Imatinib - CAS 152459-95-5
Catalog number: 152459-95-5
Category: Inhibitor
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Molecular Formula:
C29H31N7O
Molecular Weight:
493.6
COA:
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Targets:
c-Kit
Description:
Imatinib inhibits the SLF-dependent activation of wild-type c-kit kinase activity with a IC50 for these effects of approximately 0.1 μM, which is similar to the concentration required for inhibition of PDGFR.
Purity:
>98%
Synonyms:
CGP057148B, STI571
MSDS:
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InChIKey:
KTUFNOKKBVMGRW-UHFFFAOYSA-N
InChI:
InChI=1S/C29H31N7O/c1-21-5-10-25(18-27(21)34-29-31-13-11-26(33-29)24-4-3-12-30-19-24)32-28(37)23-8-6-22(7-9-23)20-36-16-14-35(2)15-17-36/h3-13,18-19H,14-17,20H2,1-2H3,(H,32,37)(H,31,33,34)
Canonical SMILES:
CC1=C(C=C(C=C1)NC(=O)C2=CC=C(C=C2)CN3CCN(CC3)C)NC4=NC=CC(=N4)C5=CN=CC=C5
1. Mathematical modelling of miRNA mediated BCR.ABL protein regulation in chronic myeloid leukaemia vis-a-vis therapeutic strategies
Malkhey Verma, Ehsan Ghayoor Karimiani, Hans V. Westerhoff* and Philip J. R. Day*. Integr. Biol., 2013, 5, 543—554
Imatinib is a competitive inhibitor of ATP binding to BCR.ABL protein. It thereby inhibits the cell proliferation signal of BCR.ABL and induces cell death in BCR.ABL positive cells. In patients with newly diagnosed CML, TKIs including imatinib are offered as a front-line therapy. While the advent of TKIs has significantly changed the management of the chronic phase of CML, these drugs are not able to entirely eradicate the disease. This could be in part due to rapidly induced or selected cytogenetic changes which occur in the majority of CML patients. imatinib may not, as was long believed, function by its binding to the BCR.ABLp ATP-binding site. With the binding of imatinib, the ABL part of the proto-oncogene may be trapped in a state without kinase activity. Despite some therapeutic success of imatinib, it fails to eradicate leukaemic cells completely.
2. In silico identification of novel kinase inhibitors targeting wild-type and T315I mutant ABL1 from FDA-approved drugs
Huai-long Xu, Zi-jie Wang, Xiao-meng Liang, Jin-ku Bao*. Mol. BioSyst., 2014, 10, 1524—1537
In order to compare the flexibility of each residue in single ABL1–inhibitor complexes, the RMSF was calculated (Fig. 7). In general, wild-type ABL1 bound with different drugs have similar RMSF profiles and it is the same for T315I ABL1. Moreover, considering the ATP binding site (residues 248–260 and 315–322) and the A-loop motif (residues 381–405), nilotinib and imatinib exhibited lower flexibility while chlorhexidine exhibited the highest flexibility in the T315I complex, indicating that bound with nilotinib and imatinib, wild-type ABL1 could maintain the ATP binding site and A-loop motif, leading to its inhibited ability. Sorafenib possessed similar flexibility to nilotinib and imatinib. However, in the T315I ABL1 complex, nicergoline and plerixafor exhibited lower flexibility than ponatinib, indicating that nicergoline and plerixafor could form a stronger interaction with T315I ABL1.
3. An expeditious synthesis of imatinib and analogues utilising flow chemistry methods
Mark D. Hopkin, Ian R. Baxendale and Steven V. Ley*. Org. Biomol.Chem., 2013, 11, 1822–1839
A flow process has been developed that leads to the preparation of imatinib without the need for any manual handling of intermediates over a three step process. The synthesis was achieved despite the poor solubility of individual components and methods were developed to overcome these. In addition the use of an in-line solvent switching technique permitted reaction solvents to be changed as part of the continuous process and this could be used for a number of different applications. Using this method enables imatinib to be synthesized in high purity in less than a day. The generic reactor set-up was then utilised to prepare a number of analogues in similaryield that were not directly obtainable using the original process route described.
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