PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
34564697-4	2021	Here, we show that combining TKI (imatinib, nilotinib, dasatinib, or asciminib) treatment with the small-molecule MCL1 inhibitor S63845 exerted strong synergistic antiviability and proapoptotic effects on CML lines and CD34+ stem/progenitor cells isolated from untreated CML patients in chronic phase.	asciminib	69-78	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	114-118
33971041-0	2021	Overcoming TKI resistance in a patient with chronic myeloid leukemia using combination BCR-ABL inhibition with asciminib and bosutinib.	asciminib	111-120	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-94
34115385-1	2021	Asciminib is an investigational, first-in-class, Specifically Targeting the ABL Myristoyl Pocket (STAMP), inhibitor of BCR-ABL1 with a new mechanism of action compared with approved ATP-competitive tyrosine kinase inhibitors.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-127
34564697-4	2021	Here, we show that combining TKI (imatinib, nilotinib, dasatinib, or asciminib) treatment with the small-molecule MCL1 inhibitor S63845 exerted strong synergistic antiviability and proapoptotic effects on CML lines and CD34+ stem/progenitor cells isolated from untreated CML patients in chronic phase.	asciminib	69-78	CD34 molecule	Homo sapiens	219-223
35583386-4	2022	Asciminib, a first-in-class BCR::ABL1 inhibitor Specifically Targeting the ABL Myristoyl Pocket (STAMP), has the potential to overcome resistance/intolerance to prior TKI treatment.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	33-37
34659899-0	2021	Asciminib and ponatinib exert synergistic anti-neoplastic effects on CML cells expressing BCR-ABL1 T315I-compound mutations.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-98
34659899-3	2021	Asciminib is a novel drug capable of targeting most BCR-ABL1 mutant-forms, including BCR-ABL1T315I, but remains ineffective against most BCR-ABL1T315I+ compound mutation-bearing sub-clones.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-60
34659899-3	2021	Asciminib is a novel drug capable of targeting most BCR-ABL1 mutant-forms, including BCR-ABL1T315I, but remains ineffective against most BCR-ABL1T315I+ compound mutation-bearing sub-clones.	asciminib	0-9	BCR activator of RhoGEF and GTPase	Homo sapiens	85-88
34659899-4	2021	We demonstrate that asciminib synergizes with ponatinib in inducing growth-arrest and apoptosis in patient-derived CML cell lines and murine Ba/F3 cells harboring BCR-ABL1 T315I or T315I-including compound mutations.	asciminib	20-29	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	167-171
34659899-5	2021	Asciminib and ponatinib also produced cooperative effects on CRKL phosphorylation in BCR-ABL1-transformed cells.	asciminib	0-9	CRK like proto-oncogene, adaptor protein	Homo sapiens	61-65
34659899-5	2021	Asciminib and ponatinib also produced cooperative effects on CRKL phosphorylation in BCR-ABL1-transformed cells.	asciminib	0-9	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	89-93
34659899-6	2021	The growth-inhibitory effects of the drug combination "asciminib+ponatinib" was further enhanced by hydroxyurea (HU), a drug which has lately been described to suppresses the proliferation of BCR-ABL1 T315I+ CML cells.	asciminib	55-64	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	196-200
34659899-8	2021	Most importantly, we were able to show that the combinations "asciminib+ponatinib" and "asciminib+ponatinib+HU" produce synergistic apoptosis-inducing effects in CD34+/CD38- CML stem cells obtained from patients with chronic phase CML or BCR-ABL1 T315I+ CML blast phase.	asciminib	62-71	CD34 molecule	Homo sapiens	162-166
34659899-8	2021	Most importantly, we were able to show that the combinations "asciminib+ponatinib" and "asciminib+ponatinib+HU" produce synergistic apoptosis-inducing effects in CD34+/CD38- CML stem cells obtained from patients with chronic phase CML or BCR-ABL1 T315I+ CML blast phase.	asciminib	62-71	CD38 molecule	Homo sapiens	168-172
34659899-8	2021	Most importantly, we were able to show that the combinations "asciminib+ponatinib" and "asciminib+ponatinib+HU" produce synergistic apoptosis-inducing effects in CD34+/CD38- CML stem cells obtained from patients with chronic phase CML or BCR-ABL1 T315I+ CML blast phase.	asciminib	62-71	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	242-246
34659899-8	2021	Most importantly, we were able to show that the combinations "asciminib+ponatinib" and "asciminib+ponatinib+HU" produce synergistic apoptosis-inducing effects in CD34+/CD38- CML stem cells obtained from patients with chronic phase CML or BCR-ABL1 T315I+ CML blast phase.	asciminib	88-97	CD34 molecule	Homo sapiens	162-166
34659899-8	2021	Most importantly, we were able to show that the combinations "asciminib+ponatinib" and "asciminib+ponatinib+HU" produce synergistic apoptosis-inducing effects in CD34+/CD38- CML stem cells obtained from patients with chronic phase CML or BCR-ABL1 T315I+ CML blast phase.	asciminib	88-97	CD38 molecule	Homo sapiens	168-172
34659899-8	2021	Most importantly, we were able to show that the combinations "asciminib+ponatinib" and "asciminib+ponatinib+HU" produce synergistic apoptosis-inducing effects in CD34+/CD38- CML stem cells obtained from patients with chronic phase CML or BCR-ABL1 T315I+ CML blast phase.	asciminib	88-97	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	242-246
34659899-9	2021	Together, asciminib, ponatinib and HU synergize in producing anti-leukemic effects in multi-resistant CML cells, including cells harboring T315I+ BCR-ABL1 compound mutations and CML stem cells.	asciminib	10-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-154
35616006-0	2022	Pharmacokinetics of asciminib in the presence of CYP3A or P-gp inhibitors, CYP3A inducers, and acid-reducing agents.	asciminib	20-29	ATP binding cassette subfamily B member 1	Homo sapiens	58-62
35616006-0	2022	Pharmacokinetics of asciminib in the presence of CYP3A or P-gp inhibitors, CYP3A inducers, and acid-reducing agents.	asciminib	20-29	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	75-80
35616006-10	2022	Taking into account the large therapeutic window of asciminib, the observed changes in asciminib PK following multiple doses of P-gp, CYP3A inhibitors, CYP3A inducers, or ARAs are not considered to be clinically meaningful.	asciminib	87-96	ATP binding cassette subfamily B member 1	Homo sapiens	128-132
35616006-1	2022	Asciminib is a first-in-class inhibitor of BCR::ABL1, specifically targeting the ABL myristoyl pocket.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-52
35616006-1	2022	Asciminib is a first-in-class inhibitor of BCR::ABL1, specifically targeting the ABL myristoyl pocket.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	81-84
35616006-2	2022	Asciminib is a substrate of CYP3A4 and P-glycoprotein (P-gp) and possesses pH-dependent solubility in aqueous solution.	asciminib	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	28-34
35616006-2	2022	Asciminib is a substrate of CYP3A4 and P-glycoprotein (P-gp) and possesses pH-dependent solubility in aqueous solution.	asciminib	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	39-53
35616006-2	2022	Asciminib is a substrate of CYP3A4 and P-glycoprotein (P-gp) and possesses pH-dependent solubility in aqueous solution.	asciminib	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	55-59
35616006-4	2022	Asciminib exposure (area under the curve (AUC)) unexpectedly decreased by ~40% when administered concomitantly with the strong CYP3A inhibitor itraconazole oral solution, whereas maximum plasma concentration (Cmax ) decreased by ~50%.	asciminib	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	127-132
35616006-5	2022	However, asciminib exposure was slightly increased in subjects receiving an itraconazole capsule (~3%) or clarithromycin (~35%), another strong CYP3A inhibitor.	asciminib	9-18	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	144-149
35616006-7	2022	The AUC of asciminib was marginally decreased by concomitant administration with the strong CYP3A inducer rifampicin (by ~13-15%) and the strong P-gp inhibitor quinidine (by ~13-16%).	asciminib	11-20	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	92-97
35616006-7	2022	The AUC of asciminib was marginally decreased by concomitant administration with the strong CYP3A inducer rifampicin (by ~13-15%) and the strong P-gp inhibitor quinidine (by ~13-16%).	asciminib	11-20	ATP binding cassette subfamily B member 1	Homo sapiens	145-149
35129779-2	2022	Asciminib has been recently (2021) approved for patients resistant to former TKIs, and because the binding site of this drug (the myristoyl pocket in the ABL1 kinase) is different from that of other TKIs (ATP-binding sites), it is, therefore, effective against T315I mutation of BCR-ABL oncoprotein.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	154-158
35468180-1	2022	Asciminib, a first-in-class allosteric inhibitor of BCR::ABL1 kinase activity, is now approved for the treatment of chronic phase CML patients who failed 2 lines of therapy or in patients with the T315I mutation.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-61
35129779-2	2022	Asciminib has been recently (2021) approved for patients resistant to former TKIs, and because the binding site of this drug (the myristoyl pocket in the ABL1 kinase) is different from that of other TKIs (ATP-binding sites), it is, therefore, effective against T315I mutation of BCR-ABL oncoprotein.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	279-286
35129779-8	2022	Not only does CYP3A4, flavin-containing monooxygenase 3 (FMO3), and uridine 5"-diphospho-glucuronosyltransferase (UGT) also metabolize dasatinib, and similarly, by glucuronidation process, asciminib gets metabolized by UGT enzymes (UGT1A3, UGT1A4, UGT2B7, and UGT2B17).	asciminib	189-198	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	14-20
35129779-8	2022	Not only does CYP3A4, flavin-containing monooxygenase 3 (FMO3), and uridine 5"-diphospho-glucuronosyltransferase (UGT) also metabolize dasatinib, and similarly, by glucuronidation process, asciminib gets metabolized by UGT enzymes (UGT1A3, UGT1A4, UGT2B7, and UGT2B17).	asciminib	189-198	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	68-112
35129779-8	2022	Not only does CYP3A4, flavin-containing monooxygenase 3 (FMO3), and uridine 5"-diphospho-glucuronosyltransferase (UGT) also metabolize dasatinib, and similarly, by glucuronidation process, asciminib gets metabolized by UGT enzymes (UGT1A3, UGT1A4, UGT2B7, and UGT2B17).	asciminib	189-198	UDP glucuronosyltransferase family 1 member A complex locus	Homo sapiens	114-117
33096322-0	2020	The specificity of asciminib, a potential treatment for chronic myeloid leukemia, as a myristate-pocket binding ABL inhibitor and analysis of its interactions with mutant forms of BCR-ABL1 kinase.	asciminib	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-115
35065232-3	2022	Asciminib is an investigational drug that specifically and potently inhibits the tyrosine kinase activity of ABL1, ABL2 and that of the chimeric BCR-ABL1 oncoprotein which causes chronic myeloid leukemia.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Rattus norvegicus	109-113
35065232-3	2022	Asciminib is an investigational drug that specifically and potently inhibits the tyrosine kinase activity of ABL1, ABL2 and that of the chimeric BCR-ABL1 oncoprotein which causes chronic myeloid leukemia.	asciminib	0-9	ABL proto-oncogene 2, non-receptor tyrosine kinase	Rattus norvegicus	115-119
35065232-3	2022	Asciminib is an investigational drug that specifically and potently inhibits the tyrosine kinase activity of ABL1, ABL2 and that of the chimeric BCR-ABL1 oncoprotein which causes chronic myeloid leukemia.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Rattus norvegicus	149-153
35021069-0	2022	Development of Asciminib, a Novel Allosteric Inhibitor of BCR-ABL1.	asciminib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-66
35021069-4	2022	Asciminib is a promising investigational agent in development that allosterically targets BCR-ABL1 in a non-ATP-competitive manner.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-98
35041175-1	2022	Asciminib (Scemblix ) is an orally administered, small molecule, selective allosteric inhibitor that targets the myristoyl pocket of the BCR-ABL1 tyrosine kinase and is being developed by Novartis for the treatment of haematological malignancies, including Philadelphia chromosome-positive (Ph+) chronic myeloid leukaemia (CML).	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-145
35041175-1	2022	Asciminib (Scemblix ) is an orally administered, small molecule, selective allosteric inhibitor that targets the myristoyl pocket of the BCR-ABL1 tyrosine kinase and is being developed by Novartis for the treatment of haematological malignancies, including Philadelphia chromosome-positive (Ph+) chronic myeloid leukaemia (CML).	asciminib	11-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	141-145
33096322-0	2020	The specificity of asciminib, a potential treatment for chronic myeloid leukemia, as a myristate-pocket binding ABL inhibitor and analysis of its interactions with mutant forms of BCR-ABL1 kinase.	asciminib	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	184-188
33096322-1	2020	Asciminib is a potent, orally bioavailable, investigational drug that specifically and potently inhibits the tyrosine kinase activity of native ABL1, together with that of the chimeric BCR-ABL1 oncoprotein which causes chronic myeloid leukemia (CML).	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	144-148
33096322-1	2020	Asciminib is a potent, orally bioavailable, investigational drug that specifically and potently inhibits the tyrosine kinase activity of native ABL1, together with that of the chimeric BCR-ABL1 oncoprotein which causes chronic myeloid leukemia (CML).	asciminib	0-9	BCR activator of RhoGEF and GTPase	Homo sapiens	185-193
33096322-2	2020	In contrast to ATP-competitive BCR-ABL1 kinase inhibitors employed to treat CML that target multiple kinases, asciminib binds to the myristate binding pocket on the kinase domains of ABL1 and BCR-ABL1.	asciminib	110-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-187
33096322-2	2020	In contrast to ATP-competitive BCR-ABL1 kinase inhibitors employed to treat CML that target multiple kinases, asciminib binds to the myristate binding pocket on the kinase domains of ABL1 and BCR-ABL1.	asciminib	110-119	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	183-187
33096322-6	2020	However, in vitro studies in cells have identified BCR-ABL1 mutations that reduce the anti-proliferative activity of asciminib, some of which are associated with clinical resistance towards the drug in patients.	asciminib	117-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	55-59
33096322-7	2020	Here we review effects of asciminib on mutant forms of BCR-ABL1, analyse their sensitivity towards the drug from a structural perspective and affirm support for employing combinations with ATP-competitive inhibitors to impede the reactivation of BCR-ABL1 kinase activity in patients receiving monotherapy.	asciminib	26-35	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	59-63
31826340-1	2019	BACKGROUND: Asciminib is an allosteric inhibitor that binds a myristoyl site of the BCR-ABL1 protein, locking BCR-ABL1 into an inactive conformation through a mechanism distinct from those for all other ABL kinase inhibitors.	asciminib	12-21	BCR activator of RhoGEF and GTPase	Homo sapiens	84-92
32657579-4	2020	Herein, we systematically designed a set of unique PROTACs by globally targeting all the three binding sites of BCR-ABL, including dasatinib-, ponatinib-, and asciminib-based PROTACs.	asciminib	159-168	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-119
32380976-3	2020	Two of these are (I) Axitinib, which inhibits the T315I mutation of BCR-ABL1, a main source of drug resistance, and (II) Asciminib, which has been developed as an allosteric BCR-ABL1 inhibitor, targeting an entirely different binding site, and as such does not compete for binding with other drugs.	asciminib	121-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	178-182
31006307-0	2020	Disposition of asciminib, a potent BCR-ABL1 tyrosine kinase inhibitor, in healthy male subjects.	asciminib	15-24	BCR activator of RhoGEF and GTPase	Homo sapiens	35-43
31006307-1	2020	Asciminib is a potent, specific BCR-ABL1 inhibitor being developed for the treatment of patients with chronic myelogenous leukemia (CML) and Philadelphia chromosome positive acute lymphoblastic leukemia (Ph + ALL).	asciminib	0-9	BCR activator of RhoGEF and GTPase	Homo sapiens	32-40
31826340-1	2019	BACKGROUND: Asciminib is an allosteric inhibitor that binds a myristoyl site of the BCR-ABL1 protein, locking BCR-ABL1 into an inactive conformation through a mechanism distinct from those for all other ABL kinase inhibitors.	asciminib	12-21	BCR activator of RhoGEF and GTPase	Homo sapiens	110-118
31826340-2	2019	Asciminib targets both native and mutated BCR-ABL1, including the gatekeeper T315I mutant.	asciminib	0-9	BCR activator of RhoGEF and GTPase	Homo sapiens	42-50
30927708-0	2019	Molecular dynamics investigation on the Asciminib resistance mechanism of I502L and V468F mutations in BCR-ABL.	asciminib	40-49	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
31543464-0	2019	Combining the Allosteric Inhibitor Asciminib with Ponatinib Suppresses Emergence of and Restores Efficacy against Highly Resistant BCR-ABL1 Mutants.	asciminib	35-44	BCR activator of RhoGEF and GTPase	Homo sapiens	131-139
31543464-3	2019	Asciminib, an allosteric inhibitor targeting the myristoyl-binding pocket of BCR-ABL1, is active against most single mutants but ineffective against all tested compound mutants.	asciminib	0-9	BCR activator of RhoGEF and GTPase	Homo sapiens	77-85
31448223-5	2019	This includes the use asciminib as first in class inhibitor targeting the myristoyl pocket of BCR-ABL, combination treatments with established non-TKI drugs such as interferon and drugs with novel targets relevant to CML biology such as gliptins and thiazolidinediones.	asciminib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
30927708-1	2019	Asciminib, a highly selective non-ATP competitive inhibitor of BCR-ABL, has demonstrated to be a promising drug for patients with chronic myeloid leukemia.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
30927708-4	2019	The obtained results indicate that the mutations have adversely influence on the binding of Asciminib to BCR-ABL, as the nonpolar contributions decline in the two mutants.	asciminib	92-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	105-112
30927708-7	2019	Our results provide the molecular insights of Asciminib resistance mechanism in BCR-ABL mutants, which may help the design of novel inhibitors.	asciminib	46-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
29325229-3	2018	Moreover, allosteric targeting has been identified to consequentially inhibit Bcr-Abl activity, which led to the recent development of ABL-001 (asciminib) that selectively binds the myristoyl pocket.	asciminib	144-153	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	78-85
29522367-8	2018	Asciminib, an allosteric ABL1 inhibitor, could demonstrate a higher capacity in overcoming common TKIs resistant mutations, including T315I, but clinical findings are needed.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-29
30877503-3	2019	Recent experimental studies show a synergistic effect in suppressing this resistance when Nilotinib and Asciminib are co-administered to target both the catalytic and allosteric binding site of BCR-ABL1 oncoprotein, respectively.	asciminib	104-113	BCR activator of RhoGEF and GTPase	Homo sapiens	194-202
31250767-4	2019	OBJECTIVE: In recent studies, the dual inhibition of BCR-ABL by Nilotinib and Asciminib has been shown to overcome drug resistance.	asciminib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
30137981-0	2018	Discovery of Asciminib (ABL001), an Allosteric Inhibitor of the Tyrosine Kinase Activity of BCR-ABL1.	asciminib	13-22	TXK tyrosine kinase	Homo sapiens	64-79
30137981-0	2018	Discovery of Asciminib (ABL001), an Allosteric Inhibitor of the Tyrosine Kinase Activity of BCR-ABL1.	asciminib	13-22	BCR activator of RhoGEF and GTPase	Homo sapiens	92-100
30137981-0	2018	Discovery of Asciminib (ABL001), an Allosteric Inhibitor of the Tyrosine Kinase Activity of BCR-ABL1.	asciminib	24-30	TXK tyrosine kinase	Homo sapiens	64-79
30137981-0	2018	Discovery of Asciminib (ABL001), an Allosteric Inhibitor of the Tyrosine Kinase Activity of BCR-ABL1.	asciminib	24-30	BCR activator of RhoGEF and GTPase	Homo sapiens	92-100
30137981-4	2018	We describe the discovery of asciminib (ABL001), the first allosteric BCR-ABL1 inhibitor to reach the clinic.	asciminib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-78
30137981-4	2018	We describe the discovery of asciminib (ABL001), the first allosteric BCR-ABL1 inhibitor to reach the clinic.	asciminib	40-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	74-78
30137981-5	2018	Asciminib binds to the myristate pocket of BCR-ABL1 and maintains activity against TKI-resistant ATP-site mutations.	asciminib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-51
29568367-0	2018	The new allosteric inhibitor asciminib is susceptible to resistance mediated by ABCB1 and ABCG2 overexpression in vitro.	asciminib	29-38	ATP binding cassette subfamily B member 1	Homo sapiens	80-85
29568367-0	2018	The new allosteric inhibitor asciminib is susceptible to resistance mediated by ABCB1 and ABCG2 overexpression in vitro.	asciminib	29-38	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	90-95
29568367-1	2018	Asciminib (previously ABL001), which binds the myristate-binding pocket of the Bcr-Abl kinase domain, is in phase I clinical trials as monotherapy and in combination with imatinib, nilotinib and dasatinib for the treatment of patients with refractory CML or Ph+ ALL.	asciminib	0-9	BCR activator of RhoGEF and GTPase	Homo sapiens	79-82
29568367-5	2018	When asciminib resistance was modelled in vitro, ABCB1 and ABCG2 overexpression was integral in the development of asciminib resistance.	asciminib	5-14	ATP binding cassette subfamily B member 1	Homo sapiens	49-54
29568367-5	2018	When asciminib resistance was modelled in vitro, ABCB1 and ABCG2 overexpression was integral in the development of asciminib resistance.	asciminib	115-124	ATP binding cassette subfamily B member 1	Homo sapiens	49-54
29568367-5	2018	When asciminib resistance was modelled in vitro, ABCB1 and ABCG2 overexpression was integral in the development of asciminib resistance.	asciminib	115-124	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	59-64
29568367-6	2018	In K562 asciminib-resistant cells, ABCG2 expression increased prior to BCR-ABL1 overexpression and remained high (up to 7.6-fold greater levels in resistant vs control cells, p < 0.001).	asciminib	8-17	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	35-40
29568367-6	2018	In K562 asciminib-resistant cells, ABCG2 expression increased prior to BCR-ABL1 overexpression and remained high (up to 7.6-fold greater levels in resistant vs control cells, p < 0.001).	asciminib	8-17	BCR activator of RhoGEF and GTPase	Homo sapiens	71-79
29568367-7	2018	K562-Dox asciminib-resistant cells had increased ABCB1 expression (2.1-fold vs control cells p = 0.0033).	asciminib	9-18	ATP binding cassette subfamily B member 1	Homo sapiens	49-54
29568367-8	2018	KU812 asciminib-resistant cells overexpressed ABCB1 (5.4-fold increase, p < 0.001) and ABCG2 (6-fold increase, p < 0.001) before emergence of a novel myristate-binding pocket mutation (F497L).	asciminib	6-15	ATP binding cassette subfamily B member 1	Homo sapiens	46-51
29568367-8	2018	KU812 asciminib-resistant cells overexpressed ABCB1 (5.4-fold increase, p < 0.001) and ABCG2 (6-fold increase, p < 0.001) before emergence of a novel myristate-binding pocket mutation (F497L).	asciminib	6-15	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	90-95
29568367-9	2018	In all three cell lines, asciminib resistance was reversible upon chemical inhibition of ABCB1, ABCG2 or both (p < 0.001).	asciminib	25-34	ATP binding cassette subfamily B member 1	Homo sapiens	89-94
29568367-9	2018	In all three cell lines, asciminib resistance was reversible upon chemical inhibition of ABCB1, ABCG2 or both (p < 0.001).	asciminib	25-34	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	96-101
28819281-0	2017	Mechanisms of resistance to the BCR-ABL1 allosteric inhibitor asciminib.	asciminib	62-71	BCR activator of RhoGEF and GTPase	Homo sapiens	32-40
28329763-5	2017	Here we characterize ABL001 (asciminib), a potent and selective allosteric ABL1 inhibitor that is undergoing clinical development testing in patients with CML and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukaemia.	asciminib	21-27	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-79
28329763-5	2017	Here we characterize ABL001 (asciminib), a potent and selective allosteric ABL1 inhibitor that is undergoing clinical development testing in patients with CML and Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukaemia.	asciminib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-79