Untitled Quiz

Cell Cycle Specific Agents

• Mechanism of Action: Drugs function by inhibiting dihydrofolate reductase, interfering with purine and thymine synthesis, or competing with enzymes within specific phases (S-phase mostly). Some drugs compete with thymidylate synthase for thymidine.

• Pharmacokinetics: Many drugs are well absorbed orally or administered intravenously (IV). Plasma protein binding, renal excretion, and other pathways vary depending on the individual drug.

• Toxicity: Common side effects include gastrointestinal disturbances, myelosuppression, and nephrotoxicity. Some drugs cause organ-specific effects like pulmonary toxicity.

• Resistance: Impaired cellular uptake, drug export by multidrug resistance protein, or enzyme mutations can lead to drug resistance.

Anti-metabolites: Pyrimidine Analogs

• Mechanism of Action: Inhibiting specific enzymes in thymidine synthesis or by mimicking natural molecules (e.g. acting as nucleosides).

• Pharmacokinetics: Variable oral or IV absorption; significant metabolism by liver or other enzymes.

• Toxicity: Common GI side effects, myelosuppression, and potential for cardiovascular issues. Other toxicities include rare cases of cerebellar or ocular toxicity.

• Resistance: Decreased enzyme activity, altered drug uptake mechanisms, and drug activation changes can lead to resistance.

Anti-metabolites: Purine Analogs

• Mechanism of Action: Acting as analogs to purine compounds, these agents block or interfere with purine synthesis at different levels.

• Pharmacokinetics: Varied oral and IV absorption and metabolism.

• Toxicity: Myelosuppression (bone marrow suppression), other organ-related toxicities.

• Resistance: Mutational changes in enzymes or alterations in drug export mechanisms can lead to resistance.

Topoisomerase Inhibitors

• Mechanism of Action: Inhibition of DNA topoisomerase enzyme, influencing DNA replication and repair.

• Pharmacokinetics: Primarily intravenous administration. Rapid and extensive metabolism by various enzymes.

• Toxicity: Myelosuppression, gastrointestinal discomfort, and potential for severe diarrhea or cholinergic syndrome.

• Resistance: Altered enzyme activity, impaired accumulation of active metabolites or altered drug export mechanisms can influence resistance.

Microtubule Inhibitors

• Mechanism of Action: Interference with microtubule assembly, crucial for cell division.

• Pharmacokinetics: Varied routes, with primary administration being intravenous.

• Toxicity: Peripheral neuropathy, myelosuppression, and/or emetogenicity are commonly seen side effects.

• Resistance: Mutations in specific cellular processes, or changes in the cellular machinery involved in the process can lead to resistance.

Other Antineoplastic Agents

• Mechanism of Action: Varies significantly; may involve alkylation, inhibition of specific enzymes (e.g. topoisomerases), or immunesystem-modulating properties.

• Pharmacokinetics: Drug administration by various routes and notable metabolic pathways.

• Toxicity: A wide range of possible toxicities including myelosuppression, gastrointestinal issues, and various organ-specific effects are possible.

• Resistance: Several mechanisms including increased drug efflux, altered drug metabolism, overexpression of drug resistance proteins and/or cellular mutations.

Genotoxic Agents

• Mechanism of Action: Alkylating agents that directly damage DNA.

• Pharmacokinetics: Can be absorbed orally or intravenously.

• Toxicity: Bone marrow suppression, nausea, vomiting, and other effects.

• Resistance: Decreased DNA damage through increased DNA repair systems.

Anthracyclines

• Mechanism of Action: Intercalate into DNA, and interfere with DNA replication and repair. Also can cause oxidative stress.

• Pharmacokinetics: Intravenous administration and metabolism.

• Toxicity: Potential cardiovascular issues, myelosuppression, and secondary cancer.

• Resistance: Altered cellular defenses against reactive oxygen species.

Molecular Targeted Agents

• Mechanism of Action: Inhibit specific enzymes or proteins involved in cell signaling and proliferation.

• Pharmacokinetics: Varies by agent, frequently requiring oral or intravenous administration.

• Toxicity: Myelosuppression, other possible organ related toxicities, cardiovascular issues, and others.

• Resistance: Genetic mutations that change the specific target of the drug, resulting in its decreased effectiveness.