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Antineoplastic Drugs

Antineoplastic Drug Classes and Mechanisms

QuestionAnswer
Antimetabolites cell cycle specific (s-phase): interfere with DNA and/or protein synthesis
Antimitotics (general) cell cycle specific (m-phase): prevents microtubules from forming and breaking down
Topoisomerase I inhibitors cell cycle non-specific: binds to topoisomerase I which prevents its binding to DNA; results in increased torsional strain and eventually causes DNA breaks
Topoisomerase II inhibitors cell cycle non-specific: binds to topoisomerase II while topoisomerase II is bound to DNA; allows DNA strand break but prevents resealing
Anthracyclines cell cycle non-specific: topoisomerase II inhibitors, produce oxygen free radicals, intercalates into DNA
Alkylating Agents cell cycle non-specific: covalently binds reactive alkyl groups to nucleic acids, can result in crosslinking of DNA (intrastrand, interstrand)
Heavy Metals cell cycle non-specific: platinum binds to DNA and chases its shape and reactivity
Biologics: Tyrosine Kinase Inhibitors cell cycle non-specific: create pro-growth signals in some cancer cells, inhibition of these enzymes block cell growth and induces apoptosis
Biologics: Monoclonal Antibodies cell cycle non-specific: antibody dependent lysis (label), complement dependent lysis (label), localized delivery of radiation, localized delivery of chemotherapy, inhibit angiogenesis
Antimitotics: Vinca Alkaloids cell cycle specific (prometaphase): inhibits spindle fiber formation by binding tubulin
Antimitotics: Taxanes cell cycle specific (prevents anaphase to telophase conversion): stabilizes microtubules, prevents them from breaking down
Antimitotics: Eribulin cell cycle specific (prevents anaphase to telophase conversion): stabilizes microtubules, prevents them from breaking down
Created by: mmendoza
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