PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
35201512-9	2022	Deletion of MCL-1 sensitized the NPC cells to BCL-XL selective inhibitor A-1331852, suggesting that MCL-1 and BCL-XL may be important for NPC cell survival.	A-1331852	73-82	BCL2 like 1	Homo sapiens	46-52	
35421634-7	2022	Live-cell fluorescence resonance energy transfer showed that A-1331852 detached the binding of Bcl-xL to BAK and promoted the oligomerization of BAK on the mitochondrial membrane.	A-1331852	61-70	BCL2 like 1	Homo sapiens	95-101	
35421634-8	2022	In conclusion, this study provides the first evidence that A-1331852 selectively promotes apoptosis in senescent chondrocytes by interfering with the interaction between Bcl-xL and BAK.	A-1331852	59-68	BCL2 like 1	Homo sapiens	170-176	
34100903-4	2021	We demonstrate that a selective BCL-XL inhibitor (A-1331852) has therapeutic potential by causing apoptosis in inflammatory human neutrophils ex vivo.	A-1331852	50-59	BCL2 like 1	Homo sapiens	32-38	
35074525-5	2022	We demonstrated in non-small-cell lung cancer (NSCLC) cells that the instability of A-1155463 in cells as well as invalid entry into mitochondria of A-1331852, two BCL-XL-selective inhibitors, accounted for their off-target problems.	A-1331852	149-158	BCL2 like 1	Homo sapiens	164-170	
35201512-9	2022	Deletion of MCL-1 sensitized the NPC cells to BCL-XL selective inhibitor A-1331852, suggesting that MCL-1 and BCL-XL may be important for NPC cell survival.	A-1331852	73-82	BCL2 like 1	Homo sapiens	110-116	
35013156-10	2022	Treatment with either the Bcl-XL inhibitor A1331852 or the Mcl-1 inhibitor S63845 increased the cytotoxicity of NK cells and reduced spheroid size, while the Bcl-2 inhibitor ABT-199 had no effect on NK cell-mediated killing.	A-1331852	43-51	BCL2 like 1	Homo sapiens	26-32	
31113936-2	2019	In this study, we show that the orally bioavailable XPO1 inhibitor KPT-330 reduced Mcl-1 protein level, by which it synergized with Bcl-xL inhibitor A-1331852 to induce apoptosis in cancer cells.	A-1331852	149-158	BCL2 like 1	Homo sapiens	132-138	
32346617-4	2020	In this present study, we used the BCL-2 selective inhibitor ABT-199 and the BCL-XL selective inhibitor A1331852 to resolve the individual antitumor activities of ABT-263 into BCL-2 and BCL-XL dependent mechanisms.	A-1331852	104-112	BCL2 like 1	Homo sapiens	77-83	
32346617-11	2020	Co-inhibition of BCL-XL and MCL-1 with A1331852 and S63845 significantly inhibited cell proliferation of all four cell lines.	A-1331852	39-47	BCL2 like 1	Homo sapiens	17-23	
33062160-0	2020	Discovery of A-1331852, a First-in-Class, Potent, and Orally-Bioavailable BCL-XL Inhibitor.	A-1331852	13-22	BCL2 like 1	Homo sapiens	74-80	
33062160-1	2020	Herein we describe the discovery of A-1331852, a first-in-class orally active BCL-XL inhibitor that selectively and potently induces apoptosis in BCL-XL-dependent tumor cells.	A-1331852	36-45	BCL2 like 1	Homo sapiens	78-84	
31772331-6	2020	Furthermore, its killing efficacy rose on combination with venetoclax, the BCL-XL-specific inhibitor A-1331852, or Bruton"s tyrosine kinase (BTK) inhibitor ibrutinib, which reduced pro-survival signals.	A-1331852	101-110	BCL2 like 1	Homo sapiens	75-81	
33017468-7	2020	However, apoptotic cell death could be consistently induced following treatment with A-1331852, a BH3-mimetic drug that specifically inhibits the prosurvival protein BCL-XL.	A-1331852	85-94	BCL2 like 1	Homo sapiens	166-172	
26939706-9	2016	In contrast, xenografts that expressed BCL-XL, MCL-1, and BCL-2 were more sensitive to the combination of bortezomib with a BCL-XL selective inhibitor (A-1331852) but not with venetoclax cotreatment when compared with monotherapies.	A-1331852	152-161	BCL2 like 1	Homo sapiens	39-45	
29928488-5	2018	However, inhibition of BCL-xL/BCL-2 by the BH3 mimetics ABT-737 and navitoclax or BCL-xL by A-1331852 induced caspase-dependent apoptosis involving activation of Bak and Bax synergistically with ruxolitinib in HEL cells.	A-1331852	92-101	BCL2 like 1	Homo sapiens	23-29	
29928488-5	2018	However, inhibition of BCL-xL/BCL-2 by the BH3 mimetics ABT-737 and navitoclax or BCL-xL by A-1331852 induced caspase-dependent apoptosis involving activation of Bak and Bax synergistically with ruxolitinib in HEL cells.	A-1331852	92-101	BCL2 like 1	Homo sapiens	82-88	
26939706-9	2016	In contrast, xenografts that expressed BCL-XL, MCL-1, and BCL-2 were more sensitive to the combination of bortezomib with a BCL-XL selective inhibitor (A-1331852) but not with venetoclax cotreatment when compared with monotherapies.	A-1331852	152-161	BCL2 like 1	Homo sapiens	124-130