The 8 Main Types of — Targeted Therapy Drugs

Chemotherapy kills any rapidly dividing cell, including healthy cells in your hair, gut and bone marrow — which is why it causes hair loss and nausea. Targeted therapy attacks a specific molecular change present in cancer cells but not in most healthy tissue. The side effect profile differs because the drugs act on different targets. Neither is universally better — the right choice depends on what your tumour testing shows and what guidelines recommend for your cancer type.

No. Both are precision treatments, but they work through completely different mechanisms. Targeted therapy blocks a molecular change inside or on the surface of the cancer cell itself. Immunotherapy works by releasing the brakes on your own immune system so it can recognise and attack cancer cells — it does not target the cancer cell directly. Some treatment plans use both together, but they are separate drug classes with different eligibility criteria, side effects and monitoring needs.

Biomarker testing on your tumour tissue is the starting point. The laboratory looks for specific mutations, protein overexpression or gene rearrangements — and each finding points to a different drug class. There is no shortcut: a drug designed for an EGFR mutation will not work against a BRCA mutation. NCCN and ASCO guidelines recommend completing this testing before starting targeted therapy wherever it is clinically indicated, because the target determines the class.

For non-small-cell lung cancer, the class depends entirely on the mutation found in your tumour. EGFR mutations are treated with tyrosine kinase inhibitors that block the EGFR signalling pathway. ALK or ROS1 rearrangements call for a different group of kinase inhibitors designed for those specific targets. KRAS mutations have more recently become targetable with newer agents in the same broad family. This is why molecular profiling of your tumour tissue is done before a treatment recommendation is made.

In breast cancer, the class depends on the subtype established by testing. HER2-positive tumours are treated with monoclonal antibodies targeting HER2, sometimes combined with tyrosine kinase inhibitors. Hormone-receptor-positive cancers may be treated with CDK 4/6 inhibitors when certain features are present. In patients with BRCA mutations and eligible tumour characteristics, PARP inhibitors may be considered. Receptor testing and genomic testing — not the breast cancer diagnosis alone — are what determine which class applies to you.

It depends on the class. Monoclonal antibodies are given as an intravenous infusion, usually in a day-care setting over a few hours. Most small-molecule inhibitors — including tyrosine kinase inhibitors, CDK 4/6 inhibitors, PARP inhibitors and mTOR inhibitors — are taken as tablets or capsules at home on a daily or twice-daily schedule. The route of administration does not determine which is more effective; that depends on what your tumour testing shows and which drug your oncologist recommends.

Yes. Most targeted therapies eventually encounter resistance — the cancer adapts by developing new mutations or activating alternative pathways that the drug does not block. How quickly this happens varies with the drug class and the individual cancer. When resistance occurs, your oncologist may recommend a repeat biopsy to identify what has changed, then switch to a different drug within the same class, a drug from a different class, or a combination. Regular monitoring matters even when treatment appears to be going well.

Yes, though the profile differs from chemotherapy because different pathways are affected. Hair loss and severe bone marrow suppression are less common, but each class has its own effects to watch for. Monoclonal antibodies can cause infusion reactions. Tyrosine kinase inhibitors commonly cause skin rash, diarrhoea or changes in liver readings. CDK 4/6 inhibitors can reduce white cell counts. PARP inhibitors often cause fatigue and nausea. Your oncology team will tell you which effects to watch for based on the specific drug prescribed, and most can be managed if reported early.