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

Pharmacology & Drug Discovery

Key Properties

• CAS Number: 220127-57-1
• MW: 589.71
• Purity: >99.99% (May vary between batches)
• Formula: C₂₉H₃₁N₇O·CH₄SO₃
• SMILES: CS(O)(=O)=O.CN1CCN(Cc2ccc(cc2)C(=O)Nc2ccc(C)c(Nc3nccc(n3)-c3cccnc3)c2)CC1
• Target: Autophagy,Bcr-Abl,PDGFR,c-Kit
• Solubility: 10% DMSO+40% PEG300+5% Tween 80+45% Saline:5 mg/mL (8.48 mM);H2O:59 mg/mL (100.05 mM);DMSO:237.5 mg/mL (402.74 mM)

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: Powder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice/Shipping at ambient temperature.
• Expiration Date: 12 months from date of receipt.
• Disclaimer: For research use only

Alternative Names

Autophagy, Bcr-Abl, BcrAbl, cKit, c-Kit, CD117, CGP-57148B, inhibit, Platelet-derived growth factor receptor, PDGFR, Imatinib Mesylate, Imatinib, Inhibitor, v-Abl, STI 571, STI571, STI-571, SCFR, ST 1571 Mesylate, ST1571 Mesylate, ST-1571 Mesylate

Compound Identifiers

PubChem CID

123596