PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
26186940-9	2015	Finally, glutaminolysis inhibition activated mitochondrial apoptosis and synergistically sensitized leukemic cells to priming with the BCL-2 inhibitor ABT-199.	venetoclax	151-158	BCL2 apoptosis regulator	Homo sapiens	135-140
26285204-9	2015	The significant upregulation of the key antiapoptotic protein Bcl-2 in Mino/FR cells was associated with the markedly increased sensitivity of the fludarabine-resistant MCL cells to Bcl-2-specific inhibitor ABT199 compared to fludarabine-sensitive cells.	venetoclax	207-213	BCL2 apoptosis regulator	Homo sapiens	62-67
26214592-7	2015	Striking on-target sensitivity was achieved with the BCL2-specific inhibitor venetoclax (ABT-199).	venetoclax	77-87	BCL2 apoptosis regulator	Homo sapiens	53-57
26214592-7	2015	Striking on-target sensitivity was achieved with the BCL2-specific inhibitor venetoclax (ABT-199).	venetoclax	89-96	BCL2 apoptosis regulator	Homo sapiens	53-57
26285204-9	2015	The significant upregulation of the key antiapoptotic protein Bcl-2 in Mino/FR cells was associated with the markedly increased sensitivity of the fludarabine-resistant MCL cells to Bcl-2-specific inhibitor ABT199 compared to fludarabine-sensitive cells.	venetoclax	207-213	BCL2 apoptosis regulator	Homo sapiens	182-187
25787766-3	2015	This prompted the generation of the BCL-2-selective inhibitor venetoclax (ABT-199/GDC-0199), which demonstrates robust activity in these cancers but spares platelets.	venetoclax	62-72	BCL2 apoptosis regulator	Homo sapiens	36-41
25582069-0	2015	The BCL2 antagonist ABT-199 triggers apoptosis, and augments ibrutinib and idelalisib mediated cytotoxicity in CXCR4 Wild-type and CXCR4 WHIM mutated Waldenstrom macroglobulinaemia cells.	venetoclax	20-27	C-X-C motif chemokine receptor 4	Homo sapiens	111-116
25582069-0	2015	The BCL2 antagonist ABT-199 triggers apoptosis, and augments ibrutinib and idelalisib mediated cytotoxicity in CXCR4 Wild-type and CXCR4 WHIM mutated Waldenstrom macroglobulinaemia cells.	venetoclax	20-27	C-X-C motif chemokine receptor 4	Homo sapiens	131-136
25880088-3	2015	Recently, ABT-199, a selective BCL-2 antagonist, was developed.	venetoclax	10-17	B cell leukemia/lymphoma 2	Mus musculus	31-36
25582069-0	2015	The BCL2 antagonist ABT-199 triggers apoptosis, and augments ibrutinib and idelalisib mediated cytotoxicity in CXCR4 Wild-type and CXCR4 WHIM mutated Waldenstrom macroglobulinaemia cells.	venetoclax	20-27	BCL2 apoptosis regulator	Homo sapiens	4-8
25804936-6	2015	Finally, a series Phase I/II studies of BCL-2 inhibitor (i.e., venetoclax, GDC-0199) used alone or in combination provide promising results in patients with relapsed/refractory CLL.	venetoclax	63-73	BCL2 apoptosis regulator	Homo sapiens	40-45
25804936-6	2015	Finally, a series Phase I/II studies of BCL-2 inhibitor (i.e., venetoclax, GDC-0199) used alone or in combination provide promising results in patients with relapsed/refractory CLL.	venetoclax	75-83	BCL2 apoptosis regulator	Homo sapiens	40-45
25739041-6	2015	In contrast, the anti-apoptotic protein Bcl2 inhibitor ABT199 enhanced cell killing after PDT+4HPR.	venetoclax	55-61	BCL2 apoptosis regulator	Homo sapiens	40-44
25486070-2	2015	Small molecules that inhibit the protein-protein interactions between prosurvival and proapoptotic Bcl-2 family members (so-called "BH3 mimetics") have a potential therapeutic value, as indicated by clinical findings obtained with ABT-263 (navitoclax), a Bcl-2/Bcl-xL antagonist, and more recently with GDC-0199/ABT-199, a more selective antagonist of Bcl-2.	venetoclax	303-311	BCL2 apoptosis regulator	Homo sapiens	99-104
25787766-3	2015	This prompted the generation of the BCL-2-selective inhibitor venetoclax (ABT-199/GDC-0199), which demonstrates robust activity in these cancers but spares platelets.	venetoclax	82-90	BCL2 apoptosis regulator	Homo sapiens	36-41
24531733-0	2014	Acute myeloid leukemia cells harboring MLL fusion genes or with the acute promyelocytic leukemia phenotype are sensitive to the Bcl-2-selective inhibitor ABT-199.	venetoclax	154-161	lysine methyltransferase 2A	Homo sapiens	39-42
25266739-6	2014	In contrast, ABT199, an inhibitor of the anti-apoptotic protein Bcl2, enhanced cell killing after PDT.	venetoclax	13-19	BCL2 apoptosis regulator	Homo sapiens	64-68
25333252-0	2014	The BCL2 inhibitor ABT-199 significantly enhances imatinib-induced cell death in chronic myeloid leukemia progenitors.	venetoclax	19-26	BCL2 apoptosis regulator	Homo sapiens	4-8
24994123-9	2014	We have discovered, through BH3 profiling, that ETP-ALL is BCL-2 dependent and is very sensitive to in vitro and in vivo treatment with ABT-199, a drug well tolerated in clinical trials.	venetoclax	136-143	BCL2 apoptosis regulator	Homo sapiens	59-64
24531733-0	2014	Acute myeloid leukemia cells harboring MLL fusion genes or with the acute promyelocytic leukemia phenotype are sensitive to the Bcl-2-selective inhibitor ABT-199.	venetoclax	154-161	BCL2 apoptosis regulator	Homo sapiens	128-133
25003352-5	2014	Through an elegant reengineering of navitoclax, ABT-199 was developed as a Bcl-2-selective small molecule inhibitor.	venetoclax	48-55	BCL2 apoptosis regulator	Homo sapiens	75-80
24778183-8	2014	The BCL2 inhibitor ABT-199 is currently in clinical trials for CLL.	venetoclax	19-26	BCL2 apoptosis regulator	Homo sapiens	4-8
25003352-1	2014	ABT-199, a second-generation BH3 mimetic, is an orally bioavailable, small molecule inhibitor that selectively targets B-cell lymphoma/leukemia 2 (Bcl-2).	venetoclax	0-7	BCL2 apoptosis regulator	Homo sapiens	119-145
23614795-5	2013	Dosing of navitoclax (ABT-263) was complicated by thrombocytopenia due to BCL-XL inhibition, but the BCL-2 specific inhibitor ABT-199 (GDC-0199) should avoid this issue, and may overcome stroma-mediated resistance to apoptosis.	venetoclax	135-143	BCL2 apoptosis regulator	Homo sapiens	101-106
25003352-1	2014	ABT-199, a second-generation BH3 mimetic, is an orally bioavailable, small molecule inhibitor that selectively targets B-cell lymphoma/leukemia 2 (Bcl-2).	venetoclax	0-7	BCL2 apoptosis regulator	Homo sapiens	147-152
23410971-1	2013	ABT-199 is a new selective small molecule inhibitor of BCL-2 that appears to spare platelets while achieving potent antitumor activity.	venetoclax	0-7	BCL2 apoptosis regulator	Homo sapiens	55-60
23291630-0	2013	ABT-199, a potent and selective BCL-2 inhibitor, achieves antitumor activity while sparing platelets.	venetoclax	0-7	BCL2 apoptosis regulator	Homo sapiens	32-37
23291630-5	2013	Here we report the re-engineering of navitoclax to create a highly potent, orally bioavailable and BCL-2-selective inhibitor, ABT-199.	venetoclax	126-133	BCL2 apoptosis regulator	Homo sapiens	99-104
29459573-11	2018	A Bcl-2 inhibitor, ABT-199, induced an apoptotic response in ASC-knockdown cells, and dasatinib, a Src inhibitor, blocked cell invasiveness.	venetoclax	19-26	BCL2 apoptosis regulator	Homo sapiens	2-7
24172207-3	2013	ABT-199 is a small molecule that selectively inhibits BCL-2, which is currently in clinical trials in lymphoid malignancies.	venetoclax	0-7	BCL2 apoptosis regulator	Homo sapiens	54-59
33822485-4	2021	The in vivo CYP3A4 induction effect of ivosidenib was quantified using 4beta-hydroxycholesterol and was subsequently verified with the PK data from an ivosidenib and venetoclax combination study.	venetoclax	166-176	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	12-18
34332791-12	2022	To our best knowledge, we have reported the first BCL2 G101V mutation in an RS patient treated with venetoclax.	venetoclax	100-110	BCL2 apoptosis regulator	Homo sapiens	50-54
25284608-0	2015	Combination of ibrutinib with ABT-199: synergistic effects on proliferation inhibition and apoptosis in mantle cell lymphoma cells through perturbation of BTK, AKT and BCL2 pathways.	venetoclax	30-37	Bruton tyrosine kinase	Homo sapiens	155-158
25284608-0	2015	Combination of ibrutinib with ABT-199: synergistic effects on proliferation inhibition and apoptosis in mantle cell lymphoma cells through perturbation of BTK, AKT and BCL2 pathways.	venetoclax	30-37	AKT serine/threonine kinase 1	Homo sapiens	160-163
25284608-0	2015	Combination of ibrutinib with ABT-199: synergistic effects on proliferation inhibition and apoptosis in mantle cell lymphoma cells through perturbation of BTK, AKT and BCL2 pathways.	venetoclax	30-37	BCL2 apoptosis regulator	Homo sapiens	168-172
34610123-7	2021	Variables that favored response to ven/aza over IC included older age, secondary AML and RUNX1 mutations.	venetoclax	35-38	RUNX family transcription factor 1	Homo sapiens	89-94
34705247-10	2022	In the study shown, venetoclax compound demonstrated excellent binding affinity to iNOS protein.	venetoclax	20-30	nitric oxide synthase 2	Homo sapiens	83-87
34767916-8	2022	Inhibition of Mcl-1 using another Mcl-1 selective inhibitor, AZD5991, also synergistically enhanced apoptosis induced by venetoclax in a caspase dependent manner.	venetoclax	121-131	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	14-19
34767916-8	2022	Inhibition of Mcl-1 using another Mcl-1 selective inhibitor, AZD5991, also synergistically enhanced apoptosis induced by venetoclax in a caspase dependent manner.	venetoclax	121-131	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	34-39
34614506-1	2021	Adding the selective BCL-2 inhibitor venetoclax to reduced intensity conditioning (RIC) chemotherapy (fludarabine and busulfan, FluBu2) may enhance anti-leukemic cytotoxicity and thereby reduce the risk of post-transplant relapse.	venetoclax	37-47	BCL2 apoptosis regulator	Homo sapiens	21-26
34930453-0	2021	Daratumumab and venetoclax in combination with chemotherapy provide sustained molecular remission in relapsed/refractory CD19, CD20, and CD22 negative acute B lymphoblastic leukemia with KMT2A-AFF1 transcript.	venetoclax	16-26	CD22 molecule	Homo sapiens	137-141
34930453-0	2021	Daratumumab and venetoclax in combination with chemotherapy provide sustained molecular remission in relapsed/refractory CD19, CD20, and CD22 negative acute B lymphoblastic leukemia with KMT2A-AFF1 transcript.	venetoclax	16-26	CD19 molecule	Homo sapiens	121-125
34728569-13	2022	Co-treatment with venetoclax can overcome BCL2-mediated resistance to S63845, and enhance efficacy of MCL1 inhibitors in BCL2-positive aggressive B-NHL.	venetoclax	18-28	BCL2 apoptosis regulator	Homo sapiens	42-46
34728569-13	2022	Co-treatment with venetoclax can overcome BCL2-mediated resistance to S63845, and enhance efficacy of MCL1 inhibitors in BCL2-positive aggressive B-NHL.	venetoclax	18-28	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	102-106
34728569-13	2022	Co-treatment with venetoclax can overcome BCL2-mediated resistance to S63845, and enhance efficacy of MCL1 inhibitors in BCL2-positive aggressive B-NHL.	venetoclax	18-28	BCL2 apoptosis regulator	Homo sapiens	121-125
34930453-0	2021	Daratumumab and venetoclax in combination with chemotherapy provide sustained molecular remission in relapsed/refractory CD19, CD20, and CD22 negative acute B lymphoblastic leukemia with KMT2A-AFF1 transcript.	venetoclax	16-26	lysine methyltransferase 2A	Homo sapiens	187-192
34930453-0	2021	Daratumumab and venetoclax in combination with chemotherapy provide sustained molecular remission in relapsed/refractory CD19, CD20, and CD22 negative acute B lymphoblastic leukemia with KMT2A-AFF1 transcript.	venetoclax	16-26	AF4/FMR2 family member 1	Homo sapiens	193-197
34930453-0	2021	Daratumumab and venetoclax in combination with chemotherapy provide sustained molecular remission in relapsed/refractory CD19, CD20, and CD22 negative acute B lymphoblastic leukemia with KMT2A-AFF1 transcript.	venetoclax	16-26	keratin 20	Homo sapiens	127-131
34976720-4	2022	We present an unusual case of de novo TP53 mutated MDS/MPN overlap with bladder MS. Due to the high-risk nature of the disease, the patient was induced with decitabine and venetoclax combination therapy, resulting in complete remission.	venetoclax	172-182	tumor protein p53	Homo sapiens	38-42
34260140-0	2021	Azacitidine and venetoclax for post-transplant relapse in a case of CBFA2T3/GLIS2 childhood acute myeloid leukaemia.	venetoclax	16-26	CBFA2/RUNX1 partner transcriptional co-repressor 3	Homo sapiens	68-75
34592197-12	2021	The Drug resistance analysis demonstrated ADAM12 and COL1A2 up-regulation among 66 overexpressed CSPs caused resistance to Venetoclax and Cyclophosphamide with a high estimate, respectively.	venetoclax	123-133	ADAM metallopeptidase domain 12	Homo sapiens	42-48
34592197-12	2021	The Drug resistance analysis demonstrated ADAM12 and COL1A2 up-regulation among 66 overexpressed CSPs caused resistance to Venetoclax and Cyclophosphamide with a high estimate, respectively.	venetoclax	123-133	collagen type I alpha 2 chain	Homo sapiens	53-59
34795418-6	2022	We found in a Swiss DLBCL cohort that ~15% of patients are projected to respond to the venetoclax/ibrutinib combination based on their high Bcl-2 expression and nuclear NF-kappaB localization.	venetoclax	87-97	BCL2 apoptosis regulator	Homo sapiens	140-145
34581757-2	2021	We report results of a phase 1b dose-escalation study of the novel, subcutaneous BET inhibitor RO6870810 (RO) combined with the BCL-2 inhibitor venetoclax, and rituximab, in recurrent/refractory DLBCL (NCT03255096).	venetoclax	144-154	BCL2 apoptosis regulator	Homo sapiens	128-133
34548471-0	2021	ASXL1 mutations are associated with distinct epigenomic alterations that lead to sensitivity to venetoclax and azacytidine.	venetoclax	96-106	ASXL transcriptional regulator 1	Homo sapiens	0-5
34255353-0	2021	Outcomes of TP53-mutant acute myeloid leukemia with decitabine and venetoclax.	venetoclax	67-77	tumor protein p53	Homo sapiens	12-16
34790781-10	2021	(III) Transcriptome sequencing showed that differentially expressed genes in the combination group compared with the venetoclax monotherapy group were mainly enriched in the PI3K-AKT pathway and JAK2/STAT3 pathway.	venetoclax	117-127	thymoma viral proto-oncogene 1	Mus musculus	179-182
34790781-10	2021	(III) Transcriptome sequencing showed that differentially expressed genes in the combination group compared with the venetoclax monotherapy group were mainly enriched in the PI3K-AKT pathway and JAK2/STAT3 pathway.	venetoclax	117-127	Janus kinase 2	Mus musculus	195-199
34790781-10	2021	(III) Transcriptome sequencing showed that differentially expressed genes in the combination group compared with the venetoclax monotherapy group were mainly enriched in the PI3K-AKT pathway and JAK2/STAT3 pathway.	venetoclax	117-127	signal transducer and activator of transcription 3	Mus musculus	200-205
34548471-2	2021	To explore the mechanisms underlying the selective sensitivity of mutant leukemia cells to VEN and AZA, we used cell-based isogenic models containing a common leukemia-associated mutation in the epigenetic regulator ASXL1.	venetoclax	91-94	ASXL transcriptional regulator 1	Homo sapiens	216-221
34424320-7	2021	Lastly, we show that the B-cell lymphoma 2 (BCL2)-dependent cytotoxicity of huXBR1-402-G5-PNU can be leveraged by combined treatment strategies with the BCL2 inhibitor venetoclax.	venetoclax	168-178	BCL2 apoptosis regulator	Homo sapiens	25-42
34083230-11	2021	CONCLUSIONS: Venetoclax monotherapy has a manageable safety profile and achieves durable responses in a subset of patients with FL, MCL, WM, and MZL, particularly in those who achieve CR.	venetoclax	13-23	C-type lectin domain family 4 member D	Homo sapiens	132-135
34467417-5	2022	Interestingly, the spleen tyrosine kinase (SYK) inhibitor entospletinib, and the phosphoinositide 3-kinase delta (PI3Kdelta) inhibitor idelalisib, reduced T cell activation, impaired the generation of leukemic cells with this aggressive phenotype, and were able to restore CLL sensitivity to venetoclax.	venetoclax	292-302	spleen associated tyrosine kinase	Homo sapiens	19-41
34467417-5	2022	Interestingly, the spleen tyrosine kinase (SYK) inhibitor entospletinib, and the phosphoinositide 3-kinase delta (PI3Kdelta) inhibitor idelalisib, reduced T cell activation, impaired the generation of leukemic cells with this aggressive phenotype, and were able to restore CLL sensitivity to venetoclax.	venetoclax	292-302	spleen associated tyrosine kinase	Homo sapiens	43-46
34467417-5	2022	Interestingly, the spleen tyrosine kinase (SYK) inhibitor entospletinib, and the phosphoinositide 3-kinase delta (PI3Kdelta) inhibitor idelalisib, reduced T cell activation, impaired the generation of leukemic cells with this aggressive phenotype, and were able to restore CLL sensitivity to venetoclax.	venetoclax	292-302	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	81-112
34467417-5	2022	Interestingly, the spleen tyrosine kinase (SYK) inhibitor entospletinib, and the phosphoinositide 3-kinase delta (PI3Kdelta) inhibitor idelalisib, reduced T cell activation, impaired the generation of leukemic cells with this aggressive phenotype, and were able to restore CLL sensitivity to venetoclax.	venetoclax	292-302	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	114-123
34080039-8	2021	Extrapolation of the vincristine mechanistic PBPK model to other P-gp substrates further suggested DDI risk when ibrutinib (area under the concentration-time curve (AUC) ratio: 1.8), but not acalabrutinib (AUC ratio: 0.92), was given orally with venetoclax or digoxin.	venetoclax	246-256	ATP binding cassette subfamily B member 1	Homo sapiens	65-69
34331013-5	2021	Because addition of the BCL2 inhibitor venetoclax resulted in compensatory upregulation of MCL1, we established a three-drug combination composed of sirolimus, venetoclax, and the MCL1 inhibitor S63845.	venetoclax	39-49	BCL2 apoptosis regulator	Homo sapiens	24-28
34331013-5	2021	Because addition of the BCL2 inhibitor venetoclax resulted in compensatory upregulation of MCL1, we established a three-drug combination composed of sirolimus, venetoclax, and the MCL1 inhibitor S63845.	venetoclax	39-49	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	91-95
34424320-7	2021	Lastly, we show that the B-cell lymphoma 2 (BCL2)-dependent cytotoxicity of huXBR1-402-G5-PNU can be leveraged by combined treatment strategies with the BCL2 inhibitor venetoclax.	venetoclax	168-178	BCL2 apoptosis regulator	Homo sapiens	44-48
34424320-7	2021	Lastly, we show that the B-cell lymphoma 2 (BCL2)-dependent cytotoxicity of huXBR1-402-G5-PNU can be leveraged by combined treatment strategies with the BCL2 inhibitor venetoclax.	venetoclax	168-178	BCL2 apoptosis regulator	Homo sapiens	153-157
34426943-9	2021	Agents of interest include the BCL2 antagonist venetoclax, the CXCR4 inhibitor mavorixafor, and the non-covalent BTK inhibitors pirtobrutinib and ARQ-531.	venetoclax	47-57	BCL2 apoptosis regulator	Homo sapiens	31-35
34424151-8	2021	Interestingly, Venetoclax binding alters the local flexibility of Mpro and exerts pronounced effect in the C-terminal as well as two loop regions (Loop-A and Loop-B) that play important roles in catalysis.	venetoclax	15-25	NEWENTRY	Severe acute respiratory syndrome-related coronavirus	66-70
34290987-7	2021	The concentration of venetoclax in CSF was approximately 1/300 of that in plasma trough concentration.	venetoclax	21-31	colony stimulating factor 2	Homo sapiens	35-38
34367701-0	2021	Combined Ruxolitinib and Venetoclax Treatment in a Patient with a BCR-JAK2 Rearranged Myeloid Neoplasm.	venetoclax	25-35	Janus kinase 2	Homo sapiens	70-74
34112754-9	2021	Synergistic activity was demonstrated when fadraciclib was combined with the BCL-2 inhibitor venetoclax, or the conventional chemotherapy agents, cytarabine, or azacitidine, with the combination of fadraciclib and azacitidine having the most favorable therapeutic window.	venetoclax	93-103	BCL2 apoptosis regulator	Homo sapiens	77-82
34173723-0	2022	A novel polyethylene glycol (PEG)-drug conjugate of Venetoclax, a Bcl-2 inhibitor, for treatment of acute myeloid leukemia (AML).	venetoclax	52-62	BCL2 apoptosis regulator	Homo sapiens	66-71
35383271-4	2022	Further, fadraciclib was synergistic with the Bcl-2 antagonist venetoclax, inducing more profound CLL cell death, especially in samples with 17p deletion.	venetoclax	63-73	BCL2 apoptosis regulator	Homo sapiens	46-51
35418613-7	2022	Collectively, these studies indicate that Wnt5a-induced ROR1-signaling can enhance resistance to venetoclax therapy.	venetoclax	97-107	Wnt family member 5A	Homo sapiens	42-47
35418613-7	2022	Collectively, these studies indicate that Wnt5a-induced ROR1-signaling can enhance resistance to venetoclax therapy.	venetoclax	97-107	receptor tyrosine kinase like orphan receptor 1	Homo sapiens	56-60
35577568-0	2022	The BCL2 Inhibitor Venetoclax Plus Rituximab Is Active in MYD88 Wild-Type Polyneuropathy With Anti-MAG Antibodies.	venetoclax	19-29	BCL2 apoptosis regulator	Homo sapiens	4-8
35598030-9	2022	In addition to changes in BCL-2 family genes, mutations in other oncogenes can also confer resistance to apoptosis induced by venetoclax.	venetoclax	126-136	BCL2 apoptosis regulator	Homo sapiens	26-31
35594184-1	2022	The oral BCL-2 inhibitor venetoclax has demonstrated promising efficacy in patients with t(11;14) plasma cell disorders, both as a single-agent and in combination.	venetoclax	25-35	BCL2 apoptosis regulator	Homo sapiens	9-14
35577568-0	2022	The BCL2 Inhibitor Venetoclax Plus Rituximab Is Active in MYD88 Wild-Type Polyneuropathy With Anti-MAG Antibodies.	venetoclax	19-29	MYD88 innate immune signal transduction adaptor	Homo sapiens	58-63
35577568-3	2022	We report on the first patient with anti-MAG polyneuropathy and MYD88 wild-type who responded to venetoclax-rituximab.	venetoclax	97-107	MYD88 innate immune signal transduction adaptor	Homo sapiens	64-69
35187951-0	2022	PALVEN: phase 1b trial of palbociclib, letrozole and venetoclax in estrogen receptor- and BCL2-positive advanced breast cancer.	venetoclax	53-63	estrogen receptor 1	Homo sapiens	67-84
35580333-0	2022	Depletion of CLL cells by venetoclax treatment reverses oxidative stress and impaired glycolysis in CD4 T cells.	venetoclax	26-36	CD4 molecule	Homo sapiens	100-103
35491624-2	2022	The approval of the antiapoptotic BCL2 antagonist venetoclax has finally validated the potential of targeting apoptotic pathways in patients with cancer.	venetoclax	50-60	BCL2 apoptosis regulator	Homo sapiens	34-38
35568072-8	2022	The BEZ235 increased the drug sensitivity of ABT199 by reducing the MCL-1 protein synthesis and promoted the degradation of MCL-1 protein, which is considered as the mechanism of reversing ABT199 resistance.	venetoclax	45-51	myeloid cell leukemia sequence 1	Mus musculus	68-73
35568072-8	2022	The BEZ235 increased the drug sensitivity of ABT199 by reducing the MCL-1 protein synthesis and promoted the degradation of MCL-1 protein, which is considered as the mechanism of reversing ABT199 resistance.	venetoclax	45-51	myeloid cell leukemia sequence 1	Mus musculus	124-129
35568072-8	2022	The BEZ235 increased the drug sensitivity of ABT199 by reducing the MCL-1 protein synthesis and promoted the degradation of MCL-1 protein, which is considered as the mechanism of reversing ABT199 resistance.	venetoclax	189-195	myeloid cell leukemia sequence 1	Mus musculus	124-129
35568072-9	2022	Furthermore, the BEZ235 and ABT199 can synergistically enhance the inhibition of PI3K/AKT/mTOR pathway.	venetoclax	28-34	thymoma viral proto-oncogene 1	Mus musculus	86-89
35568072-9	2022	Furthermore, the BEZ235 and ABT199 can synergistically enhance the inhibition of PI3K/AKT/mTOR pathway.	venetoclax	28-34	mechanistic target of rapamycin kinase	Mus musculus	90-94
35568072-10	2022	CONCLUSION: The combination of BEZ235 and ABT199 exhibits a synergistic anti-tumor effect in AML by down-regulating MCL-1 protein.	venetoclax	42-48	myeloid cell leukemia sequence 1	Mus musculus	116-121
35187951-0	2022	PALVEN: phase 1b trial of palbociclib, letrozole and venetoclax in estrogen receptor- and BCL2-positive advanced breast cancer.	venetoclax	53-63	BCL2 apoptosis regulator	Homo sapiens	90-94
35615323-4	2022	The targeted NGS analysis showed that the VEN/AZA combination led to the eradication of the FLT3-ITD and RUNX1 mutated clone/s primarily associated with AML evolution, and subsequently, the SRSF2, NRAS, and ASXL1 mutated clone/s.	venetoclax	42-45	fms related receptor tyrosine kinase 3	Homo sapiens	92-96
35352453-6	2022	Clinically relevant doses of venetoclax, a BCL-2 inhibitor, in combination with duvelisib, a PI3Kdelta/gamma dual inhibitor, resulted in significant inhibition of these compensatory pathways and apoptosis induction.	venetoclax	29-39	BCL2 apoptosis regulator	Homo sapiens	43-48
35615323-4	2022	The targeted NGS analysis showed that the VEN/AZA combination led to the eradication of the FLT3-ITD and RUNX1 mutated clone/s primarily associated with AML evolution, and subsequently, the SRSF2, NRAS, and ASXL1 mutated clone/s.	venetoclax	42-45	RUNX family transcription factor 1	Homo sapiens	105-110
35615323-4	2022	The targeted NGS analysis showed that the VEN/AZA combination led to the eradication of the FLT3-ITD and RUNX1 mutated clone/s primarily associated with AML evolution, and subsequently, the SRSF2, NRAS, and ASXL1 mutated clone/s.	venetoclax	42-45	serine and arginine rich splicing factor 2	Homo sapiens	190-195
35615323-4	2022	The targeted NGS analysis showed that the VEN/AZA combination led to the eradication of the FLT3-ITD and RUNX1 mutated clone/s primarily associated with AML evolution, and subsequently, the SRSF2, NRAS, and ASXL1 mutated clone/s.	venetoclax	42-45	NRAS proto-oncogene, GTPase	Homo sapiens	197-201
35615323-4	2022	The targeted NGS analysis showed that the VEN/AZA combination led to the eradication of the FLT3-ITD and RUNX1 mutated clone/s primarily associated with AML evolution, and subsequently, the SRSF2, NRAS, and ASXL1 mutated clone/s.	venetoclax	42-45	ASXL transcriptional regulator 1	Homo sapiens	207-212
35452083-1	2022	Two publications detailing the clinical outcomes of patients with acute myeloid leukemia and mutations in IDH1, IDH2, or FLT3 who received initial therapy with venetoclax and azacitidine provide new insights into risk stratification and set the stage for future trials integrating molecularly targeted therapy with this new standard regimen.	venetoclax	160-170	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	106-110
35515507-3	2022	Recently, the United States FDA has approved venetoclax, a selective oral BCL-2 inhibitor, for use in conjunction with hypomethylating agents (azacitidine or decitabine) or low-dose cytarabine as a first-line treatment option for those AML patients ineligible for standard induction chemotherapy.	venetoclax	45-55	BCL2 apoptosis regulator	Homo sapiens	74-79
35577753-6	2022	In the first case, a patient with CLL, complex karyotype, del 17p, and a mutation in TP53 experiences progression after ibrutinib, venetoclax, bendamustine, rituximab, and idelalisib.	venetoclax	131-141	tumor protein p53	Homo sapiens	85-89
35507786-6	2022	Other drugs used in combination with venetoclax include: FLT3 inhibitors, IDH2 inhibitors, chidamide, ibrutinib, lapatinib, mivebresib, triptolide, metabolic inhibitors, nucleoside analogs, and classical chemotherapeutics.	venetoclax	37-47	fms related receptor tyrosine kinase 3	Homo sapiens	57-61
35507786-6	2022	Other drugs used in combination with venetoclax include: FLT3 inhibitors, IDH2 inhibitors, chidamide, ibrutinib, lapatinib, mivebresib, triptolide, metabolic inhibitors, nucleoside analogs, and classical chemotherapeutics.	venetoclax	37-47	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	74-78
35452083-1	2022	Two publications detailing the clinical outcomes of patients with acute myeloid leukemia and mutations in IDH1, IDH2, or FLT3 who received initial therapy with venetoclax and azacitidine provide new insights into risk stratification and set the stage for future trials integrating molecularly targeted therapy with this new standard regimen.	venetoclax	160-170	isocitrate dehydrogenase (NADP(+)) 2	Homo sapiens	112-116
35452083-1	2022	Two publications detailing the clinical outcomes of patients with acute myeloid leukemia and mutations in IDH1, IDH2, or FLT3 who received initial therapy with venetoclax and azacitidine provide new insights into risk stratification and set the stage for future trials integrating molecularly targeted therapy with this new standard regimen.	venetoclax	160-170	fms related receptor tyrosine kinase 3	Homo sapiens	121-125
35443722-9	2022	Artesunate serves as a bridge for venetoclax and cytarabine combination by Noxa and Bim-mediated apoptosis and Mcl-1 reduction.	venetoclax	34-44	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	75-79
35443722-9	2022	Artesunate serves as a bridge for venetoclax and cytarabine combination by Noxa and Bim-mediated apoptosis and Mcl-1 reduction.	venetoclax	34-44	BCL2 like 11	Homo sapiens	84-87
35443750-9	2022	Thus, NOXA potentiates the efficacy of the BCL-2 inhibitor ABT-199 by simultaneous inhibition of MCL-1.	venetoclax	59-66	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	6-10
35443750-9	2022	Thus, NOXA potentiates the efficacy of the BCL-2 inhibitor ABT-199 by simultaneous inhibition of MCL-1.	venetoclax	59-66	BCL2 apoptosis regulator	Homo sapiens	43-48
35443722-7	2022	Silencing Mcl-1 or adding venetoclax/artesunate diminishes the cytarabine resistance pathway p-Chk1.	venetoclax	26-36	checkpoint kinase 1	Homo sapiens	95-99
35443722-9	2022	Artesunate serves as a bridge for venetoclax and cytarabine combination by Noxa and Bim-mediated apoptosis and Mcl-1 reduction.	venetoclax	34-44	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	111-116
35443750-9	2022	Thus, NOXA potentiates the efficacy of the BCL-2 inhibitor ABT-199 by simultaneous inhibition of MCL-1.	venetoclax	59-66	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	97-102
35368106-7	2022	Notably, 6 of 7 pts (86%) who received either allo-SCT3 or a combination therapy of DLIs, 5-azacytidine and venetoclax achieved CR despite poor cytogenetics post-allo-SCT2 (e.g. TP53).	venetoclax	108-118	tumor protein p53	Homo sapiens	178-182
35454865-7	2022	Combination with ABT-199 (venetoclax), an inhibitor of Bcl2, has a synergistic effect, suggesting that mitochondrial Kv1.3 inhibitors could potentially be used as combination partner to venetoclax, even in the treatment of t(11;14) negative multiple myeloma, which represent the major part of cases and are rather resistant to venetoclax alone.	venetoclax	17-24	BCL2 apoptosis regulator	Homo sapiens	55-59
35454865-7	2022	Combination with ABT-199 (venetoclax), an inhibitor of Bcl2, has a synergistic effect, suggesting that mitochondrial Kv1.3 inhibitors could potentially be used as combination partner to venetoclax, even in the treatment of t(11;14) negative multiple myeloma, which represent the major part of cases and are rather resistant to venetoclax alone.	venetoclax	17-24	potassium voltage-gated channel subfamily A member 3	Homo sapiens	117-122
35432205-21	2022	Indeed, in non-obese diabetic mice, treatment with anti-Bcl-2 inhibitors, such as ABT199, eliminates senescent pancreatic beta cells, resulting in prevention of diabetes mellitus.	venetoclax	82-88	B cell leukemia/lymphoma 2	Mus musculus	56-61
35114569-6	2022	The combination of gilteritinib and venetoclax showed synergistic effects in the FLT3-ITD/D835 positive AML cells.	venetoclax	36-46	FMS-like tyrosine kinase 3	Mus musculus	81-85
35402265-11	2022	We further described the therapeutic potential of Bax/Bcl-2/EGFR SMIs, mainly those with more potent and selectivity, including gefitinib, EGCG, ABT-737, thymoquinone, quercetin, and venetoclax.	venetoclax	183-193	BCL2 associated X, apoptosis regulator	Homo sapiens	50-53
35456528-8	2022	Additional consideration is warranted when venetoclax is administered together with agents that inhibit both CYP3A-mediated metabolism and OATP1B-mediated transport.	venetoclax	43-53	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	109-114
35241842-6	2022	Further, patients with MDS who progressed after failure to frontline HMA therapy and whose HSCs upregulated BCL-2 achieved improved clinical responses to venetoclax-based therapy in the clinical setting.	venetoclax	154-164	BCL2 apoptosis regulator	Homo sapiens	108-113
35245447-7	2022	Functional analyses reveal that Mito-AML is metabolically wired toward stronger complex I-dependent respiration and is more responsive to treatment with the BCL2 inhibitor venetoclax.	venetoclax	172-182	BCL2 apoptosis regulator	Homo sapiens	157-161
35193595-13	2022	Decreased frequencies and recovery functions of BCL-2+T cells were observed in CLL patients in complete remission after treatment with venetoclax.	venetoclax	135-145	BCL2 apoptosis regulator	Homo sapiens	48-53
35046058-0	2022	Impact of Venetoclax and Azacitidine in Treatment-Naive Patients with Acute Myeloid Leukemia and IDH1/2 mutations.	venetoclax	10-20	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	97-103
35188042-3	2022	We demonstrated the synergism of (Bis + ABT199/venetoclax) in combination with panobinostat (Pano), decitabine (DAC), or olaparib (Ola), known inhibitors of BCL2, histone deacetylase, DNA methyltransferase, and poly(ADP-ribose) polymerase, respectively, in AML cells.	venetoclax	47-57	arylacetamide deacetylase	Homo sapiens	112-115
35188042-3	2022	We demonstrated the synergism of (Bis + ABT199/venetoclax) in combination with panobinostat (Pano), decitabine (DAC), or olaparib (Ola), known inhibitors of BCL2, histone deacetylase, DNA methyltransferase, and poly(ADP-ribose) polymerase, respectively, in AML cells.	venetoclax	47-57	BCL2 apoptosis regulator	Homo sapiens	157-161
35188042-3	2022	We demonstrated the synergism of (Bis + ABT199/venetoclax) in combination with panobinostat (Pano), decitabine (DAC), or olaparib (Ola), known inhibitors of BCL2, histone deacetylase, DNA methyltransferase, and poly(ADP-ribose) polymerase, respectively, in AML cells.	venetoclax	47-57	poly(ADP-ribose) polymerase 1	Homo sapiens	211-238
35198449-0	2022	Clinical Response to Venetoclax and Decitabine in Acute Promyelocytic Leukemia With a Novel RARA-THRAP3 Fusion: A Case Report.	venetoclax	21-31	retinoic acid receptor alpha	Homo sapiens	92-96
35198449-0	2022	Clinical Response to Venetoclax and Decitabine in Acute Promyelocytic Leukemia With a Novel RARA-THRAP3 Fusion: A Case Report.	venetoclax	21-31	thyroid hormone receptor associated protein 3	Homo sapiens	97-103
35092513-9	2022	Synergistic effects between CDK9 inhibitors and either Venetoclax, Bortezomib, Lenalidomide or Erlotinib have been proven and are awaiting verification in clinical trials.	venetoclax	55-65	cyclin dependent kinase 9	Homo sapiens	28-32
35185150-1	2022	Despite high initial response rates, acute myeloid leukemia (AML) treated with the BCL-2-selective inhibitor venetoclax (VEN) alone or in combinations commonly acquires resistance.	venetoclax	109-119	BCL2 apoptosis regulator	Homo sapiens	83-88
35185150-1	2022	Despite high initial response rates, acute myeloid leukemia (AML) treated with the BCL-2-selective inhibitor venetoclax (VEN) alone or in combinations commonly acquires resistance.	venetoclax	121-124	BCL2 apoptosis regulator	Homo sapiens	83-88
35179064-12	2022	DISCUSSION: Although this report describes the safe administration of venetoclax with voriconazole, extreme caution should be exercised when administering venetoclax with any strong CYP3A4 inhibitor during the ramp-up phase in patients with CLL.	venetoclax	155-165	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	182-188
35211416-0	2022	Combination of Venetoclax and Midostaurin Efficiently Suppressed Relapsed t(8;21)Acute Myeloid Leukemia With Mutant KIT After Failure of Venetoclax Plus Azacitidine Treatment.	venetoclax	15-25	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	116-119
35153769-5	2021	Blasts t (6; 11) KMT2A-AFDN rearranged, both from cell lines and primary samples, were shown to be significantly highly responsive to the combination of venetoclax and thioridazine, with the synergy being induced by a dramatic increase of mitochondrial depolarization that triggered blast apoptosis.	venetoclax	153-163	lysine methyltransferase 2A	Homo sapiens	17-22
35153769-5	2021	Blasts t (6; 11) KMT2A-AFDN rearranged, both from cell lines and primary samples, were shown to be significantly highly responsive to the combination of venetoclax and thioridazine, with the synergy being induced by a dramatic increase of mitochondrial depolarization that triggered blast apoptosis.	venetoclax	153-163	afadin, adherens junction formation factor	Homo sapiens	23-27
35063965-0	2022	Impact of FLT3 mutation on outcomes after venetoclax and azacitidine for patients with treatment-naive acute myeloid leukemia.	venetoclax	42-52	fms related receptor tyrosine kinase 3	Homo sapiens	10-14
35063965-7	2022	Composite complete remission (CRc, complete remission (CR)+CR with incomplete hematologic recovery (CRi)) rates (venetoclax+azacitidine /azacitidine) for FLT3 mutant patients were 67%/36%, median duration of remission (DoR) was 17.3/5.0 months, and median OS was 12.5/8.6 months.	venetoclax	113-123	fms related receptor tyrosine kinase 3	Homo sapiens	154-158
35063965-9	2022	In patients treated with venetoclax+azacitidine, CRc in patients with FLT3-ITD and FLT3-TKD was 63% and 77%, median OS was 9.9 and 19.2 months, and in co-mutated FLT3-ITD+NPM1, CRc was 70%, median DoR was not reached, and median OS was 9.1 months.	venetoclax	25-35	fms related receptor tyrosine kinase 3	Homo sapiens	162-166
35063965-9	2022	In patients treated with venetoclax+azacitidine, CRc in patients with FLT3-ITD and FLT3-TKD was 63% and 77%, median OS was 9.9 and 19.2 months, and in co-mutated FLT3-ITD+NPM1, CRc was 70%, median DoR was not reached, and median OS was 9.1 months.	venetoclax	25-35	nucleophosmin 1	Homo sapiens	171-175
35063965-11	2022	CONCLUSION: When treated with venetoclax+azacitidine, patients with FLT3 mutations and FLT3 wild-type had similar outcomes.	venetoclax	30-40	fms related receptor tyrosine kinase 3	Homo sapiens	68-72
35046058-6	2022	Composite complete remission (CRc, complete remission (CR)+CR with incomplete hematologic recovery (CRi)) rates (venetoclax+azacitidine/azacitidine) among patients with IDH1/2mut were 79%/11%, median duration of remission (mDoR) was 29.5/9.5 months, and median overall survival (mOS) was 24.5/6.2 months.	venetoclax	113-123	opioid receptor, delta 1	Mus musculus	223-227
35046058-6	2022	Composite complete remission (CRc, complete remission (CR)+CR with incomplete hematologic recovery (CRi)) rates (venetoclax+azacitidine/azacitidine) among patients with IDH1/2mut were 79%/11%, median duration of remission (mDoR) was 29.5/9.5 months, and median overall survival (mOS) was 24.5/6.2 months.	venetoclax	113-123	Moloney sarcoma oncogene	Mus musculus	279-282
35046058-12	2022	CONCLUSION: Patients with IDH1/2mut who receive venetoclax+azacitidine had high response rates, durable remissions and significant OS; cytogenetic risk did not mitigate the favorable outcomes seen from this regimen for IDH1/2mut.	venetoclax	48-58	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	26-30
35046058-12	2022	CONCLUSION: Patients with IDH1/2mut who receive venetoclax+azacitidine had high response rates, durable remissions and significant OS; cytogenetic risk did not mitigate the favorable outcomes seen from this regimen for IDH1/2mut.	venetoclax	48-58	Moloney sarcoma oncogene	Mus musculus	131-133
35046058-12	2022	CONCLUSION: Patients with IDH1/2mut who receive venetoclax+azacitidine had high response rates, durable remissions and significant OS; cytogenetic risk did not mitigate the favorable outcomes seen from this regimen for IDH1/2mut.	venetoclax	48-58	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	219-223
34667127-7	2022	PREVENTION RELEVANCE: This study demonstrates that prophylactic treatment with the BCL2-specific antagonist venetoclax prevents breast cancer initiated by a mutated and activated PIK3CA, the most common breast oncogene.	venetoclax	108-118	B cell leukemia/lymphoma 2	Mus musculus	83-87
35070982-0	2021	Notch2 Increases the Resistance to Venetoclax-Induced Apoptosis in Chronic Lymphocytic Leukemia B Cells by Inducing Mcl-1.	venetoclax	35-45	notch receptor 2	Homo sapiens	0-6
34667127-7	2022	PREVENTION RELEVANCE: This study demonstrates that prophylactic treatment with the BCL2-specific antagonist venetoclax prevents breast cancer initiated by a mutated and activated PIK3CA, the most common breast oncogene.	venetoclax	108-118	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Mus musculus	179-185
33954893-8	2021	Interestingly, pibrentasvir, venetoclax, and ledipasvir were observed to show even higher binding affinities with the ABCG2 transporter with binding energies of < -80.0 kcal/mol over long MD simulations of 100 ns.	venetoclax	29-39	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	118-123
33900450-14	2021	Combined therapy of ibrutinib and venetoclax showed promising efficacy and synergistic effects in R/R DLBCL patients with non-GCB subtype and BCL2 overexpression, and the toxicities were well-tolerated.	venetoclax	34-44	BCL2 apoptosis regulator	Homo sapiens	142-146
33954893-10	2021	The current study throws new light on pibrentasvir, venetoclax, and ledipasvir as curative options for multidrug resistant cancers by inhibiting ABCG2 transporter.	venetoclax	52-62	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	145-150
33846811-1	2021	The aim of the present study was to investigate the synergistic effect of LY294002 (a PI3K inhibitor) and ABT199 (a BCL2 inhibitor) on the cell cycle in acute myeloid leukemia (AML).	venetoclax	106-112	BCL2 apoptosis regulator	Homo sapiens	116-120
33846811-4	2021	At the molecular level, LY294002 and ABT199 combination treatment significantly downregulated Skp2, Bcl2, procaspase-3 and procaspase-9 expression levels, but markedly upregulated p27, Bax, cleaved caspase-3 and caspase-9 expression levels in K562, HL-60 and KG1a cells.	venetoclax	37-43	S-phase kinase associated protein 2	Homo sapiens	94-98
33846811-4	2021	At the molecular level, LY294002 and ABT199 combination treatment significantly downregulated Skp2, Bcl2, procaspase-3 and procaspase-9 expression levels, but markedly upregulated p27, Bax, cleaved caspase-3 and caspase-9 expression levels in K562, HL-60 and KG1a cells.	venetoclax	37-43	BCL2 apoptosis regulator	Homo sapiens	100-104
33846811-4	2021	At the molecular level, LY294002 and ABT199 combination treatment significantly downregulated Skp2, Bcl2, procaspase-3 and procaspase-9 expression levels, but markedly upregulated p27, Bax, cleaved caspase-3 and caspase-9 expression levels in K562, HL-60 and KG1a cells.	venetoclax	37-43	caspase 3	Homo sapiens	106-118
33846811-4	2021	At the molecular level, LY294002 and ABT199 combination treatment significantly downregulated Skp2, Bcl2, procaspase-3 and procaspase-9 expression levels, but markedly upregulated p27, Bax, cleaved caspase-3 and caspase-9 expression levels in K562, HL-60 and KG1a cells.	venetoclax	37-43	dynactin subunit 6	Homo sapiens	180-183
33846811-4	2021	At the molecular level, LY294002 and ABT199 combination treatment significantly downregulated Skp2, Bcl2, procaspase-3 and procaspase-9 expression levels, but markedly upregulated p27, Bax, cleaved caspase-3 and caspase-9 expression levels in K562, HL-60 and KG1a cells.	venetoclax	37-43	BCL2 associated X, apoptosis regulator	Homo sapiens	185-188
33846811-4	2021	At the molecular level, LY294002 and ABT199 combination treatment significantly downregulated Skp2, Bcl2, procaspase-3 and procaspase-9 expression levels, but markedly upregulated p27, Bax, cleaved caspase-3 and caspase-9 expression levels in K562, HL-60 and KG1a cells.	venetoclax	37-43	caspase 3	Homo sapiens	109-118
33846811-4	2021	At the molecular level, LY294002 and ABT199 combination treatment significantly downregulated Skp2, Bcl2, procaspase-3 and procaspase-9 expression levels, but markedly upregulated p27, Bax, cleaved caspase-3 and caspase-9 expression levels in K562, HL-60 and KG1a cells.	venetoclax	37-43	caspase 9	Homo sapiens	126-135
33580980-0	2021	Decitabine and Venetoclax for IDH1/2-mutated Acute Myeloid Leukemia.	venetoclax	15-25	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	30-36
34036969-2	2021	A Bcl-2 inhibitor, venetoclax, can improve the clinical outcome of acute lung injury based on its pro-apoptotic effect.	venetoclax	19-29	BCL2 apoptosis regulator	Homo sapiens	2-7
34012921-7	2021	The BCL2 inhibitor venetoclax, combined with hypomethylating agents or low dose cytarabine, represents an important new therapy especially for older AML patients.	venetoclax	19-29	BCL2 apoptosis regulator	Homo sapiens	4-8
33976278-8	2021	Notably, a head-to-head comparison of Disarib to ABT199, the only FDA approved BCL2 inhibitor revealed that Disarib is as potent as ABT199.	venetoclax	49-55	B cell leukemia/lymphoma 2	Mus musculus	79-83
33954816-0	2022	Venetoclax and decitabine in refractory TP53-mutated early T-cell precursor acute lymphoblastic leukemia.	venetoclax	0-10	tumor protein p53	Homo sapiens	40-44
33926484-0	2021	Inhibition of CPT1a as a prognostic marker can synergistically enhance the antileukemic activity of ABT199.	venetoclax	100-106	carnitine palmitoyltransferase 1A	Homo sapiens	14-19
33843403-6	2021	The addition of the CXCR4 inhibitor plerixafor with ruxolitinib and venetoclax reduces clinical scores and enhances survival.	venetoclax	68-78	C-X-C motif chemokine receptor 4	Homo sapiens	20-25
32165486-3	2021	In this study, we combine venetoclax with the dual PI3K and histone deacetylase inhibitor CUDC-907, which can downregulate Mcl-1, upregulate Bim, and induce DNA damage, as well as downregulate c-Myc.	venetoclax	26-36	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	123-128
32165486-3	2021	In this study, we combine venetoclax with the dual PI3K and histone deacetylase inhibitor CUDC-907, which can downregulate Mcl-1, upregulate Bim, and induce DNA damage, as well as downregulate c-Myc.	venetoclax	26-36	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	193-198
33926484-14	2021	Moreover, we found downregulation of CPT1a sentitized BCL-2 inhibitor ABT199 and CPT1a-selective inhibitor ST1326 combined with ABT199 had a strong synergistic effect to induce apoptosis in AML cells and primary patient blasts for the first time.	venetoclax	70-76	carnitine palmitoyltransferase 1A	Homo sapiens	37-42
33926484-14	2021	Moreover, we found downregulation of CPT1a sentitized BCL-2 inhibitor ABT199 and CPT1a-selective inhibitor ST1326 combined with ABT199 had a strong synergistic effect to induce apoptosis in AML cells and primary patient blasts for the first time.	venetoclax	70-76	BCL2 apoptosis regulator	Homo sapiens	54-59
33926484-14	2021	Moreover, we found downregulation of CPT1a sentitized BCL-2 inhibitor ABT199 and CPT1a-selective inhibitor ST1326 combined with ABT199 had a strong synergistic effect to induce apoptosis in AML cells and primary patient blasts for the first time.	venetoclax	128-134	carnitine palmitoyltransferase 1A	Homo sapiens	37-42
33926484-14	2021	Moreover, we found downregulation of CPT1a sentitized BCL-2 inhibitor ABT199 and CPT1a-selective inhibitor ST1326 combined with ABT199 had a strong synergistic effect to induce apoptosis in AML cells and primary patient blasts for the first time.	venetoclax	128-134	carnitine palmitoyltransferase 1A	Homo sapiens	81-86
33926484-17	2021	CPT1a-selective inhibitor ST1326 combined with Bcl-2 inhibitor ABT199 showed strong synergistic inhibitory effects on AML.	venetoclax	63-69	BCL2 apoptosis regulator	Homo sapiens	47-52
33743079-4	2021	In general, we currently utilize a backbone regimen of a hypomethylating agent (HMA) or low-intensity chemotherapy with the BCL-2 inhibitor venetoclax for the majority of elderly patients with newly diagnosed AML.	venetoclax	140-150	BCL2 apoptosis regulator	Homo sapiens	124-129
33542074-6	2021	RESULTS: ABT199 (BCL-2 inhibitor) and IMD0354 (IKKB inhibitor), were identified as potent and selective inhibitors of cell viability in ENZ-resistant cell lines in vitro and in vivo which were further validated using loss-of-function assays of BCL-2 and IKKB.	venetoclax	9-15	BCL2 apoptosis regulator	Homo sapiens	17-22
33542074-6	2021	RESULTS: ABT199 (BCL-2 inhibitor) and IMD0354 (IKKB inhibitor), were identified as potent and selective inhibitors of cell viability in ENZ-resistant cell lines in vitro and in vivo which were further validated using loss-of-function assays of BCL-2 and IKKB.	venetoclax	9-15	BCL2 apoptosis regulator	Homo sapiens	244-249
33542074-6	2021	RESULTS: ABT199 (BCL-2 inhibitor) and IMD0354 (IKKB inhibitor), were identified as potent and selective inhibitors of cell viability in ENZ-resistant cell lines in vitro and in vivo which were further validated using loss-of-function assays of BCL-2 and IKKB.	venetoclax	9-15	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	254-258
33919958-4	2021	The Bcl-2 inhibitor venetoclax, in combination with hypomethylating agents or low dose cytarabine, has produced impressive results for newly diagnosed AML, while its role in R/R disease is not well defined yet.	venetoclax	20-30	BCL2 apoptosis regulator	Homo sapiens	4-9
33368455-0	2021	Targeting BCL-2 with venetoclax and dexamethasone in patients with relapsed/refractory t(11;14) multiple myeloma.	venetoclax	21-31	BCL2 apoptosis regulator	Homo sapiens	10-15
33687436-4	2021	In this study, we induced a mitochondrial damage model in oocytes with the Bcl-2-specific antagonist ABT-199.	venetoclax	101-108	BCL2 apoptosis regulator	Homo sapiens	75-80
33853293-3	2022	The selective BCL2 inhibitor, venetoclax (VEN) is used in combination with azacitidine (AZA), a DNA-methyltransferase inhibitor (DNMTi), to treat patients with AML.	venetoclax	30-40	BCL2 apoptosis regulator	Homo sapiens	14-18
33939107-7	2021	Current trials of IDH inhibitors include combination with standard induction chemotherapy, as maintenance therapy, and in combination with venetoclax-based regimens.	venetoclax	139-149	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	18-21
33786587-4	2021	Importantly, inhibition of AXL sensitized AML stem/progenitor cells to venetoclax treatment, with strong synergistic effects in vitro and in PDX models.	venetoclax	71-81	AXL receptor tyrosine kinase	Homo sapiens	27-30
33563904-0	2021	Triplet therapy with venetoclax, FLT3 inhibitor and decitabine for FLT3-mutated acute myeloid leukemia.	venetoclax	21-31	fms related receptor tyrosine kinase 3	Homo sapiens	67-71
32458446-5	2021	This paper highlights the promising efficacy of venetoclax-based therapy to reduce the relapse risk in patients with persistent or rising NPM1mut MRD.	venetoclax	48-58	nucleophosmin 1	Homo sapiens	138-142
33318657-1	2021	BACKGROUND: The BCL2 inhibitor venetoclax has shown efficacy in several hematologic malignancies, with the greatest response rates in indolent blood cancers such as chronic lymphocytic leukaemia.	venetoclax	31-41	BCL2 apoptosis regulator	Homo sapiens	16-20
33459064-2	2021	Venetoclax, an oral BCL-2 inhibitor, is approved by the Food and Drug Administration in combination with hypomethylating agents or low-dose cytarabine in newly-diagnosed AML patients who are ineligible to receive intensive chemotherapy.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	20-25
33480649-2	2021	The BCL-2 inhibitor venetoclax combined with hypomethylating agents like decitabine, has shown favorable responses in elderly patients with acute myeloid leukemia.	venetoclax	20-30	BCL2 apoptosis regulator	Homo sapiens	4-9
33495184-4	2021	A combination therapy including venetoclax was used based on efficacy data for Bcl-2 inhibitor venetoclax from available early-phase clinical trials in patients with relapsed multiple myeloma with t(11;14) and other published case studies.	venetoclax	32-42	BCL2 apoptosis regulator	Homo sapiens	79-84
33148670-0	2021	BET inhibition enhances the antileukemic activity of low-dose Venetoclax in acute myeloid leukemia.	venetoclax	62-72	delta/notch like EGF repeat containing	Homo sapiens	0-3
32887697-3	2021	We evaluated whether venetoclax, a selective small-molecule inhibitor of BCL-2, would influence the anti-tumor activity of immune checkpoint inhibitors (ICIs).	venetoclax	21-31	BCL2 apoptosis regulator	Homo sapiens	73-78
32404571-3	2020	In this review article, we discuss current treatment strategies for CLL patients in Japan, where the novel targeted agents, the BTK inhibitor ibrutinib and BCL2 antagonist venetoclax, now are available and increasingly used in clinical practice.	venetoclax	172-182	BCL2 apoptosis regulator	Homo sapiens	156-160
33414642-0	2020	BCL-2 Inhibitor Venetoclax Induces Autophagy-Associated Cell Death, Cell Cycle Arrest, and Apoptosis in Human Breast Cancer Cells.	venetoclax	16-26	BCL2 apoptosis regulator	Homo sapiens	0-5
33414642-8	2020	Induction of apoptosis by VCX treatment induced cell cycle arrest at G0/G1 phase with inhibition of cell proliferator genes, cyclin D1 and E2F1.	venetoclax	26-29	cyclin D1	Homo sapiens	125-134
33414642-8	2020	Induction of apoptosis by VCX treatment induced cell cycle arrest at G0/G1 phase with inhibition of cell proliferator genes, cyclin D1 and E2F1.	venetoclax	26-29	E2F transcription factor 1	Homo sapiens	139-143
33414642-9	2020	Furthermore, VCX treatment increased the formation of reactive oxygen species and the expression level of autophagy markers, Beclin 1 and LC3-II.	venetoclax	13-16	beclin 1	Homo sapiens	125-133
33414642-9	2020	Furthermore, VCX treatment increased the formation of reactive oxygen species and the expression level of autophagy markers, Beclin 1 and LC3-II.	venetoclax	13-16	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	138-141
33375215-4	2020	Personalized low dose rIL-2 in combination with either lenalidomide or venetoclax mediates natural killer stimulation and is an effective non-toxic immunotherapy administered in the outpatient setting for poor prognosis CLL.	venetoclax	71-81	interleukin 2	Rattus norvegicus	22-27
33425404-0	2020	Efficacy of Venetoclax and Dexamethasone in Refractory IgM Primary Plasma Cell Leukemia with t(11;14) and TP53 Mutation: A Case Report and Literature Review.	venetoclax	12-22	tumor protein p53	Homo sapiens	106-110
32948748-2	2020	The selective Bcl-2 inhibitor venetoclax (ABT-199) in combination therapy has been approved for the treatment of newly diagnosed AML patients who are ineligible for intensive chemotherapy, but resistance can be acquired through the upregulation of alternative antiapoptotic proteins.	venetoclax	30-40	BCL2 apoptosis regulator	Homo sapiens	14-19
33091356-8	2020	Novel BTK inhibitors (acalabrutinib, zanubrutinib, tirabrutinib) and the BCL2 antagonist venetoclax appear safe and active, and represent emerging options for the treatment of Waldenstrom macroglobulinaemia.	venetoclax	89-99	BCL2 apoptosis regulator	Homo sapiens	73-77
33121235-1	2021	Venetoclax (Ven), an orally administered, potent BCL-2 inhibitor, has demonstrated efficacy in chronic lymphocytic leukaemia (CLL) in combination with rituximab (R) or obinutuzumab (G).	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	49-54
33121235-1	2021	Venetoclax (Ven), an orally administered, potent BCL-2 inhibitor, has demonstrated efficacy in chronic lymphocytic leukaemia (CLL) in combination with rituximab (R) or obinutuzumab (G).	venetoclax	0-3	BCL2 apoptosis regulator	Homo sapiens	49-54
32519423-4	2020	By using RNA-seq analysis in two human AML cohorts made up of three patients with complete remission and three patients without remission after venetoclax treatment, we identified that upregulation of BTK enabled AML blast resistance to venetoclax.	venetoclax	144-154	Bruton tyrosine kinase	Homo sapiens	201-204
32948748-2	2020	The selective Bcl-2 inhibitor venetoclax (ABT-199) in combination therapy has been approved for the treatment of newly diagnosed AML patients who are ineligible for intensive chemotherapy, but resistance can be acquired through the upregulation of alternative antiapoptotic proteins.	venetoclax	42-49	BCL2 apoptosis regulator	Homo sapiens	14-19
32683457-5	2020	CYP3A4 is the main enzyme responsible for SMIs metabolism, and strong CYP3A4 inhibitors, such azoles, could increase drug exposure and toxicity; therefore dose adjustments (venetoclax, quizartinib, and ivosidenib) or alternative therapies or close monitoring (glasdegib, midostaurin, and gilteritinib) are recommended.	venetoclax	173-183	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	0-6
32577785-6	2020	Further multiscreen/Western blot analyses revealed that NF-kappaB was significantly downregulated in AZD9291 + ABT263/ABT199 treatment groups compared with AZD9291 or ABT263/ABT199 treatment alone, with a more significant reduction of NF-kappaB in AZD9291 + ABT199 compared with AZD9291 + ABT263.	venetoclax	118-124	nuclear factor kappa B subunit 1	Homo sapiens	56-65
32577785-6	2020	Further multiscreen/Western blot analyses revealed that NF-kappaB was significantly downregulated in AZD9291 + ABT263/ABT199 treatment groups compared with AZD9291 or ABT263/ABT199 treatment alone, with a more significant reduction of NF-kappaB in AZD9291 + ABT199 compared with AZD9291 + ABT263.	venetoclax	118-124	nuclear factor kappa B subunit 1	Homo sapiens	235-244
32577785-6	2020	Further multiscreen/Western blot analyses revealed that NF-kappaB was significantly downregulated in AZD9291 + ABT263/ABT199 treatment groups compared with AZD9291 or ABT263/ABT199 treatment alone, with a more significant reduction of NF-kappaB in AZD9291 + ABT199 compared with AZD9291 + ABT263.	venetoclax	174-180	nuclear factor kappa B subunit 1	Homo sapiens	56-65
32577785-6	2020	Further multiscreen/Western blot analyses revealed that NF-kappaB was significantly downregulated in AZD9291 + ABT263/ABT199 treatment groups compared with AZD9291 or ABT263/ABT199 treatment alone, with a more significant reduction of NF-kappaB in AZD9291 + ABT199 compared with AZD9291 + ABT263.	venetoclax	174-180	nuclear factor kappa B subunit 1	Homo sapiens	56-65
32577785-7	2020	It is also noticeable that AZD9291 + ABT263 specifically caused a significantly reduced expression of p21 compared with AZD9291 or ABT263 treatment alone while AZD9291 + ABT199 specifically caused significantly reduced expressions of SQSTM1 and survivin, but increased expression of autophagosome marker LC3-II compared with AZD9291 or ABT199 treatment alone.	venetoclax	170-176	H3 histone pseudogene 16	Homo sapiens	102-105
32577785-7	2020	It is also noticeable that AZD9291 + ABT263 specifically caused a significantly reduced expression of p21 compared with AZD9291 or ABT263 treatment alone while AZD9291 + ABT199 specifically caused significantly reduced expressions of SQSTM1 and survivin, but increased expression of autophagosome marker LC3-II compared with AZD9291 or ABT199 treatment alone.	venetoclax	170-176	sequestosome 1	Homo sapiens	234-240
32683457-5	2020	CYP3A4 is the main enzyme responsible for SMIs metabolism, and strong CYP3A4 inhibitors, such azoles, could increase drug exposure and toxicity; therefore dose adjustments (venetoclax, quizartinib, and ivosidenib) or alternative therapies or close monitoring (glasdegib, midostaurin, and gilteritinib) are recommended.	venetoclax	173-183	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	70-76
32245900-3	2020	We therefore evaluated combination therapy with ABT-199 (venetoclax), a potent and selective BCL2 inhibitor.	venetoclax	48-55	BCL2 apoptosis regulator	Homo sapiens	93-97
32504922-0	2020	Staurosporine and venetoclax induce the caspase-dependent proteolysis of MEF2D-fusion proteins and apoptosis in MEF2D-fusion (+) ALL cells.	venetoclax	18-28	myocyte enhancer factor 2D	Mus musculus	73-78
32592909-2	2020	Targeted drugs already changed the clinical practice in treatment of leukemias, such as imatinib (BCR/ABL inhibitor) in chronic myeloid leukemia (CML) and acute lymphoblastic leukemia (ALL), ibrutinib (Bruton"s tyrosine kinase inhibitor) in chronic lymphocytic leukemia (CLL), venetoclax (BCL2 inhibitor) in CLL and acute myeloid leukemia (AML) or midostaurin (FLT3 inhibitor) in AML.	venetoclax	277-287	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	98-105
32628327-0	2020	Venetoclax and hypomethylating agents in FLT3-mutated acute myeloid leukemia.	venetoclax	0-10	fms related receptor tyrosine kinase 3	Homo sapiens	41-45
32198151-0	2020	Assessment of the Efficacy of Therapies Following Venetoclax Discontinuation in CLL Reveals BTK inhibition as an Effective Strategy.	venetoclax	50-60	Bruton tyrosine kinase	Homo sapiens	92-95
33088538-1	2020	A case of an early-relapsed high-risk T-ALL with high BCL-2 expression on leukemic blasts was successfully treated with decitabine and venetoclax, achieving a CR.	venetoclax	135-145	BCL2 apoptosis regulator	Homo sapiens	54-59
33088538-2	2020	We suggest decitabine and venetoclax should be synergistic in BCL2-positive ALL.	venetoclax	26-36	BCL2 apoptosis regulator	Homo sapiens	62-66
32677976-8	2020	Furthermore, DT2216 combined with ABT199 (a selective Bcl-2 inhibitor) synergistically reduced disease burden and improved survival in a TCL PDX mouse model dependent on both Bcl-2 and Bcl-xL.	venetoclax	34-40	B cell leukemia/lymphoma 2	Mus musculus	54-59
32677976-8	2020	Furthermore, DT2216 combined with ABT199 (a selective Bcl-2 inhibitor) synergistically reduced disease burden and improved survival in a TCL PDX mouse model dependent on both Bcl-2 and Bcl-xL.	venetoclax	34-40	ras homolog family member J	Mus musculus	137-140
32677976-8	2020	Furthermore, DT2216 combined with ABT199 (a selective Bcl-2 inhibitor) synergistically reduced disease burden and improved survival in a TCL PDX mouse model dependent on both Bcl-2 and Bcl-xL.	venetoclax	34-40	B cell leukemia/lymphoma 2	Mus musculus	175-180
32677976-8	2020	Furthermore, DT2216 combined with ABT199 (a selective Bcl-2 inhibitor) synergistically reduced disease burden and improved survival in a TCL PDX mouse model dependent on both Bcl-2 and Bcl-xL.	venetoclax	34-40	BCL2-like 1	Mus musculus	185-191
32611578-0	2020	Response in patients with BIRC3-mutated relapsed/refractory chronic lymphocytic leukemia treated with fixed-duration venetoclax and rituximab.	venetoclax	117-127	baculoviral IAP repeat containing 3	Homo sapiens	26-31
32244251-8	2020	Our findings indicate that BTKi therapy can provide durable CLL control after disease progression on venetoclax.	venetoclax	101-111	inhibitor of Bruton tyrosine kinase	Homo sapiens	27-31
31439679-4	2020	Compared to other cell types, CD19+/B and CD56+/NK cells were more sensitive to dexamethasone, venetoclax and midostaurin, while monocytes were more sensitive to trametinib.	venetoclax	95-105	CD19 molecule	Homo sapiens	30-34
31439679-5	2020	Venetoclax exhibited dose dependent cell selectivity that inversely correlated to STAT3 phosphorylation.	venetoclax	0-10	signal transducer and activator of transcription 3	Homo sapiens	82-87
31439679-4	2020	Compared to other cell types, CD19+/B and CD56+/NK cells were more sensitive to dexamethasone, venetoclax and midostaurin, while monocytes were more sensitive to trametinib.	venetoclax	95-105	neural cell adhesion molecule 1	Homo sapiens	42-46
32184020-10	2020	AZD5991 exhibited the synergistic action with PNT, anti-cancer drugs and venetoclax (BCL2 inhibitor), suggesting the utility of MCL1 inhibitor alone or in combination as a future clinical option for Ph + leukemia patients.	venetoclax	73-83	BCL2 apoptosis regulator	Homo sapiens	85-89
31827241-0	2020	A novel CDK9 inhibitor increases the efficacy of venetoclax (ABT-199) in multiple models of hematologic malignancies.	venetoclax	61-68	cyclin dependent kinase 9	Homo sapiens	8-12
32184020-10	2020	AZD5991 exhibited the synergistic action with PNT, anti-cancer drugs and venetoclax (BCL2 inhibitor), suggesting the utility of MCL1 inhibitor alone or in combination as a future clinical option for Ph + leukemia patients.	venetoclax	73-83	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	128-132
31928108-1	2020	Venetoclax, a small molecule inhibitor of BCL-2, has promising pre-clinical and early clinical activity in relapsed refractory multiple myeloma (RRMM).	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	42-47
32066201-0	2020	Venetoclax, bortezomib and S63845, an MCL1 inhibitor, in multiple myeloma.	venetoclax	0-10	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	38-42
32066201-1	2020	OBJECTIVES: Venetoclax, an orally available BCL2-selective inhibitor, has demonstrated promising single-agent anti-tumour activity in myeloma especially patients with t(11;14).	venetoclax	12-22	BCL2 apoptosis regulator	Homo sapiens	44-48
31932844-1	2020	The BCL-2 inhibitor venetoclax combined with hypomethylating agents or low-dose cytarabine represents an important new therapy for older or unfit patients with acute myeloid leukemia (AML).	venetoclax	20-30	BCL2 apoptosis regulator	Homo sapiens	4-9
32089221-2	2020	Venetoclax is an orally selective BCL-2 inhibitor and BH3 mimetic approved in chronic lymphocytic leukemia and in combination with low dose cytarabine or hypomethylating agent in acute myeloid leukemia for the treatment of patients unfit for intensive chemotherapy.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	34-39
32171069-2	2020	The BCL-2 inhibitor, venetoclax, has shown promising activity in combination with hypomethylating agents and low-dose cytarabine in older adults for whom chemotherapy is not suitable with newly diagnosed acute myeloid leukaemia.	venetoclax	21-31	BCL2 apoptosis regulator	Homo sapiens	4-9
32183335-5	2020	Among them, venetoclax is a potent and selective BCL-2 inhibitor, which has demonstrated the strongest clinical activity in mature B-cell malignancies, including chronic lymphoid leukemia, mantle-cell lymphoma, and multiple myeloma.	venetoclax	12-22	BCL2 apoptosis regulator	Homo sapiens	49-54
32035785-3	2020	The clinical activity of venetoclax, a selective BCL2 inhibitor, in T-ALL is unknown.	venetoclax	25-35	BCL2 apoptosis regulator	Homo sapiens	49-53
32199933-5	2021	Venetoclax (ABT-199) is a novel, orally bioavailable small-molecule inhibitor of B-cell lymphoma 2 (BCL-2), a key regulator of the intrinsic apoptotic pathway.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	81-98
32199933-5	2021	Venetoclax (ABT-199) is a novel, orally bioavailable small-molecule inhibitor of B-cell lymphoma 2 (BCL-2), a key regulator of the intrinsic apoptotic pathway.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	100-105
32199933-5	2021	Venetoclax (ABT-199) is a novel, orally bioavailable small-molecule inhibitor of B-cell lymphoma 2 (BCL-2), a key regulator of the intrinsic apoptotic pathway.	venetoclax	12-19	BCL2 apoptosis regulator	Homo sapiens	81-98
32199933-5	2021	Venetoclax (ABT-199) is a novel, orally bioavailable small-molecule inhibitor of B-cell lymphoma 2 (BCL-2), a key regulator of the intrinsic apoptotic pathway.	venetoclax	12-19	BCL2 apoptosis regulator	Homo sapiens	100-105
32172299-4	2020	However, 17p-deleted, p53-mutated or IGHV-UM subgroups are generally resistant to FCR, and much better responses are seen with ibrutinib and venetoclax, frequently inducing MRD negativity that hopefully will be translated into durable remissions.	venetoclax	141-151	tumor protein p53	Homo sapiens	22-25
32172299-4	2020	However, 17p-deleted, p53-mutated or IGHV-UM subgroups are generally resistant to FCR, and much better responses are seen with ibrutinib and venetoclax, frequently inducing MRD negativity that hopefully will be translated into durable remissions.	venetoclax	141-151	immunoglobulin heavy variable 3-69-1 (pseudogene)	Homo sapiens	37-41
32131385-4	2020	Accordingly, the approval of venetoclax (ABT-199), a small molecule BCL-2 inhibitor, in patients with chronic lymphocytic leukemia and acute myeloid leukemia has become the proverbial torchbearer for novel candidate drug approaches selectively targeting the BCL-2 superfamily.	venetoclax	29-39	BCL2 apoptosis regulator	Homo sapiens	68-73
32144272-1	2020	The BCL-2 antagonist venetoclax is highly effective in multiple myeloma (MM) patients exhibiting the 11;14 translocation, the mechanistic basis of which is unknown.	venetoclax	21-31	BCL2 apoptosis regulator	Homo sapiens	4-9
32231817-6	2020	Venetoclax, an inhibitor of the antiapoptotic protein BCL-2 used to treat chronic lymphocytic leukemia, is currently being evaluated in clinical trials as a monotherapy in high-risk myelodysplastic syndromes/acute myeloid leukemia.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	54-59
32126142-8	2020	The strongest combination was with the B-cell lymphoma 2 (BCL2) inhibitor venetoclax.	venetoclax	74-84	BCL2 apoptosis regulator	Homo sapiens	39-56
32126142-8	2020	The strongest combination was with the B-cell lymphoma 2 (BCL2) inhibitor venetoclax.	venetoclax	74-84	BCL2 apoptosis regulator	Homo sapiens	58-62
32131385-4	2020	Accordingly, the approval of venetoclax (ABT-199), a small molecule BCL-2 inhibitor, in patients with chronic lymphocytic leukemia and acute myeloid leukemia has become the proverbial torchbearer for novel candidate drug approaches selectively targeting the BCL-2 superfamily.	venetoclax	29-39	BCL2 apoptosis regulator	Homo sapiens	258-263
31533509-1	2020	Venetoclax is an oral selective BCL2 inhibitor which is highly efficacious in a variety of B-cell lymphoproliferative diseases (B-LPDs) due to their collective dependency on BCL2 over-expression as a central feature of their pathogenesis.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	32-36
32111748-6	2020	RESULTS: We demonstrated the cytotoxic effect of BCL-2 inhibition and that dual targeting of BCL-2 and BCR-ABL1 with venetoclax and nilotinib further increases this cytotoxicity.	venetoclax	117-127	BCL2 apoptosis regulator	Homo sapiens	93-98
32111748-6	2020	RESULTS: We demonstrated the cytotoxic effect of BCL-2 inhibition and that dual targeting of BCL-2 and BCR-ABL1 with venetoclax and nilotinib further increases this cytotoxicity.	venetoclax	117-127	BCR activator of RhoGEF and GTPase	Homo sapiens	103-111
31123034-2	2020	The BCL2 selective inhibitor venetoclax has potent anti-leukemia efficacy; however, resistance can occur due to its inability to inhibit MCL1, which is stabilized by the MAPK pathway.	venetoclax	29-39	BCL2 apoptosis regulator	Homo sapiens	4-8
32885175-6	2020	Manipulation of CELSR2 recapitulated glucocorticoid resistance in human leukemia cell lines and revealed a synergistic drug combination (prednisolone and venetoclax) that mitigated resistance in mouse xenograft models.	venetoclax	154-164	cadherin EGF LAG seven-pass G-type receptor 2	Homo sapiens	16-22
32085398-0	2020	Venetoclax, a BCL-2 Inhibitor, Enhances the Efficacy of Chemotherapeutic Agents in Wild-Type ABCG2-Overexpression-Mediated MDR Cancer Cells.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	14-19
32085398-0	2020	Venetoclax, a BCL-2 Inhibitor, Enhances the Efficacy of Chemotherapeutic Agents in Wild-Type ABCG2-Overexpression-Mediated MDR Cancer Cells.	venetoclax	0-10	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	93-98
32085398-2	2020	Venetoclax is a potent and selective BCL-2 inhibitor, approved by the FDA in 2016 for the treatment of patients with chronic lymphocytic leukemia (CLL).	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	37-42
32085398-3	2020	This study showed that, at a non-toxic concentration, venetoclax at 10 microM significantly reversed multidrug resistance (MDR) mediated by wild-type ABCG2, without significantly affecting MDR mediated by mutated ABCG2 (R482G and R482T) and ABCB1, while moderate or no reversal effects were observed at lower concentrations (0.5 to 1 microM).	venetoclax	54-64	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	150-155
32085398-3	2020	This study showed that, at a non-toxic concentration, venetoclax at 10 microM significantly reversed multidrug resistance (MDR) mediated by wild-type ABCG2, without significantly affecting MDR mediated by mutated ABCG2 (R482G and R482T) and ABCB1, while moderate or no reversal effects were observed at lower concentrations (0.5 to 1 microM).	venetoclax	54-64	ATP binding cassette subfamily B member 1	Homo sapiens	241-246
32085398-4	2020	The results showed that venetoclax increased the intracellular accumulation of chemotherapeutic agents, which was the result of directly blocking the wild-type ABCG2 efflux function and inhibiting the ATPase activity of ABCG2.	venetoclax	24-34	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	160-165
32085398-4	2020	The results showed that venetoclax increased the intracellular accumulation of chemotherapeutic agents, which was the result of directly blocking the wild-type ABCG2 efflux function and inhibiting the ATPase activity of ABCG2.	venetoclax	24-34	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	220-225
32085398-5	2020	Our study demonstrated that venetoclax potentiates the efficacy of wild-type ABCG2 substrate drugs.	venetoclax	28-38	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	77-82
32045477-3	2020	Early trials with venetoclax (ABT-199), a potent, selective inhibitor of BCL2, have revealed responses across a variety of hematologic malignancies.	venetoclax	30-37	BCL2 apoptosis regulator	Homo sapiens	73-77
31533509-1	2020	Venetoclax is an oral selective BCL2 inhibitor which is highly efficacious in a variety of B-cell lymphoproliferative diseases (B-LPDs) due to their collective dependency on BCL2 over-expression as a central feature of their pathogenesis.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	174-178
31640928-4	2020	Moreover, Venetoclax, the anti-Bcl-2 drug, and Cirmtuzumab, the monoclonal antibody against ROR1, are synergistic in killing CLL cells.	venetoclax	10-20	B cell leukemia/lymphoma 2	Mus musculus	31-36
31772331-10	2020	Accordingly, sensitivity of the CD40L-stimulated cells to S63845 was substantially restored by co-treatment with venetoclax, the BCL-XL-specific inhibitor or ibrutinib.	venetoclax	113-123	CD40 ligand	Homo sapiens	32-37
31837377-7	2020	Conversely, YM155 sensitized K562 cells to ABT-199 (a BCL2/BCL2L1 inhibitor), and circumvented K562 cell resistance to ABT-199 because of its inhibitory effect on survivin and MCL1 expression.	venetoclax	43-50	BCL2 apoptosis regulator	Homo sapiens	54-58
31171817-6	2020	Finally, (-)-SDS-1-021, the most promising synthetic rocaglate, was confirmed to be highly potent as a single agent, and displayed significant synergy with the BCL2 inhibitor ABT199 in inhibiting tumor growth and survival in primary lymphoma cells in vitro and in patient-derived xenograft mouse models.	venetoclax	175-181	BCL2 apoptosis regulator	Homo sapiens	160-164
32570264-0	2020	Sustained Complete Remission with Incomplete Hematologic Recovery (CRi) in a Patient with Relapsed AML and Concurrent BCR-ABL1 and CBFB Rearrangement Treated with a Combination of Venetoclax and 5-Azacytidine.	venetoclax	180-190	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-126
32570264-0	2020	Sustained Complete Remission with Incomplete Hematologic Recovery (CRi) in a Patient with Relapsed AML and Concurrent BCR-ABL1 and CBFB Rearrangement Treated with a Combination of Venetoclax and 5-Azacytidine.	venetoclax	180-190	core-binding factor subunit beta	Homo sapiens	131-135
33477155-10	2020	The use of venetoclax as a single drug to treat DLBCL BCL2 patients deserves further investigation.	venetoclax	11-21	BCL2 apoptosis regulator	Homo sapiens	54-58
31320594-1	2019	Purpose: To investigate the efficacy of the combination of the FLT3 inhibitors midostaurin or gilteritinib with the Bcl-2 inhibitor venetoclax in FLT3-internal tandem duplication (ITD) acute myeloid leukemia (AML) and the underlying molecular mechanism.Experimental Design: Using both FLT3-ITD cell lines and primary patient samples, Annexin V-FITC/propidium iodide staining and flow cytometry analysis were used to quantify cell death induced by midostaurin or gilteritinib, alone or in combination with venetoclax.	venetoclax	132-142	BCL2 apoptosis regulator	Homo sapiens	116-121
31209657-1	2019	BACKGROUND: Venetoclax is a selective B-cell lymphoma-2 (BCL-2) inhibitor approved for use as monotherapy or with rituximab in patients with chronic lymphocytic leukemia (CLL).	venetoclax	12-22	BCL2 apoptosis regulator	Homo sapiens	38-55
31209657-1	2019	BACKGROUND: Venetoclax is a selective B-cell lymphoma-2 (BCL-2) inhibitor approved for use as monotherapy or with rituximab in patients with chronic lymphocytic leukemia (CLL).	venetoclax	12-22	BCL2 apoptosis regulator	Homo sapiens	57-62
31484706-10	2019	Thus, fenretinide + venetoclax is a synergistic combination that warrants clinical testing in high BCL-2-expressing neuroblastoma.	venetoclax	20-30	BCL2 apoptosis regulator	Homo sapiens	99-104
31808888-3	2019	The BCL2 inhibitor venetoclax in combination with low-dose cytarabine (LDAC) or hypomethylating agents (HMAs) is safe and effective in older patients with newly diagnosed AML ineligible for intensive chemotherapy.	venetoclax	19-29	BCL2 apoptosis regulator	Homo sapiens	4-8
30861214-3	2019	These include venetoclax (BCL-2 inhibitor) in combination with hypomethylating agents (azacitidine or decitabine) or low-dose cytarabine (LDAC), and glasdegib (sonic hedgehog pathway inhibitor) in combination with LDAC.	venetoclax	14-24	BCL2 apoptosis regulator	Homo sapiens	26-31
31320594-9	2019	In vivo results show that gilteritinib in combination with venetoclax has therapeutic potential.Conclusions: Inhibition of Bcl-2 via venetoclax synergistically enhances the efficacy of midostaurin and gilteritinib in FLT3-mutated AML.	venetoclax	133-143	BCL2 apoptosis regulator	Homo sapiens	123-128
31320594-9	2019	In vivo results show that gilteritinib in combination with venetoclax has therapeutic potential.Conclusions: Inhibition of Bcl-2 via venetoclax synergistically enhances the efficacy of midostaurin and gilteritinib in FLT3-mutated AML.	venetoclax	133-143	fms related receptor tyrosine kinase 3	Homo sapiens	217-221
31320594-1	2019	Purpose: To investigate the efficacy of the combination of the FLT3 inhibitors midostaurin or gilteritinib with the Bcl-2 inhibitor venetoclax in FLT3-internal tandem duplication (ITD) acute myeloid leukemia (AML) and the underlying molecular mechanism.Experimental Design: Using both FLT3-ITD cell lines and primary patient samples, Annexin V-FITC/propidium iodide staining and flow cytometry analysis were used to quantify cell death induced by midostaurin or gilteritinib, alone or in combination with venetoclax.	venetoclax	132-142	fms related receptor tyrosine kinase 3	Homo sapiens	146-150
31320594-1	2019	Purpose: To investigate the efficacy of the combination of the FLT3 inhibitors midostaurin or gilteritinib with the Bcl-2 inhibitor venetoclax in FLT3-internal tandem duplication (ITD) acute myeloid leukemia (AML) and the underlying molecular mechanism.Experimental Design: Using both FLT3-ITD cell lines and primary patient samples, Annexin V-FITC/propidium iodide staining and flow cytometry analysis were used to quantify cell death induced by midostaurin or gilteritinib, alone or in combination with venetoclax.	venetoclax	132-142	fms related receptor tyrosine kinase 3	Homo sapiens	146-150
31320594-4	2019	Lentiviral overexpression of Mcl-1 was used to confirm its role in cell death induced by midostaurin or gilteritinib with venetoclax.	venetoclax	122-132	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	29-34
31320594-5	2019	Changes of Mcl-1 transcript levels were assessed by RT-PCR.Results: The combination of midostaurin or gilteritinib with venetoclax potently and synergistically induces apoptosis in FLT3-ITD AML cell lines and primary patient samples.	venetoclax	120-130	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	11-16
31320594-7	2019	Phosphorylated-ERK expression is induced by venetoclax but abolished by the combination of venetoclax with midostaurin or gilteritinib.	venetoclax	44-54	mitogen-activated protein kinase 1	Homo sapiens	15-18
31320594-9	2019	In vivo results show that gilteritinib in combination with venetoclax has therapeutic potential.Conclusions: Inhibition of Bcl-2 via venetoclax synergistically enhances the efficacy of midostaurin and gilteritinib in FLT3-mutated AML.	venetoclax	59-69	BCL2 apoptosis regulator	Homo sapiens	123-128
30872780-0	2019	Inhibition of SYK or BTK augments venetoclax sensitivity in SHP1-negative/BCL-2-positive diffuse large B-cell lymphoma.	venetoclax	34-44	spleen associated tyrosine kinase	Homo sapiens	14-17
31515455-2	2019	The BCL2 inhibitor venetoclax enhances responses to low intensity AML chemotherapy but its activity is limited by MCL1 upregulation.	venetoclax	19-29	BCL2 apoptosis regulator	Homo sapiens	4-8
31515455-2	2019	The BCL2 inhibitor venetoclax enhances responses to low intensity AML chemotherapy but its activity is limited by MCL1 upregulation.	venetoclax	19-29	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	114-118
31515455-3	2019	FLT3 inhibitors downregulate MCL1 and synergize with venetoclax in preclinical AML models.	venetoclax	53-63	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
31764121-3	2019	The approval of the BCL-2 inhibitor venetoclax for relapsed/refractory del(17p) CLL in 2016 represented the culmination of decades of molecular and clinical research and has paved the way for new combination therapy regimens in CLL, including the venetoclax + rituximab regimen approved for relapsed/refractory CLL in 2018 and the venetoclax + obinutuzumab regimen approved for frontline CLL treatment in 2019.	venetoclax	36-46	BCL2 apoptosis regulator	Homo sapiens	20-25
31353975-9	2019	Combinations of hypomethylating agents (HMA) with other compounds, and inhibitors of bcl2, such as venetoclax are being developed for higher-risk patients.	venetoclax	99-109	BCL2 apoptosis regulator	Homo sapiens	85-89
31175323-0	2019	Elevated expression of S100A8 and S100A9 correlates with resistance to the BCL-2 inhibitor venetoclax in AML.	venetoclax	91-101	S100 calcium binding protein A8	Homo sapiens	23-29
31175323-0	2019	Elevated expression of S100A8 and S100A9 correlates with resistance to the BCL-2 inhibitor venetoclax in AML.	venetoclax	91-101	S100 calcium binding protein A9	Homo sapiens	34-40
30872780-0	2019	Inhibition of SYK or BTK augments venetoclax sensitivity in SHP1-negative/BCL-2-positive diffuse large B-cell lymphoma.	venetoclax	34-44	Bruton tyrosine kinase	Homo sapiens	21-24
31175323-0	2019	Elevated expression of S100A8 and S100A9 correlates with resistance to the BCL-2 inhibitor venetoclax in AML.	venetoclax	91-101	BCL2 apoptosis regulator	Homo sapiens	75-80
30872780-0	2019	Inhibition of SYK or BTK augments venetoclax sensitivity in SHP1-negative/BCL-2-positive diffuse large B-cell lymphoma.	venetoclax	34-44	nuclear receptor subfamily 0 group B member 2	Homo sapiens	60-64
30872780-0	2019	Inhibition of SYK or BTK augments venetoclax sensitivity in SHP1-negative/BCL-2-positive diffuse large B-cell lymphoma.	venetoclax	34-44	BCL2 apoptosis regulator	Homo sapiens	74-79
30872780-1	2019	The BCL-2 inhibitor venetoclax has only limited activity in DLBCL despite frequent BCL-2 overexpression.	venetoclax	20-30	BCL2 apoptosis regulator	Homo sapiens	4-9
30872780-1	2019	The BCL-2 inhibitor venetoclax has only limited activity in DLBCL despite frequent BCL-2 overexpression.	venetoclax	20-30	BCL2 apoptosis regulator	Homo sapiens	83-88
30872780-3	2019	We report that pharmacological inhibition of SYK or BTK synergistically enhances venetoclax sensitivity in BCL-2-positive DLBCL cell lines with an activated BCR pathway in vitro and in a xenograft model in vivo, despite the only modest direct cytotoxic effect.	venetoclax	81-91	spleen associated tyrosine kinase	Homo sapiens	45-48
30872780-3	2019	We report that pharmacological inhibition of SYK or BTK synergistically enhances venetoclax sensitivity in BCL-2-positive DLBCL cell lines with an activated BCR pathway in vitro and in a xenograft model in vivo, despite the only modest direct cytotoxic effect.	venetoclax	81-91	Bruton tyrosine kinase	Homo sapiens	52-55
30872780-3	2019	We report that pharmacological inhibition of SYK or BTK synergistically enhances venetoclax sensitivity in BCL-2-positive DLBCL cell lines with an activated BCR pathway in vitro and in a xenograft model in vivo, despite the only modest direct cytotoxic effect.	venetoclax	81-91	BCL2 apoptosis regulator	Homo sapiens	107-112
31187237-2	2019	We hypothesized that the addition of venetoclax, a BCL-2 inhibitor, to AML patients who previously failed HMA might overcome resistance.	venetoclax	37-47	BCL2 apoptosis regulator	Homo sapiens	51-56
31233483-6	2019	BTK inhibitors have emerged as most important agents for the treatment of relapsed/refractory disease, but many other options exist, including rituximab, chemotherapy, immunomodulators, bortezomib and venetoclax that can be used in combination and sequentially.	venetoclax	201-211	Bruton tyrosine kinase	Homo sapiens	0-3
31182435-6	2019	We observed synergistic activity when YK-4-279 and TK-216 were combined with the BCL2 inhibitor venetoclax and with the immunomodulatory drug lenalidomide.	venetoclax	96-106	BCL2 apoptosis regulator	Homo sapiens	81-85
31542870-5	2019	Hence, with its novel mechanism of action and convenient oral once-daily regimen, venetoclax monotherapy or fixed 24-month combination therapy with rituximab represents an important option for treating RR CLL, including in patients with del(17p) or TP53 mutation and those failing a B cell receptor (BCR) inhibitor and/or chemotherapy.	venetoclax	82-92	tumor protein p53	Homo sapiens	249-253
30623427-0	2019	The Bcl-2 inhibitor venetoclax inhibits Nrf2 antioxidant pathway activation induced by hypomethylating agents in AML.	venetoclax	20-30	BCL2 apoptosis regulator	Homo sapiens	4-9
30949874-0	2019	Pharmacokinetics of the BCL-2 Inhibitor Venetoclax in Subjects with Hepatic Impairment.	venetoclax	40-50	BCL2 apoptosis regulator	Homo sapiens	24-29
31449511-0	2019	Venetoclax, the first BCL-2 inhibitor for use in patients with chronic lymphocytic leukemia.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	22-27
30623427-0	2019	The Bcl-2 inhibitor venetoclax inhibits Nrf2 antioxidant pathway activation induced by hypomethylating agents in AML.	venetoclax	20-30	NFE2 like bZIP transcription factor 2	Homo sapiens	40-44
30523053-2	2019	In this study, we showed the potential benefit of the BCL2 inhibitor venetoclax in the treatment of this disease.	venetoclax	69-79	BCL2 apoptosis regulator	Homo sapiens	54-58
31327069-2	2019	B cell receptor inhibitors that target either bruton tyrosine kinase (ibrutinib) or phosphatidylinositol 3-kinases (idelalisib and duvelisib) and BCL-2 inhibitor venetoclax have become the mainstay of treatment.	venetoclax	162-172	BCL2 apoptosis regulator	Homo sapiens	146-151
31048321-2	2019	Venetoclax, a selective BCL2 inhibitor, has received FDA approval for the treatment of AML.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	24-28
31048321-6	2019	We demonstrated that CLPB is upregulated in human AML, it is further induced upon acquisition of venetoclax resistance, and its ablation sensitizes AML to venetoclax.	venetoclax	97-107	caseinolytic mitochondrial matrix peptidase chaperone subunit B	Homo sapiens	21-25
31048321-11	2019	Targeting CLPB synergizes with venetoclax and the venetoclax/azacitidine combination in AML in a p53-independent manner.See related commentary by Savona and Rathmell, p. 831.This article is highlighted in the In This Issue feature, p. 813.	venetoclax	31-41	caseinolytic mitochondrial matrix peptidase chaperone subunit B	Homo sapiens	10-14
31048321-11	2019	Targeting CLPB synergizes with venetoclax and the venetoclax/azacitidine combination in AML in a p53-independent manner.See related commentary by Savona and Rathmell, p. 831.This article is highlighted in the In This Issue feature, p. 813.	venetoclax	31-41	tumor protein p53	Homo sapiens	97-100
31048321-11	2019	Targeting CLPB synergizes with venetoclax and the venetoclax/azacitidine combination in AML in a p53-independent manner.See related commentary by Savona and Rathmell, p. 831.This article is highlighted in the In This Issue feature, p. 813.	venetoclax	50-60	caseinolytic mitochondrial matrix peptidase chaperone subunit B	Homo sapiens	10-14
31048321-11	2019	Targeting CLPB synergizes with venetoclax and the venetoclax/azacitidine combination in AML in a p53-independent manner.See related commentary by Savona and Rathmell, p. 831.This article is highlighted in the In This Issue feature, p. 813.	venetoclax	50-60	tumor protein p53	Homo sapiens	97-100
31358732-4	2019	Here, we investigated the activity of the BCL-2 inhibitor venetoclax (VEN, ABT-199) in B-cell precursor acute lymphoblastic leukemia and found heterogeneous sensitivities in BCP-ALL cell lines and in a series of patient-derived primografts.	venetoclax	58-68	BCL2 apoptosis regulator	Homo sapiens	42-47
31308179-7	2019	Due to progression on initial treatment, she was treated with decitabine and venetoclax (BCL-2 inhibitor).	venetoclax	77-87	BCL2 apoptosis regulator	Homo sapiens	89-94
31167506-0	2019	The Novel TORC1/2 Kinase Inhibitor PQR620 Has Anti-Tumor Activity in Lymphomas as a Single Agent and in Combination with Venetoclax.	venetoclax	121-131	CREB regulated transcription coactivator 1	Homo sapiens	10-15
31154862-3	2019	Venetoclax selectively inhibits the B-cell lymphoma-2 (Bcl-2) protein, an anti-apoptotic protein that can be overexpressed in most B-cell lymphoid malignancies.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	36-53
31154862-3	2019	Venetoclax selectively inhibits the B-cell lymphoma-2 (Bcl-2) protein, an anti-apoptotic protein that can be overexpressed in most B-cell lymphoid malignancies.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	55-60
31293422-0	2019	Efficacy and Safety of Bcl-2 Inhibitor Venetoclax in Hematological Malignancy: A Systematic Review and Meta-Analysis of Clinical Trials.	venetoclax	39-49	BCL2 apoptosis regulator	Homo sapiens	23-28
31293422-2	2019	Venetoclax (ABT-199/GDC-0199) is a highly selective bioavailable inhibitor of BCL-2 protein, which is more effective and less valid against BCL-xL in BCL2-dependent leukemia and lymphoma cell.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	78-83
31293422-2	2019	Venetoclax (ABT-199/GDC-0199) is a highly selective bioavailable inhibitor of BCL-2 protein, which is more effective and less valid against BCL-xL in BCL2-dependent leukemia and lymphoma cell.	venetoclax	0-10	BCL2 like 1	Homo sapiens	140-146
31293422-2	2019	Venetoclax (ABT-199/GDC-0199) is a highly selective bioavailable inhibitor of BCL-2 protein, which is more effective and less valid against BCL-xL in BCL2-dependent leukemia and lymphoma cell.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	150-154
31293422-2	2019	Venetoclax (ABT-199/GDC-0199) is a highly selective bioavailable inhibitor of BCL-2 protein, which is more effective and less valid against BCL-xL in BCL2-dependent leukemia and lymphoma cell.	venetoclax	20-28	BCL2 apoptosis regulator	Homo sapiens	78-83
31293422-2	2019	Venetoclax (ABT-199/GDC-0199) is a highly selective bioavailable inhibitor of BCL-2 protein, which is more effective and less valid against BCL-xL in BCL2-dependent leukemia and lymphoma cell.	venetoclax	20-28	BCL2 apoptosis regulator	Homo sapiens	150-154
31209350-2	2019	Venetoclax is the first FDA-approved drug to reactivate apoptosis in cancer by selectively targeting an anti-apoptotic BCL-2 family member.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	119-124
31167506-5	2019	PQR620 was largely cytostatic, but the combination with the BCL2 inhibitor venetoclax led to cytotoxicity.	venetoclax	75-85	BCL2 apoptosis regulator	Homo sapiens	60-64
31115744-10	2019	Although vosaroxin could partially abrogate the increase of Mcl-1 protein induced by venetoclax, it could not abrogate the increased binding of Bim to Mcl-1 induced by venetoclax.	venetoclax	85-95	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	60-65
31166681-1	2019	BACKGROUND: The BCL2 inhibitor venetoclax has shown activity in patients with chronic lymphocytic leukemia (CLL), but its efficacy in combination with other agents in patients with CLL and coexisting conditions is not known.	venetoclax	31-41	BCL2 apoptosis regulator	Homo sapiens	16-20
31160589-4	2019	The pose of venetoclax in its binding site on BCL-2 reveals small but unexpected differences as compared to published structures of complexes with venetoclax analogues.	venetoclax	12-22	BCL2 apoptosis regulator	Homo sapiens	46-51
31115744-4	2019	Venetoclax (ABT-199), a selective Bcl-2 inhibitor, was recently approved for the treatment of acute myeloid leukemia.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	34-39
30487125-7	2019	As a consequence of enhanced canonical NF-kappaB target gene activation, both anti- and proapoptotic Bcl-2 family members were upregulated in BIRC3low primary CLL cells, which was associated with higher sensitivity to venetoclax treatment in vitro.	venetoclax	218-228	nuclear factor kappa B subunit 1	Homo sapiens	39-48
31115744-4	2019	Venetoclax (ABT-199), a selective Bcl-2 inhibitor, was recently approved for the treatment of acute myeloid leukemia.	venetoclax	12-19	BCL2 apoptosis regulator	Homo sapiens	34-39
30862722-4	2019	ABT-199, a selective Bcl-2 inhibitor, was effective in reducing leukemic burden in vitro and in vivo in patient-derived xenograft models of hypodiploid B-ALL.	venetoclax	0-7	BCL2 apoptosis regulator	Homo sapiens	21-26
30608891-8	2019	However, the potential synergistic anti-neoplastic effects of lenalidomide in combination with other biological agents, i.e. ibrutinib and venetoclax, especially in the management of p53-mutated cases, still remain an open issue.	venetoclax	139-149	tumor protein p53	Homo sapiens	183-186
30972300-2	2019	Recently, venetoclax, an inhibitor of the anti-apoptotic protein BCL-2, has been approved for the treatment of upfront AML in an unfit, elderly population.	venetoclax	10-20	BCL2 apoptosis regulator	Homo sapiens	65-70
30763062-3	2019	Here, we demonstrate that GLI1 imparts resistance to ~40 compounds, including FDA-approved drugs with disparate chemotypes ( e.g., methotrexate and venetoclax).	venetoclax	148-158	GLI family zinc finger 1	Homo sapiens	26-30
30850381-2	2019	Here, we report a phase 1b study investigating dose escalation of the BCL2 inhibitor, venetoclax, in combination with rituximab or obinutuzumab and cyclophosphamide, doxorubicin, vincristine, and prednisone (R-/G-CHOP) chemotherapy in B-cell NHL.	venetoclax	86-96	BCL2 apoptosis regulator	Homo sapiens	70-74
30850381-2	2019	Here, we report a phase 1b study investigating dose escalation of the BCL2 inhibitor, venetoclax, in combination with rituximab or obinutuzumab and cyclophosphamide, doxorubicin, vincristine, and prednisone (R-/G-CHOP) chemotherapy in B-cell NHL.	venetoclax	86-96	DNA damage inducible transcript 3	Homo sapiens	213-217
30725494-2	2019	The BCL-2 inhibitor venetoclax demonstrated activity as monotherapy and in combination with chemotherapy or HMA in AML.	venetoclax	20-30	BCL2 apoptosis regulator	Homo sapiens	4-9
31118772-1	2019	Venetoclax (ABT-199), a BH3-mimetic and selective BCL-2 inhibitor, was recently approved by the US Food and Drug Administration (FDA) for the treatment of acute myeloid leukemia (AML) in adult patients aged 75 years or older, or otherwise unable to tolerate intensive induction chemotherapy, in combination with either hypomethylating agents or low-dose cytarabine.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	50-55
31118772-1	2019	Venetoclax (ABT-199), a BH3-mimetic and selective BCL-2 inhibitor, was recently approved by the US Food and Drug Administration (FDA) for the treatment of acute myeloid leukemia (AML) in adult patients aged 75 years or older, or otherwise unable to tolerate intensive induction chemotherapy, in combination with either hypomethylating agents or low-dose cytarabine.	venetoclax	12-19	BCL2 apoptosis regulator	Homo sapiens	50-55
30487125-7	2019	As a consequence of enhanced canonical NF-kappaB target gene activation, both anti- and proapoptotic Bcl-2 family members were upregulated in BIRC3low primary CLL cells, which was associated with higher sensitivity to venetoclax treatment in vitro.	venetoclax	218-228	BCL2 apoptosis regulator	Homo sapiens	101-106
30487125-7	2019	As a consequence of enhanced canonical NF-kappaB target gene activation, both anti- and proapoptotic Bcl-2 family members were upregulated in BIRC3low primary CLL cells, which was associated with higher sensitivity to venetoclax treatment in vitro.	venetoclax	218-228	baculoviral IAP repeat containing 3	Homo sapiens	142-147
32009829-2	2019	Recently, a selective BCL-2 inhibitor ABT-199, venetoclax, has demonstrated remarkable activity in relapsed/refractory chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), both as a single agent and in combination with anti-CD20 immunotherapies, such as rituximab.	venetoclax	38-45	BCL2 apoptosis regulator	Homo sapiens	22-27
32009829-2	2019	Recently, a selective BCL-2 inhibitor ABT-199, venetoclax, has demonstrated remarkable activity in relapsed/refractory chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL), both as a single agent and in combination with anti-CD20 immunotherapies, such as rituximab.	venetoclax	38-45	solute carrier family 35 member B2	Homo sapiens	176-183
30415007-0	2019	Combined treatment of ABT199 and irinotecan suppresses KRAS-mutant lung cancer cells.	venetoclax	22-28	KRAS proto-oncogene, GTPase	Homo sapiens	55-59
31016071-7	2019	This time, the patient was started on venetoclax (BCL-2 inhibitor) and rituximab which he is tolerating well without any complications.	venetoclax	38-48	BCL2 apoptosis regulator	Homo sapiens	50-55
30514704-1	2019	The BCL2 inhibitor venetoclax induces high rates of durable remission in patients with previously treated chronic lymphocytic leukemia (CLL).	venetoclax	19-29	BCL2 apoptosis regulator	Homo sapiens	4-8
30514704-8	2019	SIGNIFICANCE: Why CLL recurs in patients who achieve remission with the BCL2 inhibitor venetoclax has been unknown.	venetoclax	87-97	BCL2 apoptosis regulator	Homo sapiens	72-76
30518523-0	2019	A Phase Ib Dose-Escalation and Expansion Study of the BCL2 Inhibitor Venetoclax Combined with Tamoxifen in ER and BCL2-Positive Metastatic Breast Cancer.	venetoclax	69-79	BCL2 apoptosis regulator	Homo sapiens	54-58
30518523-0	2019	A Phase Ib Dose-Escalation and Expansion Study of the BCL2 Inhibitor Venetoclax Combined with Tamoxifen in ER and BCL2-Positive Metastatic Breast Cancer.	venetoclax	69-79	BCL2 apoptosis regulator	Homo sapiens	114-118
30518523-1	2019	Venetoclax, a potent and selective BCL2 inhibitor, synergizes with endocrine therapy in preclinical models of ER-positive breast cancer.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	35-39
30741367-10	2019	Combination therapy that includes venetoclax (BCL2 inhibitor) with hypomethylating agents may also be appropriate for such patients.	venetoclax	34-44	BCL2 apoptosis regulator	Homo sapiens	46-50
30824486-2	2019	In this issue, Lok and colleagues diverge from this paradigm by combining the BCL2 inhibitor venetoclax with tamoxifen in a phase Ib clinical trial, building on preclinical work to demonstrate that targeting apoptosis could represent a promising new strategy in the treatment of breast cancer.See related article by Lok et al., p. 354.	venetoclax	93-103	serine/threonine kinase 10	Homo sapiens	15-18
30824486-2	2019	In this issue, Lok and colleagues diverge from this paradigm by combining the BCL2 inhibitor venetoclax with tamoxifen in a phase Ib clinical trial, building on preclinical work to demonstrate that targeting apoptosis could represent a promising new strategy in the treatment of breast cancer.See related article by Lok et al., p. 354.	venetoclax	93-103	BCL2 apoptosis regulator	Homo sapiens	78-82
30824486-2	2019	In this issue, Lok and colleagues diverge from this paradigm by combining the BCL2 inhibitor venetoclax with tamoxifen in a phase Ib clinical trial, building on preclinical work to demonstrate that targeting apoptosis could represent a promising new strategy in the treatment of breast cancer.See related article by Lok et al., p. 354.	venetoclax	93-103	serine/threonine kinase 10	Homo sapiens	316-319
30508305-14	2019	All 3 patients with disease progression received venetoclax and demonstrated suppression of BTK mutations.	venetoclax	49-59	Bruton tyrosine kinase	Homo sapiens	92-95
30647052-1	2019	The BCL2 inhibitor venetoclax plus the MDM2 inhibitor idasanutlin may be effective in treating relapsed/refractory acute myeloid leukemia.	venetoclax	19-29	BCL2 apoptosis regulator	Homo sapiens	4-8
30715623-6	2019	The addition of the BCL2 inhibitor venetoclax appears to markedly improve the results of hypomethylating agents.	venetoclax	35-45	BCL2 apoptosis regulator	Homo sapiens	20-24
29930300-4	2019	RPL10 R98S selective sensitivity to the clinically available Bcl-2 inhibitor Venetoclax (ABT-199) was supported by suppression of splenomegaly and the absence of human leukemia cells in the blood of T-ALL xenografted mice.	venetoclax	77-87	BCL2 apoptosis regulator	Homo sapiens	61-66
30190341-0	2019	Efficacy of venetoclax monotherapy in patients with relapsed, refractory mantle cell lymphoma after Bruton tyrosine kinase inhibitor therapy.	venetoclax	12-22	Bruton tyrosine kinase	Homo sapiens	100-122
29930300-4	2019	RPL10 R98S selective sensitivity to the clinically available Bcl-2 inhibitor Venetoclax (ABT-199) was supported by suppression of splenomegaly and the absence of human leukemia cells in the blood of T-ALL xenografted mice.	venetoclax	77-87	ribosomal protein L10	Homo sapiens	0-5
30701031-4	2018	This study investigated the potential synergistic relationship between Venetoclax and the MCL-1 inhibitor S63845 in AML cells.	venetoclax	71-81	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	90-95
30611710-4	2019	A corollary of this is that CLL is very sensitive to the anti BCL2 drug venetoclax that can induce complete remission in CLL patients.	venetoclax	72-82	BCL2 apoptosis regulator	Homo sapiens	62-66
31084767-3	2019	Venetoclax, a BCL-2 inhibitor is a promising agent, as BCL-2 overexpression is present in 84% of acute myeloid leukemia patients at diagnosis and 95% of patients at relapse and has been associated with leukemia cell survival, chemotherapy resistance and poor prognosis.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	14-19
31084767-3	2019	Venetoclax, a BCL-2 inhibitor is a promising agent, as BCL-2 overexpression is present in 84% of acute myeloid leukemia patients at diagnosis and 95% of patients at relapse and has been associated with leukemia cell survival, chemotherapy resistance and poor prognosis.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	55-60
29846950-5	2019	In the first section, the design and development of BCL-2/BCL-XL dual inhibitor navitoclax, as well as the recent advances and clinical experience with selective BCL-2 inhibitor venetoclax, were synopsized.	venetoclax	178-188	BCL2 apoptosis regulator	Homo sapiens	162-167
30008477-0	2019	The MCL1-specific inhibitor S63845 acts synergistically with venetoclax/ABT-199 to induce apoptosis in T-cell acute lymphoblastic leukemia cells.	venetoclax	61-71	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	4-8
30008477-0	2019	The MCL1-specific inhibitor S63845 acts synergistically with venetoclax/ABT-199 to induce apoptosis in T-cell acute lymphoblastic leukemia cells.	venetoclax	72-79	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	4-8
30572618-0	2018	Synergistic AML Cell Death Induction by Marine Cytotoxin (+)-1(R), 6(S), 1"(R), 6"(S), 11(R), 17(S)-Fistularin-3 and Bcl-2 Inhibitor Venetoclax.	venetoclax	133-143	BCL2 apoptosis regulator	Homo sapiens	117-122
30537511-5	2018	The BCL-2 inhibitor venetoclax has been approved for treatment of refractory chronic lymphocytic leukemia and this drug and inhibitors of pro-survival MCL-1 and BCL-XL are being tested in diverse malignancies.	venetoclax	20-30	BCL2 apoptosis regulator	Homo sapiens	4-9
30466743-2	2018	This year, 2018, already has seen the regulatory approval of the BCL2 inhibitor venetoclax in the form of breakthrough designation and the IDH1 inhibitor ivosidenib received full FDA approval.	venetoclax	80-90	BCL2 apoptosis regulator	Homo sapiens	65-69
30152528-0	2018	Biclonal IGHV-4-34 hairy cell leukemia variant and CLL - successful treatment with ibrutinib and venetoclax.	venetoclax	97-107	immunoglobulin heavy variable 4-34	Homo sapiens	9-18
30185627-2	2018	Induced myeloid leukemia cell differentiation protein (MCL1), an antiapoptotic BCL2 family member, is commonly upregulated in AML cells and is often a primary mode of resistance to treatment with the BCL2 inhibitor venetoclax.	venetoclax	215-225	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	55-59
30185627-2	2018	Induced myeloid leukemia cell differentiation protein (MCL1), an antiapoptotic BCL2 family member, is commonly upregulated in AML cells and is often a primary mode of resistance to treatment with the BCL2 inhibitor venetoclax.	venetoclax	215-225	BCL2 apoptosis regulator	Homo sapiens	79-83
30185627-2	2018	Induced myeloid leukemia cell differentiation protein (MCL1), an antiapoptotic BCL2 family member, is commonly upregulated in AML cells and is often a primary mode of resistance to treatment with the BCL2 inhibitor venetoclax.	venetoclax	215-225	BCL2 apoptosis regulator	Homo sapiens	200-204
30527922-7	2018	The kinase inhibitor idelalisib (plus rituximab) and the bcl2 inhibitor venetoclax are other novel compounds, which showed great efficacy in relapsed CLL even in unfit patients.	venetoclax	72-82	BCL2 apoptosis regulator	Homo sapiens	57-61
30510014-1	2018	Unleashing blocked apoptosis has emerged as an important tool in treating cancer as shown by the recent success of the BCL2 inhibitor venetoclax.	venetoclax	134-144	BCL2 apoptosis regulator	Homo sapiens	119-123
30428277-2	2018	Venetoclax (ABT-199) is a BCL-2 inhibitor recently approved by the US food and drug administration for treatment of chronic lymphocytic leukemia but the drug has shown activity in a number of hematological malignancies.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	26-31
30155839-4	2018	METHODS: The synergistic effect of gemcitabine combined with specific B cell CLL/lymphoma 2 (Bcl-2) inhibitor ABT-199 against pancreatic cancer was tested using cell viability, cell cycle, and apoptosis assays in vitro and in an MIA Paca-2 xenograft model in vivo.	venetoclax	110-117	B cell leukemia/lymphoma 2	Mus musculus	70-91
30155839-4	2018	METHODS: The synergistic effect of gemcitabine combined with specific B cell CLL/lymphoma 2 (Bcl-2) inhibitor ABT-199 against pancreatic cancer was tested using cell viability, cell cycle, and apoptosis assays in vitro and in an MIA Paca-2 xenograft model in vivo.	venetoclax	110-117	B cell leukemia/lymphoma 2	Mus musculus	93-98
29912596-5	2018	In this review, we will discuss the currently most active two drugs: ibrutinib and venetoclax, both of which have shown high response rates in R/R MCL.	venetoclax	83-93	C-type lectin domain family 4 member D	Homo sapiens	147-150
30417424-7	2018	Indeed, low doses of the BCL2 inhibitor, venetoclax, in combination with the BETi was a potent combination in t(8;21) containing cells.	venetoclax	41-51	BCL2 apoptosis regulator	Homo sapiens	25-29
30420752-3	2018	In this report, we show that treatment of older patients with AML with the B cell lymphoma 2 (BCL-2) inhibitor venetoclax in combination with azacitidine results in deep and durable remissions and is superior to conventional treatments.	venetoclax	111-121	BCL2 apoptosis regulator	Homo sapiens	75-92
30420752-3	2018	In this report, we show that treatment of older patients with AML with the B cell lymphoma 2 (BCL-2) inhibitor venetoclax in combination with azacitidine results in deep and durable remissions and is superior to conventional treatments.	venetoclax	111-121	BCL2 apoptosis regulator	Homo sapiens	94-99
30417424-8	2018	Thus, BET inhibitors that affect MYC and BCL2 expression should be considered for combination therapy with venetoclax.	venetoclax	107-117	delta/notch like EGF repeat containing	Homo sapiens	6-9
30417424-8	2018	Thus, BET inhibitors that affect MYC and BCL2 expression should be considered for combination therapy with venetoclax.	venetoclax	107-117	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	33-36
30278333-1	2018	By taking advantage of the apoptosis-inducing capacity of artemisinin derivatives, we developed several series of compounds by merging the basic structural elements of the natural product artemisinin into the P2 interaction pocket of the clinically prescribed Bcl-2 inhibitor venetoclax.	venetoclax	276-286	BCL2 apoptosis regulator	Homo sapiens	260-265
30278333-5	2018	Though further structural optimization is needed to improve the cellular absorptive permeability, the current approach represents an alternative strategy to develop novel Bcl-2 inhibitors with greater selectivity over Bcl-xL, which is related to the off-target adverse effects of venetoclax.	venetoclax	280-290	BCL2 apoptosis regulator	Homo sapiens	171-176
30278333-5	2018	Though further structural optimization is needed to improve the cellular absorptive permeability, the current approach represents an alternative strategy to develop novel Bcl-2 inhibitors with greater selectivity over Bcl-xL, which is related to the off-target adverse effects of venetoclax.	venetoclax	280-290	BCL2 like 1	Homo sapiens	218-224
30264382-2	2018	This study evaluated the effect of azithromycin, a commonly used antibiotic in cancer patients and a P-gp inhibitor, on the pharmacokinetics of venetoclax.	venetoclax	144-154	ATP binding cassette subfamily B member 1	Homo sapiens	101-105
30021909-3	2018	MCL1 was also targeted directly using RNAi, CRISPR, or an MCL1-specific BH3 mimetic, S63845.Results: We initially found that MCL1 depletion or inhibition markedly sensitized prostate cancer cells to apoptosis mediated by navitoclax, but not venetoclax, in vitro and in vivo, indicating that they are primed to undergo apoptosis and protected by MCL1 and BCLXL.	venetoclax	241-251	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	0-4
30264382-0	2018	Effect of Azithromycin on Venetoclax Pharmacokinetics in Healthy Volunteers: Implications for Dosing Venetoclax with P-gp Inhibitors.	venetoclax	101-111	ATP binding cassette subfamily B member 1	Homo sapiens	117-121
30021909-1	2018	Purpose: Clinically available BH3 mimetic drugs targeting BCLXL and/or BCL2 (navitoclax and venetoclax, respectively) are effective in some hematologic malignancies, but have limited efficacy in solid tumors.	venetoclax	92-102	BCL2 like 1	Homo sapiens	58-63
30406027-4	2018	The BCL-2-selective inhibitor venetoclax has been approved for use in chronic lymphocytic leukemia and is now being studied in a number of other hematologic malignancies.	venetoclax	30-40	BCL2 apoptosis regulator	Homo sapiens	4-9
30021909-1	2018	Purpose: Clinically available BH3 mimetic drugs targeting BCLXL and/or BCL2 (navitoclax and venetoclax, respectively) are effective in some hematologic malignancies, but have limited efficacy in solid tumors.	venetoclax	92-102	BCL2 apoptosis regulator	Homo sapiens	71-75
29785506-4	2018	Venetoclax, a BCL-2 inhibitor, has been approved for the treatment of relapsed and/or refractory chronic lymphoid leukemia.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	14-19
30012635-4	2018	The US Food and Drug Administration (FDA)-approved BCL-2 inhibitor venetoclax was first proven to be highly effective in chronic lymphocytic leukemia and some B-cell non-Hodgkin lymphoma subtypes.	venetoclax	67-77	BCL2 apoptosis regulator	Homo sapiens	51-56
29333561-0	2018	Pharmacokinetics of the B-Cell Lymphoma 2 (Bcl-2) Inhibitor Venetoclax in Female Subjects with Systemic Lupus Erythematosus.	venetoclax	60-70	BCL2 apoptosis regulator	Homo sapiens	24-41
30055346-1	2018	Several newly developed drugs including JQ1 (BET inhibitor), ABT199 (BCL2 inhibitor), and bortezomib (proteasome inhibitor) may offer novel therapeutic strategies for aggressive diffuse large B-cell lymphoma (DLBCL).	venetoclax	61-67	BCL2 apoptosis regulator	Homo sapiens	69-73
30017199-10	2018	Given that ABT-199 induces apoptosis in NPC cells through the Bcl-2/Noxa/Mcl-1 axis, treatment avenues further targeting this pathway should be promising.	venetoclax	11-18	B cell leukemia/lymphoma 2	Mus musculus	62-67
30017199-10	2018	Given that ABT-199 induces apoptosis in NPC cells through the Bcl-2/Noxa/Mcl-1 axis, treatment avenues further targeting this pathway should be promising.	venetoclax	11-18	phorbol-12-myristate-13-acetate-induced protein 1	Mus musculus	68-72
30017199-10	2018	Given that ABT-199 induces apoptosis in NPC cells through the Bcl-2/Noxa/Mcl-1 axis, treatment avenues further targeting this pathway should be promising.	venetoclax	11-18	myeloid cell leukemia sequence 1	Mus musculus	73-78
29895707-1	2018	Purpose: The oral BCL-2 inhibitor venetoclax is an effective therapy for patients with relapsed/refractory (R/R) chronic lymphocytic leukemia (CLL), including disease with high-risk genomic features such as chromosome 17p deletion [del(17p)] or progressive disease following B-cell receptor pathway inhibitors.Patients and Methods: We conducted a comprehensive analysis of the safety of 400 mg daily venetoclax monotherapy in 350 patients with CLL using an integrated dataset from three phase I/II studies.Results: Median age was 66 years and 60% had del(17p).	venetoclax	34-44	BCL2 apoptosis regulator	Homo sapiens	18-23
29895707-1	2018	Purpose: The oral BCL-2 inhibitor venetoclax is an effective therapy for patients with relapsed/refractory (R/R) chronic lymphocytic leukemia (CLL), including disease with high-risk genomic features such as chromosome 17p deletion [del(17p)] or progressive disease following B-cell receptor pathway inhibitors.Patients and Methods: We conducted a comprehensive analysis of the safety of 400 mg daily venetoclax monotherapy in 350 patients with CLL using an integrated dataset from three phase I/II studies.Results: Median age was 66 years and 60% had del(17p).	venetoclax	400-410	BCL2 apoptosis regulator	Homo sapiens	18-23
29333561-0	2018	Pharmacokinetics of the B-Cell Lymphoma 2 (Bcl-2) Inhibitor Venetoclax in Female Subjects with Systemic Lupus Erythematosus.	venetoclax	60-70	BCL2 apoptosis regulator	Homo sapiens	43-48
29333561-1	2018	BACKGROUND AND OBJECTIVE: Venetoclax is an oral selective Bcl-2 inhibitor approved for the treatment of patients with chronic lymphocytic leukemia with 17p deletion.	venetoclax	26-36	BCL2 apoptosis regulator	Homo sapiens	58-63
30076373-3	2018	The oral drug venetoclax is the first-in-class Bcl-2-specific BH3 mimetic.	venetoclax	14-24	BCL2 apoptosis regulator	Homo sapiens	47-52
29880613-1	2018	Venetoclax is a BCL2 inhibitor approved for 17p-deleted relapsed/refractory chronic lymphocytic leukemia with activity following kinase inhibitors.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	16-20
29595064-1	2018	Venetoclax is a highly selective, potent BCL-2 inhibitor that is approved for some patients previously treated for chronic lymphocytic leukemia, and has shown promising activity in adult studies across several hematologic malignancies.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	41-46
29027832-3	2018	Since venetoclax is an inhibitor of P glycoprotein (P-gp) transporter, a study was conducted in healthy, female volunteers to evaluate the effect of venetoclax on the pharmacokinetics of digoxin, a P-gp probe substrate.	venetoclax	6-16	ATP binding cassette subfamily B member 1	Homo sapiens	36-50
29027832-3	2018	Since venetoclax is an inhibitor of P glycoprotein (P-gp) transporter, a study was conducted in healthy, female volunteers to evaluate the effect of venetoclax on the pharmacokinetics of digoxin, a P-gp probe substrate.	venetoclax	6-16	ATP binding cassette subfamily B member 1	Homo sapiens	52-56
29027832-11	2018	The results of this study indicate that venetoclax can increase the concentrations of P-gp substrates.	venetoclax	40-50	ATP binding cassette subfamily B member 1	Homo sapiens	86-90
29027832-12	2018	Narrow therapeutic index P-gp substrates should be administered six hours prior to venetoclax to minimise the potential interaction.	venetoclax	83-93	ATP binding cassette subfamily B member 1	Homo sapiens	25-29
29982865-4	2018	Herein, we will discuss the mechanism and rationale of BCL-2 inhibition in acute myeloid leukemia (AML) and myelodysplastic syndromes (MDS) with an overview of the selective BCL-2 inhibitor venetoclax.	venetoclax	190-200	BCL2 apoptosis regulator	Homo sapiens	174-179
30067771-6	2018	Synergy with duvelisib was prominent in lymphoma lines with approved and emerging drugs used to treat HM, including dexamethasone, ibrutinib, and the BCL-2 inhibitor venetoclax.	venetoclax	166-176	BCL2 apoptosis regulator	Homo sapiens	150-155
29944468-9	2018	The Bcl-2 selective inhibitor ABT-199 reduces particulate matter-induced lung inflammation by inducing the apoptosis of neutrophils and might be a promising drug for the treatment of particulate matter-induced lung inflammation.	venetoclax	30-37	B cell leukemia/lymphoma 2	Mus musculus	4-9
29882807-7	2018	In addition, IDH1 inhibitors are in ongoing clinical studies, and the oral BCL-2 inhibitor venetoclax shows preliminary efficacy in this subset of patients.	venetoclax	91-101	BCL2 apoptosis regulator	Homo sapiens	75-80
29559471-2	2018	Here, we assessed the efficacy of coadministration of the PI3K/mTOR inhibitor GDC-0980 or the p110beta-sparing PI3K inhibitor taselisib with the selective BCL-2 antagonist venetoclax in AML cells.	venetoclax	172-182	BCL2 apoptosis regulator	Homo sapiens	155-160
29559471-4	2018	Venetoclax/GDC-0980 coadministration induced rapid and pronounced BAX mitochondrial translocation, cytochrome c release, and apoptosis in various AML cell lines in association with AKT/mTOR inactivation and MCL-1 downregulation; ectopic expression of MCL-1 significantly protected cells from this regimen.	venetoclax	0-10	BCL2 associated X, apoptosis regulator	Homo sapiens	66-69
29559471-4	2018	Venetoclax/GDC-0980 coadministration induced rapid and pronounced BAX mitochondrial translocation, cytochrome c release, and apoptosis in various AML cell lines in association with AKT/mTOR inactivation and MCL-1 downregulation; ectopic expression of MCL-1 significantly protected cells from this regimen.	venetoclax	0-10	cytochrome c, somatic	Homo sapiens	99-111
29559471-4	2018	Venetoclax/GDC-0980 coadministration induced rapid and pronounced BAX mitochondrial translocation, cytochrome c release, and apoptosis in various AML cell lines in association with AKT/mTOR inactivation and MCL-1 downregulation; ectopic expression of MCL-1 significantly protected cells from this regimen.	venetoclax	0-10	AKT serine/threonine kinase 1	Homo sapiens	181-184
29559471-4	2018	Venetoclax/GDC-0980 coadministration induced rapid and pronounced BAX mitochondrial translocation, cytochrome c release, and apoptosis in various AML cell lines in association with AKT/mTOR inactivation and MCL-1 downregulation; ectopic expression of MCL-1 significantly protected cells from this regimen.	venetoclax	0-10	mechanistic target of rapamycin kinase	Homo sapiens	185-189
29559471-4	2018	Venetoclax/GDC-0980 coadministration induced rapid and pronounced BAX mitochondrial translocation, cytochrome c release, and apoptosis in various AML cell lines in association with AKT/mTOR inactivation and MCL-1 downregulation; ectopic expression of MCL-1 significantly protected cells from this regimen.	venetoclax	0-10	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	207-212
29559471-4	2018	Venetoclax/GDC-0980 coadministration induced rapid and pronounced BAX mitochondrial translocation, cytochrome c release, and apoptosis in various AML cell lines in association with AKT/mTOR inactivation and MCL-1 downregulation; ectopic expression of MCL-1 significantly protected cells from this regimen.	venetoclax	0-10	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	251-256
29559471-6	2018	Venetoclax/GDC-0980 markedly induced apoptosis in primitive CD34+/38-/123+ AML cell populations but not in normal hematopoietic progenitor CD34+ cells.	venetoclax	0-10	CD34 molecule	Homo sapiens	60-64
29559471-11	2018	Collectively, these studies demonstrate that venetoclax/GDC-0980 exhibits potent anti-AML activity primarily through BAX and, to a lesser extent, BAK.	venetoclax	45-55	BCL2 associated X, apoptosis regulator	Homo sapiens	117-120
28838268-1	2018	Venetoclax (ABT-199) is a Bcl-2-specific BH3-mimetic that has shown significant promise in certain subtypes of CLL as well as in several other hematologic malignancies.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	26-31
29058801-0	2018	Pharmacokinetics of the BCL-2 Inhibitor Venetoclax in Healthy Chinese Subjects.	venetoclax	40-50	BCL2 apoptosis regulator	Homo sapiens	24-29
29561706-4	2018	Among these new drugs, venetoclax, an orally bioavailable BCL2 inhibitor, has shown high efficacy also in relapsed/refractory CLL with TP53 disruption.	venetoclax	23-33	BCL2 apoptosis regulator	Homo sapiens	58-62
29561706-4	2018	Among these new drugs, venetoclax, an orally bioavailable BCL2 inhibitor, has shown high efficacy also in relapsed/refractory CLL with TP53 disruption.	venetoclax	23-33	tumor protein p53	Homo sapiens	135-139
29561706-9	2018	Venetoclax has achieved responses also in patients with TP53 disruption.	venetoclax	0-10	tumor protein p53	Homo sapiens	56-60
29666304-2	2018	A recent phase I first-in-human study of the BCL-2 inhibitor venetoclax in non-Hodgkin lymphoma showed an overall response rate of 44%.	venetoclax	61-71	BCL2 apoptosis regulator	Homo sapiens	45-50
29666304-5	2018	We demonstrate that DLBCL and MCL cell lines, primary patient samples, and PDX mouse models expressing high BCL-2 levels are extremely sensitive to venetoclax treatment.	venetoclax	148-158	B cell leukemia/lymphoma 2	Mus musculus	108-113
29666304-7	2018	Short- and long-term exposure to venetoclax inhibited PTEN expression, leading to enhanced AKT pathway activation and concomitant susceptibility to PI3K/AKT inhibition.	venetoclax	33-43	phosphatase and tensin homolog	Homo sapiens	54-58
29666304-7	2018	Short- and long-term exposure to venetoclax inhibited PTEN expression, leading to enhanced AKT pathway activation and concomitant susceptibility to PI3K/AKT inhibition.	venetoclax	33-43	AKT serine/threonine kinase 1	Homo sapiens	91-94
29666304-7	2018	Short- and long-term exposure to venetoclax inhibited PTEN expression, leading to enhanced AKT pathway activation and concomitant susceptibility to PI3K/AKT inhibition.	venetoclax	33-43	AKT serine/threonine kinase 1	Homo sapiens	153-156
29767411-0	2018	MEK1/2 inhibition by binimetinib is effective as a single agent and potentiates the actions of Venetoclax and ABT-737 under conditions that mimic the chronic lymphocytic leukaemia (CLL) tumour microenvironment.	venetoclax	95-105	mitogen-activated protein kinase kinase 1	Homo sapiens	0-6
30073206-0	2018	BCL2 inhibitor ABT-199 and JNK inhibitor SP600125 exhibit synergistic cytotoxicity against imatinib-resistant Ph+ ALL cells.	venetoclax	15-22	BCL2 apoptosis regulator	Homo sapiens	0-4
29752258-2	2018	The availability novel agents, including the B-cell receptor inhibitors ibrutinib, acalabrutinib, and idelalisib, as well as venetoclax, which targets the BCL2 pathway, and the success of these agents in treating high-risk disease patients have made it more difficult to assess who should be considered for allo-SCT and when in the treatment course.	venetoclax	125-135	BCL2 apoptosis regulator	Homo sapiens	155-159
29899021-3	2018	We report that inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) using statins enhances the proapoptotic activity of the B cell lymphoma-2 (BCL2) inhibitor venetoclax (ABT-199) in primary leukemia and lymphoma cells but not in normal human peripheral blood mononuclear cells.	venetoclax	176-186	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	29-76
29899021-3	2018	We report that inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) using statins enhances the proapoptotic activity of the B cell lymphoma-2 (BCL2) inhibitor venetoclax (ABT-199) in primary leukemia and lymphoma cells but not in normal human peripheral blood mononuclear cells.	venetoclax	176-186	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	78-83
29899021-3	2018	We report that inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) using statins enhances the proapoptotic activity of the B cell lymphoma-2 (BCL2) inhibitor venetoclax (ABT-199) in primary leukemia and lymphoma cells but not in normal human peripheral blood mononuclear cells.	venetoclax	176-186	BCL2 apoptosis regulator	Homo sapiens	141-158
29899021-3	2018	We report that inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) using statins enhances the proapoptotic activity of the B cell lymphoma-2 (BCL2) inhibitor venetoclax (ABT-199) in primary leukemia and lymphoma cells but not in normal human peripheral blood mononuclear cells.	venetoclax	176-186	BCL2 apoptosis regulator	Homo sapiens	160-164
29899021-3	2018	We report that inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) using statins enhances the proapoptotic activity of the B cell lymphoma-2 (BCL2) inhibitor venetoclax (ABT-199) in primary leukemia and lymphoma cells but not in normal human peripheral blood mononuclear cells.	venetoclax	188-195	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	29-76
29899021-3	2018	We report that inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) using statins enhances the proapoptotic activity of the B cell lymphoma-2 (BCL2) inhibitor venetoclax (ABT-199) in primary leukemia and lymphoma cells but not in normal human peripheral blood mononuclear cells.	venetoclax	188-195	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	78-83
29899021-3	2018	We report that inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) using statins enhances the proapoptotic activity of the B cell lymphoma-2 (BCL2) inhibitor venetoclax (ABT-199) in primary leukemia and lymphoma cells but not in normal human peripheral blood mononuclear cells.	venetoclax	188-195	BCL2 apoptosis regulator	Homo sapiens	141-158
29899021-3	2018	We report that inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR) using statins enhances the proapoptotic activity of the B cell lymphoma-2 (BCL2) inhibitor venetoclax (ABT-199) in primary leukemia and lymphoma cells but not in normal human peripheral blood mononuclear cells.	venetoclax	188-195	BCL2 apoptosis regulator	Homo sapiens	160-164
29761903-2	2018	ABT-199 is a specific Bcl-2 inhibitor in clinical trials for MM; however, its activity as a single agent was limited to myeloma patients with the t(11;14) translocation who acquire resistance due to co-expression of Mcl-1 and Bcl-xL.	venetoclax	0-7	BCL2 apoptosis regulator	Homo sapiens	22-27
29761903-2	2018	ABT-199 is a specific Bcl-2 inhibitor in clinical trials for MM; however, its activity as a single agent was limited to myeloma patients with the t(11;14) translocation who acquire resistance due to co-expression of Mcl-1 and Bcl-xL.	venetoclax	0-7	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	216-221
29761903-2	2018	ABT-199 is a specific Bcl-2 inhibitor in clinical trials for MM; however, its activity as a single agent was limited to myeloma patients with the t(11;14) translocation who acquire resistance due to co-expression of Mcl-1 and Bcl-xL.	venetoclax	0-7	BCL2 like 1	Homo sapiens	226-232
29477371-2	2018	Whereas nonselective agents have been limited by their affinity to different BCL2 members, thus inducing excessive toxicity, the highly selective BCL2 inhibitor venetoclax (ABT-199, Venclexta ) has an acceptable safety profile.	venetoclax	161-171	BCL2 apoptosis regulator	Homo sapiens	146-150
29477371-2	2018	Whereas nonselective agents have been limited by their affinity to different BCL2 members, thus inducing excessive toxicity, the highly selective BCL2 inhibitor venetoclax (ABT-199, Venclexta ) has an acceptable safety profile.	venetoclax	173-180	BCL2 apoptosis regulator	Homo sapiens	146-150
29477371-2	2018	Whereas nonselective agents have been limited by their affinity to different BCL2 members, thus inducing excessive toxicity, the highly selective BCL2 inhibitor venetoclax (ABT-199, Venclexta ) has an acceptable safety profile.	venetoclax	182-191	BCL2 apoptosis regulator	Homo sapiens	146-150
29982865-8	2018	BCL-2 inhibition with venetoclax is well tolerated and active in older patients with newly diagnosed AML and in the relapsed setting has activity that may be improved in combination with other therapies.	venetoclax	22-32	BCL2 apoptosis regulator	Homo sapiens	0-5
29353886-0	2018	The BET bromodomain inhibitor CPI203 overcomes resistance to ABT-199 (venetoclax) by downregulation of BFL-1/A1 in in vitro and in vivo models of MYC+/BCL2+ double hit lymphoma.	venetoclax	61-68	delta/notch like EGF repeat containing	Homo sapiens	4-7
29477250-5	2018	The impressive efficacy of kinase inhibitors ibrutinib and idelalisib and the BCL-2 antagonist venetoclax have changed the standard of care in specific subsets of patients.	venetoclax	95-105	BCL2 apoptosis regulator	Homo sapiens	78-83
29305552-2	2018	Venetoclax is a selective, orally bioavailable BCL-2 inhibitor with activity in patients with CLL, including those who are heavily pretreated or have 17p deletion.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	47-52
29644450-1	2018	PURPOSE REVIEW: B cell signaling agents, including ibrutinib, idelalisib, and the BCL-2 inhibitor venetoclax have become an integral part of therapy for patients with non-Hodgkin"s lymphomas.	venetoclax	98-108	BCL2 apoptosis regulator	Homo sapiens	82-87
29302721-1	2018	PURPOSE: Venetoclax is a selective BCL-2 inhibitor indicated for the treatment of patients with chronic lymphocytic leukemia (CLL).	venetoclax	9-19	BCL2 apoptosis regulator	Homo sapiens	35-40
29302721-10	2018	CONCLUSION: After completion of the dose ramp-up, venetoclax dose reductions of at least 75% are recommended when administered concomitantly with strong CYP3A inhibitors to maintain venetoclax exposures within the established therapeutic window for CLL treatment.	venetoclax	50-60	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	153-158
29099493-6	2018	Among several CLL-targeted agents, venetoclax, when combined with acalabrutinib, showed optimal complementary activity in vitro, ex vivo and in vivo in TCL-1 adoptive transfer mouse model system of CLL.	venetoclax	35-45	T cell lymphoma breakpoint 1	Mus musculus	152-157
29353886-0	2018	The BET bromodomain inhibitor CPI203 overcomes resistance to ABT-199 (venetoclax) by downregulation of BFL-1/A1 in in vitro and in vivo models of MYC+/BCL2+ double hit lymphoma.	venetoclax	61-68	BCL2 related protein A1	Homo sapiens	103-108
29353886-4	2018	ABT-199 (venetoclax) is a potent and selective small-molecule antagonist of BCL-2 recently approved for the treatment of a specific subtype of lymphoid neoplasm.	venetoclax	0-7	BCL2 apoptosis regulator	Homo sapiens	76-81
29353886-4	2018	ABT-199 (venetoclax) is a potent and selective small-molecule antagonist of BCL-2 recently approved for the treatment of a specific subtype of lymphoid neoplasm.	venetoclax	9-19	BCL2 apoptosis regulator	Homo sapiens	76-81
29218851-0	2018	Clinical experience with the BCL2-inhibitor venetoclax in combination therapy for relapsed and refractory acute myeloid leukemia and related myeloid malignancies.	venetoclax	44-54	BCL2 apoptosis regulator	Homo sapiens	29-33
29590547-1	2018	BACKGROUND: Both the BTK inhibitor ibrutinib and the BCL2 inhibitor venetoclax are active as monotherapy in the treatment of mantle-cell lymphoma.	venetoclax	68-78	BCL2 apoptosis regulator	Homo sapiens	53-57
29590547-19	2018	CONCLUSIONS: In this study involving historical controls, dual targeting of BTK and BCL2 with ibrutinib and venetoclax was consistent with improved outcomes in patients with mantle-cell lymphoma who had been predicted to have poor outcomes with current therapy.	venetoclax	108-118	Bruton tyrosine kinase	Homo sapiens	76-79
29590547-19	2018	CONCLUSIONS: In this study involving historical controls, dual targeting of BTK and BCL2 with ibrutinib and venetoclax was consistent with improved outcomes in patients with mantle-cell lymphoma who had been predicted to have poor outcomes with current therapy.	venetoclax	108-118	BCL2 apoptosis regulator	Homo sapiens	84-88
29854301-10	2018	Venetoclax, an inhibitor of BCL-2, showed activity against the transformed cell line in vitro and could be combined with ruxolitinib in vivo.	venetoclax	0-10	B cell leukemia/lymphoma 2	Mus musculus	28-33
29218851-1	2018	INTRODUCTION: Venetoclax (VEN), a selective BCL2 inhibitor, has single-agent activity in relapsed and refractory (R/R) acute myeloid leukemia (AML), and efficacy in lower intensity combinations for treatment-naive elderly AML patients.	venetoclax	14-24	BCL2 apoptosis regulator	Homo sapiens	44-48
29218851-1	2018	INTRODUCTION: Venetoclax (VEN), a selective BCL2 inhibitor, has single-agent activity in relapsed and refractory (R/R) acute myeloid leukemia (AML), and efficacy in lower intensity combinations for treatment-naive elderly AML patients.	venetoclax	26-29	BCL2 apoptosis regulator	Homo sapiens	44-48
28549767-3	2018	Venetoclax, an inhibitor of BCL-2 known to play an important role in regulating cell death, has been approved recently for treatment of patients with chronic lymphocytic leukemia with Del17p who have received at least one prior therapy.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	28-33
29333953-0	2018	The irreversible ERBB1/2/4 inhibitor neratinib interacts with the BCL-2 inhibitor venetoclax to kill mammary cancer cells.	venetoclax	82-92	epidermal growth factor receptor	Homo sapiens	17-26
29333953-0	2018	The irreversible ERBB1/2/4 inhibitor neratinib interacts with the BCL-2 inhibitor venetoclax to kill mammary cancer cells.	venetoclax	82-92	BCL2 apoptosis regulator	Homo sapiens	66-71
29333953-2	2018	Venetoclax (ABT199) is a BCL-2 inhibitor.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	25-30
29333953-2	2018	Venetoclax (ABT199) is a BCL-2 inhibitor.	venetoclax	12-18	BCL2 apoptosis regulator	Homo sapiens	25-30
29333953-3	2018	At physiologic concentrations neratinib interacted in a synergistic fashion with venetoclax to kill HER2 + and TNBC mammary carcinoma cells.	venetoclax	81-91	erb-b2 receptor tyrosine kinase 2	Homo sapiens	100-104
29382644-1	2018	The BCL2 inhibitor venetoclax is approved in the United States for only a subset of patients with refractory chronic lymphocytic leukemia.	venetoclax	19-29	BCL2 apoptosis regulator	Homo sapiens	4-8
28663582-7	2018	Cotreatment of ARV-771 with ibrutinib or the BCL2 antagonist venetoclax or CDK4/6 inhibitor palbociclib synergistically induced apoptosis of MCL cells.	venetoclax	61-71	B cell leukemia/lymphoma 2	Mus musculus	45-49
29463802-2	2018	To this end, we analyzed whole-exome sequencing data of eight chronic lymphocytic leukemia (CLL) patients that developed resistance upon BCL2-inhibition by venetoclax.	venetoclax	156-166	BCL2 apoptosis regulator	Homo sapiens	137-141
29257139-10	2018	Venetoclax, an oral BH3 mimetic inhibiting BCL2, showed single agent activity in MM with t(11;14), and is being studied in combination with bortezomib/dexamethasone.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	43-47
29386360-4	2018	BCL2 activation in mouse Emu-myc lymphomas antagonized tigecycline-induced cell death, which was specifically restored by combined treatment with the BCL2 inhibitor venetoclax.	venetoclax	165-175	B cell leukemia/lymphoma 2	Mus musculus	0-4
28691866-2	2018	The safety, tolerability, and pharmacodynamics of the selective Bcl-2 inhibitor venetoclax (ABT-199) were assessed in women with systemic lupus erythematosus.	venetoclax	80-90	BCL2 apoptosis regulator	Homo sapiens	64-69
28751770-3	2018	Preclinical and clinical studies indicate modest single-agent activity with selective BCL-2 inhibitors (for example, venetoclax).	venetoclax	117-127	BCL2 apoptosis regulator	Homo sapiens	86-91
29386360-0	2018	Therapeutic synergy between tigecycline and venetoclax in a preclinical model of MYC/BCL2 double-hit B cell lymphoma.	venetoclax	44-54	myelocytomatosis oncogene	Mus musculus	81-84
29386360-0	2018	Therapeutic synergy between tigecycline and venetoclax in a preclinical model of MYC/BCL2 double-hit B cell lymphoma.	venetoclax	44-54	B cell leukemia/lymphoma 2	Mus musculus	85-89
29386360-4	2018	BCL2 activation in mouse Emu-myc lymphomas antagonized tigecycline-induced cell death, which was specifically restored by combined treatment with the BCL2 inhibitor venetoclax.	venetoclax	165-175	myelocytomatosis oncogene	Mus musculus	29-32
29386360-4	2018	BCL2 activation in mouse Emu-myc lymphomas antagonized tigecycline-induced cell death, which was specifically restored by combined treatment with the BCL2 inhibitor venetoclax.	venetoclax	165-175	B cell leukemia/lymphoma 2	Mus musculus	150-154
29386360-5	2018	In line with these findings, tigecycline and two related antibiotics, tetracycline and doxycycline, synergized with venetoclax in killing human MYC/BCL2 DHL cells.	venetoclax	116-126	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	144-147
29386360-5	2018	In line with these findings, tigecycline and two related antibiotics, tetracycline and doxycycline, synergized with venetoclax in killing human MYC/BCL2 DHL cells.	venetoclax	116-126	BCL2 apoptosis regulator	Homo sapiens	148-152
29118061-2	2018	Despite notable advances in SCLC genomics, new therapies remain elusive, largely due to a lack of druggable targets.Experimental Design: We used a high-throughput drug screen to identify a venetoclax-sensitive SCLC subpopulation and validated the findings with multiple patient-derived xenografts of SCLC.Results: Our drug screen consisting of a very large collection of cell lines demonstrated that venetoclax, an FDA-approved BCL-2 inhibitor, was found to be active in a substantial fraction of SCLC cell lines.	venetoclax	189-199	BCL2 apoptosis regulator	Homo sapiens	428-433
29118061-3	2018	Venetoclax induced BIM-dependent apoptosis in vitro and blocked tumor growth and induced tumor regressions in mice bearing high BCL-2-expressing SCLC tumors in vivo BCL-2 expression was a predictive biomarker for sensitivity in SCLC cell lines and was highly expressed in a subset of SCLC cell lines and tumors, suggesting that a substantial fraction of patients with SCLC could benefit from venetoclax.	venetoclax	0-10	B cell leukemia/lymphoma 2	Mus musculus	128-133
29118061-3	2018	Venetoclax induced BIM-dependent apoptosis in vitro and blocked tumor growth and induced tumor regressions in mice bearing high BCL-2-expressing SCLC tumors in vivo BCL-2 expression was a predictive biomarker for sensitivity in SCLC cell lines and was highly expressed in a subset of SCLC cell lines and tumors, suggesting that a substantial fraction of patients with SCLC could benefit from venetoclax.	venetoclax	0-10	B cell leukemia/lymphoma 2	Mus musculus	165-170
28984869-8	2018	Very recently, a specific BCL2 inhibitor ABT-199 (Venetoclax) was developed and approved by FDA for CLL treatment.	venetoclax	41-48	BCL2 apoptosis regulator	Homo sapiens	26-30
28984869-8	2018	Very recently, a specific BCL2 inhibitor ABT-199 (Venetoclax) was developed and approved by FDA for CLL treatment.	venetoclax	50-60	BCL2 apoptosis regulator	Homo sapiens	26-30
29246803-3	2018	Venetoclax is a selective, orally bioavailable inhibitor of BCL-2 active in previously treated patients with relapsed or refractory chronic lymphocytic leukaemia.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	60-65
28993217-5	2018	Model predictions of oral venetoclax pharmacokinetics were verified against clinical studies of fed and fasted healthy volunteers, and clinical drug interaction studies with strong CYP3A inhibitor (ketoconazole) and inducer (rifampicin).	venetoclax	26-36	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	181-186
29877243-3	2018	Furthermore, venetoclax, a selective BCL-2 inhibitor, and chimeric antigen receptor (CAR) T-cell therapy that work against B-cell maturation antigen (BCMA) have reportedly shown great efficacy in phase 1 studies.	venetoclax	13-23	BCL2 apoptosis regulator	Homo sapiens	37-42
30069633-4	2018	Venetoclax (ABT-199) is a novel, orally bioavailable small-molecule inhibitor for selective targeting of B-cell lymphoma 2 (BCL2).	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	105-122
30069633-4	2018	Venetoclax (ABT-199) is a novel, orally bioavailable small-molecule inhibitor for selective targeting of B-cell lymphoma 2 (BCL2).	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	124-128
30069633-4	2018	Venetoclax (ABT-199) is a novel, orally bioavailable small-molecule inhibitor for selective targeting of B-cell lymphoma 2 (BCL2).	venetoclax	12-19	BCL2 apoptosis regulator	Homo sapiens	105-122
30069633-4	2018	Venetoclax (ABT-199) is a novel, orally bioavailable small-molecule inhibitor for selective targeting of B-cell lymphoma 2 (BCL2).	venetoclax	12-19	BCL2 apoptosis regulator	Homo sapiens	124-128
29877243-3	2018	Furthermore, venetoclax, a selective BCL-2 inhibitor, and chimeric antigen receptor (CAR) T-cell therapy that work against B-cell maturation antigen (BCMA) have reportedly shown great efficacy in phase 1 studies.	venetoclax	13-23	TNF receptor superfamily member 17	Homo sapiens	123-148
29877243-3	2018	Furthermore, venetoclax, a selective BCL-2 inhibitor, and chimeric antigen receptor (CAR) T-cell therapy that work against B-cell maturation antigen (BCMA) have reportedly shown great efficacy in phase 1 studies.	venetoclax	13-23	TNF receptor superfamily member 17	Homo sapiens	150-154
29416779-11	2018	Co-administration of the Bcl-2 inhibitor GDC-0199 further potentiated ABC294640"s anti-tumor activity.	venetoclax	41-49	BCL2 apoptosis regulator	Homo sapiens	25-30
28972015-4	2017	To test this, we developed a screening assay for evaluating the sensitivity of CTCL cells to targeted molecular agents, and compared a novel BCL2 inhibitor, venetoclax, alone and in combination with a histone deacetylase (HDAC) inhibitor, vorinostat or romidepsin.	venetoclax	157-167	BCL2 apoptosis regulator	Homo sapiens	141-145
29269870-3	2017	While clinical inhibition of BCL-2 has been achieved with the BH3 mimetic venetoclax, anti-tumor efficacy is limited by compensatory induction of MCL-1.	venetoclax	74-84	BCL2 apoptosis regulator	Homo sapiens	29-34
28972014-0	2017	First-in-human response of BCL-2 inhibitor venetoclax in T-cell prolymphocytic leukemia.	venetoclax	43-53	BCL2 apoptosis regulator	Homo sapiens	27-32
28972014-3	2017	We found that the B-cell lymphoma 2 (BCL-2) inhibitor venetoclax (ABT-199) demonstrated the strongest T-PLL-specific response when comparing individual ex vivo drug response in 86 patients with refractory hematologic malignancies.	venetoclax	54-64	BCL2 apoptosis regulator	Homo sapiens	18-35
28972014-3	2017	We found that the B-cell lymphoma 2 (BCL-2) inhibitor venetoclax (ABT-199) demonstrated the strongest T-PLL-specific response when comparing individual ex vivo drug response in 86 patients with refractory hematologic malignancies.	venetoclax	54-64	BCL2 apoptosis regulator	Homo sapiens	37-42
29146569-0	2017	Found in Translation: How Preclinical Research Is Guiding the Clinical Development of the BCL2-Selective Inhibitor Venetoclax.	venetoclax	115-125	BCL2 apoptosis regulator	Homo sapiens	90-94
29146569-4	2017	We review a number of preclinical studies that have deepened our understanding of BCL2 biology and facilitated the clinical development of venetoclax.Significance: Basic research into the pathways governing programmed cell death have paved the way for the discovery of apoptosis-inducing agents such as venetoclax, a BCL2-selective inhibitor that was recently approved by the FDA and the European Medicines Agency.	venetoclax	139-149	BCL2 apoptosis regulator	Homo sapiens	317-321
29250930-7	2017	In the relapsed or refractory setting, patients with del(17p) or TP53 aberrations should be offered treatment with a novel agent, such as ibrutinib, idelalisib-rituximab or venetoclax.	venetoclax	173-183	tumor protein p53	Homo sapiens	65-69
29390581-9	2017	OUTCOMES: The patient was treated with venetoclax, a Bcl-2 inhibitor, and exhibits complete resolution of prior skin findings and continues to remain free of new cutaneous lesions 10 months posttreatment initiation with venetoclax.	venetoclax	39-49	BCL2 apoptosis regulator	Homo sapiens	53-58
28847998-2	2017	Venetoclax is a selective, orally bioavailable small-molecule BCL-2 inhibitor; bortezomib can indirectly inhibit MCL-1.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	62-67
28847998-3	2017	In preclinical studies, venetoclax enhanced bortezomib activity, suggesting that cotargeting of BCL-2 and MCL-1 could be an effective treatment strategy in myeloma.	venetoclax	24-34	BCL2 apoptosis regulator	Homo sapiens	96-101
28847998-3	2017	In preclinical studies, venetoclax enhanced bortezomib activity, suggesting that cotargeting of BCL-2 and MCL-1 could be an effective treatment strategy in myeloma.	venetoclax	24-34	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	106-111
29018077-1	2017	Venetoclax is a selective, orally bioavailable BCL-2 inhibitor that induces cell death in multiple myeloma (MM) cells, particularly in those harboring t(11;14), which express high levels of BCL-2 relative to BCL-XL and MCL-1.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	47-52
29018077-1	2017	Venetoclax is a selective, orally bioavailable BCL-2 inhibitor that induces cell death in multiple myeloma (MM) cells, particularly in those harboring t(11;14), which express high levels of BCL-2 relative to BCL-XL and MCL-1.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	190-195
29018077-1	2017	Venetoclax is a selective, orally bioavailable BCL-2 inhibitor that induces cell death in multiple myeloma (MM) cells, particularly in those harboring t(11;14), which express high levels of BCL-2 relative to BCL-XL and MCL-1.	venetoclax	0-10	BCL2 like 1	Homo sapiens	208-214
29018077-1	2017	Venetoclax is a selective, orally bioavailable BCL-2 inhibitor that induces cell death in multiple myeloma (MM) cells, particularly in those harboring t(11;14), which express high levels of BCL-2 relative to BCL-XL and MCL-1.	venetoclax	0-10	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	219-224
29018077-14	2017	Venetoclax monotherapy at a daily dose up to 1200 mg has an acceptable safety profile and evidence of single-agent antimyeloma activity in patients with relapsed/refractory MM, predominantly in patients with t(11;14) abnormality and those with a favorable BCL2 family profile.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	256-260
28972015-7	2017	Furthermore, this anti-BCL2 effect was markedly potentiated by concurrent HDAC inhibition with 93% of samples treated with venetoclax and vorinostat and 73% of samples treated with venetoclax and romidepsin showing synergistic effects.	venetoclax	123-133	BCL2 apoptosis regulator	Homo sapiens	23-27
28972015-7	2017	Furthermore, this anti-BCL2 effect was markedly potentiated by concurrent HDAC inhibition with 93% of samples treated with venetoclax and vorinostat and 73% of samples treated with venetoclax and romidepsin showing synergistic effects.	venetoclax	123-133	histone deacetylase 9	Homo sapiens	74-78
28972015-7	2017	Furthermore, this anti-BCL2 effect was markedly potentiated by concurrent HDAC inhibition with 93% of samples treated with venetoclax and vorinostat and 73% of samples treated with venetoclax and romidepsin showing synergistic effects.	venetoclax	181-191	BCL2 apoptosis regulator	Homo sapiens	23-27
28972015-7	2017	Furthermore, this anti-BCL2 effect was markedly potentiated by concurrent HDAC inhibition with 93% of samples treated with venetoclax and vorinostat and 73% of samples treated with venetoclax and romidepsin showing synergistic effects.	venetoclax	181-191	histone deacetylase 9	Homo sapiens	74-78
29291023-2	2017	Anti-apoptotic BCL-2 family inhibitors, such as venetoclax, are promising therapies for AML.	venetoclax	48-58	BCL2 apoptosis regulator	Homo sapiens	15-20
29291023-7	2017	CDK9 inhibition predominantly mediated venetoclax sensitization, while CDK4/6 inhibition with palbociclib did not potentiate venetoclax activity.	venetoclax	39-49	cyclin dependent kinase 9	Homo sapiens	0-4
29291023-8	2017	Combined, venetoclax and alvocidib modulate the balance of BCL-2 family proteins through complementary, yet variable mechanisms favoring apoptosis, highlighting this combination as a promising therapy for AML or high-risk MDS with the capacity to overcome intrinsic apoptosis mechanisms of resistance.	venetoclax	10-20	BCL2 apoptosis regulator	Homo sapiens	59-64
27357816-5	2017	Venetoclax (ABT-199), the recently FDA-approved BCL2 inhibitor, as well as several other agents and therapy combinations in the pipeline offer great promise for patients with chronic lymphocytic leukemia, particularly in the relapsed/refractory setting.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	48-52
28972395-1	2017	INTRODUCTION: Venetoclax, an orally bioavailable inhibitor of BCL-2, was approved in 2016 by the United States Food and Drug Administration (FDA) for the treatment of chronic lymphocytic leukemia (CLL) patients with 17p deletion [del(17p)], who have received at least one prior therapy.	venetoclax	14-24	BCL2 apoptosis regulator	Homo sapiens	62-67
29061914-2	2017	Clinical utility for selective inhibition of specific anti-apoptotic Bcl-2 family proteins has recently been realized with the Food and Drug Administration (FDA) approval of venetoclax (formerly ABT-199/GDC-0199) in relapsed chronic lymphocytic leukemia (CLL) with 17p deletion.	venetoclax	174-184	BCL2 apoptosis regulator	Homo sapiens	69-74
29061914-2	2017	Clinical utility for selective inhibition of specific anti-apoptotic Bcl-2 family proteins has recently been realized with the Food and Drug Administration (FDA) approval of venetoclax (formerly ABT-199/GDC-0199) in relapsed chronic lymphocytic leukemia (CLL) with 17p deletion.	venetoclax	203-211	BCL2 apoptosis regulator	Homo sapiens	69-74
29064593-3	2018	Results from early phase clinical trials utilizing the selective Bcl-2 inhibitor, venetoclax, as a single agent in patients with relapsed MM have had remarkable efficacy among patients with t (11;14) abnormality.	venetoclax	82-92	BCL2 apoptosis regulator	Homo sapiens	65-70
27357816-5	2017	Venetoclax (ABT-199), the recently FDA-approved BCL2 inhibitor, as well as several other agents and therapy combinations in the pipeline offer great promise for patients with chronic lymphocytic leukemia, particularly in the relapsed/refractory setting.	venetoclax	12-19	BCL2 apoptosis regulator	Homo sapiens	48-52
29025288-5	2017	New classes of drugs like kinase inhibitors and BCL-2 inhibitors (ibrutinib, idelalisib and venetoclax) are the treatment of choice in CLL patients with relapsed/refractory disease, with the exception of high risk disease, where the optimal treatment is frontline ibrutinib monotherapy.	venetoclax	92-102	BCL2 apoptosis regulator	Homo sapiens	48-53
28111464-7	2017	In contrast, treatment with the selective BCL-2 inhibitor venetoclax enhanced overall mitochondrial priming without increasing BCL-2 dependence.	venetoclax	58-68	BCL2 apoptosis regulator	Homo sapiens	42-47
28111464-8	2017	Pre-treatment of CLL cells with either BTK inhibitor, whether ex vivo or in vivo in patients, enhanced killing by venetoclax.	venetoclax	114-124	Bruton tyrosine kinase	Homo sapiens	39-42
28482721-4	2017	A potential partner to ibrutinib with a distinct mechanism of action that is likely to lead to deeper responses is the BCL-2 inhibitor venetoclax.	venetoclax	135-145	BCL2 apoptosis regulator	Homo sapiens	119-124
28782884-14	2017	Patients with a del(17p) or TP53 mutation can be treated with ibrutinib, venetoclax, or a combination of idelalisib and rituximab.	venetoclax	73-83	tumor protein p53	Homo sapiens	28-32
28619845-0	2017	The prohibitin-binding compound fluorizoline induces apoptosis in chronic lymphocytic leukemia cells through the upregulation of NOXA and synergizes with ibrutinib, 5-aminoimidazole-4-carboxamide riboside or venetoclax.	venetoclax	208-218	prohibitin 1	Homo sapiens	4-14
28562380-1	2017	Venetoclax is a first-in-class orally available, B-cell lymphoma (BCL)-2 inhibitor indicated for the treatment of patients with relapsed/refractory chronic lymphocytic leukemia (CLL) harboring the 17p deletion.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	49-72
28646646-4	2017	ARTS lowered cellular BCL-2 level via ROS induction and increased the cytotoxicity of the BCL-2 inhibitor venetoclax (ABT-199).	venetoclax	106-116	BCL2 apoptosis regulator	Homo sapiens	90-95
28017967-6	2017	The BCL2 inhibitor venetoclax induced greater apoptosis in ex vivo-cultured CLL cells obtained from patients on duvelisib compared with pre-treatment CLL cells from the same patients.	venetoclax	19-29	BCL2 apoptosis regulator	Homo sapiens	4-8
28140720-1	2017	The approval of venetoclax, a "BH3-mimetic" antagonist of the BCL-2 anti-apoptotic protein, for chronic lymphocytic leukemia represents a major milestone in translational apoptosis research.	venetoclax	16-26	BCL2 apoptosis regulator	Homo sapiens	62-67
28619982-8	2017	Moreover, the JAK1/2 inhibitor ruxolitinib restored sensitivity to the BCL2 inhibitor venetoclax in AML patient cells ex vivo in different model systems and in vivo in an AML xenograft mouse model.	venetoclax	86-96	Janus kinase 1	Homo sapiens	14-20
28619982-8	2017	Moreover, the JAK1/2 inhibitor ruxolitinib restored sensitivity to the BCL2 inhibitor venetoclax in AML patient cells ex vivo in different model systems and in vivo in an AML xenograft mouse model.	venetoclax	86-96	BCL2 apoptosis regulator	Homo sapiens	71-75
28449207-4	2017	The first BCL2-specific inhibitor, venetoclax, has shown extraordinary single agent activity in chronic lymphocytic leukaemia (CLL), with surprisingly little toxicity given the expression of BCL2 in normal tissues.	venetoclax	35-45	BCL2 apoptosis regulator	Homo sapiens	10-14
28449207-4	2017	The first BCL2-specific inhibitor, venetoclax, has shown extraordinary single agent activity in chronic lymphocytic leukaemia (CLL), with surprisingly little toxicity given the expression of BCL2 in normal tissues.	venetoclax	35-45	BCL2 apoptosis regulator	Homo sapiens	191-195
28646646-4	2017	ARTS lowered cellular BCL-2 level via ROS induction and increased the cytotoxicity of the BCL-2 inhibitor venetoclax (ABT-199).	venetoclax	118-125	BCL2 apoptosis regulator	Homo sapiens	90-95
28455421-7	2017	Accordingly, we found that combining the BCL-2/BCL-XL inhibitors ABT-263/ABT199 with the CDK7 inhibitor THZ1 synergized in producing growth inhibition and apoptosis of human TNBC cells.	venetoclax	73-79	BCL2 apoptosis regulator	Homo sapiens	41-46
28522442-11	2017	A highly selective BCL2 inhibitor, venetoclax, was recently introduced as breakthrough therapy.	venetoclax	35-45	BCL2 apoptosis regulator	Homo sapiens	19-23
28714472-6	2017	As doxorubicin and dinaciclib also reduced BCL-XL, the combinations of BCL-2 inhibitor ABT-199 (venetoclax) with doxorubicin or dinaciclib provided effective therapeutic strategies for SCLC.	venetoclax	87-94	BCL2 apoptosis regulator	Homo sapiens	71-76
28714472-6	2017	As doxorubicin and dinaciclib also reduced BCL-XL, the combinations of BCL-2 inhibitor ABT-199 (venetoclax) with doxorubicin or dinaciclib provided effective therapeutic strategies for SCLC.	venetoclax	96-106	BCL2 apoptosis regulator	Homo sapiens	71-76
28119366-8	2017	BLI and PB were subsequently used to evaluate efficacy of the Bcl-2 inhibitor venetoclax.Results: BLI considerably accelerated and enhanced detection of leukemia burden compared with PB and identified sites of residual disease during treatment in a quantitative manner, highlighting limitations in current PB-based scoring criteria.	venetoclax	78-88	BCL2 apoptosis regulator	Homo sapiens	62-67
28915653-3	2017	To this purpose we evaluated 15 targeted drugs in combination with idasanutlin in three p53 wild type neuroblastoma cell lines and identified the BCL2 inhibitor venetoclax (ABT-199) as a promising interaction partner.	venetoclax	161-171	transformation related protein 53, pseudogene	Mus musculus	88-91
28915653-3	2017	To this purpose we evaluated 15 targeted drugs in combination with idasanutlin in three p53 wild type neuroblastoma cell lines and identified the BCL2 inhibitor venetoclax (ABT-199) as a promising interaction partner.	venetoclax	161-171	B cell leukemia/lymphoma 2	Mus musculus	146-150
28915653-4	2017	The venetoclax/idasanutlin combination was consistently found to be highly synergistic in a diverse panel of neuroblastoma cell lines, including cells with high MCL1 expression levels.	venetoclax	4-14	myeloid cell leukemia sequence 1	Mus musculus	161-165
28389687-6	2017	New options include two agents targeting B cell receptor (BCR) signaling pathways (ibrutinib and idelalisib) and a B cell lymphoma-2 (BCL-2) inhibitor (venetoclax).	venetoclax	152-162	BCL2 apoptosis regulator	Homo sapiens	134-139
28536906-11	2017	Combination trials of ibrutinib with venetoclax, a Bcl-2 inhibitor, are underway and are supported by sound preclinical rationale.	venetoclax	37-47	BCL2 apoptosis regulator	Homo sapiens	51-56
27808579-1	2017	Treatment options for chronic lymphocytic leukemia (CLL) have improved with the introduction of the B-cell receptor inhibitors ibrutinib and idelalisib, and of the BCL2 inhibitor venetoclax.	venetoclax	179-189	BCL2 apoptosis regulator	Homo sapiens	164-168
28473407-1	2017	The BCL2 inhibitor venetoclax achieves responses in ~79% of patients with relapsed or refractory chronic lymphocytic leukemia/small lymphocytic lymphoma (RR-CLL/SLL), irrespective of risk factors associated with poor response to chemoimmunotherapy.	venetoclax	19-29	BCL2 apoptosis regulator	Homo sapiens	4-8
28473407-1	2017	The BCL2 inhibitor venetoclax achieves responses in ~79% of patients with relapsed or refractory chronic lymphocytic leukemia/small lymphocytic lymphoma (RR-CLL/SLL), irrespective of risk factors associated with poor response to chemoimmunotherapy.	venetoclax	19-29	solute carrier family 35 member B2	Homo sapiens	154-164
29034364-2	2017	To identify such combinations, we previously performed a combinatorial drug screen and identified the Bcl-2 inhibitor venetoclax (VEN) as a promising partner for combination with IBR in Mantle Cell Lymphoma (MCL).	venetoclax	118-128	BCL2 apoptosis regulator	Homo sapiens	102-107
28578655-1	2017	BACKGROUND: Venetoclax (ABT-199), a first-in-class orally bioavailable BCL-2-selective inhibitor, was recently approved by the FDA for use in patients with 17p-deleted chronic lymphocytic leukemia who have received prior therapy.	venetoclax	12-22	BCL2 apoptosis regulator	Homo sapiens	71-76
28578655-9	2017	For resistant cell lines showing elevations in BCL-XL or MCL-1, strong synergistic cell killing was observed when venetoclax was combined with either BCL-XL- or MCL-1-selective inhibitors, respectively.	venetoclax	114-124	BCL2 like 1	Homo sapiens	47-53
28578655-9	2017	For resistant cell lines showing elevations in BCL-XL or MCL-1, strong synergistic cell killing was observed when venetoclax was combined with either BCL-XL- or MCL-1-selective inhibitors, respectively.	venetoclax	114-124	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	57-62
27913204-0	2017	The selective Bcl-2 inhibitor venetoclax, a BH3 mimetic, does not dysregulate intracellular Ca2+ signaling.	venetoclax	30-40	BCL2 apoptosis regulator	Homo sapiens	14-19
27913204-4	2017	Venetoclax (1muM) did neither trigger Ca2+ release by itself nor affect agonist-induced Ca2+ release in a variety of intact cell models.	venetoclax	0-10	latexin	Homo sapiens	13-16
27913204-9	2017	Furthermore, venetoclax-induced cell death in Bcl-2-dependent cancer cells is not mediated by intracellular Ca2+ overload.	venetoclax	13-23	BCL2 apoptosis regulator	Homo sapiens	46-51
28416490-5	2017	Apoptosis induced by ABBV-075 was mediated in part by modulation of the intrinsic apoptotic pathway, exhibiting synergy with the BCL-2 inhibitor venetoclax in preclinical models of AML.	venetoclax	145-155	BCL2 apoptosis regulator	Homo sapiens	129-134
28492339-1	2017	Venetoclax is a potent, selective inhibitor of BCL-2, a key regulator of the intrinsic pathway of apoptosis.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	47-52
28492339-2	2017	In preclinical studies, venetoclax bound to BCL-2 with high affinity and rapidly induced apoptosis in chronic lymphocytic leukemia (CLL) cells.	venetoclax	24-34	BCL2 apoptosis regulator	Homo sapiens	44-49
28052338-7	2017	Model simulations indicated no effect of weak CYP3A inhibitors or inducers on Cmax or AUC  , while both moderate and strong CYP3A inducers were estimated to decrease venetoclax exposure.	venetoclax	166-176	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	124-129
28052338-9	2017	The recommended venetoclax dose reductions of at least 50% and 75% when coadministered with moderate and strong CYP3A inhibitors, respectively, maintain venetoclax exposures between therapeutic and maximally administered safe doses.	venetoclax	16-26	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	112-117
28052338-9	2017	The recommended venetoclax dose reductions of at least 50% and 75% when coadministered with moderate and strong CYP3A inhibitors, respectively, maintain venetoclax exposures between therapeutic and maximally administered safe doses.	venetoclax	153-163	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	112-117
28548645-6	2017	Cytotoxicity studies using the AKT inhibitor, MK2206+-ibrutinib, and the Bcl-2-specific inhibitor, venetoclax+-ibrutinib, demonstrated synergistic loss of cell viability when either MK22016 or venetoclax were used in combination with ibrutinib.	venetoclax	99-109	BCL2 apoptosis regulator	Homo sapiens	73-78
28331083-6	2017	This effect can be overcome by treating cells with the clinically approved BCL2 antagonist venetoclax, which prevents Casp8p41 from binding BCL2, thereby allowing Casp8p41 to bind Bak and kill the infected cell.	venetoclax	91-101	BCL2 apoptosis regulator	Homo sapiens	75-79
28331083-6	2017	This effect can be overcome by treating cells with the clinically approved BCL2 antagonist venetoclax, which prevents Casp8p41 from binding BCL2, thereby allowing Casp8p41 to bind Bak and kill the infected cell.	venetoclax	91-101	caspase 8	Homo sapiens	118-124
28331083-6	2017	This effect can be overcome by treating cells with the clinically approved BCL2 antagonist venetoclax, which prevents Casp8p41 from binding BCL2, thereby allowing Casp8p41 to bind Bak and kill the infected cell.	venetoclax	91-101	BCL2 apoptosis regulator	Homo sapiens	140-144
28331083-6	2017	This effect can be overcome by treating cells with the clinically approved BCL2 antagonist venetoclax, which prevents Casp8p41 from binding BCL2, thereby allowing Casp8p41 to bind Bak and kill the infected cell.	venetoclax	91-101	caspase 8	Homo sapiens	163-169
28331083-6	2017	This effect can be overcome by treating cells with the clinically approved BCL2 antagonist venetoclax, which prevents Casp8p41 from binding BCL2, thereby allowing Casp8p41 to bind Bak and kill the infected cell.	venetoclax	91-101	BCL2 antagonist/killer 1	Homo sapiens	180-183
28056525-0	2017	Venetoclax: A First-in-Class Oral BCL-2 Inhibitor for the Management of Lymphoid Malignancies.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	34-39
28468776-9	2017	Indeed, strong synergy was observed both in vitro and in vivo when cotreating the cells with BET inhibitor and the BH3-mimetic, BCL2 inhibitor venetoclax (ABT-199).	venetoclax	143-153	BCL2 apoptosis regulator	Homo sapiens	128-132
28566329-2	2017	The BCL-2 small-molecule inhibitor venetoclax shows promising clinical response rates in several lymphomas, but is not curative as monotherapy.	venetoclax	35-45	B cell leukemia/lymphoma 2	Mus musculus	4-9
28455421-7	2017	Accordingly, we found that combining the BCL-2/BCL-XL inhibitors ABT-263/ABT199 with the CDK7 inhibitor THZ1 synergized in producing growth inhibition and apoptosis of human TNBC cells.	venetoclax	73-79	BCL2 like 1	Homo sapiens	47-53
27859472-0	2017	Effect of ketoconazole, a strong CYP3A inhibitor, on the pharmacokinetics of venetoclax, a BCL-2 inhibitor, in patients with non-Hodgkin lymphoma.	venetoclax	77-87	BCL2 apoptosis regulator	Homo sapiens	91-96
29263915-0	2017	Inhibition of Mcl-1 enhances cell death induced by the Bcl-2-selective inhibitor ABT-199 in acute myeloid leukemia cells.	venetoclax	81-88	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	14-19
29263915-0	2017	Inhibition of Mcl-1 enhances cell death induced by the Bcl-2-selective inhibitor ABT-199 in acute myeloid leukemia cells.	venetoclax	81-88	BCL2 apoptosis regulator	Homo sapiens	55-60
27859472-1	2017	AIMS: To examine the effect of a strong cytochrome P450 (CYP) 3A inhibitor, ketoconazole, on the pharmacokinetics, safety and tolerability of venetoclax.	venetoclax	142-152	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	40-64
27859472-7	2017	CONCLUSIONS: Coadministration of venetoclax with multiple doses of ketoconazole resulted in a significant increase of venetoclax exposures, strongly suggesting that CYP3A plays a major role in elimination of venetoclax in patients.	venetoclax	33-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	165-170
27859472-7	2017	CONCLUSIONS: Coadministration of venetoclax with multiple doses of ketoconazole resulted in a significant increase of venetoclax exposures, strongly suggesting that CYP3A plays a major role in elimination of venetoclax in patients.	venetoclax	118-128	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	165-170
27859472-7	2017	CONCLUSIONS: Coadministration of venetoclax with multiple doses of ketoconazole resulted in a significant increase of venetoclax exposures, strongly suggesting that CYP3A plays a major role in elimination of venetoclax in patients.	venetoclax	118-128	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	165-170
27859472-9	2017	For patients who have completed the ramp-up phase, a modification in venetoclax dose for use with strong and moderate inhibitors or inducers of CYP3A is recommended.	venetoclax	69-79	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	144-149
28095146-2	2017	A phase I trial in patients with NHL was conducted to determine safety, pharmacokinetics, and efficacy of venetoclax, a selective, potent, orally bioavailable BCL-2 inhibitor.	venetoclax	106-116	BCL2 apoptosis regulator	Homo sapiens	159-164
28209992-4	2017	Clinical experience with navitoclax prompted the generation of the highly selective BCL-2 inhibitor venetoclax, which is now approved in the United States for the treatment of patients with chronic lymphocytic leukaemia with 17p deletion who have received at least one prior therapy.	venetoclax	100-110	BCL2 apoptosis regulator	Homo sapiens	84-89
28122742-6	2017	The BCL2-inhibitor venetoclax was highly active below 10 nM in B-cell precursor ALL (BCP-ALL) subsets, including MLL-AF4 and TCF3-HLF ALL, and in some T-cell ALLs (T-ALLs), predicting in vivo activity as a single agent and in combination with dexamethasone and vincristine.	venetoclax	19-29	BCL2 apoptosis regulator	Homo sapiens	4-8
28122742-6	2017	The BCL2-inhibitor venetoclax was highly active below 10 nM in B-cell precursor ALL (BCP-ALL) subsets, including MLL-AF4 and TCF3-HLF ALL, and in some T-cell ALLs (T-ALLs), predicting in vivo activity as a single agent and in combination with dexamethasone and vincristine.	venetoclax	19-29	lysine methyltransferase 2A	Homo sapiens	113-116
28122742-6	2017	The BCL2-inhibitor venetoclax was highly active below 10 nM in B-cell precursor ALL (BCP-ALL) subsets, including MLL-AF4 and TCF3-HLF ALL, and in some T-cell ALLs (T-ALLs), predicting in vivo activity as a single agent and in combination with dexamethasone and vincristine.	venetoclax	19-29	AF4/FMR2 family member 1	Homo sapiens	117-120
28331288-2	2017	Venetoclax (Venclexta , formerly ABT-199, GDC-0199) is a highly selective BCL-2 inhibitor, which mimics its BCL-2 homology 3-domain to induce apoptosis.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	74-79
28331288-2	2017	Venetoclax (Venclexta , formerly ABT-199, GDC-0199) is a highly selective BCL-2 inhibitor, which mimics its BCL-2 homology 3-domain to induce apoptosis.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	108-113
28331288-2	2017	Venetoclax (Venclexta , formerly ABT-199, GDC-0199) is a highly selective BCL-2 inhibitor, which mimics its BCL-2 homology 3-domain to induce apoptosis.	venetoclax	12-21	BCL2 apoptosis regulator	Homo sapiens	74-79
27558232-0	2017	Pharmacokinetics of Venetoclax, a Novel BCL-2 Inhibitor, in Patients With Relapsed or Refractory Chronic Lymphocytic Leukemia or Non-Hodgkin Lymphoma.	venetoclax	20-30	BCL2 apoptosis regulator	Homo sapiens	40-45
27558232-1	2017	Venetoclax is a selective BCL-2 inhibitor that is approved in the United States for the treatment of patients with chronic lymphocytic leukemia (CLL) with 17p deletion who have received at least 1 prior therapy.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	26-31
28095146-12	2017	Conclusion Selective targeting of BCL-2 with venetoclax was well tolerated, and single-agent activity varied among NHL subtypes.	venetoclax	45-55	BCL2 apoptosis regulator	Homo sapiens	34-39
28331288-2	2017	Venetoclax (Venclexta , formerly ABT-199, GDC-0199) is a highly selective BCL-2 inhibitor, which mimics its BCL-2 homology 3-domain to induce apoptosis.	venetoclax	12-21	BCL2 apoptosis regulator	Homo sapiens	108-113
28331288-2	2017	Venetoclax (Venclexta , formerly ABT-199, GDC-0199) is a highly selective BCL-2 inhibitor, which mimics its BCL-2 homology 3-domain to induce apoptosis.	venetoclax	42-50	BCL2 apoptosis regulator	Homo sapiens	74-79
28331288-2	2017	Venetoclax (Venclexta , formerly ABT-199, GDC-0199) is a highly selective BCL-2 inhibitor, which mimics its BCL-2 homology 3-domain to induce apoptosis.	venetoclax	42-50	BCL2 apoptosis regulator	Homo sapiens	108-113
27993930-0	2017	Metabolism and Disposition of a Novel B-Cell Lymphoma-2 Inhibitor Venetoclax in Humans and Characterization of Its Unusual Metabolites.	venetoclax	66-76	BCL2 apoptosis regulator	Homo sapiens	38-55
27993930-1	2017	Venetoclax (ABT-199), a B-cell lymphoma-2 (Bcl-2) protein inhibitor, is currently in clinical development for the treatment of hematologic malignancies.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	24-41
27993930-1	2017	Venetoclax (ABT-199), a B-cell lymphoma-2 (Bcl-2) protein inhibitor, is currently in clinical development for the treatment of hematologic malignancies.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	43-48
28161120-1	2017	PURPOSE: The effect of posaconazole, a strong cytochrome P450 3A (CYP3A) inhibitor and commonly used antifungal agent, on the pharmacokinetic properties of venetoclax, a CYP3A substrate, was evaluated in patients with acute myeloid leukemia to determine the dose adjustments needed to manage this potential interaction.	venetoclax	156-166	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	46-64
27749061-6	2017	Indeed, the selective Bcl-2 inhibitor venetoclax (Venclexta) recently received FDA approval for the treatment of a specific subset of patients with chronic lymphocytic leukemia.	venetoclax	38-48	BCL2 apoptosis regulator	Homo sapiens	22-27
27749061-6	2017	Indeed, the selective Bcl-2 inhibitor venetoclax (Venclexta) recently received FDA approval for the treatment of a specific subset of patients with chronic lymphocytic leukemia.	venetoclax	50-59	BCL2 apoptosis regulator	Homo sapiens	22-27
27986708-2	2017	We found that primary BPDCN cells were dependent on the antiapoptotic protein BCL2 and were uniformly sensitive to the BCL2 inhibitor venetoclax, as measured by direct cytotoxicity, apoptosis assays, and dynamic BH3 profiling.	venetoclax	134-144	BCL2 apoptosis regulator	Homo sapiens	119-123
28161120-1	2017	PURPOSE: The effect of posaconazole, a strong cytochrome P450 3A (CYP3A) inhibitor and commonly used antifungal agent, on the pharmacokinetic properties of venetoclax, a CYP3A substrate, was evaluated in patients with acute myeloid leukemia to determine the dose adjustments needed to manage this potential interaction.	venetoclax	156-166	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	66-71
28161120-8	2017	IMPLICATIONS: The results are consistent with inhibition of CYP3A-mediated metabolism of venetoclax.	venetoclax	89-99	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	60-65
28089635-1	2017	BACKGROUND: Selective BCL2 inhibition with venetoclax has substantial activity in patients with relapsed or refractory chronic lymphocytic leukaemia.	venetoclax	43-53	BCL2 apoptosis regulator	Homo sapiens	22-26
27499136-1	2017	Inhibitors of B-cell lymphoma-2 (BCL-2) such as venetoclax (ABT-199) and navitoclax (ABT-263) are clinically explored in several cancer types, including acute myeloid leukemia (AML), to selectively induce apoptosis in cancer cells.	venetoclax	48-58	BCL2 apoptosis regulator	Homo sapiens	14-31
27499136-1	2017	Inhibitors of B-cell lymphoma-2 (BCL-2) such as venetoclax (ABT-199) and navitoclax (ABT-263) are clinically explored in several cancer types, including acute myeloid leukemia (AML), to selectively induce apoptosis in cancer cells.	venetoclax	48-58	BCL2 apoptosis regulator	Homo sapiens	33-38
28079887-1	2017	The concept of using BH3 mimetics as anticancer agents has been substantiated by the efficacy of selective drugs, such as Navitoclax and Venetoclax, in treating BCL-2-dependent haematological malignancies.	venetoclax	137-147	BCL2 apoptosis regulator	Homo sapiens	161-166
28653191-4	2017	Thus, loss of miR-15/16 leads to overexpression of BCL2 that can be targeted by the new drug, venetoclax, that was recently approved by the FDA for the treatment of aggressive CLLs.	venetoclax	94-104	BCL2 apoptosis regulator	Homo sapiens	51-55
27913471-7	2016	These recently approved drugs (ibrutinib, idelalisib, and venetoclax) are reporting excellent outcomes, including patients with high-risk disease such as 17p deletion (17p-) or TP53 mutations (TP53mut).	venetoclax	58-68	tumor protein p53	Homo sapiens	177-181
28185174-1	2017	OPINION STATEMENT: A number of new treatment options have recently emerged for chronic lymphocytic leukemia (CLL) patients, including the Bruton"s tyrosine kinase (BTK) inhibitor ibrutinib, phosphatidylinositol-3-kinase (PI3K) delta isoform inhibitor idelalisib combined with rituximab, the Bcl-2 antagonist venetoclax, and the new anti-CD20 antibodies obinutuzumab and ofatumumab.	venetoclax	308-318	Bruton tyrosine kinase	Homo sapiens	138-162
28185174-1	2017	OPINION STATEMENT: A number of new treatment options have recently emerged for chronic lymphocytic leukemia (CLL) patients, including the Bruton"s tyrosine kinase (BTK) inhibitor ibrutinib, phosphatidylinositol-3-kinase (PI3K) delta isoform inhibitor idelalisib combined with rituximab, the Bcl-2 antagonist venetoclax, and the new anti-CD20 antibodies obinutuzumab and ofatumumab.	venetoclax	308-318	Bruton tyrosine kinase	Homo sapiens	164-167
27693384-3	2016	Here, we have investigated the mechanism of Disarib-induced cytotoxicity, and compared its efficacy with a well-established BCL2 inhibitor, ABT199.	venetoclax	140-146	B cell leukemia/lymphoma 2	Mus musculus	124-128
27990281-2	2016	Here we summarize recent advances in understanding of the biology of BCL2 family members that shed light on the action of BH3 mimetics, review preclinical and clinical studies leading to the regulatory approval of venetoclax, and discuss future investigation of this new class of antineoplastic agent.	venetoclax	214-224	BCL2 apoptosis regulator	Homo sapiens	69-73
27233802-1	2016	Venetoclax (ABT-199/GDC-0199) is a selective, potent, first-in-class BCL-2 inhibitor that restores apoptosis in cancer cells and has demonstrated clinical efficacy in a variety of hematological malignancies.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	69-74
27029823-0	2016	Effect of Low- and High-Fat Meals on the Pharmacokinetics of Venetoclax, a Selective First-in-Class BCL-2 Inhibitor.	venetoclax	61-71	BCL2 apoptosis regulator	Homo sapiens	100-105
27520294-1	2016	We present a phase II, single-arm study evaluating 800 mg daily venetoclax, a highly selective, oral small-molecule B-cell leukemia/lymphoma-2 (BCL2) inhibitor in patients with high-risk relapsed/refractory acute myelogenous leukemia (AML) or unfit for intensive chemotherapy.	venetoclax	64-74	BCL2 apoptosis regulator	Homo sapiens	116-142
27520294-1	2016	We present a phase II, single-arm study evaluating 800 mg daily venetoclax, a highly selective, oral small-molecule B-cell leukemia/lymphoma-2 (BCL2) inhibitor in patients with high-risk relapsed/refractory acute myelogenous leukemia (AML) or unfit for intensive chemotherapy.	venetoclax	64-74	BCL2 apoptosis regulator	Homo sapiens	144-148
27695617-1	2016	Venetoclax (VEN, ABT-199/GDC-0199) is an orally bioavailable BH3-mimetic that specifically inhibits the anti-apoptotic B-cell lymphoma/leukemia 2 (BCL2) protein.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	119-145
27695617-1	2016	Venetoclax (VEN, ABT-199/GDC-0199) is an orally bioavailable BH3-mimetic that specifically inhibits the anti-apoptotic B-cell lymphoma/leukemia 2 (BCL2) protein.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	147-151
27695617-1	2016	Venetoclax (VEN, ABT-199/GDC-0199) is an orally bioavailable BH3-mimetic that specifically inhibits the anti-apoptotic B-cell lymphoma/leukemia 2 (BCL2) protein.	venetoclax	12-15	BCL2 apoptosis regulator	Homo sapiens	119-145
27695617-1	2016	Venetoclax (VEN, ABT-199/GDC-0199) is an orally bioavailable BH3-mimetic that specifically inhibits the anti-apoptotic B-cell lymphoma/leukemia 2 (BCL2) protein.	venetoclax	12-15	BCL2 apoptosis regulator	Homo sapiens	147-151
27695617-1	2016	Venetoclax (VEN, ABT-199/GDC-0199) is an orally bioavailable BH3-mimetic that specifically inhibits the anti-apoptotic B-cell lymphoma/leukemia 2 (BCL2) protein.	venetoclax	25-33	BCL2 apoptosis regulator	Homo sapiens	119-145
27695617-1	2016	Venetoclax (VEN, ABT-199/GDC-0199) is an orally bioavailable BH3-mimetic that specifically inhibits the anti-apoptotic B-cell lymphoma/leukemia 2 (BCL2) protein.	venetoclax	25-33	BCL2 apoptosis regulator	Homo sapiens	147-151
27617850-3	2016	Drugging the BH3-binding pockets of anti-apoptotic proteins has become a highest-priority goal, fueled by the clinical success of ABT-199, a selective BCL-2 inhibitor, in reactivating apoptosis in BCL-2-dependent cancers.	venetoclax	130-137	BCL2 apoptosis regulator	Homo sapiens	151-156
27617850-3	2016	Drugging the BH3-binding pockets of anti-apoptotic proteins has become a highest-priority goal, fueled by the clinical success of ABT-199, a selective BCL-2 inhibitor, in reactivating apoptosis in BCL-2-dependent cancers.	venetoclax	130-137	BCL2 apoptosis regulator	Homo sapiens	197-202
27725868-3	2016	While the Bcl-2-selective inhibitor ABT-199 has demonstrated promising preclinical anti-leukemic activities, intrinsic drug resistance remains a problem.	venetoclax	36-43	BCL2 apoptosis regulator	Homo sapiens	10-15
27343252-5	2016	We demonstrate that in contrast to the clear dependence of CLL on BCL-2 alone, effective antileukemic activity in the majority of ALL xenografts requires concurrent inhibition of both BCL-2 and BCL-XL We identify BCL-XL expression as a key predictor of poor response to venetoclax and demonstrate that concurrent inhibition of both BCL-2 and BCL-XL results in synergistic killing in the majority of ALL xenografts.	venetoclax	270-280	BCL2 like 1	Homo sapiens	213-219
27343252-5	2016	We demonstrate that in contrast to the clear dependence of CLL on BCL-2 alone, effective antileukemic activity in the majority of ALL xenografts requires concurrent inhibition of both BCL-2 and BCL-XL We identify BCL-XL expression as a key predictor of poor response to venetoclax and demonstrate that concurrent inhibition of both BCL-2 and BCL-XL results in synergistic killing in the majority of ALL xenografts.	venetoclax	270-280	BCL2 like 1	Homo sapiens	213-219
27469405-6	2016	Finally, we showed that low concentrations of dinaciclib enhanced cell sensitivity to ibrutinib and the BCL2 inhibitor ABT-199, two drugs with known effects on CLL.	venetoclax	119-126	BCL2 apoptosis regulator	Homo sapiens	104-108
26953185-0	2016	Evaluation of Rifampin"s Transporter Inhibitory and CYP3A Inductive Effects on the Pharmacokinetics of Venetoclax, a BCL-2 Inhibitor: Results of a Single- and Multiple-Dose Study.	venetoclax	103-113	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	52-57
26953185-0	2016	Evaluation of Rifampin"s Transporter Inhibitory and CYP3A Inductive Effects on the Pharmacokinetics of Venetoclax, a BCL-2 Inhibitor: Results of a Single- and Multiple-Dose Study.	venetoclax	103-113	BCL2 apoptosis regulator	Homo sapiens	117-122
26953185-2	2016	A single-dose and multiple-dose rifampin study was conducted to evaluate the effect of CYP3A induction and transporter inhibition on the pharmacokinetics of venetoclax.	venetoclax	157-167	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	87-92
27661108-2	2016	This study investigates activity of the BH3 mimetic venetoclax (ABT-199), which targets BCL-2, and mechanisms of acquired resistance in FL.The sensitivity of FL cells to venetoclax treatment correlated with BCL-2/BIM ratio.	venetoclax	52-62	BCL2 apoptosis regulator	Homo sapiens	88-93
27661108-2	2016	This study investigates activity of the BH3 mimetic venetoclax (ABT-199), which targets BCL-2, and mechanisms of acquired resistance in FL.The sensitivity of FL cells to venetoclax treatment correlated with BCL-2/BIM ratio.	venetoclax	52-62	BCL2 apoptosis regulator	Homo sapiens	207-212
27661108-2	2016	This study investigates activity of the BH3 mimetic venetoclax (ABT-199), which targets BCL-2, and mechanisms of acquired resistance in FL.The sensitivity of FL cells to venetoclax treatment correlated with BCL-2/BIM ratio.	venetoclax	52-62	BCL2 like 11	Homo sapiens	213-216
27661108-4	2016	Venetoclax induced dissociation of BCL-2/ BIM complex and a decrease in mitochondrial potential.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	35-40
27661108-4	2016	Venetoclax induced dissociation of BCL-2/ BIM complex and a decrease in mitochondrial potential.	venetoclax	0-10	BCL2 like 11	Homo sapiens	42-45
27661108-5	2016	Interestingly the population of cells that survived venetoclax treatment showed increased p-ERK1/2 and p-BIM (S69), as well as a decrease in total BIM levels.	venetoclax	52-62	mitogen-activated protein kinase 3	Homo sapiens	92-98
27661108-5	2016	Interestingly the population of cells that survived venetoclax treatment showed increased p-ERK1/2 and p-BIM (S69), as well as a decrease in total BIM levels.	venetoclax	52-62	BCL2 like 11	Homo sapiens	105-108
27661108-5	2016	Interestingly the population of cells that survived venetoclax treatment showed increased p-ERK1/2 and p-BIM (S69), as well as a decrease in total BIM levels.	venetoclax	52-62	BCL2 like 11	Homo sapiens	147-150
27233802-1	2016	Venetoclax (ABT-199/GDC-0199) is a selective, potent, first-in-class BCL-2 inhibitor that restores apoptosis in cancer cells and has demonstrated clinical efficacy in a variety of hematological malignancies.	venetoclax	20-28	BCL2 apoptosis regulator	Homo sapiens	69-74
27233802-5	2016	The terminal half-life in cancer subjects was estimated to be approximately 26 h. Moderate and strong CYP3A inhibitors decreased venetoclax apparent clearance by 19% and 84%, respectively, while weak CYP3A inhibitors and inducers did not affect clearance.	venetoclax	129-139	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	102-107
27233802-12	2016	In conclusion, the concomitant administration of moderate and strong CYP3A inhibitors and rituximab as well as food were the main factors impacting venetoclax pharmacokinetics, while patient characteristics had only minimal impact.	venetoclax	148-158	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	69-74
27520705-6	2016	Finally, Birinapant and AT-406 can synergise with BCL-2 inhibitor ABT-199 to reduce viability of adenocarcinoma cells with high BCL-2 expression.	venetoclax	66-73	BCL2 apoptosis regulator	Homo sapiens	50-55
27582059-5	2016	Recently, a selective inhibitor of B cell lymphoma 2 (BCL-2), ABT-199 (venetoclax), has shown impressive activity against hematologic malignancies.	venetoclax	62-69	BCL2 apoptosis regulator	Homo sapiens	35-52
27582059-5	2016	Recently, a selective inhibitor of B cell lymphoma 2 (BCL-2), ABT-199 (venetoclax), has shown impressive activity against hematologic malignancies.	venetoclax	62-69	BCL2 apoptosis regulator	Homo sapiens	54-59
27297795-1	2016	Novel agents such as the Bcl-2 inhibitor venetoclax (ABT-199) are changing treatment paradigms for chronic lymphocytic leukemia (CLL) but important problems remain.	venetoclax	41-51	BCL2 apoptosis regulator	Homo sapiens	25-30
27297795-1	2016	Novel agents such as the Bcl-2 inhibitor venetoclax (ABT-199) are changing treatment paradigms for chronic lymphocytic leukemia (CLL) but important problems remain.	venetoclax	53-60	BCL2 apoptosis regulator	Homo sapiens	25-30
27520705-6	2016	Finally, Birinapant and AT-406 can synergise with BCL-2 inhibitor ABT-199 to reduce viability of adenocarcinoma cells with high BCL-2 expression.	venetoclax	66-73	BCL2 apoptosis regulator	Homo sapiens	128-133
27166183-0	2016	Inhibition of CHK1 enhances cell death induced by the Bcl-2-selective inhibitor ABT-199 in acute myeloid leukemia cells.	venetoclax	80-87	checkpoint kinase 1	Homo sapiens	14-18
27235137-7	2016	Proliferation induced by CD40(+) interleukin-21 stimulation was completely blocked by CC-115, and CD40-mediated resistance to fludarabine and venetoclax could be reverted by CC-115.	venetoclax	142-152	CD40 molecule	Homo sapiens	98-102
27069256-0	2016	The BCL2 selective inhibitor venetoclax induces rapid onset apoptosis of CLL cells in patients via a TP53-independent mechanism.	venetoclax	29-39	BCL2 apoptosis regulator	Homo sapiens	4-8
27069256-0	2016	The BCL2 selective inhibitor venetoclax induces rapid onset apoptosis of CLL cells in patients via a TP53-independent mechanism.	venetoclax	29-39	tumor protein p53	Homo sapiens	101-105
27069256-2	2016	Venetoclax (ABT-199) is a small-molecule selective inhibitor of BCL2 currently in clinical trials for CLL and other malignancies.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	64-68
27283158-1	2016	ABT-199, a potent and selective small-molecule antagonist of BCL-2, is being clinically vetted as pharmacotherapy for the treatment of acute myeloid leukemia (AML).	venetoclax	0-7	BCL2 apoptosis regulator	Homo sapiens	61-66
27353420-0	2016	Superior anti-tumor activity of the MDM2 antagonist idasanutlin and the Bcl-2 inhibitor venetoclax in p53 wild-type acute myeloid leukemia models.	venetoclax	88-98	B cell leukemia/lymphoma 2	Mus musculus	72-77
27353420-0	2016	Superior anti-tumor activity of the MDM2 antagonist idasanutlin and the Bcl-2 inhibitor venetoclax in p53 wild-type acute myeloid leukemia models.	venetoclax	88-98	transformation related protein 53, pseudogene	Mus musculus	102-105
27353420-1	2016	BACKGROUND: Venetoclax, a small molecule BH3 mimetic which inhibits the anti-apoptotic protein Bcl-2, and idasanutlin, a selective MDM2 antagonist, have both shown activity as single-agent treatments in pre-clinical and clinical studies in acute myeloid leukemia (AML).	venetoclax	12-22	B cell leukemia/lymphoma 2	Mus musculus	95-100
27353420-2	2016	In this study, we deliver the rationale and molecular basis for the combination of idasanutlin and venetoclax for treatment of p53 wild-type AML.	venetoclax	99-109	transformation related protein 53, pseudogene	Mus musculus	127-130
27353420-6	2016	RESULTS: Combination treatment with venetoclax and idasanutlin results in synergistic anti-tumor activity compared with the respective single-agent treatments in vitro, in p53 wild-type AML cell lines, and leads to strongly superior efficacy in vivo, in subcutaneous and orthotopic AML models.	venetoclax	36-46	transformation related protein 53, pseudogene	Mus musculus	172-175
27353420-11	2016	Protein expression studies demonstrated that inhibition of the anti-apoptotic protein Mcl-1 contributed to the activity of venetoclax and idasanutlin, with earlier inhibition of Mcl-1 in response to combination treatment contributing to the superior combined activity.	venetoclax	123-133	myeloid cell leukemia sequence 1	Mus musculus	86-91
27069256-2	2016	Venetoclax (ABT-199) is a small-molecule selective inhibitor of BCL2 currently in clinical trials for CLL and other malignancies.	venetoclax	12-19	BCL2 apoptosis regulator	Homo sapiens	64-68
27095788-1	2016	The Bcl-2 antagonist ABT-199 (venetoclax) has demonstrated promising clinical activity in patients with chronic lymphocytic leukemia (CLL).	venetoclax	21-28	BCL2 apoptosis regulator	Homo sapiens	4-9
27095788-9	2016	The finding that BCR signaling inhibitors differ in their ability to target Mcl-1 is relevant for the design of clinical trials combining these agents with ABT-199.	venetoclax	156-163	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	76-81
27166183-0	2016	Inhibition of CHK1 enhances cell death induced by the Bcl-2-selective inhibitor ABT-199 in acute myeloid leukemia cells.	venetoclax	80-87	BCL2 apoptosis regulator	Homo sapiens	54-59
27166183-2	2016	The Bcl-2-selective inhibitor ABT-199 has demonstrated encouraging preclinical results, drug resistance remains a concern.	venetoclax	30-37	BCL2 apoptosis regulator	Homo sapiens	4-9
26707935-0	2016	Dexamethasone treatment promotes Bcl-2 dependence in multiple myeloma resulting in sensitivity to venetoclax.	venetoclax	98-108	BCL2 apoptosis regulator	Homo sapiens	33-38
27056887-0	2016	High efficacy of the BCL-2 inhibitor ABT199 (venetoclax) in BCL-2 high-expressing neuroblastoma cell lines and xenografts and rational for combination with MCL-1 inhibition.	venetoclax	37-43	BCL2 apoptosis regulator	Homo sapiens	21-26
27056887-0	2016	High efficacy of the BCL-2 inhibitor ABT199 (venetoclax) in BCL-2 high-expressing neuroblastoma cell lines and xenografts and rational for combination with MCL-1 inhibition.	venetoclax	37-43	BCL2 apoptosis regulator	Homo sapiens	60-65
27056887-0	2016	High efficacy of the BCL-2 inhibitor ABT199 (venetoclax) in BCL-2 high-expressing neuroblastoma cell lines and xenografts and rational for combination with MCL-1 inhibition.	venetoclax	45-55	BCL2 apoptosis regulator	Homo sapiens	21-26
27056887-0	2016	High efficacy of the BCL-2 inhibitor ABT199 (venetoclax) in BCL-2 high-expressing neuroblastoma cell lines and xenografts and rational for combination with MCL-1 inhibition.	venetoclax	45-55	BCL2 apoptosis regulator	Homo sapiens	60-65
27056887-2	2016	In this study, the selective BCL-2 inhibitor ABT199 was tested in a panel of neuroblastoma cell lines with diverse expression levels of BCL-2 and other BCL-2 family proteins.	venetoclax	45-51	BCL2 apoptosis regulator	Homo sapiens	29-34
27056887-2	2016	In this study, the selective BCL-2 inhibitor ABT199 was tested in a panel of neuroblastoma cell lines with diverse expression levels of BCL-2 and other BCL-2 family proteins.	venetoclax	45-51	BCL2 apoptosis regulator	Homo sapiens	136-141
27056887-2	2016	In this study, the selective BCL-2 inhibitor ABT199 was tested in a panel of neuroblastoma cell lines with diverse expression levels of BCL-2 and other BCL-2 family proteins.	venetoclax	45-51	BCL2 apoptosis regulator	Homo sapiens	136-141
27056887-3	2016	ABT199 caused apoptosis more potently in neuroblastoma cell lines expressing high BCL-2 and BIM/BCL-2 complex levels than low expressing cell lines.	venetoclax	0-6	BCL2 apoptosis regulator	Homo sapiens	82-87
27056887-3	2016	ABT199 caused apoptosis more potently in neuroblastoma cell lines expressing high BCL-2 and BIM/BCL-2 complex levels than low expressing cell lines.	venetoclax	0-6	BCL2 like 11	Homo sapiens	92-95
27056887-3	2016	ABT199 caused apoptosis more potently in neuroblastoma cell lines expressing high BCL-2 and BIM/BCL-2 complex levels than low expressing cell lines.	venetoclax	0-6	BCL2 apoptosis regulator	Homo sapiens	96-101
27056887-6	2016	We showed that neuroblastoma cells might survive ABT199 treatment due to its acute upregulation of the anti-apoptotic BCL-2 family protein myeloid cell leukaemia sequence 1 (MCL-1) and BIM sequestration by MCL-1.	venetoclax	49-55	BCL2 apoptosis regulator	Homo sapiens	118-123
27056887-6	2016	We showed that neuroblastoma cells might survive ABT199 treatment due to its acute upregulation of the anti-apoptotic BCL-2 family protein myeloid cell leukaemia sequence 1 (MCL-1) and BIM sequestration by MCL-1.	venetoclax	49-55	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	139-172
27056887-6	2016	We showed that neuroblastoma cells might survive ABT199 treatment due to its acute upregulation of the anti-apoptotic BCL-2 family protein myeloid cell leukaemia sequence 1 (MCL-1) and BIM sequestration by MCL-1.	venetoclax	49-55	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	174-179
27056887-6	2016	We showed that neuroblastoma cells might survive ABT199 treatment due to its acute upregulation of the anti-apoptotic BCL-2 family protein myeloid cell leukaemia sequence 1 (MCL-1) and BIM sequestration by MCL-1.	venetoclax	49-55	BCL2 like 11	Homo sapiens	185-188
27056887-6	2016	We showed that neuroblastoma cells might survive ABT199 treatment due to its acute upregulation of the anti-apoptotic BCL-2 family protein myeloid cell leukaemia sequence 1 (MCL-1) and BIM sequestration by MCL-1.	venetoclax	49-55	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	206-211
27056887-8	2016	Our findings suggest that neuroblastoma patients with high BCL-2 and BIM/BCL-2 complex levels might benefit from combination treatment with ABT199 and compounds that inhibit MCL-1 expression.	venetoclax	140-146	BCL2 apoptosis regulator	Homo sapiens	59-64
27056887-8	2016	Our findings suggest that neuroblastoma patients with high BCL-2 and BIM/BCL-2 complex levels might benefit from combination treatment with ABT199 and compounds that inhibit MCL-1 expression.	venetoclax	140-146	BCL2 like 11	Homo sapiens	69-72
27056887-8	2016	Our findings suggest that neuroblastoma patients with high BCL-2 and BIM/BCL-2 complex levels might benefit from combination treatment with ABT199 and compounds that inhibit MCL-1 expression.	venetoclax	140-146	BCL2 apoptosis regulator	Homo sapiens	73-78
27178240-2	2016	Venetoclax is an oral small-molecule BCL2 inhibitor that induces chronic lymphocytic leukaemia cell apoptosis.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	37-41
26707935-1	2016	Venetoclax (ABT-199), a specific inhibitor of the anti-apoptotic protein Bcl-2, is currently in phase I clinical trials for multiple myeloma.	venetoclax	0-10	BCL2 apoptosis regulator	Homo sapiens	73-78
26707935-1	2016	Venetoclax (ABT-199), a specific inhibitor of the anti-apoptotic protein Bcl-2, is currently in phase I clinical trials for multiple myeloma.	venetoclax	12-19	BCL2 apoptosis regulator	Homo sapiens	73-78
26639348-16	2016	CONCLUSIONS: Selective targeting of BCL2 with venetoclax had a manageable safety profile and induced substantial responses in patients with relapsed CLL or SLL, including those with poor prognostic features.	venetoclax	46-56	BCL2 apoptosis regulator	Homo sapiens	36-40
26939706-0	2016	Expression Profile of BCL-2, BCL-XL, and MCL-1 Predicts Pharmacological Response to the BCL-2 Selective Antagonist Venetoclax in Multiple Myeloma Models.	venetoclax	115-125	BCL2 apoptosis regulator	Homo sapiens	22-27
26939706-0	2016	Expression Profile of BCL-2, BCL-XL, and MCL-1 Predicts Pharmacological Response to the BCL-2 Selective Antagonist Venetoclax in Multiple Myeloma Models.	venetoclax	115-125	BCL2 like 1	Homo sapiens	29-35
26939706-0	2016	Expression Profile of BCL-2, BCL-XL, and MCL-1 Predicts Pharmacological Response to the BCL-2 Selective Antagonist Venetoclax in Multiple Myeloma Models.	venetoclax	115-125	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	41-46
26939706-0	2016	Expression Profile of BCL-2, BCL-XL, and MCL-1 Predicts Pharmacological Response to the BCL-2 Selective Antagonist Venetoclax in Multiple Myeloma Models.	venetoclax	115-125	BCL2 apoptosis regulator	Homo sapiens	88-93
26939706-2	2016	Indeed, multiple myeloma cells are sensitive to antagonists that selectively target prosurvival proteins such as BCL-2/BCL-XL (ABT-737 and ABT-263/navitoclax) or BCL-2 only (ABT-199/GDC-0199/venetoclax).	venetoclax	182-190	BCL2 apoptosis regulator	Homo sapiens	113-118
26939706-2	2016	Indeed, multiple myeloma cells are sensitive to antagonists that selectively target prosurvival proteins such as BCL-2/BCL-XL (ABT-737 and ABT-263/navitoclax) or BCL-2 only (ABT-199/GDC-0199/venetoclax).	venetoclax	191-201	BCL2 apoptosis regulator	Homo sapiens	113-118
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).	venetoclax	73-83	BCL2 apoptosis regulator	Homo sapiens	38-43
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).	venetoclax	73-83	BCL2 like 1	Homo sapiens	48-54
26939706-8	2016	Resistance to venetoclax was mitigated by cotreatment with bortezomib in xenografts that coexpressed BCL-2 and MCL-1 due to upregulation of NOXA, a proapoptotic factor that neutralizes MCL-1.	venetoclax	14-24	BCL2 apoptosis regulator	Homo sapiens	101-106
26939706-8	2016	Resistance to venetoclax was mitigated by cotreatment with bortezomib in xenografts that coexpressed BCL-2 and MCL-1 due to upregulation of NOXA, a proapoptotic factor that neutralizes MCL-1.	venetoclax	14-24	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	111-116
26939706-8	2016	Resistance to venetoclax was mitigated by cotreatment with bortezomib in xenografts that coexpressed BCL-2 and MCL-1 due to upregulation of NOXA, a proapoptotic factor that neutralizes MCL-1.	venetoclax	14-24	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	140-144
26939706-8	2016	Resistance to venetoclax was mitigated by cotreatment with bortezomib in xenografts that coexpressed BCL-2 and MCL-1 due to upregulation of NOXA, a proapoptotic factor that neutralizes MCL-1.	venetoclax	14-24	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	185-190
26842479-10	2016	Antagonizing BCL-2 with venetoclax derepresses this antagonism, resulting in death, preferentially in HIV DNA containing cells, since only these cells generate Casp8p41.	venetoclax	24-34	BCL2 apoptosis regulator	Homo sapiens	13-18
26842479-10	2016	Antagonizing BCL-2 with venetoclax derepresses this antagonism, resulting in death, preferentially in HIV DNA containing cells, since only these cells generate Casp8p41.	venetoclax	24-34	caspase 8	Homo sapiens	160-165
26842479-10	2016	Antagonizing BCL-2 with venetoclax derepresses this antagonism, resulting in death, preferentially in HIV DNA containing cells, since only these cells generate Casp8p41.	venetoclax	24-34	erythrocyte membrane protein band 4.1	Homo sapiens	165-168
26701089-1	2016	Results from an international phase II study show that the investigational BCL2 inhibitor venetoclax is effective in patients with chronic lymphocytic leukemia and the chromosome 17p deletion, whose prognosis is particularly poor.	venetoclax	90-100	BCL2 apoptosis regulator	Homo sapiens	75-79
26899021-3	2016	Both navitoclax (BCL-2/BCL-XL antagonist) and ABT-199/venetoclax (BCL-2-selective inhibitor) have demonstrated therapeutic efficacy especially in chronic lymphocytic leukemia (CLL).	venetoclax	54-64	BCL2 apoptosis regulator	Homo sapiens	66-71
26967820-0	2016	Loss in MCL-1 function sensitizes non-Hodgkin"s lymphoma cell lines to the BCL-2-selective inhibitor venetoclax (ABT-199).	venetoclax	101-111	BCL2 apoptosis regulator	Homo sapiens	75-80
27076234-9	2016	ABT-199 is another novel drug; it inhibits BCL2 signaling, not the BCR pathway, and can be administered orally.	venetoclax	0-7	BCL2 apoptosis regulator	Homo sapiens	43-47
26874859-6	2016	This led to the creation of a Bcl-2 selective inhibitor, ABT-199 (Venetoclax).	venetoclax	57-64	BCL2 apoptosis regulator	Homo sapiens	30-35
26874859-6	2016	This led to the creation of a Bcl-2 selective inhibitor, ABT-199 (Venetoclax).	venetoclax	66-76	BCL2 apoptosis regulator	Homo sapiens	30-35
26874859-16	2016	In contrast, Bcl-2 dependent xenografts responded to ABT-199 alone and had sustained complete remission (CR) to the ABT-199/cyclophosphamide combination, with one recurrent tumor maintaining Bcl-2 dependence and obtaining a second CR after a second course of therapy.	venetoclax	53-60	BCL2 apoptosis regulator	Homo sapiens	13-18
26859456-3	2016	Using data from our large drug screen we predicted, and subsequently demonstrated, that MYCN-amplified neuroblastomas are sensitive to the BCL-2 inhibitor ABT-199.	venetoclax	155-162	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	88-92
26859456-3	2016	Using data from our large drug screen we predicted, and subsequently demonstrated, that MYCN-amplified neuroblastomas are sensitive to the BCL-2 inhibitor ABT-199.	venetoclax	155-162	BCL2 apoptosis regulator	Homo sapiens	139-144
26859456-5	2016	Screening for enhancers of ABT-199 sensitivity in MYCN-amplified neuroblastomas, we demonstrate that the Aurora Kinase A inhibitor MLN8237 combines with ABT-199 to induce widespread apoptosis.	venetoclax	27-34	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	50-54
26859456-5	2016	Screening for enhancers of ABT-199 sensitivity in MYCN-amplified neuroblastomas, we demonstrate that the Aurora Kinase A inhibitor MLN8237 combines with ABT-199 to induce widespread apoptosis.	venetoclax	27-34	aurora kinase A	Homo sapiens	105-120
26766586-2	2016	A recent paper by Roberts and colleagues describes an additional therapeutic target by reporting encouraging clinical results with venetoclax, an inhibitor of the antiapoptotic protein BCL2.	venetoclax	131-141	BCL2 apoptosis regulator	Homo sapiens	185-189
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.	venetoclax	72-82	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	138-143
26841018-6	2016	Adding the Bcl-2 antagonist venetoclax could further intensify the treatment of CLL.	venetoclax	28-38	BCL2 apoptosis regulator	Homo sapiens	11-16
26567361-6	2015	Here, we discuss the biology of the intrinsic pathway of apoptosis, an assay known as BH3 profiling that can interrogate this pathway, early attempts to target BCL-2 clinically, and the recent promising results with the BCL-2 antagonist venetoclax (ABT-199) in clinical trials in hematologic malignancies.	venetoclax	237-247	BCL2 apoptosis regulator	Homo sapiens	220-225
26153654-3	2016	To overcome the acquired apoptotic resistance in high-risk MDS, we investigated the induction of apoptosis by inhibition of pro-survival BCL-2 proteins using the BCL-2/-XL/-W inhibitor ABT-737 or the BCL-2-selective inhibitor ABT-199.	venetoclax	226-233	BCL2 apoptosis regulator	Homo sapiens	137-142
27889784-5	2016	Additionally, the observation of high expression levels of the anti-apoptotic mitochondrial protein Bcl-2 in CLL has led to the development of venetoclax, a BH3 mimetic compound that inhibits Bcl-2 and has shown high efficacy in CLL.	venetoclax	143-153	BCL2 apoptosis regulator	Homo sapiens	100-105
27889784-5	2016	Additionally, the observation of high expression levels of the anti-apoptotic mitochondrial protein Bcl-2 in CLL has led to the development of venetoclax, a BH3 mimetic compound that inhibits Bcl-2 and has shown high efficacy in CLL.	venetoclax	143-153	BCL2 apoptosis regulator	Homo sapiens	192-197
26565405-0	2015	Loss in MCL-1 function sensitizes non-Hodgkin"s lymphoma cell lines to the BCL-2-selective inhibitor venetoclax (ABT-199).	venetoclax	101-111	BCL2 apoptosis regulator	Homo sapiens	75-80
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.	venetoclax	72-82	BCL2 apoptosis regulator	Homo sapiens	46-51
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.	venetoclax	72-82	BCL2 apoptosis regulator	Homo sapiens	148-153
26516589-1	2015	The Bcl-2 family inhibitors venetoclax and navitoclax demonstrated potent antitumor activity in chronic lymphocytic leukemia patients, notably in reducing marrow load and adenopathy.	venetoclax	28-38	BCL2 apoptosis regulator	Homo sapiens	4-9
26537004-2	2015	We have reported that acquired resistance to the BCL-2 inhibitor ABT-199 (venetoclax) is associated with increased BCL-xL expression.	venetoclax	65-72	BCL2 apoptosis regulator	Homo sapiens	49-54
26537004-2	2015	We have reported that acquired resistance to the BCL-2 inhibitor ABT-199 (venetoclax) is associated with increased BCL-xL expression.	venetoclax	65-72	BCL2 like 1	Homo sapiens	115-121
26537004-2	2015	We have reported that acquired resistance to the BCL-2 inhibitor ABT-199 (venetoclax) is associated with increased BCL-xL expression.	venetoclax	74-84	BCL2 apoptosis regulator	Homo sapiens	49-54
26537004-2	2015	We have reported that acquired resistance to the BCL-2 inhibitor ABT-199 (venetoclax) is associated with increased BCL-xL expression.	venetoclax	74-84	BCL2 like 1	Homo sapiens	115-121
26430964-5	2015	Furthermore, ABT199, a BH-3 specific inhibitor of Bcl-2, as well as silencing of Bcl-2 blocked STAT3 phosphorylation.	venetoclax	13-19	BCL2 apoptosis regulator	Homo sapiens	50-55
26430964-5	2015	Furthermore, ABT199, a BH-3 specific inhibitor of Bcl-2, as well as silencing of Bcl-2 blocked STAT3 phosphorylation.	venetoclax	13-19	signal transducer and activator of transcription 3	Homo sapiens	95-100
26254443-8	2015	Cotreatment with BA and panobinostat (pan-histone deacetylase inhibitor) or palbociclib (CDK4/6 inhibitor) or ABT-199 (BCL2 antagonist) synergistically induced apoptosis of the ibrutinib-resistant MCL cells.	venetoclax	110-117	B cell leukemia/lymphoma 2	Mus musculus	119-123