Big Chemical Encyclopedia

Chemical substances, components, reactions, process design ...

Articles Figures Tables About

Tyrosine kinase inhibitors imatinib mesylate

Conventional cytogenetics, FISH, and RT-PCR have been reliably used for the laboratory detection of the t(9 22). RT-PCR detection is possible in up to 95% of cases, and may detect up to 10% of cases missed by conventional cytogenetics, and is an important modality for minimal residual disease detection. Recently, quantitative real-time PCR-based approaches have improved the ability to detect and quantify BCR-ABL transcripts in CML patients (Figure 39-15 Color Plate 4]). The recent availability the tyrosine kinase inhibitor imatinib mesylate for CML is an important development in the treatment of CML and further underscores the importance of methods for sensitive and specific identification and quantification of the BCR-ABL fusions in patients with a clinical suspicion of a CML. [Pg.1470]

Fig. 13.3 Structures of the tyrosine kinase inhibitors imatinib, a phenylaminopyrimidine derivative, and the 4-aminoquinazoline derivatives, gefitinib and erlotinib. Imatinib is marketed as the mesylate salt... Fig. 13.3 Structures of the tyrosine kinase inhibitors imatinib, a phenylaminopyrimidine derivative, and the 4-aminoquinazoline derivatives, gefitinib and erlotinib. Imatinib is marketed as the mesylate salt...
Imatinib Mesylate (Gleevec) Tyrosine kinase inhibitor bcr-abl, c-kit Chronic myelogenous leukemia Hematologic and cytogenetic response rate. Phase III GIST ... [Pg.447]

Imatinib mesylate (Gleevec, Novartis) tyrosine kinase inhibitor for the treatment of chronic myeloid leukemia (refer to Exhibit 7.3)... [Pg.35]

Imatinib mesylate is a tyrosine kinase inhibitor (see Chapter 2 on receptors). It is used to block the growth of white blood cells. [Pg.214]

Protein kinases can be classified according to the amino acid residue that is phosphorylated in the cellular process. Consequently, there are tyrosine-specific kinases and serine/threonine kinases. Tyrosine kinases are a family of tightly regulated enzymes, and the aberrant activation of various members of this family is one of the hallmarks of cancer. Tyrosine phosphorylation has been linked to multiple cell growth and differentiation pathways. Imatinib mesylate (1) is a tyrosine kinase inhibitor (TKI). An important characteristic of imatinib mesylate (1) is that it is an ATP-competitive inhibitor. It binds at the ATP binding site and blocks ATP binding thereby inhibiting kinase activities. [Pg.31]

Imatinib mesylate is a new tyrosine kinase inhibitor designed for the treatment of CML. It inhibits the Bcr-AbI tyrosine kinase leading to inhibition of proliferation and induction of apoptosis in Bcr-Abl-positive cells. Imatinib is indicated for treatment of CML in blast crisis, accelerated phase, or chronic phase in patients who have failed interferon therapy. Response rates have been evaluated in terms of hematologic and cytogenetic (decrease or disappearance of Philadelphia chromosome) responses. [Pg.158]

Imatinib mesylate was the first tyrosine kinase inhibitor to be approved for treatment of cancer (see Table 124—18). It inhibits deregulated bcr-abl tyrosine kinase, the molecular abnormality in patients with chronic myelogenous leukemia that results from the characteristic Philadelphia chromosome translocation. The deregulated tyrosine kinase constantly drives leukemic cell proliferation. Imatinib inhibits cell proliferation and induces apoptosis in the Philadelphia chromosome-positive cells. It is relatively, but not completely, selective for these cells. °°... [Pg.2317]

The bcr-abl fusion gene produces a mutant tyrosine kinase that is involved in both the increased proliferation of the CML clone, and in the reduction in FAS-mediated apoptosis. The characterization of the adenosine triphosphate (ATP) binding site on the tyrosine kinase has led to a new class of inhibitors. The first of these inhibitors, imatinib mesylate (Gleevec), was approved in 2001 for patients in chronic phase who had failed interferon alfa (IFN-a), and in accelerated phase or blast crisis. It obtained additional FDA approval in 2002 for first-line treatment in newly diagnosed CML. The clinical results associated with imatinib have changed the way CML is treated, and will be discussed in more detail under the treatment section of this chapter. "... [Pg.2514]

States, acrivastine (18) is the active ingredient in the Semprex-D brand. Imatinib mesylate (Gleevec, 19) is a tyrosine kinase inhibitor and was approved for the treatment of ten different cancers including chronic myelogenous leukemia (CML) by 2001. Atazanavir (Reyataz, 20) is a once-daily, anti-viral drug of the protein kinase class, and, it is prescribed for human immunodeficiency virus (HIV). [Pg.402]

Gefitinib is a tyrosine kinase inhibitor used in the treatment of refractory non-small cell carcinoma of the lung. Respiratory failure has been observed in 1 % of the cases with a 30% fatality rate and corresponds histologically to DAD with possible progression to fibrosis (4). Diffuse alveolar hemorrhage has also been reported. Rare cases of pulmonary complications with imatinib mesylate (used in chronic myelogenous leukemia) have also been described. [Pg.816]

Dr. Guy B. Faguet is particularly keen on imatinib mesylate, or Gleevec, against CML and is an advocate of the more fundamental gene therapy rather than the cell-toxic chemotherapy (e.g., Faguet, 2005, p. 46). He also notes it to be an inhibitor for tyrosine kinase. Interestingly, he skips the Warburg theory about cancer metabolism vs. normal cell metabolism and of enzymes and enzyme inhibitors. [Pg.412]

Imatinib mesylate (Gleevee, A -(4-methyl-3-(4-(pyridin-3-yl)-pyrimidin-2-ylamino) phenyl)-4-((4-methyl piperazin-l-yl)methyl) benzamide methane-sulfonate, STI571) is known as an inhibitor of tyrosine kinases and is used for the treatment of chronic myeloid leukemia and gastrointestinal stromal tumors. It was developed by Novartis Pharma AG and is a 2-phenylamino-pyrimidine derivative. [Pg.592]

Some neuroblastoma cells overexpress the c-Kit receptor for its ligand, stem cell factor (SCF), and release SCF in an autocrine loop for self-stimulation of mitoses. Imatinib mesylate suppresses PDGF and tyrosine kinase c-Kit (GDI 17) expression. Somatostatin inhibited PDGF-induced phosphorylation of PDGFR and inhibited ras gene amplification. For local invasion, these tumor cells release MMP2/9. The synthetic MMP inhibitor, prinomastat, suppresses MMP production and tumor cell locomotion. However, MMP expression is promotional for neuroblastoma cell differentiation. The presence of MMP is necessary for the neurite formation of retinoic acid-treated neuroblastoma cells neurite formation is the first sign of differentiation induction (vide infra) [1624]. [Pg.360]


See other pages where Tyrosine kinase inhibitors imatinib mesylate is mentioned: [Pg.54]    [Pg.793]    [Pg.399]    [Pg.400]    [Pg.416]    [Pg.54]    [Pg.793]    [Pg.399]    [Pg.400]    [Pg.416]    [Pg.31]    [Pg.31]    [Pg.235]    [Pg.491]    [Pg.703]    [Pg.2502]    [Pg.316]    [Pg.16]    [Pg.703]    [Pg.132]    [Pg.196]    [Pg.410]    [Pg.760]    [Pg.59]    [Pg.132]    [Pg.627]    [Pg.1562]    [Pg.401]    [Pg.639]    [Pg.171]    [Pg.452]    [Pg.201]   
See also in sourсe #XX -- [ Pg.410 ]




SEARCH



Kinase imatinib

Kinase inhibitors

Kinase, kinases inhibitors

Mesylate

Mesylation

Tyrosine inhibitors

Tyrosine kinases

Tyrosines tyrosine kinase

© 2024 chempedia.info