Imatinib mesylate

SKU: orb1307991

Description

Imatinib Mesylate is an orally active, multi-targeted tyrosine kinase inhibitor that potently suppresses BCR-ABL, PDGFR, and c-Kit. It is a foundational research tool for studying oncogenic signaling and has demonstrated efficacy in both in vitro assays and in vivo models of chronic myeloid leukemia and other cancers.

Research Area

Cell Biology

Key Properties

• CAS Number: 220127-57-1
• MW: 493.62 ∙ 96.11
• Purity: >98%
• Formula: C₂₉H₃₁N₇O ∙ CH₃SO₃H
• SMILES: CS(O)(=O)=O.CN1CCN(Cc2ccc(cc2)C(=O)Nc2ccc(C)c(Nc3nccc(n3)-c3cccnc3)c2)CC1
• Target: Kinase
• Solubility: Soluble in DMSO (up to 50 mg/ml) or in Water (up to 50 mg/ml).

Bioactivity

• Target IC50:
  OSRGA cells:9 μM|MOS-J cells:23 µM|HOS cells:11 µM|Vero C1008 cells:3.24 μM|SGC-7901 cells:0.208 μM|c-Kit:0.1 μM|POS-1 cells:15 µM|PDGFR:0.3 μM|MG-63 cells:20 µM
• In Vivo:
  The treatment of imatinib significantly reduced the incidence of adenocarcinomas (47.1% vs. 76.9% of untreated TRAMP mice) but had no effect against NE tumors, which instead significantly increased in frequency (23.5% vs. 15.4% of untreated TRAMP mice) . In the imatinib group, lung function was improved with a lower W/D ratio. Perivascular edema and neutrophil infiltration were ameliorated. The imatinib group demonstrated maintained expression of VEC, inhibition of pCrkL, and a significantly higher level of interleukin (IL)-10 .
• In Vitro:
  Inhibition of Steel factor (SLF)-induced c-kit autophosphorylation by STI 571 was dose-dependent, with complete inhibition observed at both 10 and 1.0 μmol/L. Inhibition was also apparent at a dose of 0.5 μmol/L, although limited c-kit autophosphorylation still occurred. Complete inhibition of MAP kinase activation occurred at 10- and 1.0-μmol/L concentrations of STI 571. Partial inhibition was observed at a dose of 0.1 μmol/L, and no inhibition occurred at a dose of 0.01 μmol/L. Total MAP kinase expression was not altered by treatment with STI 571 . Exposure of cells to 1 μM STI571 for 24 hours before lysis resulted in a reduction of cellular tyrosine phosphorylation in general and of TEL/ARG specifically . Imatinib had a more similar effect on Bcr/Abl- and c-Kit–dependent proliferation, with an IC50 of 19 nM in R10(-) cells and 82 nM in MO7e cells growing in the presence of SCF (KL, Kit ligand), respectively .
• Cell Research:
  Cells were added to 96-well plates at a density of 20 000 cells/well for HMC-1 and 50 000 cells/well for M-07e. Experiments with M-07e were performed with the use of GM-CSF or SLF as a growth factor supplement. Experiments using HMC-1 were performed without growth factor supplementation. Proliferation at 48 hours was measured with an XTT-based assay .
• Animal Research:
  Heterozygous experimental TRAMP mice were obtained by breeding wild-type C57BL/6 male mice and heterozygous female TRAMP mice. MC-deficient C57BL/6-KitW-sh/W-sh mice were intercrossed over 12 generations with TRAMP mice to obtain MC-deficient KitWsh-TRAMP mice. Cromolyn (10 mg/kg dissolved in saline; Sigma Aldrich) or imatinib (50 mg/kg dissolved in saline) were administered intraperitoneally in TRAMP mice for 5 days/week. Treatments started at 8 or 16 weeks, as indicated in text and figures, and continued for the duration of the experiment. Mice were sacrificed at 25 weeks and their urogenital apparatus collected for IHC .

Storage & Handling

• Storage: -20°C
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

Gleevec; STI571

Compound Identifiers

PubChem CID

123596