Bcr-Abl tyrosine-kinase inhibitors (TKI) are the first-line therapy for most patients with chronic myelogenous leukemia (CML).A chromosomal abnormality that results in the formation of a so-called Philadelphia chromosome is the root cause of more than 90% of CML cases. This abnormality results from the fusion of the break point cluster (Bcr) gene at chromosome 22 with the Abelson (Abl) tyrosine kinase gene at chromosome 9, creating a chimeric oncogene (Bcr-Abl) and a constitutively active Bcr-Abl tyrosine kinase that has been linked to the pathogenesis of CML. The tyrosine kinase has been selectively inhibited by substances.
| Structure | Cat No. | Product Name | CAS No. | Product Description |
|---|---|---|---|---|
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V122167 | (S)-Embibatinib | 2412969-12-9 | (S)-Embibatinib is an isomer of TERN-701 and is a selective BCR-ABL allosteric inhibitor. |
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V118988 | ABL1 E255K Recombinant Human Active Protein Kinase | Mutations in the BCR::ABL1 kinase domain (KD) weaken its binding affinity to imatinib mesylate, leading to resistance to imatinib mesylate. | |
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V118790 | ABL1 F317I Recombinant Human Active Protein Kinase | Mutations in the BCR::ABL1 kinase domain (KD) weaken its binding affinity to imatinib mesylate, leading to resistance to imatinib mesylate. | |
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V118929 | ABL1 G250E Recombinant Human Active Protein Kinase | Mutations in the BCR::ABL1 kinase domain (KD) weaken the binding affinity of imatinib mesylate, leading to resistance to imatinib mesylate. | |
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V118949 | ABL1 H396P Recombinant Human Active Protein Kinase | Mutations in the BCR::ABL1 kinase domain (KD) weaken the binding affinity of imatinib mesylate, leading to resistance to imatinib mesylate. | |
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V118956 | ABL1 M351T Recombinant Human Active Protein Kinase | Mutations in the BCR::ABL1 kinase domain (KD) weaken its binding affinity to imatinib mesylate, leading to resistance to imatinib mesylate. | |
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V118872 | ABL1 Q252H Recombinant Human Active Protein Kinase | Mutations in the BCR::ABL1 kinase domain (KD) weaken its binding affinity to imatinib mesylate, leading to resistance to imatinib mesylate. | |
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V118971 | ABL1 T315I Recombinant Human Active Protein Kinase | Mutations in the BCR::ABL1 kinase domain (KD) weaken its binding affinity to imatinib mesylate, leading to resistance to imatinib mesylate. | |
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V118850 | ABL1 Y253F Recombinant Human Active Protein Kinase | Mutations in the BCR::ABL1 kinase domain (KD) weaken its binding affinity to imatinib mesylate, leading to resistance to imatinib mesylate. | |
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V10305 | Adaphostin | 241127-58-2 | Adaphostin(NSC-680410) is the adamantyl ester of AG957, acting as anovel and potent activator of Fas-mediated death pathwayin Bcr/Abl-positive leukaemia. |
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V84226 | AK-HW-90 | ||
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V85947 | AKE-72 | 2566525-18-4 | |
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V69652 | AP 24149 | 926922-29-4 | AP 24149 is a potent Src-Abl dual (bifunctional) inhibitor (antagonist) with IC50s of 9.1 and 3.6 nM for Src and Abl respectively. |
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V110394 | Arg-PEG1-Dasa | 3037776-67-0 | Arg-PEG1-Dasa is a miniature PROTAC that targets BCR-ABL. |
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V109138 | Asciminib-NH2 | 3106065-83-9 | Asciminib-NH2 is a BCR-ABL ligand that can be used to synthesize PROTACs, such as P19A. |
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V109878 | Azo-PROTAC-4C-cis | Azo-PROTAC-4C-cis is a BCR-ABL protein degrader that exhibits significantly reduced degradation efficiency for BCR-ABL compared to its trans isomer, Azo-PROTAC-4C-trans. | |
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V110013 | Azo-PROTAC-4C-trans | Azo-PROTAC-4C-trans is a BCR-ABL PROTAC degrader that can efficiently degrade BCR-ABL fusion proteins and ABL proteins. | |
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V110419 | BCR-ABL degrader 1 | BCR-ABL degrader 1 (compound 23) is a HyT-based BCR-ABL degrader with a DC50 value of 19.9 μM. | |
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V85499 | BCR-ABL kinase-IN-3 | 2699634-21-2 | |
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V85510 | BCR-ABL kinase-IN-3 (dihydrocholide) |