imatinib
Glivec (imatinib) is the pioneering tyrosine kinase inhibitor from Novartis. By blocking the abnormal BCR-ABL protein it turned chronic myeloid leukaemia from a fatal disease into a manageable one, and it also treats GIST and other kinase-driven cancers.
This page is based on the EMA medicine record for imatinib, cross-checked with MedlinePlus and the National Cancer Institute dictionary; the mechanism is explained in plain language, and analogies are used only where they stay accurate.
How it works
Explains what the medicine does in the body, not dosing, side effects, or safety.
An analogy
In chronic myeloid leukaemia a genetic accident fuses two genes into one faulty switch, BCR-ABL, stuck permanently in the "on" position, telling blood cells to multiply. Imatinib is a precisely shaped wedge that slots into the switch's energy socket, so it cannot fire. With the signal off, the leukaemia cells stop multiplying and die at the end of their natural lifespan.
In simple terms
Chronic myeloid leukaemia is caused by a gene swap, the Philadelphia chromosome, that creates an abnormal protein called BCR-ABL. This protein acts like a growth signal that never turns off. Imatinib fits into BCR-ABL and blocks its energy supply, switching the signal off. Leukaemia cells stop dividing and gradually die, while normal cells are largely spared because they do not carry the abnormal protein.
In depth
Imatinib mesylate is a 2-phenylaminopyrimidine small molecule that occupies the ATP-binding site of the BCR-ABL fusion kinase, inhibiting phosphorylation of downstream substrates. It also inhibits c-KIT and PDGFR kinases, explaining activity in gastrointestinal stromal tumours and dermatofibrosarcoma protuberans. Imatinib established the paradigm of targeted cancer therapy; resistance commonly arises via ABL kinase domain mutations such as T315I.
See it in motion
A schematic animation of the mechanism — simplified for clarity, not drawn to scale.
In chronic myeloid leukaemia a genetic accident fuses two genes into one faulty switch, BCR-ABL, stuck permanently in the "on" position, telling blood cells to multiply.
- Chronic myeloid leukaemia is caused by a gene swap, the Philadelphia chromosome, that creates an abnormal protein called BCR-ABL.
- This protein acts like a growth signal that never turns off.
- Imatinib fits into BCR-ABL and blocks its energy supply, switching the signal off.
- Leukaemia cells stop dividing and gradually die, while normal cells are largely spared because they do not carry the abnormal protein.
Target: BCR-ABL tyrosine kinase
An abnormal fusion protein created by the Philadelphia chromosome that constantly signals leukaemia cells to divide; blocking its ATP pocket shuts the signal off.
Approved uses
Approved uses differ by country and change over time. Always follow your local prescribing information.
Approved uses in European Union
EMA- Newly diagnosed Philadelphia-chromosome-positive chronic myeloid leukaemia in adults and children for whom bone-marrow transplantation is not considered as the first-line treatment
- Philadelphia-chromosome-positive chronic myeloid leukaemia in chronic phase after failure of interferon-alpha therapy, or in accelerated phase or blast crisis
Official sources
The statements on this page trace back to these records.
- Glivec (imatinib) — Summary of product characteristics and package leaflet, English version
European Medicines Agency
- MedlinePlus: imatinib
MedlinePlus, U.S. National Library of Medicine
- National Cancer Institute: imatinib mesylate
National Cancer Institute
This page explains how the medicine works — it isn’t the patient leaflet. For anything that applies to you, read the leaflet that came with your medicine or ask your pharmacist.
MedUnfold provides educational content and is not medical advice. Always follow your local prescribing information and healthcare professional.