There are six major types of traditional chemotherapy, grouped by how the drugs attack cancer cells. Within those six categories, roughly 250 FDA-approved cancer-fighting drugs exist, though not all of them are classic chemotherapy. The categories matter because each type works at a different stage of cell growth, which is why oncologists often combine drugs from multiple classes to hit cancer from several angles at once.
The Six Main Types of Chemotherapy
Chemotherapy drugs are classified by their mechanism: how they interfere with a cancer cell’s ability to grow and divide. The six standard categories are alkylating agents, antimetabolites, antitumor antibiotics, topoisomerase inhibitors, mitotic inhibitors, and a miscellaneous group that doesn’t fit neatly elsewhere. Some of these drugs work only during a specific phase of cell division, while others damage DNA regardless of what the cell is doing at the time. That distinction shapes how they’re dosed and how toxic they are to healthy tissue.
Alkylating Agents
Alkylating agents are one of the oldest and most widely used classes. They work by chemically attaching small molecular groups directly to DNA strands, creating cross-links that prevent the double helix from separating. A cell that can’t unzip its DNA can’t copy itself, so it dies.
Because alkylating agents attack DNA at any point in the cell cycle, they don’t need to catch a cancer cell in a particular phase of division. That makes them broadly effective but also more toxic to healthy cells than some other classes. The alkylating family itself breaks down into several subgroups: nitrogen mustards (cyclophosphamide, melphalan, chlorambucil), platinum compounds (cisplatin, carboplatin, oxaliplatin), nitrosoureas (carmustine, lomustine), and others like temozolomide. Platinum-based drugs are a cornerstone of treatment for lung, ovarian, bladder, and testicular cancers.
Antimetabolites
Antimetabolites are molecular imposters. They closely resemble the building blocks a cell needs to construct DNA and RNA, so the cell absorbs them as if they were the real thing. Once incorporated, they sabotage the genetic code and prevent the cell from making functional copies of itself.
These drugs are active during the S phase (the synthesis phase) of the cell cycle, when DNA is being copied. There are three subtypes based on which building block they mimic. Purine antagonists block the cell from making purines, one of the two families of DNA bases. Pyrimidine antagonists do the same for pyrimidines. Folic acid antagonists, sometimes called antifolates, prevent the cell from using folic acid, a vitamin essential for building DNA and RNA. This class includes some of the most commonly prescribed chemotherapy drugs across many cancer types.
Antitumor Antibiotics
Despite the name, these aren’t antibiotics for infections. They’re derived from natural substances, often fungi, and they interfere with cancer cell DNA in several ways at once. The most important subgroup is the anthracyclines, which include doxorubicin and daunorubicin.
Anthracyclines wedge themselves between DNA base pairs, physically uncoiling the double helix and preventing the cell from reading or copying its genetic instructions. They also block a key enzyme that helps DNA strands coil and uncoil properly, and they generate oxygen-based molecules called free radicals that directly damage the cell membrane and DNA. This multi-pronged attack makes them powerful but comes with a well-known risk: cumulative heart damage. Oncologists track the total lifetime dose carefully because exceeding certain thresholds raises the risk of weakened heart muscle.
Topoisomerase Inhibitors
When a cell copies its DNA, specialized enzymes called topoisomerases help untangle and separate the tightly wound strands. Topoisomerase inhibitors block those enzymes, leaving the DNA in a tangled state the cell can’t resolve. Without functioning topoisomerases, the cell can’t replicate its genetic material and eventually dies.
There are two subtypes. Topoisomerase I inhibitors interfere with one version of the enzyme, while topoisomerase II inhibitors target a different version and are most active during the synthesis and pre-division phases of the cell cycle. These drugs are used across a range of solid tumors and certain leukemias.
Mitotic Inhibitors
Mitotic inhibitors target the final act of cell division itself: mitosis. When a cell is ready to split into two, it builds a scaffolding of tiny protein tubes called microtubules to pull the chromosomes apart. Mitotic inhibitors disrupt that scaffolding, trapping the cell mid-division so it can’t complete the process.
The two best-known subgroups take opposite approaches. Vinca alkaloids, originally derived from the periwinkle plant (vincristine, vinblastine, vinorelbine), prevent microtubules from assembling in the first place. Taxanes (paclitaxel, docetaxel) do the reverse: they lock microtubules into a rigid state so they can’t disassemble when needed. Either way, the cell is stuck. A newer class called epothilones works similarly to taxanes but through a slightly different binding mechanism, which can sometimes help when cancer cells have developed resistance to taxane drugs.
Miscellaneous Agents
A handful of chemotherapy drugs don’t fit into the five categories above. Some work through unique mechanisms. For example, one class breaks down a specific amino acid that certain leukemia cells depend on but can’t manufacture themselves, essentially starving the cancer. Corticosteroids are also sometimes grouped here. While their exact anticancer mechanism isn’t fully understood, they appear to make cancer cells more vulnerable to other chemotherapy drugs and are commonly used alongside cytotoxic treatment for blood cancers like lymphoma, leukemia, and multiple myeloma.
How Chemotherapy Differs From Targeted Therapy
Traditional chemotherapy kills cells that are actively growing and dividing, which is why it affects healthy fast-growing tissues like hair follicles, the gut lining, and bone marrow alongside cancer. Targeted therapies are a newer, separate category. They interfere with specific proteins or genetic mutations that drive a particular tumor’s growth, largely sparing normal cells. Immunotherapy is yet another distinct approach, training the immune system to recognize and attack cancer.
The total count of 250 FDA-approved oncology therapies includes targeted drugs and immunotherapies alongside traditional chemotherapy agents. New approvals continue at a steady pace. In 2025 alone, the FDA approved multiple new oncology drugs, including antibody-drug conjugates for breast cancer, lung cancer treatments targeting specific mutations, and new formulations of existing immunotherapy drugs. The trend has been toward more precise treatments, but traditional cytotoxic chemotherapy remains a core part of treatment for many cancers, often combined with these newer agents.
How Chemotherapy Is Delivered
Most people picture an IV drip when they think of chemotherapy, and intravenous delivery through a vein is the most common method. But chemotherapy also comes as oral pills or capsules, topical creams for certain skin cancers, and injections into muscle or under the skin.
For cancers in specific locations, doctors sometimes deliver chemotherapy directly to the site. Intra-arterial chemotherapy sends the drug into an artery feeding a tumor. Intracavitary chemotherapy places it inside a body cavity, such as the abdomen or bladder. One specialized version, called HIPEC, delivers heated chemotherapy directly into the abdominal cavity during surgery. Intrathecal chemotherapy goes into the fluid surrounding the brain and spinal cord, which is necessary because many drugs given through a vein can’t cross the blood-brain barrier. The delivery method depends on the cancer’s location, the specific drug being used, and whether the goal is to treat the whole body or a targeted area.
Why Oncologists Combine Multiple Types
Because each category attacks cancer cells at a different stage of their life cycle, combining drugs from two or more classes increases the chance of catching every cancer cell, no matter what phase it’s in when treatment arrives. A drug that works during DNA synthesis pairs well with one that works during cell division, for instance. Combination regimens also reduce the odds of the cancer developing resistance to any single drug. The tradeoff is more potential side effects, which is why treatment plans balance effectiveness against the toll on the body’s healthy tissues.