Anti-neoplastic drugs

Anti-neoplastic drugs treat cancer by interfering with the growth and division of malignant cells. Traditional cytotoxic agents act on rapidly dividing cells generally, which is why they also damage bone marrow, gastrointestinal mucosa, and hair follicles — the source of the characteristic toxicities of myelosuppression, mucositis, nausea, and alopecia. Newer targeted agents and monoclonal antibodies act on specific molecular features of tumor cells and have different, often more selective, side effect profiles.

The traditional classes are organized by mechanism. Alkylating agents such as cyclophosphamide add alkyl groups to DNA, creating cross-links that block replication. Antimetabolites such as methotrexate and 5-fluorouracil mimic normal nucleotide precursors and jam DNA and RNA synthesis. Antitumor antibiotics such as doxorubicin and bleomycin intercalate into DNA or generate free radicals. Mitotic inhibitors act on microtubules — vinca alkaloids block their assembly while taxanes prevent their disassembly. Topoisomerase inhibitors prevent the unwinding and religation of DNA strands. Hormonal agents such as tamoxifen and aromatase inhibitors act on hormone-dependent tumors.

Handling is a defining practical issue. Most anti-neoplastics are classified as hazardous drugs, so preparation requires containment primary engineering controls, personal protective equipment, and dedicated compounding areas, with strict spill and waste procedures. Dosing is frequently based on body surface area, narrow therapeutic indices leave little room for error, and many regimens require verification of laboratory values before each cycle. Class-specific toxicities also have to be monitored, such as cardiotoxicity with anthracyclines and pulmonary fibrosis with bleomycin.

Anti-neoplastic drugs appear on the PTCE within medications by organ system and in the federal requirements material governing hazardous drug handling and USP standards. They are also tested on USMLE Step 1 pharmacology, where questions typically pair a drug with its mechanism, its cell-cycle specificity, or its signature adverse effect.