treatment of relapsed multiple myeloma

Tafamidis MOA

binding to Transthyretin (TTR)'s tetramer> stabilized, potentially inhibit aggregation, arrest disease progression prevents fam from breaking up

Tafamidis use

Transthyretin (TTR) aggregation treatment

Ivacaftor MOA

treats missense mutations, binding to misfolded CFTR, forces it into native state "caft"= crafty

Ivacaftor use

Cystic Fibrosis

tunicamycin

blocks N-linked glycosylation, inhibits 1st sugar being added tuna sugar

bactitracin MOA

inhibits phosphorylation of Dol-PP to Dol-P bacteria in your Dole whip

b-lactams MOA

inhibit transpeptidase (breask cross linking peptidoglycan chains) milk melting cell wall

DGAT-1 inhibitors MOA

inhibits DAG 2 fncs: last step in esterification of TAGs serves as precursor for phospholipid synthesis

DGAT-1 inhibitors use

obesity/metabolic syndrome

statins MOA

targets HMG-CoA reductase | HMG-CoA>Mevalonate>>squalene>>cholesterol/isoprenoids eg dolichol

CYP19A1 (aromatase) inhibitors MOA

blocks conversion of testosterone (androgens) >aromatase>estrogen eg letrozole "-zole" usually CYP inhibitor

CYP19A1 (aromatase) inhibitors use

hormone-receptor-positive breast cancer

tetrodotoxin MOA

fugu toxin, inhibits voltage gated NA channels

Ca channel blockers MOA

inhibit VDCCs in heart muscle>decr influx of Ca2+ into cardiac/smooth muscle> decr cardiac contractibility and causes vasodilation> lowers bp eg amlodipine "am low in Ca">hurts heart

Ca channel blockers use

hypertension

diazepam/zolpidem MOA

enhance GABA receptor activity, allosterically

nAChR inhibitors/antagonists

Non-depolarizing neuromuscular junction agents bind to the nAChR and competitively inhibit ACh binding eg d-turbocurarine, atracurium "cur" Ach

P-gp (P-glycoprotein) inhibitor

P-gp pumps xenobiotic compounds out of cytoplasm, ATP dep eg quinidine P=Potter and quidditch

cardiac glycosides

incr intensity of heart muscle contraction eg digoxin digging (digo) makes dogs heart race

mAbs (monoclonal antibodies)

EGFR-targeting | egcetuximab, erlotinib

cetuximab MOA

inhibit EGF binding

erlotinib MOA

inhibit autophosphorylation and downstream signaling

bevacizumab/ranibizumab MOA

bind to VEGF, prevent recognition by VEGFR

GPCR targeted by

loratadine, ranitidine, perphenazine