Gleevec FDA Approval History
Last updated by Judith Stewart, BPharm on May 25, 2025.
FDA Approved: Yes (First approved May 10, 2001)
Brand name: Gleevec
Generic name: imatinib mesylate
Dosage form: Tablets
Company: Novartis Pharmaceuticals Corporation
Treatment for: Acute Lymphoblastic Leukemia, Chronic Myelogenous Leukemia, Myelodysplastic Diseases, Dermatofibrosarcoma Protuberans, Gastrointestinal Stromal Tumor, Systemic Mastocytosis, Hypereosinophilic Syndrome
Gleevec (imatinib mesylate) is a kinase inhibitor indicated for the treatment of chronic myeloid leukemia, acute lymphoblastic leukemia, myelodysplastic/ myeloproliferative diseases, systemic mastocytosis, hypereosinophilic syndrome, dermatofibrosarcoma protuberans and gastrointestinal stromal tumors.
- Gleevec is indicated for the treatment of:
- newly diagnosed adult and pediatric patients with Philadelphia chromosome positive chronic myeloid leukemia (Ph+ CML) in chronic phase.
- patients with Philadelphia chromosome positive chronic myeloid leukemia (Ph+ CML) in blast crisis (BC), accelerated phase (AP), or in chronic phase (CP) after failure of interferon-alpha therapy.
- adult patients with relapsed or refractory Philadelphia chromosome positive acute lymphoblastic leukemia (Ph+ ALL).
- pediatric patients with newly diagnosed Philadelphia chromosome positive acute lymphoblastic leukemia (Ph+ ALL) in combination with chemotherapy.
- adult patients with myelodysplastic/myeloproliferative diseases (MDS/MPD) associated with platelet-derived growth factor receptor (PDGFR) gene re-arrangements.
- adult patients with aggressive systemic mastocytosis (ASM) without the D816V c-Kit mutation or with c-Kit mutational status unknown.
- adult patients with hypereosinophilic syndrome (HES) and/or chronic eosinophilic leukemia (CEL) who have the FIP1L1-PDGFRα fusion kinase (mutational analysis or fluorescence in situ hybridization [FISH] demonstration of CHIC2 allele deletion) and for patients with HES and/or CEL who are FIP1L1-PDGFRα fusion kinase negative or unknown.
- adult patients with unresectable, recurrent and/or metastatic dermatofibrosarcoma protuberans (DFSP).
- patients with Kit (CD117) positive unresectable and/or metastatic malignant gastrointestinal stromal tumors (GIST).
- adjuvant treatment of adult patients following resection of Kit (CD117) positive GIST.
History of Gleevec from the Novartis Archive
The story of Gleevec began in 1960, when two researchers in Philadelphia identified a genetic mutation in patients with CML. They found that a section of DNA was missing from chromosome 22, an alteration that became known as the Philadelphia (Ph) chromosome.
In the late 1980s, two researchers from the California Institute of Technology identified the principal cause of CML: the Ph chromosome produced an enzyme that played a central role in aberrant cell growth and division. The enzyme, a tyrosine kinase known as Bcr-Abl, changed the cell’s normal genetic instructions, jamming the signal that tells the body to stop producing white blood cells. The massive increase in the number of white blood cells characterizes Ph+ CML.
Bcr-Abl inhibitors were discovered in early 1990, and a team at Ciba-Geigy, one of the Novartis predecessor companies, spent two years turning one candidate compound into a potent, specific Bcr-Abl inhibitor. Crucially, the compound – STI571, now known as Gleevec – did not demonstrate significant activity against normal cells, a distinguishing factor from traditional cancer treatments.
In the mid-to-late 1990s, Ciba-Geigy and then Novartis prepared for Gleevec’s clinical trials, and the first Phase I study with Gleevec began in June 1998. It was designed to determine optimal dosing for safety and efficacy. But between September 1998 and April 1999, investigators noticed that nearly every CML patient who took the drug was responding. Novartis then committed unprecedented resources to accelerate the development and production of Gleevec.
Recognizing Gleevec’s potential, the U.S. Food and Drug Administration granted a fast-track designation for treatment of patients with the most advanced stage of CML, for which at that time there were few, if any, treatment options that were effective and well tolerated.
The presentation of the initial Phase I clinical trial results took the oncology-hematology community by storm. At the December 1999 meeting of the American Society of Hematology, it was reported that at certain doses, 31 of 31 patients who had taken Gleevec long enough to be included in the presentation of the Phase I findings had a significant reduction in the number of white blood cells, and one-third had a reduction or disappearance of cells containing the Ph chromosome, a major goal of CML treatment. Updated Phase I data published in The New England Journal of Medicine validated the early responses.
The demand for Gleevec skyrocketed as the news spread worldwide. Within two days, Novartis received more than 2,000 telephone requests for information on the agent. On May 10, 2001, only 10 weeks after submission of a New Drug Application, the FDA granted approval of Gleevec – marking the FDA’s fastest review period of any cancer drug.
Source: Novartis
Development timeline for Gleevec
| Date | Article |
|---|---|
| Jan 25, 2013 | Approval FDA Approves Gleevec for Children with Acute Lymphoblastic Leukemia |
| Jan 31, 2012 | Approval FDA Approves Gleevec for Expanded Use in Patients with Rare Gastrointestinal Cancer |
| Dec 22, 2008 | Approval FDA Approves Gleevec to Prevent Recurrence of Rare Gastrointestinal Cancer |
| Dec 8, 2003 | Approval FDA Converts Gleevec in Second Line Setting to Regular Approval |
| May 20, 2003 | Approval FDA Approves Gleevec for Pediatric Leukemia Treatment |
| Dec 20, 2002 | Approval Gleevec Approved for First Line Treatment of Chronic Myeloid Leukemia (CML) |
| May 10, 2001 | Approval FDA Approves Gleevec for Leukemia Treatment |
Further information
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