Imatinib is an oral medication used for treating chronic myeloid leukemia and acute lymphoblastic leukemia. It is classified as a kinase inhibitor. Kinase inhibitors include dasatinib (Sprycel), erlotinib (Tarceva), gefitinib (Iressa), nilotinib (Tasigna), pazopanib (Votrient), sunitinib (Sutent), and vandetanib (Caprelsa).
What is imatinib used to treat?
Summary. Imatinib (Gleevec) is a kinase inhibitor prescribed for the treatment of chronic myeloid leukemia and acute lymphoblastic leukemia. Side effects, drug interactions, dosing information, and warnings and precautions should be reviewed prior to taking any medication.
What is im imatinib (Gleevec)?
Imatinib (Gleevec) is a kinase inhibitor prescribed for the treatment of chronic myeloid leukemia and acute lymphoblastic leukemia. Side effects, drug interactions, dosing information, and warnings and precautions should be reviewed prior to taking any medication.
Is im imatinib a kinase inhibitor?
Imatinib is an oral medication used for treating chronic myeloid leukemia and acute lymphoblastic leukemia. It is classified as a kinase inhibitor. Kinase inhibitors include dasatinib (Sprycel), erlotinib (Tarceva), gefitinib (Iressa), nilotinib (Tasigna), pazopanib (Votrient), sunitinib (Sutent), and vandetanib (Caprelsa).
What is the difference between IM imatinib and rituximab?
Imatinib acts by targeting the BCR-ABL protein, which is commonly found in patients with chronic myelogenous leukemia. Rituximab acts by binding to B-cell antigens (CD20) and is used to treat chronic lymphocytic leukemia.
What is the mechanism of action of imatinib?
Mechanism of Action Imatinib mesylate is a protein-tyrosine kinase inhibitor that inhibits the bcr-abl tyrosine kinase, the constitutive abnormal tyrosine kinase created by the Philadelphia chromosome abnormality in chronic myeloid leukemia (CML).
How does imatinib Gleevec work?
Gleevec, known generically as imatinib, works by slowing or stopping the growth of certain cancer cells. Gleevec inhibits (or blocks) specific enzymes in the body called tyrosine kinases. Tyrosine kinase enzymes are involved in many cell functions, including cell signaling (communication), growth, and division.
What is imatinib used to treat?
Imatinib mesylate is approved to treat: Acute lymphoblastic leukemia in adults and children that is Philadelphia chromosome positive. In adults, it is used for disease that has recurred (come back) or is refractory (does not respond to treatment).
How does imatinib work in CML?
Imatinib binds to BCR-ABL kinase domain by preventing the transfer of a phosphate group to tyrosine on the protein substrate and the subsequent activation of phosphorylated protein. As the result, the transmission of proliferative signals to the nucleus is blocked and leukemic cell apoptosis is induced.
How does Gleevec work for leukemia?
Gleevec, the thin molecule shown here in blue, has a specific shape which blocks the active site of the abnormal protein. By binding to the active site, Gleevec prevents the trigger protein from causing the release the white blood cells and alleviates the symptoms of the disease.
What type of inhibitor is imatinib?
Imatinib is a member of the class of small molecule tyrosine kinase inhibitors with selectivity for the Abl kinase. Imatinib is a potent competitive inhibitor of ATP binding to Abl kinase, as well as to the c-Kit and PDGF receptor tyrosine kinases.
Which mechanism of action for imatinib makes it effective in treating chronic myelogenous leukemia?
Imatinib inhibits proliferation and induces apoptosis in cells positive for BCR/ABL. For patients with chronic-phase CML, imatinib at 400 mg/day is the best dosage for primary therapy, because it induces a complete hematologic response in almost all patients and causes a high cytogenetic response rate.
What type of molecule is imatinib?
Imatinib is a benzamide obtained by formal condensation of the carboxy group of 4-[(4-methylpiperazin-1-yl)methyl]benzoic acid with the primary aromatic amino group of 4-methyl-N(3)-[4-(pyridin-3-yl)pyrimidin-2-yl]benzene-1,3-diamine.
How is imatinib metabolism?
Imatinib is metabolised mainly by the cytochrome P450 (CYP) 3A4 or CYP3A5 and can competitively inhibit the metabolism of drugs that are CYP3A4 or CYP3A5 substrates.
How effective is imatinib?
Among the patients in the imatinib group, the estimated overall survival rate at 10 years was 83.3%. Approximately half the patients (48.3%) who had been randomly assigned to imatinib completed study treatment with imatinib, and 82.8% had a complete cytogenetic response.
Does imatinib cure CML?
Imatinib mesylate has transformed the treatment for chronic myeloid leukemia (CML). The vast majority of patients obtain hematologic remission, with a low probability of progression of disease. Yet imatinib rarely cures CML, and current recommendations dictate lifelong treatment with imatinib.
What is deep molecular response in CML?
A deep molecular response is commonly defined as BCR-ABL1 values of ≤0.01% IS and is described as various BCR-ABL1 cutoff values, where molecular response 4 (MR4) is ≤0.01% IS, MR4. 5 ≤0.0032% IS, and MR5 <0.001%.
What is imatinib used for?
Imatinib was the first signal transduction inhibitor (STI), used in a clinical setting. It prevents a BCR-ABL protein from exerting its role in the oncogenic pathway in chronic myeloid leukemia (CML). Imatinib directly inhibits the constitutive tyrosine kinase activity, which results in the modification of the function of various genes involved in ...
When was imatinib approved?
The FDA has approved imatinib as first-line treatment for newly diagnosed CML in December 2002 following an International Randomized Study (IRIS), initiated in June 2000, comparing imatinib at a single daily dose 400 mg to IFN alpha plus cytarabine in newly diagnosed patients with CML in CP.
Does imatinib inhibit tyrosine kinase?
Imatinib directly inhibits the constitutive tyrosine kinase activity. Imatinib binds to BCR-ABL kinase domain by preventing the transfer of a phosphate group to tyrosine on the protein substrate and the subsequent activation of phosphorylated protein.
What is the purpose of imatinib?
In addition to transforming the outcome for patients with CML, the discovery of imatinib helped establish a group of cancer drugs, called targeted therapies, that are designed to attack cancer cells with specific genetic abnormalities.
What is the name of the drug that has been used to treat chronic myelogenous leukemia?
NCI-supported research led to a series of discoveries that resulted in the development of imatinib (Gleevec), a landmark drug that has vastly improved the outcomes of patients with a type of blood cancer called chronic myelogenous leukemia. These discoveries also helped establish a new group of drugs (known as targeted therapy) ...
What is the cause of CML?
CML is caused by one translocation that creates a singular mutation, the BCR-ABL fusion gene or Philadelphia chromosome. The discovery of the Philadelphia chromosome and BCR-ABL, supported in part by NCI, demonstrated for the first time that a genetic alteration could cause cancer.
How have targeted therapies changed cancer?
Targeted therapies have immensely changed how cancer is studied and treated, and have fostered the precision medicine approach: treatment tailored to the unique genetic changes in an individual’s cancer cells.