bcr-abl(t315i)

BCR-ABL-IN-7 is a WT and T315I mutant ABL kinase inhibitor.BCR-ABL-IN-7 potently inhibits WT and T315I mutant ABL kinase activity.BCR-ABL-IN-7 can be used in chronic myelogenous leukemia (CML) research.

BCR-ABL-IN-2 is a BCR-ABL1 tyrosine kinase inhibitor (IC50s: 57 nM, 773 nM for ABL1 native and ABL1 T315I).

BCR-ABL-IN-4 is a BCR-ABL inhibitor exhibiting anticancer activity with an inhibitory effect on cancer cell growth, specifically on K562 cells (IC50: 0.67 nM) and BCR-ABL T315I-transfected Ba F3 cells (IC50: 16 nM).

BCR-ABL-IN-5 is a Bcr-Abl (Breakpoint cluster region-Abelson) kinase inhibitor that acts on Bcr-AblWT (IC50: 0.014 μM) and Bcr-AblT3151 (IC50: 0.45 μM) and exhibits some anti-proliferative effects on leukemic cells. effect.

BCR-ABL-IN-6 (9h) is an imatinib derivative and a selective inhibitor of Bcr-Abl kinase, showing activity on Bcr-AblWT (IC50: 4.6 nM) and Bcr-AblT3151 (IC50: 277 nM). BCR-ABL-IN-6 (9h) is utilized in studying chronic myeloid leukemia treatment.

BCR-ABL-IN-8 (compound 26f) is a BCR-ABL inhibitor characterized by a trimethoxy group [1].

BCR-ABL-IN-3 is a highly effective, irreversible inhibitor of Bcr-Abl, with an IC50 value of ≤100 nM for Ba F3 Bcr-Abl T3151, displaying significant anti-cancer activity.

PSMA I&T is a PSMA-targeting radiocompound that serves as a diagnostic agent for prostate-specific membrane antigen-targeted therapy, often coupled with radioactivity.

BCR-ABL-IN-1 is a BCR-ABL tyrosine kinase inhibitor (pIC50: 6.46) and may be used in the research of chronic myelogenous leukemia.

PROTAC BCR-ABL Degrader-1 (compound PROTAC 1), featuring a 2-oxoethyl linker, induces Bcr-Abl degradation via the ubiquitin-proteasome pathway and exhibits antiproliferative effects on K562 cells, indicating its potential in cancer research [1].

Vamotinib (PF-114) is an orally active and specific tyrosine kinase inhibitor with antiproliferative and antitumour activity.Vamotinib inhibits the phosphorylation of BCR/ABL and BCR/ABL-T315I, which promotes apoptosis. Vamotinib is used to study drug-resistant Philadelphia chromosome-positive (Ph+) leukaemia and Alzheimer's disease.

BGG463 (K 0859) can inhibit c-ABL-T334I, BCR-ABL and BCR-ABL-T315I variants with a 50% inhibitory concentration (IC50) of 0.25 μM, 0.09 μM and 0.590 μM, respectively.

Olverembatinib (GZD 824) is an orally bioavailable Bcr-Abl inhibitor for Bcr-Abl(WT, IC50: 0.34 nM) and Bcr-Abl(T315I, IC50: 0.68 nM).

DCC-2036 (Rebastinib (DCC-2036)) is a conformational control Bcr-Abl inhibitor for Abl1(WT, IC50: 0.8 nM) and Abl1(T315I, IC50: 4 nM), also inhibits LYN, SRC, HCK, FGR, FLT3, KDR, and Tie-2, and low activity to c-Kit. Rebastinib aimed at the Angiopoietin2-Tie2 pathway.

Bafetinib (INNO-406) (INNO-406) is an effective and specific dual Bcr-Abl Lyn inhibitor (IC50: 5.8 19 nM), and no inhibition of the phosphorylation of the T315I mutant and less effective to c-Kit and PDGFR.

AKI603 is a novel small molecule inhibitor of Aurora kinase A (AurA)(IC50 = 12.3 nM). AKI603 is developed to overcome resistance mediated by BCR-ABL-T315I mutation. AKI603 exhibits strong anti-proliferative activity in leukemic cells[1][2].

BV02 is an inhibitor of 14-3-3 protein-protein interactions and can be used in studies about the treatment of chronic myeloid leukemia. BV02 disrupts hematopoietic cells expressing the IM-resistant T315I mutation and the IM-sensitive wild-type Bcr-Abl.

HS-438 inhibits imatinib-resistant BCR-ABL T315I mutation in chronic myeloid leukemia.

DB07107 is a potent inhibitor of drug resistant T315I mutant Bcr-Abl tyrosine kinase and a potent Akt1 inhibitor (IC50: 360 nM).

GZD856 is an orally bioavailable PDGFRα/β inhibitor (IC50s: 68.6 and 136.6 nM) with anti-lung cancer activities.

ON012380 is a non-ATP-competitive Bcr-Abl inhibitor, potently inhibiting imatinib-resistant Bcr-Abl mutants such as T315I.

Olverembatinib dimesylate (GZD824 Dimesylate) is a novel orally bioavailable Bcr-Abl inhibitor for Bcr-Abl(WT) and Bcr-Abl(T315I).

c-ABL-IN-4, a potent inhibitor of c-Abl, exhibits strong activity in inhibiting the Bcr-Abl (IC50 = 4.5 nM) kinase activity and proliferation (IC50 = 0.41-2.12 μM) of Bcr-Abl(T315I) cell lines.

MPT0B002 is a microtubule inhibitor that acts by downregulating T315I mutant Bcr-Abl and inducing apoptosis of imatinib-resistant chronic myeloid leukemia cells.

HG-7-85-01 is a type II ATP competitive inhibitor targeting wild-type and gatekeeper mutations of Bcr-Abl, PDGFRα, Kit, and Src kinases. It effectively inhibits T315I mutant Bcr-Abl kinase, as well as KDR and RET kinases with IC50 values of 3 nM, 20 nM, and 30 nM, respectively. HG-7-85-01 exhibits weak or no inhibition towards other kinases (IC50 >2 μM). Additionally, this compound inhibits cell proliferation by inducing apoptosis and impeding cell-cycle progression.

AKE-72 is a Pan-BCR-ABL inhibitor with anti-leukemic activity.AKE-72 inhibits the proliferation of Ba/F3 cells expressing natural BCR-ABL or its T315I mutant.

AP23464 is a potent adenosine 5'-triphosphate (ATP)-based inhibitor of Src and Abl kinases, displays antiproliferative activity against a human CML cell line and Bcr-Abl-transduced Ba/F3 cells (IC(50) = 14 nM. AP23464 ablates Bcr-Abl tyrosine phosphorylation, blocks cell cycle progression, and promotes apoptosis of Bcr-Abl-expressing cells. Biochemical assays with purified glutathione S transferase (GST)-Abl kinase domain confirmed that AP23464 directly inhibits Abl activity. Importantly, the low nanomolar cellular and biochemical inhibitory properties of AP23464 extend to frequently observed imatinib mesylate-resistant Bcr-Abl mutants, including nucleotide binding P-loop mutants Q252H, Y253F, E255K, C-terminal loop mutant M351T, and activation loop mutant H396P. AP23464 was ineffective against mutant T315I, an imatinib mesylate contact residue. The potency of AP23464 against imatinib mesylate-refractory Bcr-Abl and its distinct binding mode relative to imatinib mesylate warr......

GNF-7 is Bcr-Abl WT and Bcr-Abl T315I inhibitor with IC50 of 133 nM and 61 nM, respectively.

GZD856 formic is a potent, orally active inhibitor of PDGFRα/β and Bcr-Abl T315I, demonstrating IC50 values of 68.6 nM and 136.6 nM for PDGFRα/β, respectively, and 19.9 nM and 15.4 nM for native Bcr-Abl and the T315I mutant, respectively. This compound exhibits significant antitumor activity.