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 Isoform Specific Products
All Product Categories
-
Bcr-Abl Inhibitors
(201)
View all products
-
Bcr-Abl Antagonist
(1)
View all products
-
Bcr-Abl Activator
(1)
View all products
-
Bcr-Abl Modulators
(2)
View all products
-
Bcr-Abl Degraders
(24)
View all products
-
Bcr-Abl Control
(1)
View all products
-
Bcr-Abl Substrate
(1)
View all products
-
ABL1 Proteins
(7)
View all products
-
Bcr-Abl Related Products (249)
Related Products (249)
-
Recombinant Proteins (7)
-
Antibodies (6)
-
Bcr-Abl Isoform Comparison
-
SNIPER(ABL)-015
0 ImagesCat. No.: HY-111854SNIPER(ABL)-015, conjugating GNF5 (ABL inhibitor) to MV-1 (IAP ligand) with a linker, induces the reduction of BCR-ABL protein with a DC50 of 5 μM .
-
SNIPER(ABL)-049
0 ImagesCat. No.: HY-111851SNIPER(ABL)-049, conjugating Imatinib (ABL inhibitor) to Bestatin (IAP ligand) with a linker, induces the reduction of BCR-ABL protein with a DC50 of 100 μM.
-
c-ABL-IN-1
0 ImagesCat. No.: HY-139730CAS No.: 2304918-82-7c-ABL-IN-1 is a novel selective c-Abl inhibitor that prevents neurodegeneration in parkinson’s disease.
-
ABL1 Q252H Recombinant Human Active Protein Kinase
0 ImagesCat. No.: HY-E70639The emergence of mutations in the BCR::ABL1 kinase domain (KD) impairs Imatinib Mesylate (HY-50946) binding capacity, thus contributing to Imatinib Mesylate resistance. Identification of these mutations is important for treatment decisions and precision medicine in chronic myeloid leukaemia (CML). ABL1 Q252H Recombinant Human Active Protein Kinase is a recombinant ABL1 Q252H protein that can be used to study ABL1 Q252H-related functions.
-
EphB4-IN-1
0 ImagesCat. No.: HY-185227CAS No.: 1394837-94-5EphB4-IN-1 is a selective EphB4 tyrosine kinase inhibitor with IC50 values of 0.16-0.30 μM. EphB4-IN-1 binds to the ATP binding site of EphB4 in a DFG-in conformation, forming four stable intermolecular hydrogen bonds. EphB4-IN-1 also inhibits Src, Abl1, Lck, and EGFR kinases. EphB4-IN-1 inhibits EphB4 autophosphorylation. EphB4-IN-1 can be used for the research of cancer, such as non small cell lung cancer.
-
EAPB0503
0 ImagesCat. No.: HY-171184CAS No.: 1140627-77-5EAPB0503 is a quinoline compound with anti-tumor activity, showing strong cytotoxicity against melanoma cells in vitro (IC50=200 nM). EAPB0503 can induce specific cell cycle arrest in mitosis of CML cells and directly activate apoptosis, leading to an increase in the G0 cell population, disruption of mitochondrial membrane potential, PARP cleavage, and DNA fragmentation. EAPB0503 also reduces the levels of BCR-ABL protein .
-
AP 24149
0 ImagesCat. No.: HY-10363CAS No.: 926922-29-4AP 24149 is a potent Src-Abl dual inhibitor with IC50 values of 9.1, 3.6 nM for Src and Abl, respectively.
-
IM-12 (GMP)
0 ImagesCat. No.: HY-12292GCAS No.: 1129669-05-1IM-12 GMP is IM-12 (HY-12292) produced by using GMP guidelines. GMP small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. IM-12 is an orally active anti-inflammatory agent that targets and inhibits the NF-κB and STAT3 signaling pathways. IM-12 activates the Wnt signaling pathway and promotes the nuclear translocation of β-catenin by inhibiting GSK3β, while also blocking the tyrosine kinase activity of p210BCR/ABL. IM-12 reduces the levels of IL-6, IL-17, NO, prostaglandin E2, iNOS and COX-2, and induces ER stress, Ca2+ release, autophagy and apoptosis. IM-12 is heat-sensitive and does not induce autophagy in IM-resistant p210BCR/ABLT315I mutant cells. IM-12 is also a component of the 5iLA medium used for naive pluripotent stem cell research. IM-12 has been applied in studies related to carrageenan (HY-125474)-induced hind paw edema, TNBS-induced colitis, and acute and chronic myeloid leukemia.
-
DosatiLink-1
0 ImagesCat. No.: HY-155288CAS No.: 2941512-37-2DosatiLink-1 is an Abelson murine leukemia (ABL) enzyme inhibitor.
-
Leu-PEG1-Dasa
0 ImagesCat. No.: HY-180925CAS No.: 3037776-72-7Leu-PEG1-Dasa is a potent BCR-ABL PROTAC degrader with a DC50 of 0.48 nM. Leu-PEG1-Dasa uses a single amino acid as the E3 ligand and belongs to a mini-PROTAC, functioning through the N-terminal canonical pathway. Leu-PEG1-Dasa exhibits potent anti-proliferative activity against K562 cells. Leu-PEG1-Dasa can be used for the study of chronic myeloid leukemia (CML).
-
Antiproliferative agent-30
0 ImagesCat. No.: HY-155112CAS No.: 2713553-88-7Antiproliferative agent-30 (Compound 8g) inhibits tubulin assembly and inhibits FLT3 and Abl1. Antiproliferative agent-30 has vascular-disrupting activity. Antiproliferative agent-30 has broad antiproliferative activities against cancer cell lines (IC50s: 0.054 nM, 0.008 nM, 0.144 nM for HCT-116, K562, MV-4-11 cells respectively). Antiproliferative agent-30 also has anticancer effect against AML with FLT3-ITD-TKD mutation.
-
Dasatinib (GMP Like)
0 ImagesCat. No.: HY-10181GLCAS No.: 302962-49-8Synonyms: BMS-354825 (GMP Like)Dasatinib (GMP Like) (BMS-354825 (GMP Like)) is Dasatinib (HY-10181) produced by using GMP like guidelines. GMP Like small molecules works appropriately as an auxiliary reagent for cell therapy manufacture. 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.
-
DS-PPE-GW
0 ImagesCat. No.: HY-180218DS-PPE-GW is a BCR-ABL ATTEC degrader. DS-PPE-GW connects BCR-ABL and LC3B, thereby tethering BCR-ABL to the autophagosome membrane. DS-PPE-GW shows potent BCR-ABL degradation. DS-PPE-GW has anticancer activity against chronic myeloid leukemia (Pink: LC3B ligand (HY-10542); Blue: BCR-ABL ligand (HY-107447); Black: Linker (HY-W001860)).
-
ABL1 T315I Recombinant Human Active Protein Kinase
0 ImagesCat. No.: HY-E70640The emergence of mutations in the BCR::ABL1 kinase domain (KD) impairs Imatinib Mesylate (HY-50946) binding capacity, thus contributing to Imatinib Mesylate resistance. Identification of these mutations is important for treatment decisions and precision medicine in chronic myeloid leukaemia (CML). ABL1 T315I Recombinant Human Active Protein Kinase is a recombinant ABL1 T315I protein that can be used to study ABL1 T315I-related functions.
-
Azo-PROTAC-4C-cis
0 ImagesCat. No.: HY-180985Azo-PROTAC-4C-cis is a BCR-ABL PROTAC degrader, and its degradation efficiency of BCR-ABL is much lower than that of its trans isomer Azo-PROTAC-4C-trans (HY-180983). Azo-PROTAC-4C-cis is the product of the conformational transformation of Azo-PROTAC-4C-trans under ultraviolet (UV) light irradiation. Azo-PROTAC-4C-cis can be converted into highly active Azo-PROTAC-4C-trans under visible light, thereby initiating protein degradation. Azo-PROTAC-4C-cis can be used for the study of myeloid leukemia.
-
FGFRs-IN-1
0 ImagesCat. No.: HY-170846FGFRs-IN-1 (Compound A16) is the orally active inhibitor for FGFR, that inhibits FGFR1/2/3/4 with IC50s of 2.3, 7, 11, and 163 nM, respectively. FGFRs-IN-1 also inhibits VEGFR1/2/3, Abl, and Flt3 with IC50s of 61, 176, 112, 26, and 353 nM, respectively. FGFRs-IN-1 exhibits weak inhibitory efficacy against CYP enzymes. FGFRs-IN-1 reduces the expression of α-SMA and collagen I, and inhibits epithelial-mesenchymal transition (EMT) in TGF-β1 stimulated A549 cell. FGFRs-IN-1 exhibits anti-inflammatory activity in Bleomycin (HY-17565)-induced mouse pulmonary fibrosis model and CCl4 (HY-Y0298)-induced mouse liver fibrosis model.
