t315i

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

KW-2449 is a multiple-targeted inhibitor, mostly for Flt3 (IC50: 6.6 nM), modestly effective to Bcr-Abl, FGFR1, and Aurora A; little inhibitory on PDGFRβ, IGF-1R, EGFR.

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

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.

Nocodazole (Oncodazole) is a reversible inhibitor of microtubule polymerization and an inhibitor of Bcr-Abl. Nocodazole has antitumor activity, blocks the cell cycle and induces apoptosis.

AT9283 (J-504568) is an effective multi-targeted inhibitor of JAK2(IC50=1.2 nM) and JAK3(IC50=1.1 nM), Aurora A, Aurora B and Abl(T315I).

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).

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.

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.

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

GZD856 is an orally bioavailable inhibitor of PDGFRα and PDGFRβ with IC50 values of 68.6 and 136.6 nM, respectively. GZD856 has demonstrated anti-lung cancer activities in experimental studies. The molecular activity profile of GZD856 supports its utilization in research investigating PDGFR-associated signaling pathways, tumor biology, kinase inhibition, and mechanisms relevant to lung cancer progression.

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

AT-9283 L-lactate is an inhibitor of aurora kinase.

BCR-ABL-IN-13 is a dual c-Src and Abl inhibitor, with a Ki value of 0.55 μM against c-Src, 0.10 μM against wild-type Abl, and 0.40 μM against the AblT315I mutant. BCR-ABL-IN-13 exerts competitive/mixed-type inhibitory effects on wild-type Abl, and non-competitive inhibitory effects on the drug-resistant AblT315I mutant. BCR-ABL-IN-13 is used in chronic myeloid leukemia research models to study kinase inhibition profiles, resistance-associated Abl mutations, and signaling pathway modulation in oncogenic tyrosine kinase systems.

HG-7-85-01 is a novel ATP-competitive and type II tyrosine kinase inhibitor targeting both wild-type and watchman mutant BCR-ABL, PDGFRα, Kit, and Src kinases, with inhibitory effects on the proliferation of a variety of cancer cell lines, leading to G0/G1-phase blockade and apoptosis induction in BCR-ABL-expressing cells.

URMC-099 is an orally bioavailable, brain penetrant MLK inhibitor (IC50: 19/42/14/150 nM, for MLK1/MLK2/MLK3/DLK), and also inhibits LRRK2 activity (IC50: 11 nM).

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.

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.

VS1150 (Compound 11) is a phosphorylation-inducing chimeric small molecule (PHICS) designed to target BCR-ABL. It effectively hinders oncogenic kinase BCR-ABL signaling through inhibitory phosphorylation at the Y253 site (EC50: 69 nM), leading to apoptosis. Additionally, VS1150 can inhibit other oncogenic ABL fusion proteins and resistant mutants, such as T315I. This compound is applicable in research on chronic myeloid leukemia (CML) and other cancers driven by ABL fusion proteins.

BIIB021 (CNF2024) mesylate is the mesylate salt form of BIIB021. BIIB021 is an orally active Hsp90 inhibitor. It suppresses the proliferation of drug-resistant chronic myeloid leukemia (CML) cells, with IC50 values for K562, K562/G, 32Dp210, and 32Dp210-T315I cells recorded at 513.99, 603.53, 110.08, and 148.07 nM, respectively. BIIB021 induces the degradation of BCR-ABL protein and inhibits the β-catenin/c-Myc pathway. Furthermore, BIIB021 can induce autophagy in CML cells and is applicable for CML research.

P19As is a BCR-ABL PROTAC degrader based on Asciminib, with a DC50 of approximately 200 nM for the wild-type BCR-ABL protein. It is capable of degrading the T315I mutant and demonstrates strong antiproliferative activity in BaF3-BCR-ABL (T315I) cells. P19As is applicable for research in chronic myeloid leukemia and acute lymphoblastic leukemia.

PROTACBCR-ABLDegrader-2 is a selective Bcr-Abl T315I PROTAC degrader with a DC50 of 108.7 nM in Ba/F3 Bcr-AblT315I cells. It demonstrates potent degradation activity with rates of 69.89% at 100 nM and 94.23% at 300 nM concentrations. In vivo, PROTACBCR-ABLDegrader-2 exhibits good plasma exposure, induces significant tumor regression, triggers apoptosis (apoptosis), and maintains a favorable safety profile. This compound is suitable for chronic myelogenous leukemia research.

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

TG101114 is the T315I mutant enzyme inhibitor that acts by exhibiting reasonable in vivo efficacy in a xenograft mouse model harboring T315I.