Drugs aimed at a tumor's specific weakness
Targeted therapies differ from conventional chemotherapy by exploiting a defined molecular feature of a cancer rather than broadly attacking dividing cells. The diagram groups the major classes. Tyrosine kinase inhibitors are small molecules that block hyperactive signaling enzymes inside the cell. Monoclonal antibodies bind targets on the cell surface or in the environment, marking cells for destruction or interrupting signals.
mTOR inhibitors interrupt a growth and metabolism pathway that many tumors depend on. PARP inhibitors block a DNA repair enzyme, which is especially damaging to cancers that already have a repair defect such as BRCA mutation, an example of synthetic lethality. The common thread is matching a drug to a vulnerability the tumor actually carries.
Why biomarker testing comes first
Because these drugs work only when the relevant target or vulnerability is present, they are usually paired with a test. A TKI aimed at a specific mutation helps only tumors carrying it, and resistance often emerges when the tumor evolves around the blocked pathway. This is why targeted therapy is tied to molecular profiling rather than given empirically.
Matching each class to its target
This is general educational information, not medical advice. Which targeted agent fits a given cancer depends on its molecular profile and is decided by an oncology team; the classes here describe mechanisms, not prescriptions.