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Targeted therapy

How Does Sunitinib — Block Tumour Growth?

If sunitinib has just been prescribed to you, understanding what it does — and what it does not do — is a reasonable place to start.

Medically reviewed by Dr. C. Raghavendra Reddy, Medical Oncologist, MBBS (Gold Medal) · DNB · DM (Medical Oncology, Gold Medal) · Last reviewed August 2026

  • Not chemotherapy — Sunitinib targets specific molecular switches rather than attacking all dividing cells the way chemotherapy does.
  • Blocks blood supply — Tumours depend on growing new blood vessels to survive. Sunitinib cuts off the signals that drive that process.
  • Hits multiple targets at once — It blocks several kinases simultaneously, which is why it is called a multi-kinase inhibitor.
  • Taken as a tablet at home — Sunitinib is an oral medicine you take yourself — you do not need to come in for an infusion every cycle.
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Sunitinib blocks a family of proteins called kinases that cancer cells depend on to grow new blood vessels and multiply. Without that blood supply, the tumour cannot expand. It is an oral tablet taken at home, and it is classified as a targeted therapy, not chemotherapy.

What does sunitinib actually do inside your body?

Sunitinib blocks kinases — proteins that act as on/off switches in the signalling chains cells use to grow. It targets the kinases that tumour blood vessels depend on most, particularly the receptors for a chemical signal called VEGF.

When those receptors are blocked, the tumour cannot send the message that builds new blood vessels. A tumour without a growing blood supply cannot get the oxygen and nutrients it needs to expand.

Sunitinib also blocks kinases on certain tumour cell types directly, which is why it is active in cancers such as gastrointestinal stromal tumour as well as kidney cancer.

Terms your doctor may use

Kinase
A protein inside cells that passes signals along by switching other proteins on or off. Many cancers depend on overactive kinases to grow.
VEGF (vascular endothelial growth factor)
The chemical signal that tells the body to grow new blood vessels. Tumours release large amounts of VEGF to build their own blood supply.
VEGFR (VEGF receptor)
The docking port on blood vessel cells where VEGF attaches. Sunitinib fits into this receptor and blocks it, preventing the signal from getting through.
Angiogenesis
The process by which new blood vessels grow. Tumours hijack this process to feed themselves. Blocking angiogenesis is the main way sunitinib slows tumour growth.
Tyrosine kinase inhibitor (TKI)
A class of drugs — including sunitinib — that block kinase proteins. They are oral, targeted medicines, distinct from chemotherapy.
Multi-kinase inhibitor
A drug that blocks more than one kinase at the same time. Sunitinib targets several, which gives it activity across more than one type of cancer cell and blood vessel signal.

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Why does targeting blood vessels matter more than attacking cancer cells directly?

A solid tumour cannot grow beyond a few millimetres without building its own blood supply. Cutting that supply starves the tumour without needing to reach every individual cancer cell.

This is why anti-angiogenic drugs like sunitinib can work across several cancer types — the blood vessel signalling they target is something most solid tumours share.

It also explains some of sunitinib's side effects. VEGF is not only used by tumours; the body uses the same pathway to maintain normal blood pressure and the health of the skin on the palms and soles. Blocking VEGF signalling is why hypertension and hand-foot syndrome are common on this drug.

Did you know?

Tumours actively release VEGF to grow their own blood supply — a process they cannot survive without. Sunitinib was among the first oral drugs approved to specifically block this pathway in kidney cancer.

The same mechanism that makes it effective is why your blood pressure needs monitoring from the start of treatment.

Source: ESMO Clinical Practice Guidelines: Renal Cell Carcinoma

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Common questions

Frequently asked questions

Is sunitinib the same as chemotherapy?

No. Chemotherapy works by damaging or killing cells that divide quickly, which means it affects normal fast-dividing cells — in hair follicles and the gut lining — as well as cancer cells. Sunitinib works differently: it blocks specific proteins that tumour blood vessels and certain cancer cells need to grow. The side effects reflect this difference. Hair loss is uncommon on sunitinib, whereas hand-foot syndrome and high blood pressure are not typical of chemotherapy. Your oncologist may use the term 'targeted therapy' or 'TKI' to distinguish it.

Why does sunitinib cause hand-foot syndrome and high blood pressure?

Both side effects happen because VEGF — the signal sunitinib blocks — is not only used by tumours. The same growth signal maintains tiny blood vessels in the palms and soles, and helps regulate blood vessel tone throughout the body. Blocking it affects those normal vessels too. Redness, soreness, and peeling on the palms and soles is hand-foot syndrome, and it is the most common reason for dose adjustments. Blood pressure tends to rise early in treatment and is monitored closely. Neither side effect means the drug is not working — both are a consequence of the same mechanism that makes sunitinib active against tumours.

How long does sunitinib take to start working?

Response is assessed after the first full treatment cycle, which is typically several weeks. You will not feel the drug working day-to-day. The way your oncologist checks whether it is effective is through imaging — usually a CT scan — comparing tumour size before and after the first cycles. Do not interpret a lack of obvious change in how you feel as a sign the drug is not working. Tumour stability, where the cancer is neither growing nor shrinking noticeably, is also a meaningful response with sunitinib.

Does sunitinib kill cancer cells directly?

Primarily it deprives the tumour of its blood supply, which starves cancer cells indirectly. In some cancer types — particularly gastrointestinal stromal tumour — sunitinib also directly blocks kinases on the cancer cells themselves. For kidney cancer, the anti-angiogenic effect is considered the main mechanism. The distinction matters less to most patients than the outcome, but it helps explain why sunitinib's side effects differ from those of medicines that attack dividing cells directly.

Why does sunitinib come as a tablet rather than an infusion?

Sunitinib is a small molecule — small enough to be absorbed through the gut wall and enter the bloodstream after swallowing. Many older cancer drugs are large protein molecules that cannot survive the digestive system and must be given by infusion. Taking sunitinib at home is more convenient, but it also means that consistency of timing and food intake matters. Your oncologist or pharmacist will advise you on when to take it relative to meals and what to avoid.

Can sunitinib stop working over time?

Yes, and this is a known pattern with most targeted therapies. Tumours can develop or select for cells that find ways around the blocked signalling pathway — a process called acquired resistance. NCCN and ESMO guidance addresses this and includes second-line treatment options for when sunitinib is no longer controlling the disease. The goal of monitoring and follow-up imaging is to detect this change early, so that a switch in treatment can be made before there is significant progression. If your disease has been stable on sunitinib and then changes, ask your oncologist specifically what the next option is.

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