1. Signaling Pathways
  2. Protein Tyrosine Kinase/RTK
  3. Bcr-Abl

Bcr-Abl

Bcr-Abl tyrosine-kinase inhibitors (TKI) are the first-line therapy for most patients with chronic myelogenous leukemia (CML). More than 90% of CML cases are caused by a chromosomal abnormality that results in the formation of a so-called Philadelphia chromosome. This abnormality is a consequence of fusion between the Abelson (Abl) tyrosine kinase gene at chromosome 9 and the break point cluster (Bcr) gene at chromosome 22, resulting in a chimeric oncogene (Bcr-Abl) and a constitutively active Bcr-Abl tyrosine kinase that has been implicated in the pathogenesis of CML. Compounds have been developed to selectively inhibit the tyrosine kinase.

Bcr-Abl Related Products (89):

Cat. No. Product Name Effect Purity
  • HY-10181
    Dasatinib
    Inhibitor 99.85%
    Dasatinib (BMS-354825) is a highly potent, ATP competitive, orally active dual Src/Bcr-Abl inhibitor with potent antitumor activity. The Kis are 16 pM and 30 pM for Src and Bcr-Abl, respectively. Dasatinib inhibits Bcr-Abl and Src with IC50s of <1.0 nM and 0.5 nM, respectively. Dasatinib also induces apoptosis and autophagy.
  • HY-13520
    Nocodazole
    Inhibitor 99.66%
    Nocodazole (Oncodazole) is a rapidly-reversible inhibitor of microtubule. Nocodazole binds to β-tubulin and disrupts microtubule assembly/disassembly dynamics, which prevents mitosis and induces apoptosis in tumor cells. Nocodazole inhibits Bcr-Abl, and activates CRISPR/Cas9.
  • HY-15463
    Imatinib
    Inhibitor 99.95%
    Imatinib (STI571) is an orally bioavailable tyrosine kinases inhibitor that selectively inhibits BCR/ABL, v-Abl, PDGFR and c-kit kinase activity. Imatinib (STI571) works by binding close to the ATP binding site, locking it in a closed or self-inhibited conformation, therefore inhibiting the enzyme activity of the protein semicompetitively. Imatinib also is an inhibitor of SARS-CoV and MERS-CoV.
  • HY-12047
    Ponatinib
    Inhibitor 99.43%
    Ponatinib (AP24534) is an orally active multi-targeted kinase inhibitor with IC50s of 0.37 nM, 1.1 nM, 1.5 nM, 2.2 nM, and 5.4 nM for Abl, PDGFRα, VEGFR2, FGFR1, and Src, respectively.
  • HY-10159
    Nilotinib
    Inhibitor 99.96%
    Nilotinib is an orally available Bcr-Abl tyrosine kinase inhibitor with antineoplastic activity.
  • HY-108766
    Ponatinib hydrochloride
    Inhibitor 99.26%
    Ponatinib (AP24534) hydrochloride is a hydrochloride of ponatinib. Ponatinib is an orally active multi-targeted kinase inhibitor with IC50s of 0.37 nM, 1.1 nM, 1.5 nM, 2.2 nM, and 5.4 nM for Abl, PDGFRα, VEGFR2, FGFR1, and Src, respectively.
  • HY-104010A
    Asciminib hydrochloride
    Inhibitor 99.93%
    Asciminib (ABL001) hydrochloride is a potent and selective allosteric BCR-ABL1 inhibitor, which inhibits Ba/F3 cells grown with an IC50 of 0.25 nM.
  • HY-10159B
    Nilotinib hydrochloride
    Inhibitor
    Nilotinib (AMN107) hydrochloride is an orally active Bcr-Abl tyrosine kinase inhibitor with antineoplastic activity and can be used in studies of chronic myelogenous leukaemia.
  • HY-50946
    Imatinib Mesylate
    Inhibitor 99.98%
    Imatinib Mesylate (STI571 Mesylate) is a tyrosine kinases inhibitor that inhibits c-Kit, Bcr-Abl, and PDGFR (IC50=100 nM) tyrosine kinases.
  • HY-10158
    Bosutinib
    Inhibitor 99.96%
    Bosutinib is an oral Src/Abl tyrosine kinase inhibito with IC50 of 1.2 nM and 1 nM, respectively.
  • HY-104010
    Asciminib
    Inhibitor 99.78%
    Asciminib (ABL001) is a potent and selective allosteric BCR-ABL1 inhibitor, which inhibits Ba/F3 cells grown with an IC50 of 0.25 nM.
  • HY-13264
    Degrasyn
    Inhibitor 99.70%
    Degrasyn (WP1130) is a cell-permeable deubiquitinase (DUB) inhibitor, directly inhibiting DUB activity of USP9x, USP5, USP14, and UCH37. Degrasyn has been shown to downregulate the antiapoptotic proteins Bcr-Abl and JAK2.
  • HY-13024
    Rebastinib
    Inhibitor 99.91%
    Rebastinib (DCC-2036) is an orally active, non-ATP-competitive Bcr-Abl inhibitor for Abl1WT and Abl1T315I with IC50s of 0.8 nM and 4 nM, respectively. Rebastinib also inhibits SRC, KDR, FLT3, and Tie-2, and has low activity to seen towards c-Kit.
  • HY-50514
    AT9283
    Inhibitor 99.70%
    AT9283 is a multi-targeted kinase inhibitor with potent activity against Aurora A/B, JAK2/3, Abl (T315I) and Flt3 (IC50s ranging from 1 to 30 nM). AT9283 inhibits growth and survival of multiple solid tumors in vitro and in vivo.
  • HY-15666
    Olverembatinib
    Inhibitor 99.78%
    Olverembatinib (GZD824) is a potent and orally active pan-Bcr-Abl inhibitor. Olverembatinib potently inhibits a broad spectrum of Bcr-Abl mutants. Olverembatinib strongly inhibits native Bcr-Abl and Bcr-AblT315I with IC50s of 0.34 nM and 0.68 nM, respectively. Olverembatinib has antitumor activity.
  • HY-10339
    KW-2449
    Inhibitor 99.85%
    KW-2449 is a multi-targeted kinase inhibitor of FLT3, ABL, ABLT315I and Aurora kinase with IC50s of 6.6, 14, 4 and 48 nM, respectively.
  • HY-10181A
    Dasatinib hydrochloride
    Inhibitor 98.86%
    Dasatinib (BMS-354825) hydrochloride is a highly potent, ATP competitive, orally active dual Src/Bcr-Abl inhibitor with potent antitumor activity. The Kis are 16 pM and 30 pM for Src and Bcr-Abl, respectively. Dasatinib hydrochloride inhibits Bcr-Abl and Src with IC50s of <1.0 nM and 0.5 nM, respectively. Dasatinib hydrochloride also induces apoptosis and autophagy.
  • HY-112089
    LXH254
    Inhibitor 99.95%
    LXH254 is a potent, selective, orally active, type II BRAF and CRAF inhibitor, with IC50 values of 0.072 and 0.21 nM against CRAF and BRAF, respectively.
  • HY-50868
    Bafetinib
    Inhibitor 99.76%
    Bafetinib is a potent and orally active Lyn/Bcr-Abl tyrosine kinase inhibitor. Bafetinib augments the activities of several proapoptotic Bcl-2 homology (BH)3-only proteins (Bim, Bad, Bmf and Bik) and induces apoptosis in Ph+ leukemia cells via Bcl-2 family-regulated intrinsic apoptosis pathway.
  • HY-12070
    DPH
    Activator 99.20%
    DPH is a potent cell permeable c-Abl activator, which displays potent enzymatic and cellular activity in stimulating c-Abl activation.