Bcr-Abl
BCR-ABL1 is a Philadelphia chromosome-derived fusion oncogene that encodes a constitutively active tyrosine kinase and drives chronic myeloid leukemia (CML) pathophysiology[1]. Mechanistically, BCR-ABL1 coordinates malignant signaling with pathways linked to proliferation, apoptosis resistance, hematopoietic stem cell alteration, and leukemia stem cell persistence[2][3]. In disease models and clinical monitoring, CML is defined by BCR-ABL1 transcripts, most commonly e13a2 and e14a2, which encode p210 BCR-ABL1[4]. Compared with these common isoforms, rare transcripts such as e1a2, e19a2, e6a2, e8a2, e13a3, and e14a3 show structural divergence that can alter leukemogenic activity, diagnostic detection, and tyrosine kinase inhibitor response[5][6]. Transcript subtype also has practical research value, because e14a2 showed faster or deeper molecular responses than e13a2 in imatinib- or nilotinib-treated cohorts, while survival did not differ between transcripts[4]. For experimental applications, imatinib targets ABL kinase activity, whereas nilotinib and dasatinib show stronger BCR-ABL inhibition and retain activity against multiple imatinib-resistant mutants[1].
References:
- [1]. Kantarjian HM, et al. Important therapeutic targets in chronic myelogenous leukemia. Clin Cancer Res. 2007 Feb 15;13(4):1089-97. [Content Brief]
- [2]. Mencalha AL, et al. Role of calcium-dependent protein kinases in chronic myeloid leukemia: combined effects of PKC and BCR-ABL signaling on cellular alterations during leukemia development. Onco Targets Ther. 2014 Jul 8;7:1247-54. [Content Brief]
- [3]. Moradi F, et al. Signaling pathways involved in chronic myeloid leukemia pathogenesis: The importance of targeting Musashi2-Numb signaling to eradicate leukemia stem cells. Iran J Basic Med Sci. 2019 Jun;22(6):581-589. [Content Brief]
- [4]. Su YJ, et al. Comparison of molecular responses and outcomes between BCR::ABL1 e14a2 and e13a2 transcripts in chronic myeloid leukemia. Cancer Sci. 2022 Oct;113(10):3518-3527. [Content Brief]
- [5]. Zhou X, et al. The silent players: Atypical BCR‑ABL isoforms as biomarkers and therapeutic hurdles in CML pathogenesis (Review). Oncol Rep. 2025 Dec;54(6):162. [Content Brief]
- [6]. Massimino M, et al. Impact of the Breakpoint Region on the Leukemogenic Potential and the TKI Responsiveness of Atypical BCR-ABL1 Transcripts. Front Pharmacol. 2021 Jun 30;12:669469. [Content Brief]
All Product Categories
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Bcr-Abl Related Products (197)
Related Products (197)
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SNIPER(ABL)-024
0 ImagesCat. No.: HY-111861CAS No.: 2222355-77-1SNIPER(ABL)-024, conjugating GNF5 (ABL inhibitor) to LCL161 derivative (IAP ligand) with a linker, induces the reduction of BCR-ABL protein with a DC50 of 5μM.
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SGX393
0 ImagesCat. No.: HY-165532CAS No.: 1030610-86-6Synonyms: SGX70393SGX393 (SGX70393) is a Bcr-Abl kinase inhibitor. SGX393 binds to the active conformation of the kinase domains of both wild-type and T315I mutant Bcr-Abl, thereby inhibiting kinase activity. SGX393 exhibits antiproliferative effects in cells expressing wild-type or T315I mutant Bcr-Abl, and suppresses T315I-driven tumor growth. SGX393 can be used for the research of chronic myeloid leukemia.
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SNIPER(ABL)-058
0 ImagesCat. No.: HY-111859CAS No.: 2222354-61-0SNIPER(ABL)-058, conjugating Imatinib (ABL inhibitor) to LCL161 derivative (IAP ligand) with a linker, induces the reduction of BCR-ABL protein with a DC50 of 10 μM.
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BCR-ABL degrader 1
0 ImagesCat. No.: HY-180798BCR-ABL degrader 1 is a hydrophobic tag degrader with GNF‑2 (HY-11007) as the ligand and Boc2His (HY-185595) as the hydrophobic tag. BCR-ABL degrader 1 mediates the degradation of BCR‑ABL with a DC50 of 19.9 μM. BCR-ABL degrader 1 induces the degradation of BCR-ABL fusion protein via the ubiquitin-proteasome pathway, a process involving Hsp70 and Hsp90. BCR-ABL degrader 1 downregulates p‑STAT5 and p‑SHP2, the downstream signaling molecules of BCR‑ABL. BCR-ABL degrader 1 can be used in the research of chronic myeloid leukemia.
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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.
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BCR-ABL1-IN-2
0 ImagesCat. No.: HY-179247BCR-ABL1-IN-2 (compound 8) is a potent BCR-ABL1 tyrosine kinase inhibitor. BCR-ABL1-IN-2 exhibits activity in Imatinib (HY-15463) resistant K562/DOX cells with LC50 of 5.29 μM. BCR-ABL1-IN-2 shows no significant toxicity in nontumor cells. BCR-ABL1-IN-2 can be used for chronic myeloid leukemia research.
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GMB-805
0 ImagesCat. No.: HY-180968CAS No.: 2489876-41-5
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P19As
0 ImagesCat. No.: HY-180981CAS No.: 2635386-55-7P19As is a BCR-ABL PROTAC degrader based on Asciminib (HY-104010), with a DC50 value of approximately 200 nM for the wild-type BCR-ABL protein. P19As can degrade the T315I mutant and exhibits potent anti-proliferative activity in BaF3-BCR-ABL (T315I) cells. P19As can be used for the study of chronic myeloid leukemia and acute lymphoblastic leukemia.
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P19P
0 ImagesCat. No.: HY-180977CAS No.: 2512843-74-0P19P is a BCR-ABL PROTAC degrader based on Ponatinib (HY-12047), with a DC50 value of approximately 20 nM for the wild-type BCR-ABL protein. P19P can effectively degrade various drug-resistant mutants such as T315I, E255K, H396R, and V468F, and exhibits potent anti-proliferative activity in BaF3-BCR-ABL (T315I) cells. P19P maintains strong inhibitory activity against ABL (T315I), with a IC50 of 13.1 nM. P19P does not inhibit the formation of vascular lumens in HUVEC. P19P can be used for research on chronic myeloid leukemia and acute lymphoblastic leukemia.
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SIAIS056
0 ImagesCat. No.: HY-180969CAS No.: 2378581-37-2SIAIS056 is a BCR-ABL PROTAC degrader with a DC50 value of 0.18 nM. SIAIS056 time-dependently inhibits the BCR-ABL signaling pathway, accompanied by decreased phosphorylation of BCR-ABL and the downstream molecules STAT5 and CRKL in K562 cells. SIAIS056 induces the degradation of several clinically relevant resistance-conferring mutations of BCR-ABL. SIAIS056 exhibits anti-proliferative activity and induces substantial tumor regression in K562 xenograft models. SIAIS056 can be used for leukemia research.
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VS1150
0 ImagesCat. No.: HY-176269CAS No.: 2855238-97-8VS1150 (Compound 11) is a BCR-ABL-targeting phosphorylation-inducing chimeric small molecule (PHICS). VS1150 significantly inhibits oncogenic kinase BCR-ABL signaling by inducing inhibitory phosphorylation at its Y253 (EC50: 69 nM), subsequently triggering cell apoptosis. VS1150 also inhibits other oncogenic ABL fusions and drug-resistant mutants like T315I. VS1150 can be used for chronic myeloid leukemia (CML) and other ABL fusion-driven cancers research.
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P22D
0 ImagesCat. No.: HY-180979CAS No.: 2635386-51-3P22D is a BCR-ABL PROTAC degrader based on Dasatinib (HY-10181), with a DC50 value of approximately 10 nM for the wild-type BCR-ABL protein. P22D cannot degrade the BCR-ABL T315I mutant. P22D has inhibitory activity against K562 cells (wild type), but is ineffective against BaF3-BCR-ABL (T315I) cells. P22D can be used for research on chronic myeloid leukemia and acute lymphocytic leukemia.
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BCR-ABL-IN-14
0 ImagesCat. No.: HY-185916CAS No.: 2412969-11-8BCR-ABL-IN-14 is a tyrosine kinase inhibitor targeting BCR-ABL1, ABL1 and ABL2. BCR-ABL-IN-14 inhibits chronic myeloid leukemia cells. It is applicable to research related to chronic myeloid leukemia, acute myeloid leukemia and acute lymphoblastic leukemia.
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Azo-PROTAC-4C-trans
0 ImagesCat. No.: HY-180983Azo-PROTAC-4C-trans is a BCR-ABL PROTAC degrader that can efficiently degrade the BCR-ABL fusion protein and ABL protein. Azo-PROTAC-4C-trans exhibits potent selective anti-proliferative activity against K562 cells. Azo-PROTAC-4C-trans allows real-time, reversible regulation of its activity via UV (to inactivate it) /visible light (to activate it) irradiation. Azo-PROTAC-4C-trans can be used for the study of myeloid leukemia.
