Targeted Therapy
Targeted therapies are drugs designed to switch off a specific broken protein that a cancer depends on.
Small-molecule kinase inhibitors, monoclonal antibodies, hormone-pathway agents, PARP inhibitors, degraders (PROTACs, molecular glues), and synthetic-lethality approaches. Matched to a molecular alteration by a companion diagnostic. Resistance is the central problem; next-generation and combination strategies are the response.
Anti-angiogenic therapy cuts off the tumour's blood supply; it is now mostly used to help immunotherapy work better.
An ADC that carries a gene-silencing strand instead of a chemotherapy, so it can switch a protein off rather than poison the cell.
A bispecific antibody is one antibody with two different grabbing arms, so it can block two targets at once or pull an immune cell onto a cancer cell.
Tumours recruit nerves and use nerve signals to grow. Blocking that traffic, with beta-blockers or botulinum toxin, is being tested.
Pills that stop the cell-division engine, added to hormone therapy for the most common type of breast cancer.
Designing a protein from scratch on a computer to grip a chosen target, instead of finding one in an animal or a library.
An ADC that delivers a protein-destroying molecule instead of chemotherapy, hitting targets inside the cell that were previously unreachable.
Folded DNA machines that open only when they touch a tumour, releasing a payload or clotting the tumour's blood supply.
Loading the tiny vesicles cells naturally use to talk to each other with a cancer drug, so the body treats the carrier as its own.
Switching a gene off for good without changing the DNA sequence, by writing chemical marks onto it.
A harmless molecule that turns into a poison only where there is no oxygen, which in the body means inside a tumour.
In vivo base and prime editing would rewrite a cancer's DNA letter by letter inside the body. It works in the liver for inherited disease; nobody has yet corrected a cancer this way in a person.
Drugs against the most common cancer gene, considered impossible to target until sotorasib in 2021.
Cells or drugs that fire only when two conditions are true at once, so healthy tissue expressing just one of them is spared.
Removing an amino acid or nutrient that certain tumours cannot make for themselves, while normal cells can.
Molecular glues are small molecules that stick two proteins together so the cell destroys one of them. They are smaller and more drug-like than bifunctional degraders.
Lab-made immune proteins that lock onto one target, either blocking it or flagging the cell for destruction.
Oligonucleotide therapeutics are short synthetic strands of genetic code that silence a specific cancer gene.
Pills that block a DNA repair backup, killing cancer cells that already lost their main repair system (BRCA).
Programmable DNA-targeting therapeutics are an experimental idea: a drug that reads a cell's DNA, recognises a cancer-specific sequence, and kills only cells that carry it. Change the guide, and the same drug becomes a new drug.
Instead of blocking a protein, these drugs tag it for the cell's own garbage disposal, removing it entirely.
Adding a PARP or ATR inhibitor to a radioactive drug so the tumour cannot repair the damage the radiation causes.
Chemotherapy leaves behind zombie cells that will not divide but poison their neighbours. Senolytics aim to clear them.
Pills that block the specific enzyme a cancer relies on. Imatinib in 2001 proved a cancer could be switched off by design.
Finding a second gene that a cancer needs only because its first gene is broken, then hitting the second one.
Some tumours contain bacteria and fungi that shelter cancer cells and break down chemotherapy. Killing them may make treatment work.
Stiff, high-pressure tumours squeeze their own blood vessels shut, keeping drugs out. Softening them is a way in.
The dose on the label is often not the best dose for patients; it is the highest one that was tolerable for a few weeks. Project Optimus means new cancer drugs should arrive with evidence on dose, and it gives clinicians licence to consider dose reduction for toxicity. For older drugs, the evidence gap persists.
The most frequently mutated oncogene in cancer stopped being undruggable, and patients with KRAS G12C lung and bowel cancers now have targeted pills. The approach, exploiting a mutation-created chemical handle and an inactive-state pocket, has become a template for other hard targets.
Instead of blocking a cancer protein, a drug can now remove it entirely, which works even for proteins without a druggable active site and can overcome resistance driven by target overexpression or mutation. Several degraders are in late-stage trials for breast and prostate cancer.