Loading
The lung-cancer pill whose dramatic responses in a few patients led to the discovery of EGFR mutations in 2004.
Gefitinib is a reversible first-generation EGFR tyrosine kinase inhibitor selective for sensitising mutations. It received accelerated US approval in 2003 in unselected NSCLC after chemotherapy, but the ISEL trial (2005) failed to show a survival benefit in that population and US use was restricted. The dramatic responses seen in a minority of patients led Lynch and Paez in 2004 to discover activating EGFR mutations in responders, one of the founding discoveries of precision oncology. IPASS (NEJM 2009) then proved that mutation-selected first-line gefitinib was superior to chemotherapy, and the EU approved it for EGFR-mutant NSCLC in 2009; the US re-approved it in 2015 for first-line exon 19 deletion or L858R disease. Rash, diarrhoea and rare interstitial lung disease are the main toxicities. Gefitinib's story is the reason EGFR testing is now routine at diagnosis.
Reversible EGFR kinase inhibitor selective for sensitising mutations. Connects to EGFR.
1.Gefitinib slips into a pocket on EGFR.
Oral, self-administered, so it is a Part D drug: covered through a stand-alone Part D plan or Medicare Advantage drug benefit, usually on the specialty tier with 25 to 33% coinsurance until the annual cap ($2,000 in 2025, $2,100 in 2026). Generic gefitinib is available.
Multi-source generic on low-cost tiers; usually no prior authorisation. Cash prices without insurance are modest.
Sources: Medicare.gov: Drug coverage (Part D) · Medicare.gov: Costs for Medicare drug coverage (annual out-of-pocket cap). Not medical or financial advice; verify with your plan.
Sources: NICE TA192 · SMC advice: gefitinib. Funding decisions are indication-specific and change monthly; verify with NICE and your treating team.
As monotherapy for locally advanced or metastatic NSCLC after failure of platinum-based and docetaxel chemotherapy
Accelerated approval on a surrogate endpoint, with a confirmatory trial required.
As monotherapy for locally advanced or metastatic NSCLC after failure of platinum-based and docetaxel chemotherapy
Withdrawn: the indication came off the label 9.0 years after its accelerated approval.
| Region | Year | Indication |
|---|---|---|
| US | 2003 | NSCLC after chemotherapy (accelerated; restricted 2005) |
| EU | 2009 | EGFR-mutant NSCLC |
| US | 2015 | First-line NSCLC with EGFR exon 19 del or L858R |
Country and place are remembered in this browser only. A postcode is sent to OpenStreetMap's Nominatim service to find coordinates when you press the button; nothing else leaves your device.
This is the separate paper behind the survival figure quoted for dacomitinib. It is a real but modest gain, and the US label notes that overall survival was not formally tested because the response rate comparison earlier in the testing order was not significant, so the P value is descriptive.
ARCHER 1050 supported dacomitinib's 2018 US first-line approval and was the first head-to-head win of a second-generation EGFR inhibitor over a first-generation one on progression-free survival. FLAURA, reported the same year, made osimertinib the usual first choice, so dacomitinib is now rarely used.
It is the reference frequency table for resistance to first-generation EGFR inhibitors, and it made rebiopsy at progression standard rather than exceptional, because the mechanism decides the next treatment and cannot be guessed.
The case for re-biopsy at progression, for treating resistance as a diagnosis rather than an endpoint, and for the idea of a drug holiday. It is also the origin of resistance-directed sequencing: what you give next should depend on what the tumour became.
The trial that turned EGFR testing into a standard of care rather than a research assay, and the clearest demonstration in oncology that a clinically selected population can hide two opposite treatment effects inside one positive result.
It defined bypass resistance as a category and set the treatment rule that follows from it: keep blocking the original target and add an inhibitor of the bypass, which is the logic of every EGFR plus MET combination since.
It generalised the single-patient finding and made the point that drug-resistant subclones are selected by treatment rather than created by it, which is the model the whole field now works with.
Resistance to a targeted drug usually has a cause you can read off a sequence, which means it can be targeted in turn. Osimertinib exists because of this paper.
Query for this drug: (TITLE:"Gefitinib" OR ABSTRACT:"Gefitinib" OR TITLE:"Iressa" OR ABSTRACT:"Iressa") AND (cancer OR tumor OR tumour OR oncology OR carcinoma OR lymphoma OR leukemia OR leukaemia OR myeloma OR sarcoma OR melanoma OR glioma). Results are unfiltered search hits about Gefitinib, not a curated reading list.
Shares Adenosquamous carcinoma of the lung, A Study of Ramucirumab (LY3009806) in Combination With Erlotinib in Previously Untreated Participants With EGFR Mutation-Positive Metastatic NSCLC (RE, Acquired resistance of lung adenocarcinomas to gefitinib or erlotinib is associated with a second mutation in the EGFR kinase domain, EGFR exon 19 deletion & L858R and the tag generic.
Shares Lung cancer (all types), Non-small-cell lung cancer and the tag generic.
Shares AstraZeneca and the tag generic.
Shares Lung cancer (all types), Non-small-cell lung cancer and the tag generic.
Shares Lung cancer (all types) and the tag generic.
Shares Lung cancer (all types) and the tag generic.
Shares Lung cancer (all types), Non-small-cell lung cancer and the tag generic.
Shares Dacomitinib versus gefitinib as first-line treatment for patients with EGFR-mutation-positive non-small-cell lung cancer (ARCHER 1050): a randomised, open-label, phase 3 trial, Improvement in overall survival in a randomized study that compared dacomitinib with gefitinib in patients with advanced non-small-cell lung cancer and EGFR-activating mutations, ARCHER 1050, EGFR L858R.