PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34734676-7	2021	Combinations incorporating propofol with A-1155463 (a selective Bcl2l1 inhibitor) or MMP9 antagomir reduced Bcl2l1 and promoted apoptosis.	A-1155463	41-50	BCL2 like 1	Homo sapiens	64-70	
34734676-7	2021	Combinations incorporating propofol with A-1155463 (a selective Bcl2l1 inhibitor) or MMP9 antagomir reduced Bcl2l1 and promoted apoptosis.	A-1155463	41-50	BCL2 like 1	Homo sapiens	108-114	
35112436-5	2022	Simultaneous treatment of A549 cells with CCC-021-TPP and the BCL-XL selective inhibitor A-1155463 resulted in apoptosis induction.	A-1155463	89-98	BCL2 like 1	Homo sapiens	62-68	
34141086-3	2021	This molecule contains structural elements of selective BCL-XL inhibitor A-1155463 and the dual BCL-XL/BCL-2 inhibitors ABT-737 and navitoclax, while representing a distinct pharmacophore as assessed by an objective cheminformatic evaluation.	A-1155463	73-82	BCL2 like 1	Homo sapiens	56-62	
35172148-3	2022	Here, we screen a compound library for synergy with low-dose BCL-XL inhibitor A-1155463 to identify pathways that regulate sensitivity to BCL-XL inhibition and reveal that fibroblast growth factor receptor (FGFR)4 inhibition effectively sensitizes to A-1155463 both in vitro and in vivo.	A-1155463	78-87	BCL2 like 1	Homo sapiens	61-67	
35172148-3	2022	Here, we screen a compound library for synergy with low-dose BCL-XL inhibitor A-1155463 to identify pathways that regulate sensitivity to BCL-XL inhibition and reveal that fibroblast growth factor receptor (FGFR)4 inhibition effectively sensitizes to A-1155463 both in vitro and in vivo.	A-1155463	78-87	BCL2 like 1	Homo sapiens	138-144	
35172148-3	2022	Here, we screen a compound library for synergy with low-dose BCL-XL inhibitor A-1155463 to identify pathways that regulate sensitivity to BCL-XL inhibition and reveal that fibroblast growth factor receptor (FGFR)4 inhibition effectively sensitizes to A-1155463 both in vitro and in vivo.	A-1155463	251-260	BCL2 like 1	Homo sapiens	138-144	
33980597-5	2021	Infection of primary CD4+ T-cells with HIV resulted in increased BCL-XL protein expression, and treatment with two selective BCL-XL antagonists, A-1155463 and A-1551852, led to selective death of productively infected CD4+ T-cells.	A-1155463	145-154	BCL2 like 1	Homo sapiens	125-131	
33859162-4	2021	MPM cells harboring genetic alterations that inactivate the NF2/LATS1/2 signaling are associated with increased sensitivity to A-1155463, a BCL-XL-selective BH3 mimetic.	A-1155463	127-136	BCL2 like 1	Homo sapiens	140-146	
33859162-5	2021	Importantly, BCL-XL inhibition elicits protective autophagy, and concomitant blockade of BCL-XL and autophagic machinery with A-1155463 and hydroxychloroquine (HCQ), the US Food and Drug Administration (FDA)-approved autophagy inhibitor, synergistically enhances anti-MPM effects in vitro and in vivo.	A-1155463	126-135	BCL2 like 1	Homo sapiens	13-19	
33859162-5	2021	Importantly, BCL-XL inhibition elicits protective autophagy, and concomitant blockade of BCL-XL and autophagic machinery with A-1155463 and hydroxychloroquine (HCQ), the US Food and Drug Administration (FDA)-approved autophagy inhibitor, synergistically enhances anti-MPM effects in vitro and in vivo.	A-1155463	126-135	BCL2 like 1	Homo sapiens	89-95	
26565405-4	2015	Chemical segregation of this synergy with the BCL-2-selective inhibitor venetoclax or BCL-XL-selective inhibitor A-1155463 indicated that MCL-1 and BCL-2 are the two key anti-apoptotic targets for sensitization.	A-1155463	113-122	BCL2 like 1	Homo sapiens	86-92	
25313317-1	2014	A-1155463, a highly potent and selective BCL-XL inhibitor, was discovered through nuclear magnetic resonance (NMR) fragment screening and structure-based design.	A-1155463	0-9	BCL2 like 1	Homo sapiens	41-47	
32708132-10	2020	Indeed, Riva VR cells could be resensitized to venetoclax by A-1155463, a selective BH3 mimetic Bcl-XL inhibitor.	A-1155463	61-70	BCL2 like 1	Homo sapiens	96-102	
33062160-2	2020	This molecule was generated by re-engineering our previously reported BCL-XL inhibitor A-1155463 using structure-based drug design.	A-1155463	87-96	BCL2 like 1	Homo sapiens	70-76	
28273655-5	2017	Here we report that fisetin, a naturally-occurring flavone with low toxicity, and A1331852 and A1155463, selective BCL-XL inhibitors that may have less hematological toxicity than the less specific BCL-2 family inhibitor navitoclax, are senolytic.	A-1155463	95-103	BCL2 like 1	Homo sapiens	115-121	
26939706-6	2016	Multiple myeloma cells that coexpress BCL-2 and BCL-XL were resistant to venetoclax but sensitive to a BCL-XL-selective inhibitor (A-1155463).	A-1155463	131-140	BCL2 like 1	Homo sapiens	48-54	
26939706-6	2016	Multiple myeloma cells that coexpress BCL-2 and BCL-XL were resistant to venetoclax but sensitive to a BCL-XL-selective inhibitor (A-1155463).	A-1155463	131-140	BCL2 like 1	Homo sapiens	103-109