bcr-abl1

PROTAC BCR-ABL1 ligand 1 is the ligand of PROTAC .

PPY A is a potent inhibitor of T315l mutant and wild-type Abl kinase (IC50 of 9 and 20 nM, respectively).PPY A also inhibits the growth of Bcr-Abl T315l mutant or wild-type Bcr-Abl genetically transformed cells.

Radotinib (IY-5511), and sometimes referred to by its investigational name IY5511, is a drug for the treatment of different types of Y, most notably Philadelphia chromosome-positive (Ph+) chronic myeloid leukemia (CML) with resistance or intolerance of other tyrosine kinase Bcr-Abl inhibitors

GMB-475 is a BCR-ABL1 tyrosine kinase degrader based on PROTAC, overcoming BCR-ABL1-dependent drug resistance. GMB-475 targets BCR-ABL1 protein and recruits the E3 ligase Von Hippel Lindau (VHL).resulting in ubiquitination and subsequent degradation of th

Vodobatinib (K-0706) is a novel 3rd generation (3G) TKI effective against wild-type and mutated BCR-ABL1 with limited off-target activity.

GMB-475, also known as PROTAC BCR-ABL1 ligand 1, allosterically targets and binds to the BCR-ABL1 protein. It effectively recruits the E3 ligase Von Hippel-Lindau, leading to the ubiquitination and subsequent degradation of BCR-ABL1 [1].

cSRC/BCR-ABL1-IN-1 (compound 16a) is a dual-target inhibitor of the cSRC/BCR-ABL1 kinases.

BCR-ABL1-IN-1 is a highly potent, orally bioavailable inhibitor with remarkable specificity towards ABL kinase, showing significant promise for elucidating the precise role of ABL kinases in the central nervous system, particularly in preclinical investigations [1].

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

(S,R,S)-AHPC TFA (VHL ligand 1 TFA) (VH032-NH2 TFA) is a VH032-based ligand designed for von Hippel-Lindau (VHL) protein recruitment. This compound can be linked to protein ligands (e.g., BCR-ABL1) using a linker to create PROTACs (e.g., GMB-475), which effectively induce the degradation of BCR-ABL1, demonstrated by an IC50 of 1.11 μM in Ba/F3 cells.

Tyrosine kinase-IN-8 (compound 4e) is a BCR‐ABL1 tyrosine kinase inhibitor (TKI) exhibiting antiproliferative activity against the chronic myeloid leukemia (CML) cell line K562, with a CC50 of 0.8 µM. Tyrosine kinase-IN-8 is applicable for research in chronic leukemia.

(S,R,S)-AHPC-Me-piperazine-acetyl-PIP-AcOH is a conjugate of the VHL ligand of the E3 ubiquitin ligase VH032 and a linker. This linker component of (S,R,S)-AHPC-Me-piperazine-acetyl-PIP-AcOH can be further conjugated with a target protein ligand (such as BCR-ABL1) to form a PROTAC molecule.

CHMFL-ABL-053 (Compound 18a) is a potent, selective, and orally available inhibitor of BCR-ABL, SRC, and p38 kinases, with IC50 values of 70, 90, and 62 nM against ABL1, SRC, and p38, respectively. CHMFL-ABL-053 is a potentially useful drug candidate for Chronic Myeloid Leukemia (CML) [1].

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.

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).

Asciminib (ABL001) (ABL001) is a potent and selective Bcr-Abl inhibitor (Kd: 0.5–0.8nM).

Asciminib hydrochloride is described as a "STAMP inhibitor," specifically targeting the ABL myristoyl pocket, Asciminib hydrochloride, marketed as Scemblix, are applied in research in Philadelphia chromosome-positive chronic myeloid leukemia (Ph+ CML) by binding to the allosteric site of wild-type ABL N-terminus, which is myristoylated, whereas the ABL fusion protein lacks this domain, enabling selective modulation of oncogenic signaling pathways and serving as a targeted therapeutic tool in hematologic cancer research.

BP-5-087 is a STAT3 inhibitor, combining with BCR-ABL1 inhibition to overcome kinase-independent resistance in chronic myeloid leukemia.