PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
26627013-5	2016	Treatment of MLL-rearranged leukemic cells with dinaciclib resulted in rapidly decreased expression of the prosurvival protein Mcl-1, and accordingly, overexpression of Mcl-1 protected AML cells from dinaciclib-induced apoptosis.	dinaciclib	48-58	lysine methyltransferase 2A	Homo sapiens	13-16
26627013-5	2016	Treatment of MLL-rearranged leukemic cells with dinaciclib resulted in rapidly decreased expression of the prosurvival protein Mcl-1, and accordingly, overexpression of Mcl-1 protected AML cells from dinaciclib-induced apoptosis.	dinaciclib	48-58	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	127-132
26627013-5	2016	Treatment of MLL-rearranged leukemic cells with dinaciclib resulted in rapidly decreased expression of the prosurvival protein Mcl-1, and accordingly, overexpression of Mcl-1 protected AML cells from dinaciclib-induced apoptosis.	dinaciclib	48-58	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	169-174
26627013-5	2016	Treatment of MLL-rearranged leukemic cells with dinaciclib resulted in rapidly decreased expression of the prosurvival protein Mcl-1, and accordingly, overexpression of Mcl-1 protected AML cells from dinaciclib-induced apoptosis.	dinaciclib	200-210	lysine methyltransferase 2A	Homo sapiens	13-16
26627013-5	2016	Treatment of MLL-rearranged leukemic cells with dinaciclib resulted in rapidly decreased expression of the prosurvival protein Mcl-1, and accordingly, overexpression of Mcl-1 protected AML cells from dinaciclib-induced apoptosis.	dinaciclib	200-210	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	169-174
26585571-0	2016	Dinaciclib, a Cyclin-Dependent Kinase Inhibitor Promotes Proteasomal Degradation of Mcl-1 and Enhances ABT-737-Mediated Cell Death in Malignant Human Glioma Cell Lines.	dinaciclib	0-10	cyclin dependent kinase inhibitor 3	Homo sapiens	14-47
26585571-0	2016	Dinaciclib, a Cyclin-Dependent Kinase Inhibitor Promotes Proteasomal Degradation of Mcl-1 and Enhances ABT-737-Mediated Cell Death in Malignant Human Glioma Cell Lines.	dinaciclib	0-10	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	84-89
26585571-8	2016	The synergistic killing by ABT-737 with dinaciclib led to cell death accompanied by the hallmarks of apoptosis, including an early loss of the mitochondrial transmembrane potential; the release of cytochrome c, smac/DIABLO, and apoptosis-inducing factor; phosphatidylserine exposure on the plasma membrane surface and activation of caspases and poly ADP-ribose polymerase.	dinaciclib	40-50	cytochrome c, somatic	Homo sapiens	197-209
26585571-8	2016	The synergistic killing by ABT-737 with dinaciclib led to cell death accompanied by the hallmarks of apoptosis, including an early loss of the mitochondrial transmembrane potential; the release of cytochrome c, smac/DIABLO, and apoptosis-inducing factor; phosphatidylserine exposure on the plasma membrane surface and activation of caspases and poly ADP-ribose polymerase.	dinaciclib	40-50	diablo IAP-binding mitochondrial protein	Homo sapiens	211-215
26585571-8	2016	The synergistic killing by ABT-737 with dinaciclib led to cell death accompanied by the hallmarks of apoptosis, including an early loss of the mitochondrial transmembrane potential; the release of cytochrome c, smac/DIABLO, and apoptosis-inducing factor; phosphatidylserine exposure on the plasma membrane surface and activation of caspases and poly ADP-ribose polymerase.	dinaciclib	40-50	diablo IAP-binding mitochondrial protein	Homo sapiens	216-222
26585571-8	2016	The synergistic killing by ABT-737 with dinaciclib led to cell death accompanied by the hallmarks of apoptosis, including an early loss of the mitochondrial transmembrane potential; the release of cytochrome c, smac/DIABLO, and apoptosis-inducing factor; phosphatidylserine exposure on the plasma membrane surface and activation of caspases and poly ADP-ribose polymerase.	dinaciclib	40-50	poly(ADP-ribose) polymerase 1	Homo sapiens	345-371
26719576-0	2016	A Cyclin-Dependent Kinase Inhibitor, Dinaciclib, Impairs Homologous Recombination and Sensitizes Multiple Myeloma Cells to PARP Inhibition.	dinaciclib	37-47	poly (ADP-ribose) polymerase family, member 1	Mus musculus	123-127
26719576-7	2016	Here, we show that a CDK inhibitor, dinaciclib, impairs HR repair and sensitizes multiple myeloma cells to the PARP1/2 inhibitor ABT-888.	dinaciclib	36-46	poly (ADP-ribose) polymerase family, member 12	Mus musculus	111-118
26719576-10	2016	Cotreatment with dinaciclib and ABT-888 in vitro resulted in synthetic lethality of multiple myeloma cells, but not normal CD19(+) B cells, and slowed growth of multiple myeloma xenografts in SCID mice almost two-fold.	dinaciclib	17-27	CD19 antigen	Mus musculus	123-127
25962959-2	2015	Dinaciclib, a novel small molecule inhibitor of CDK1, CDK2, CDK5 and CDK9, is assessed in clinical trials for the treatment of several types of cancers.	dinaciclib	0-10	cyclin dependent kinase 1	Homo sapiens	48-52
26300056-0	2015	Dinaciclib, a cyclin-dependent kinase inhibitor, is a substrate of human ABCB1 and ABCG2 and an inhibitor of human ABCC1 in vitro.	dinaciclib	0-10	cyclin dependent kinase inhibitor 3	Homo sapiens	14-47
26300056-0	2015	Dinaciclib, a cyclin-dependent kinase inhibitor, is a substrate of human ABCB1 and ABCG2 and an inhibitor of human ABCC1 in vitro.	dinaciclib	0-10	ATP binding cassette subfamily B member 1	Homo sapiens	73-78
26300056-0	2015	Dinaciclib, a cyclin-dependent kinase inhibitor, is a substrate of human ABCB1 and ABCG2 and an inhibitor of human ABCC1 in vitro.	dinaciclib	0-10	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	83-88
26300056-0	2015	Dinaciclib, a cyclin-dependent kinase inhibitor, is a substrate of human ABCB1 and ABCG2 and an inhibitor of human ABCC1 in vitro.	dinaciclib	0-10	ATP binding cassette subfamily C member 1	Homo sapiens	115-120
26300056-1	2015	Dinaciclib is a novel cyclin-dependent kinase inhibitor (CDKI) with significant activity against various cancers in vitro and in vivo.	dinaciclib	0-10	cyclin dependent kinase inhibitor 3	Homo sapiens	22-55
26300056-1	2015	Dinaciclib is a novel cyclin-dependent kinase inhibitor (CDKI) with significant activity against various cancers in vitro and in vivo.	dinaciclib	0-10	cyclin dependent kinase inhibitor 3	Homo sapiens	57-61
26300056-9	2015	Moreover, dinaciclib significantly inhibited ABCC1-mediated efflux of daunorubicin (EC50=18 muM).	dinaciclib	10-20	ATP binding cassette subfamily C member 1	Homo sapiens	45-50
26300056-10	2015	The inhibition of ABCC1 further led to a synergistic effect of dinaciclib in both MDCKII-ABCC1 and human cancer T47D cells, when applied in combination with anticancer drugs.	dinaciclib	63-73	ATP binding cassette subfamily C member 1	Homo sapiens	18-23
26300056-10	2015	The inhibition of ABCC1 further led to a synergistic effect of dinaciclib in both MDCKII-ABCC1 and human cancer T47D cells, when applied in combination with anticancer drugs.	dinaciclib	63-73	ATP binding cassette subfamily C member 1	Homo sapiens	82-94
25947565-2	2015	CDK1/CDK2 inhibitors, such as dinaciclib, combined with anthracyclines, were synergistic in decreasing viability of TNBC cell lines.	dinaciclib	30-40	cyclin dependent kinase 1	Homo sapiens	0-4
25947565-2	2015	CDK1/CDK2 inhibitors, such as dinaciclib, combined with anthracyclines, were synergistic in decreasing viability of TNBC cell lines.	dinaciclib	30-40	cyclin dependent kinase 2	Homo sapiens	5-9
26219338-8	2015	CDK inhibition by dinaciclib resulted in Bim release from Mcl-1 in ABT-737-resistant cells.	dinaciclib	18-28	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	58-63
26766294-5	2016	Clinical studies of the drugs flavopiridol, dinaciclib, seliciclib, SNS-032 and RGB-286638 used as CDK9 inhibitors are also reviewed, with their additional targets and their relative IC50 values.	dinaciclib	44-54	cyclin dependent kinase 9	Homo sapiens	99-103
25882699-3	2015	Here we explore drugs that cause loss of MCL1, particularly the potent new cyclin-dependent kinase inhibitor dinaciclib, which knocks down MCL1 by inhibiting CDK9.	dinaciclib	109-119	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	41-45
25882699-3	2015	Here we explore drugs that cause loss of MCL1, particularly the potent new cyclin-dependent kinase inhibitor dinaciclib, which knocks down MCL1 by inhibiting CDK9.	dinaciclib	109-119	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	139-143
25882699-3	2015	Here we explore drugs that cause loss of MCL1, particularly the potent new cyclin-dependent kinase inhibitor dinaciclib, which knocks down MCL1 by inhibiting CDK9.	dinaciclib	109-119	cyclin dependent kinase 9	Homo sapiens	158-162
25882699-4	2015	Dinaciclib induces apoptosis in DLBCL cells but is completely overcome by increased activity of BCL2.	dinaciclib	0-10	BCL2 apoptosis regulator	Homo sapiens	96-100
25962959-2	2015	Dinaciclib, a novel small molecule inhibitor of CDK1, CDK2, CDK5 and CDK9, is assessed in clinical trials for the treatment of several types of cancers.	dinaciclib	0-10	cyclin dependent kinase 2	Homo sapiens	54-58
25962959-2	2015	Dinaciclib, a novel small molecule inhibitor of CDK1, CDK2, CDK5 and CDK9, is assessed in clinical trials for the treatment of several types of cancers.	dinaciclib	0-10	cyclin dependent kinase 5	Homo sapiens	60-64
25962959-2	2015	Dinaciclib, a novel small molecule inhibitor of CDK1, CDK2, CDK5 and CDK9, is assessed in clinical trials for the treatment of several types of cancers.	dinaciclib	0-10	cyclin dependent kinase 9	Homo sapiens	69-73
25962959-4	2015	Dinaciclib alone actively induced cell growth inhibition, cell cycle arrest and apoptosis with the increased intracellular ROS levels, which were accompanied by obvious alterations of related proteins such as CDKs, Cyclins, Mcl-1, XIAP and survivin.	dinaciclib	0-10	cyclin dependent kinase 1	Homo sapiens	209-213
25962959-4	2015	Dinaciclib alone actively induced cell growth inhibition, cell cycle arrest and apoptosis with the increased intracellular ROS levels, which were accompanied by obvious alterations of related proteins such as CDKs, Cyclins, Mcl-1, XIAP and survivin.	dinaciclib	0-10	cyclin L2	Homo sapiens	215-222
25962959-4	2015	Dinaciclib alone actively induced cell growth inhibition, cell cycle arrest and apoptosis with the increased intracellular ROS levels, which were accompanied by obvious alterations of related proteins such as CDKs, Cyclins, Mcl-1, XIAP and survivin.	dinaciclib	0-10	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	224-229
25962959-4	2015	Dinaciclib alone actively induced cell growth inhibition, cell cycle arrest and apoptosis with the increased intracellular ROS levels, which were accompanied by obvious alterations of related proteins such as CDKs, Cyclins, Mcl-1, XIAP and survivin.	dinaciclib	0-10	X-linked inhibitor of apoptosis	Homo sapiens	231-235
26059440-0	2015	Maritoclax and dinaciclib inhibit MCL-1 activity and induce apoptosis in both a MCL-1-dependent and -independent manner.	dinaciclib	15-25	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	34-39
25578475-0	2015	CDK9 inhibition by dinaciclib potently suppresses Mcl-1 to induce durable apoptotic responses in aggressive MYC-driven B-cell lymphoma in vivo.	dinaciclib	19-29	cyclin dependent kinase 9	Homo sapiens	0-4
25578475-0	2015	CDK9 inhibition by dinaciclib potently suppresses Mcl-1 to induce durable apoptotic responses in aggressive MYC-driven B-cell lymphoma in vivo.	dinaciclib	19-29	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	50-55
25578475-0	2015	CDK9 inhibition by dinaciclib potently suppresses Mcl-1 to induce durable apoptotic responses in aggressive MYC-driven B-cell lymphoma in vivo.	dinaciclib	19-29	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	108-111
26059440-0	2015	Maritoclax and dinaciclib inhibit MCL-1 activity and induce apoptosis in both a MCL-1-dependent and -independent manner.	dinaciclib	15-25	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	80-85
26059440-3	2015	In this report, the selectivity and potency of two putative MCL-1 inhibitors, dinaciclib and maritoclax, were assessed.	dinaciclib	78-88	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	60-65
26059440-4	2015	Although both compounds induced Bax/Bak- and caspase-9-dependent apoptosis, dinaciclib was more potent than maritoclax in downregulating MCL-1 and also in inducing apoptosis.	dinaciclib	76-86	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	137-142
26059440-9	2015	Although dinaciclib is clearly not a specific MCL-1 inhibitor, its ability to rapidly downregulate MCL-1 may be beneficial in many clinical settings, where it may reverse chemoresistance or sensitize to other chemotherapeutic agents.	dinaciclib	9-19	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	99-104
25107301-2	2014	Dinaciclib (MK-7965, formerly SCH727965) is a relatively novel CDK 1/2/5/9 inhibitor that has shown promising results in preclinical studies and an acceptable safety profile in Phase I clinical trials.	dinaciclib	0-10	cyclin dependent kinase 1	Homo sapiens	63-74
25217392-1	2014	PURPOSE: Dinaciclib is a novel selective inhibitor of cyclin-dependent kinase (CDK)1, CDK2, CDK5, and CDK9.	dinaciclib	9-19	cyclin dependent kinase 1	Homo sapiens	79-84
25217392-1	2014	PURPOSE: Dinaciclib is a novel selective inhibitor of cyclin-dependent kinase (CDK)1, CDK2, CDK5, and CDK9.	dinaciclib	9-19	cyclin dependent kinase 2	Homo sapiens	86-90
25217392-1	2014	PURPOSE: Dinaciclib is a novel selective inhibitor of cyclin-dependent kinase (CDK)1, CDK2, CDK5, and CDK9.	dinaciclib	9-19	cyclin dependent kinase 5	Homo sapiens	92-96
25217392-1	2014	PURPOSE: Dinaciclib is a novel selective inhibitor of cyclin-dependent kinase (CDK)1, CDK2, CDK5, and CDK9.	dinaciclib	9-19	cyclin dependent kinase 9	Homo sapiens	102-106
25289887-1	2014	Dinaciclib is a potent CDK1, 2, 5 and 9 inhibitor being developed for the treatment of cancer.	dinaciclib	0-10	cyclin dependent kinase 1	Homo sapiens	23-27
25289887-4	2014	This was further underscored by kinetics of dinaciclib-induced downregulation of the antiapoptotic BCL2 family member MCL1 and correlation of sensitivity with the MCL1-to-BCL-xL mRNA ratio or MCL1 amplification in solid tumor models in vitro and in vivo.	dinaciclib	44-54	BCL2 apoptosis regulator	Homo sapiens	99-103
25289887-4	2014	This was further underscored by kinetics of dinaciclib-induced downregulation of the antiapoptotic BCL2 family member MCL1 and correlation of sensitivity with the MCL1-to-BCL-xL mRNA ratio or MCL1 amplification in solid tumor models in vitro and in vivo.	dinaciclib	44-54	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	118-122
25395429-0	2015	Dinaciclib, a novel CDK inhibitor, demonstrates encouraging single-agent activity in patients with relapsed multiple myeloma.	dinaciclib	0-10	cyclin dependent kinase 1	Homo sapiens	20-23
25395429-2	2015	Dinaciclib is a novel potent small molecule inhibitor of cyclin-dependent kinases (CDK)1, CDK2, CDK5, and CDK9.	dinaciclib	0-10	cyclin dependent kinase 1	Homo sapiens	83-88
25395429-2	2015	Dinaciclib is a novel potent small molecule inhibitor of cyclin-dependent kinases (CDK)1, CDK2, CDK5, and CDK9.	dinaciclib	0-10	cyclin dependent kinase 2	Homo sapiens	90-94
25395429-2	2015	Dinaciclib is a novel potent small molecule inhibitor of cyclin-dependent kinases (CDK)1, CDK2, CDK5, and CDK9.	dinaciclib	0-10	cyclin dependent kinase 5	Homo sapiens	96-100
25395429-2	2015	Dinaciclib is a novel potent small molecule inhibitor of cyclin-dependent kinases (CDK)1, CDK2, CDK5, and CDK9.	dinaciclib	0-10	cyclin dependent kinase 9	Homo sapiens	106-110
25107301-2	2014	Dinaciclib (MK-7965, formerly SCH727965) is a relatively novel CDK 1/2/5/9 inhibitor that has shown promising results in preclinical studies and an acceptable safety profile in Phase I clinical trials.	dinaciclib	12-19	cyclin dependent kinase 1	Homo sapiens	63-74
25107301-2	2014	Dinaciclib (MK-7965, formerly SCH727965) is a relatively novel CDK 1/2/5/9 inhibitor that has shown promising results in preclinical studies and an acceptable safety profile in Phase I clinical trials.	dinaciclib	30-39	cyclin dependent kinase 1	Homo sapiens	63-74
21768777-2	2011	Flavopiridol and dinaciclib are cyclin-dependent kinase 7 and 9 inhibitors that transcriptionally inhibit expression of Mcl-1.	dinaciclib	17-27	cyclin dependent kinase 7	Homo sapiens	32-57
24007471-2	2013	Dinaciclib is a potent inhibitor of cyclin-dependent kinases (CDKs), which recently advanced to Phase III clinical trials for the treatment of leukemia.	dinaciclib	0-10	cyclin dependent kinase 2	Homo sapiens	62-66
24007471-3	2013	We determined the crystal structure of dinaciclib in complex with CDK2 at 1.7 A resolution, revealing an elaborate network of binding interactions in the ATP site, which explains the extraordinary potency and selectivity of this inhibitor.	dinaciclib	39-49	cyclin dependent kinase 2	Homo sapiens	66-70
24007471-4	2013	Remarkably, dinaciclib also interacted with the acetyl-lysine recognition site of the bromodomain testis-specific protein BRDT, a member of the BET family of bromodomains.	dinaciclib	12-22	bromodomain testis associated	Homo sapiens	122-126
24007471-5	2013	The binding mode of dinaciclib to BRDT at 2.0 A resolution suggests that general kinase inhibitors ("hinge binders") possess a previously unrecognized potential to act as protein-protein inhibitors of bromodomains.	dinaciclib	20-30	bromodomain testis associated	Homo sapiens	34-38
23527225-0	2013	The anti-melanoma activity of dinaciclib, a cyclin-dependent kinase inhibitor, is dependent on p53 signaling.	dinaciclib	30-40	tumor protein p53	Homo sapiens	95-98
23527225-6	2013	Further mechanistic studies revealed that dinaciclib induces p53 expression whilst simultaneously downregulating the expression of the anti-apoptotic factors Mcl-1 and XIAP.	dinaciclib	42-52	tumor protein p53	Homo sapiens	61-64
23527225-6	2013	Further mechanistic studies revealed that dinaciclib induces p53 expression whilst simultaneously downregulating the expression of the anti-apoptotic factors Mcl-1 and XIAP.	dinaciclib	42-52	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	158-163
23527225-6	2013	Further mechanistic studies revealed that dinaciclib induces p53 expression whilst simultaneously downregulating the expression of the anti-apoptotic factors Mcl-1 and XIAP.	dinaciclib	42-52	X-linked inhibitor of apoptosis	Homo sapiens	168-172
23527225-8	2013	Knockdown of p53 completely abolished the induction of apoptosis seen following dinaciclib treatment as shown by a lack of annexin-V staining and caspase-3 cleavage.	dinaciclib	80-90	tumor protein p53	Homo sapiens	13-16
23527225-9	2013	Altogether, these data show that dinaciclib induces apoptosis in a large panel of melanoma cell lines through a mechanism requiring p53 expression.	dinaciclib	33-43	tumor protein p53	Homo sapiens	132-135
21768779-3	2011	Dinaciclib (SCH727965) is a novel small molecule multi-CDK inhibitor with low nanomolar potency against CDK1, CDK2, CDK5 and CDK9 that has shown favorable toxicity and efficacy in preliminary mouse experiments, and has been well tolerated in Phase I clinical trials.	dinaciclib	0-10	cyclin-dependent kinase 1	Mus musculus	104-108
21768779-3	2011	Dinaciclib (SCH727965) is a novel small molecule multi-CDK inhibitor with low nanomolar potency against CDK1, CDK2, CDK5 and CDK9 that has shown favorable toxicity and efficacy in preliminary mouse experiments, and has been well tolerated in Phase I clinical trials.	dinaciclib	0-10	cyclin-dependent kinase 2	Mus musculus	110-114
21768779-3	2011	Dinaciclib (SCH727965) is a novel small molecule multi-CDK inhibitor with low nanomolar potency against CDK1, CDK2, CDK5 and CDK9 that has shown favorable toxicity and efficacy in preliminary mouse experiments, and has been well tolerated in Phase I clinical trials.	dinaciclib	0-10	cyclin-dependent kinase 5	Mus musculus	116-120
21768779-3	2011	Dinaciclib (SCH727965) is a novel small molecule multi-CDK inhibitor with low nanomolar potency against CDK1, CDK2, CDK5 and CDK9 that has shown favorable toxicity and efficacy in preliminary mouse experiments, and has been well tolerated in Phase I clinical trials.	dinaciclib	0-10	cyclin-dependent kinase 9 (CDC2-related kinase)	Mus musculus	125-129
21768779-3	2011	Dinaciclib (SCH727965) is a novel small molecule multi-CDK inhibitor with low nanomolar potency against CDK1, CDK2, CDK5 and CDK9 that has shown favorable toxicity and efficacy in preliminary mouse experiments, and has been well tolerated in Phase I clinical trials.	dinaciclib	12-21	cyclin-dependent kinase 1	Mus musculus	104-108
21768779-3	2011	Dinaciclib (SCH727965) is a novel small molecule multi-CDK inhibitor with low nanomolar potency against CDK1, CDK2, CDK5 and CDK9 that has shown favorable toxicity and efficacy in preliminary mouse experiments, and has been well tolerated in Phase I clinical trials.	dinaciclib	12-21	cyclin-dependent kinase 2	Mus musculus	110-114
21768779-3	2011	Dinaciclib (SCH727965) is a novel small molecule multi-CDK inhibitor with low nanomolar potency against CDK1, CDK2, CDK5 and CDK9 that has shown favorable toxicity and efficacy in preliminary mouse experiments, and has been well tolerated in Phase I clinical trials.	dinaciclib	12-21	cyclin-dependent kinase 5	Mus musculus	116-120
21768779-3	2011	Dinaciclib (SCH727965) is a novel small molecule multi-CDK inhibitor with low nanomolar potency against CDK1, CDK2, CDK5 and CDK9 that has shown favorable toxicity and efficacy in preliminary mouse experiments, and has been well tolerated in Phase I clinical trials.	dinaciclib	12-21	cyclin-dependent kinase 9 (CDC2-related kinase)	Mus musculus	125-129
21768779-10	2011	Gene Set Enrichment Analysis identified overrepresentation of the Notch and Transforming Growth Factor-beta (TGF-beta) signaling pathways in the xenografts least responsive to SCH727965 treatment.	dinaciclib	176-185	transforming growth factor beta 1	Homo sapiens	76-107
21768779-10	2011	Gene Set Enrichment Analysis identified overrepresentation of the Notch and Transforming Growth Factor-beta (TGF-beta) signaling pathways in the xenografts least responsive to SCH727965 treatment.	dinaciclib	176-185	transforming growth factor beta 1	Homo sapiens	109-117
24393852-0	2014	Randomized phase II trial of the cyclin-dependent kinase inhibitor dinaciclib (MK-7965) versus capecitabine in patients with advanced breast cancer.	dinaciclib	67-77	cyclin dependent kinase inhibitor 3	Homo sapiens	33-66
24393852-0	2014	Randomized phase II trial of the cyclin-dependent kinase inhibitor dinaciclib (MK-7965) versus capecitabine in patients with advanced breast cancer.	dinaciclib	79-86	cyclin dependent kinase inhibitor 3	Homo sapiens	33-66
24393852-2	2014	Dinaciclib (MK-7965, formerly SCH727965), a small-molecule cyclin-dependent kinase inhibitor, has demonstrated antitumor activity in phase I studies with solid-tumor patients.	dinaciclib	0-10	cyclin dependent kinase inhibitor 3	Homo sapiens	59-92
24393852-2	2014	Dinaciclib (MK-7965, formerly SCH727965), a small-molecule cyclin-dependent kinase inhibitor, has demonstrated antitumor activity in phase I studies with solid-tumor patients.	dinaciclib	12-19	cyclin dependent kinase inhibitor 3	Homo sapiens	59-92
24393852-2	2014	Dinaciclib (MK-7965, formerly SCH727965), a small-molecule cyclin-dependent kinase inhibitor, has demonstrated antitumor activity in phase I studies with solid-tumor patients.	dinaciclib	30-39	cyclin dependent kinase inhibitor 3	Homo sapiens	59-92
24393852-6	2014	Dinaciclib treatment demonstrated antitumor activity in 2 of 7 patients with estrogen receptor-positive and human epidermal growth factor receptor 2-negative metastatic breast cancer (1 confirmed and 1 unconfirmed partial response), as well as acceptable safety and tolerability.	dinaciclib	0-10	erb-b2 receptor tyrosine kinase 2	Homo sapiens	114-148
24362465-2	2014	Here, effects of cyclin-dependent kinase (CDK) inhibitor SCH727965 (dinaciclib) on the IRE1 arm of the UPR were examined in human leukemia and myeloma cells.	dinaciclib	57-66	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	87-91
24362465-3	2014	Exposure of cells to extremely low (e.g., nmol/L) concentrations of SCH727965, a potent inhibitor of CDKs 1/2/5/9, diminished XBP-1s and Grp78 induction by the endoplasmic reticulum (ER) stress-inducers thapsigargin and tunicamycin, while sharply inducing cell death.	dinaciclib	68-77	cyclin dependent kinase 1	Homo sapiens	101-113
24362465-3	2014	Exposure of cells to extremely low (e.g., nmol/L) concentrations of SCH727965, a potent inhibitor of CDKs 1/2/5/9, diminished XBP-1s and Grp78 induction by the endoplasmic reticulum (ER) stress-inducers thapsigargin and tunicamycin, while sharply inducing cell death.	dinaciclib	68-77	X-box binding protein 1	Homo sapiens	126-131
24362465-3	2014	Exposure of cells to extremely low (e.g., nmol/L) concentrations of SCH727965, a potent inhibitor of CDKs 1/2/5/9, diminished XBP-1s and Grp78 induction by the endoplasmic reticulum (ER) stress-inducers thapsigargin and tunicamycin, while sharply inducing cell death.	dinaciclib	68-77	heat shock protein family A (Hsp70) member 5	Homo sapiens	137-142
23949430-7	2013	Pharmacodynamic studies demonstrated in vivo inhibition of Mcl-1 expression and induction of PARP cleavage in patients" peripheral blood mononuclear cells 4 h after dinaciclib infusion, but the effects were lost by 24 h and did not correlate with clinical outcome.	dinaciclib	165-175	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	59-64
23949430-7	2013	Pharmacodynamic studies demonstrated in vivo inhibition of Mcl-1 expression and induction of PARP cleavage in patients" peripheral blood mononuclear cells 4 h after dinaciclib infusion, but the effects were lost by 24 h and did not correlate with clinical outcome.	dinaciclib	165-175	poly(ADP-ribose) polymerase 1	Homo sapiens	93-97
23053255-1	2012	PURPOSE: Dinaciclib, a selective inhibitor of cyclin-dependent kinase (CDK) 1, CDK2, CDK5, and CDK9, is metabolized via CYP3A4.	dinaciclib	9-19	cyclin dependent kinase 1	Homo sapiens	46-77
23053255-1	2012	PURPOSE: Dinaciclib, a selective inhibitor of cyclin-dependent kinase (CDK) 1, CDK2, CDK5, and CDK9, is metabolized via CYP3A4.	dinaciclib	9-19	cyclin dependent kinase 2	Homo sapiens	79-83
23053255-1	2012	PURPOSE: Dinaciclib, a selective inhibitor of cyclin-dependent kinase (CDK) 1, CDK2, CDK5, and CDK9, is metabolized via CYP3A4.	dinaciclib	9-19	cyclin dependent kinase 5	Homo sapiens	85-89
23053255-1	2012	PURPOSE: Dinaciclib, a selective inhibitor of cyclin-dependent kinase (CDK) 1, CDK2, CDK5, and CDK9, is metabolized via CYP3A4.	dinaciclib	9-19	cyclin dependent kinase 9	Homo sapiens	95-99
23053255-1	2012	PURPOSE: Dinaciclib, a selective inhibitor of cyclin-dependent kinase (CDK) 1, CDK2, CDK5, and CDK9, is metabolized via CYP3A4.	dinaciclib	9-19	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	120-126
21768777-2	2011	Flavopiridol and dinaciclib are cyclin-dependent kinase 7 and 9 inhibitors that transcriptionally inhibit expression of Mcl-1.	dinaciclib	17-27	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	120-125
34534577-9	2022	Dinaciclib did not affect MEK signaling but decreased the expression of several prosurvival proteins, including survivin and CDK1, to induce apoptosis and inhibit mitosis.	dinaciclib	0-10	cyclin dependent kinase 1	Homo sapiens	125-129
33589591-5	2021	We, therefore, tested whether the CDK inhibitor, dinaciclib, could block MCL-1 in preclinical HER2-amplified breast cancer models and therefore sensitize these cancers to dual HER2/EGFR inhibitors neratinib and lapatinib, as well as to the novel selective HER2 inhibitor tucatinib.	dinaciclib	49-59	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	73-78
33589591-5	2021	We, therefore, tested whether the CDK inhibitor, dinaciclib, could block MCL-1 in preclinical HER2-amplified breast cancer models and therefore sensitize these cancers to dual HER2/EGFR inhibitors neratinib and lapatinib, as well as to the novel selective HER2 inhibitor tucatinib.	dinaciclib	49-59	erb-b2 receptor tyrosine kinase 2	Homo sapiens	94-98
33589591-5	2021	We, therefore, tested whether the CDK inhibitor, dinaciclib, could block MCL-1 in preclinical HER2-amplified breast cancer models and therefore sensitize these cancers to dual HER2/EGFR inhibitors neratinib and lapatinib, as well as to the novel selective HER2 inhibitor tucatinib.	dinaciclib	49-59	erb-b2 receptor tyrosine kinase 2	Homo sapiens	176-180
33589591-5	2021	We, therefore, tested whether the CDK inhibitor, dinaciclib, could block MCL-1 in preclinical HER2-amplified breast cancer models and therefore sensitize these cancers to dual HER2/EGFR inhibitors neratinib and lapatinib, as well as to the novel selective HER2 inhibitor tucatinib.	dinaciclib	49-59	epidermal growth factor receptor	Homo sapiens	181-185
33589591-5	2021	We, therefore, tested whether the CDK inhibitor, dinaciclib, could block MCL-1 in preclinical HER2-amplified breast cancer models and therefore sensitize these cancers to dual HER2/EGFR inhibitors neratinib and lapatinib, as well as to the novel selective HER2 inhibitor tucatinib.	dinaciclib	49-59	erb-b2 receptor tyrosine kinase 2	Homo sapiens	176-180
33030957-4	2021	Inhibition of MEK/ERK by cobimetinib or CDK inhibitor dinaciclib was shown to attenuate mutant BRAF-induced PD-L1 coincident with reduced c-JUN and YAP expression whose combined knockdown reduced PD-L1.	dinaciclib	54-64	mitogen-activated protein kinase kinase 7	Homo sapiens	14-17
33030957-4	2021	Inhibition of MEK/ERK by cobimetinib or CDK inhibitor dinaciclib was shown to attenuate mutant BRAF-induced PD-L1 coincident with reduced c-JUN and YAP expression whose combined knockdown reduced PD-L1.	dinaciclib	54-64	mitogen-activated protein kinase 1	Homo sapiens	18-21
33030957-4	2021	Inhibition of MEK/ERK by cobimetinib or CDK inhibitor dinaciclib was shown to attenuate mutant BRAF-induced PD-L1 coincident with reduced c-JUN and YAP expression whose combined knockdown reduced PD-L1.	dinaciclib	54-64	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	95-99
33030957-4	2021	Inhibition of MEK/ERK by cobimetinib or CDK inhibitor dinaciclib was shown to attenuate mutant BRAF-induced PD-L1 coincident with reduced c-JUN and YAP expression whose combined knockdown reduced PD-L1.	dinaciclib	54-64	CD274 molecule	Homo sapiens	108-113
33030957-4	2021	Inhibition of MEK/ERK by cobimetinib or CDK inhibitor dinaciclib was shown to attenuate mutant BRAF-induced PD-L1 coincident with reduced c-JUN and YAP expression whose combined knockdown reduced PD-L1.	dinaciclib	54-64	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	138-143
33030957-4	2021	Inhibition of MEK/ERK by cobimetinib or CDK inhibitor dinaciclib was shown to attenuate mutant BRAF-induced PD-L1 coincident with reduced c-JUN and YAP expression whose combined knockdown reduced PD-L1.	dinaciclib	54-64	Yes1 associated transcriptional regulator	Homo sapiens	148-151
33030957-4	2021	Inhibition of MEK/ERK by cobimetinib or CDK inhibitor dinaciclib was shown to attenuate mutant BRAF-induced PD-L1 coincident with reduced c-JUN and YAP expression whose combined knockdown reduced PD-L1.	dinaciclib	54-64	CD274 molecule	Homo sapiens	196-201
34688130-3	2021	The 7-(4-Bromo-phenyl)-3-(3-chloro/2-chloro-phenylazo)-pyrazolo(1,5-a)pyrimidin-2-ylamines 5 h and 5i revealed the best CDK2 inhibitory activity with comparable potency (IC50 = 22 and 24 nM, respectively) to that of dinaciclib (IC50 = 18 nM).	dinaciclib	216-226	cyclin dependent kinase 2	Homo sapiens	120-124
34688130-10	2021	The molecular docking simulations indicated, as expected, that the dinaciclib analogues can well-accommodate the CDK2 binding site, forming a variety of interactions.	dinaciclib	67-77	cyclin dependent kinase 2	Homo sapiens	113-117
33777535-15	2021	In addition, the anti-tumor activity of a potential CDC20 inhibitor, namely dinaciclib, was investigated in CCA cell lines.	dinaciclib	76-86	cell division cycle 20	Homo sapiens	52-57
33800911-6	2021	Dinaciclib was shown to elicit a bimodal action in EC cell lines, disrupting both cell cycle progression and phosphorylation of the RNA polymerase carboxy terminal domain, with a concomitant reduction in Bcl-2 expression.	dinaciclib	0-10	BCL2 apoptosis regulator	Homo sapiens	204-209
33589591-6	2021	Indeed, we found dinaciclib suppresses MCL-1 RNA and is highly effective at sensitizing HER2 inhibitors both in vitro and in vivo.	dinaciclib	17-27	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	39-44
33589591-6	2021	Indeed, we found dinaciclib suppresses MCL-1 RNA and is highly effective at sensitizing HER2 inhibitors both in vitro and in vivo.	dinaciclib	17-27	erb-b2 receptor tyrosine kinase 2	Homo sapiens	88-92
34972202-2	2022	The multicohort, phase 1 KEYNOTE-155 study evaluated the safety and antitumor activity of the PD-1 inhibitor pembrolizumab plus the CDK9 inhibitor dinaciclib in patients with relapsed or refractory (rr) chronic lymphocytic leukemia (CLL), diffuse large B-cell lymphoma (DLBCL) and multiple myeloma (MM).	dinaciclib	147-157	cyclin dependent kinase 9	Homo sapiens	132-136
34722256-8	2021	Among 1278 significantly correlated gene-drug pairs, copy number of GNA13 and DNA damage response genes CBL, DNMT3A, and PPM1D were most significantly correlated with cytotoxicity; the drugs most commonly associated with these genes were PI3K/mTOR inhibitor PIK-75, and CDK inhibitors P276-00, SNS-032, AT7519, flavopiridol and dinaciclib.	dinaciclib	328-338	G protein subunit alpha 13	Homo sapiens	68-73
35417031-0	2022	Dinaciclib inhibits the stemness of two subtypes of human breast cancer cells by targeting the FoxM1 and Hedgehog signaling pathway.	dinaciclib	0-10	forkhead box M1	Homo sapiens	95-100
35417031-4	2022	Dinaciclib, a CDK1/2/5/9 inhibitor, is currently being evaluated in clinical trials against various cancer types, including BC.	dinaciclib	0-10	cyclin dependent kinase 1	Homo sapiens	14-24
35417031-8	2022	Moreover, the dinaciclib-induced decrease of Oct4 and Nanog protein expression was able to be restored by co-treatment with MG-132, a proteasome inhibitor.	dinaciclib	14-24	POU class 5 homeobox 1	Homo sapiens	45-49
35190631-6	2022	Moreover, the CDK inhibitor dinaciclib and O-GlcNAcylation inhibitor OSMI1 reduced the number of CSCs derived from these cells.	dinaciclib	28-38	cyclin-dependent kinase 1	Mus musculus	14-17
35170591-1	2022	Extracellular vesicle (EV) delivery of TNF-related apoptosis-inducing ligand (TRAIL) (EV-T) has been shown to be highly efficient for cancer treatment when combined with the potent cyclin-dependent kinase (CDK) inhibitor dinaciclib (SCH727965, Dina).	dinaciclib	221-231	TNF superfamily member 10	Homo sapiens	39-76
35170591-1	2022	Extracellular vesicle (EV) delivery of TNF-related apoptosis-inducing ligand (TRAIL) (EV-T) has been shown to be highly efficient for cancer treatment when combined with the potent cyclin-dependent kinase (CDK) inhibitor dinaciclib (SCH727965, Dina).	dinaciclib	221-231	TNF superfamily member 10	Homo sapiens	78-83
35170591-1	2022	Extracellular vesicle (EV) delivery of TNF-related apoptosis-inducing ligand (TRAIL) (EV-T) has been shown to be highly efficient for cancer treatment when combined with the potent cyclin-dependent kinase (CDK) inhibitor dinaciclib (SCH727965, Dina).	dinaciclib	233-242	TNF superfamily member 10	Homo sapiens	39-76
35170591-1	2022	Extracellular vesicle (EV) delivery of TNF-related apoptosis-inducing ligand (TRAIL) (EV-T) has been shown to be highly efficient for cancer treatment when combined with the potent cyclin-dependent kinase (CDK) inhibitor dinaciclib (SCH727965, Dina).	dinaciclib	233-242	TNF superfamily member 10	Homo sapiens	78-83
32816920-10	2021	CDK1/2/5 inhibition by dinaciclib provides a novel strategy to overcome IFNG-triggered acquired resistance in pancreatic tumour immunity.	dinaciclib	23-33	interferon gamma	Homo sapiens	72-76
35053380-10	2022	As well-known CDK inhibitors, dinaciclib and kenpaullone stabilize PXR and result in elevated expression and activity of PXR-targeted DMETs, including carboxylesterases, CYP3A4 and P-gp.	dinaciclib	30-40	cyclin dependent kinase 2	Homo sapiens	14-17
35053380-10	2022	As well-known CDK inhibitors, dinaciclib and kenpaullone stabilize PXR and result in elevated expression and activity of PXR-targeted DMETs, including carboxylesterases, CYP3A4 and P-gp.	dinaciclib	30-40	nuclear receptor subfamily 1 group I member 2	Homo sapiens	67-70
35053380-10	2022	As well-known CDK inhibitors, dinaciclib and kenpaullone stabilize PXR and result in elevated expression and activity of PXR-targeted DMETs, including carboxylesterases, CYP3A4 and P-gp.	dinaciclib	30-40	nuclear receptor subfamily 1 group I member 2	Homo sapiens	121-124
35053380-10	2022	As well-known CDK inhibitors, dinaciclib and kenpaullone stabilize PXR and result in elevated expression and activity of PXR-targeted DMETs, including carboxylesterases, CYP3A4 and P-gp.	dinaciclib	30-40	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	170-176
35053380-10	2022	As well-known CDK inhibitors, dinaciclib and kenpaullone stabilize PXR and result in elevated expression and activity of PXR-targeted DMETs, including carboxylesterases, CYP3A4 and P-gp.	dinaciclib	30-40	phosphoglycolate phosphatase	Homo sapiens	181-185
35053380-11	2022	The suppressed degradation of PXR by CDK2 inhibitors denotes dinaciclib-induced promotion of PXR-targeted genes.	dinaciclib	61-71	nuclear receptor subfamily 1 group I member 2	Homo sapiens	30-33
35053380-11	2022	The suppressed degradation of PXR by CDK2 inhibitors denotes dinaciclib-induced promotion of PXR-targeted genes.	dinaciclib	61-71	nuclear receptor subfamily 1 group I member 2	Homo sapiens	93-96
32816920-4	2021	We evaluated the ability of the cyclin-dependent kinase (CDK) inhibitor dinaciclib to block IFNG-induced IDO1 and CD274 expression in 24 human and mouse cancer cell lines as well as in primary cancer cells from patients with PDAC or ovarian carcinoma.	dinaciclib	72-82	cyclin dependent kinase 1	Homo sapiens	57-60
32816920-4	2021	We evaluated the ability of the cyclin-dependent kinase (CDK) inhibitor dinaciclib to block IFNG-induced IDO1 and CD274 expression in 24 human and mouse cancer cell lines as well as in primary cancer cells from patients with PDAC or ovarian carcinoma.	dinaciclib	72-82	interferon gamma	Homo sapiens	92-96
33125153-11	2020	In conclusion, the CDK1/2/5/9 inhibitor dinaciclib, irreversible pan-HER TKI afatinib and SRC targeting TKI dasatinib were most effective at inhibiting the proliferation and migration of HPCCLs and the combination of afatinib with dasatinib and gemcitabine with dasatinib led to synergistic tumor growth inhibition in all HPCCLs examined.	dinaciclib	40-50	cyclin dependent kinase 1	Homo sapiens	19-29
32816920-4	2021	We evaluated the ability of the cyclin-dependent kinase (CDK) inhibitor dinaciclib to block IFNG-induced IDO1 and CD274 expression in 24 human and mouse cancer cell lines as well as in primary cancer cells from patients with PDAC or ovarian carcinoma.	dinaciclib	72-82	indoleamine 2,3-dioxygenase 1	Homo sapiens	105-109
32816920-4	2021	We evaluated the ability of the cyclin-dependent kinase (CDK) inhibitor dinaciclib to block IFNG-induced IDO1 and CD274 expression in 24 human and mouse cancer cell lines as well as in primary cancer cells from patients with PDAC or ovarian carcinoma.	dinaciclib	72-82	CD274 molecule	Homo sapiens	114-119
32816920-10	2021	CDK1/2/5 inhibition by dinaciclib provides a novel strategy to overcome IFNG-triggered acquired resistance in pancreatic tumour immunity.	dinaciclib	23-33	cyclin dependent kinase 1	Homo sapiens	0-8
33686114-6	2021	We found that dinaciclib-triggered apoptosis is triggered by CDK9 inhibition and the resultant reduction in RNA pol II phosphorylation, which leads to the downregulation of the oncogenic marker MYC, and the anti-apoptotic protein MCL-1.	dinaciclib	14-24	cyclin dependent kinase 9	Homo sapiens	61-65
33686114-6	2021	We found that dinaciclib-triggered apoptosis is triggered by CDK9 inhibition and the resultant reduction in RNA pol II phosphorylation, which leads to the downregulation of the oncogenic marker MYC, and the anti-apoptotic protein MCL-1.	dinaciclib	14-24	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	194-197
33686114-6	2021	We found that dinaciclib-triggered apoptosis is triggered by CDK9 inhibition and the resultant reduction in RNA pol II phosphorylation, which leads to the downregulation of the oncogenic marker MYC, and the anti-apoptotic protein MCL-1.	dinaciclib	14-24	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	230-235
33838899-7	2021	Several genes were potential Bromodomain-containing protein 4 (Brd4) targets, making Brd4 inhibitors - JQ1, AZD5153 - and cyclin-dependent kinase (Brd4"s binding partner) inhibitors - dinaciclib - potential therapeutic agents.	dinaciclib	184-194	bromodomain containing 4	Homo sapiens	29-61
33838899-7	2021	Several genes were potential Bromodomain-containing protein 4 (Brd4) targets, making Brd4 inhibitors - JQ1, AZD5153 - and cyclin-dependent kinase (Brd4"s binding partner) inhibitors - dinaciclib - potential therapeutic agents.	dinaciclib	184-194	bromodomain containing 4	Homo sapiens	63-67
33838899-7	2021	Several genes were potential Bromodomain-containing protein 4 (Brd4) targets, making Brd4 inhibitors - JQ1, AZD5153 - and cyclin-dependent kinase (Brd4"s binding partner) inhibitors - dinaciclib - potential therapeutic agents.	dinaciclib	184-194	bromodomain containing 4	Homo sapiens	85-89
33838899-7	2021	Several genes were potential Bromodomain-containing protein 4 (Brd4) targets, making Brd4 inhibitors - JQ1, AZD5153 - and cyclin-dependent kinase (Brd4"s binding partner) inhibitors - dinaciclib - potential therapeutic agents.	dinaciclib	184-194	bromodomain containing 4	Homo sapiens	85-89
33838899-11	2021	Dinaciclib-AZD5153 combination therapy can be effective against MYCN-amplified and TERT-overexpressing neuroblastoma tumors.	dinaciclib	0-10	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	64-68
33838899-11	2021	Dinaciclib-AZD5153 combination therapy can be effective against MYCN-amplified and TERT-overexpressing neuroblastoma tumors.	dinaciclib	0-10	telomerase reverse transcriptase	Homo sapiens	83-87
32375399-0	2020	Extracellular Vesicle Delivery of TRAIL Eradicates Resistant Tumor Growth in Combination with CDK Inhibition by Dinaciclib.	dinaciclib	112-122	TNF superfamily member 10	Homo sapiens	34-39
33116269-0	2020	Dinaciclib, a cyclin-dependent kinase inhibitor, suppresses cholangiocarcinoma growth by targeting CDK2/5/9.	dinaciclib	0-10	cyclin dependent kinase 2	Homo sapiens	99-107
33116269-5	2020	Treatment with dinaciclib significantly suppressed cell proliferation, induced caspase 3/7 levels and apoptotic activity in PDXC and CCA cell lines.	dinaciclib	15-25	caspase 3	Homo sapiens	79-90
32934219-5	2020	Small-molecule drugs targeting the CDK9 kinase, dinaciclib, flavopiridol, roscovitine, AT-7519, SNS-032, and DRB, diminished MDM4 levels and activated p53 in A375 melanoma and MCF7 breast carcinoma cells with only a limited effect on MDM2.	dinaciclib	48-58	MDM4 regulator of p53	Homo sapiens	125-129
32934219-5	2020	Small-molecule drugs targeting the CDK9 kinase, dinaciclib, flavopiridol, roscovitine, AT-7519, SNS-032, and DRB, diminished MDM4 levels and activated p53 in A375 melanoma and MCF7 breast carcinoma cells with only a limited effect on MDM2.	dinaciclib	48-58	tumor protein p53	Homo sapiens	151-154
32433863-3	2020	Here, we detail the positive cooperativity between ANS and orthosteric Cdk2 inhibitors dinaciclib and roscovitine, which increase the affinity of ANS toward Cdk2 5-fold to 10-fold, and the relatively noncooperative effects of ATP.	dinaciclib	87-97	cyclin dependent kinase 2	Homo sapiens	71-75
32433863-3	2020	Here, we detail the positive cooperativity between ANS and orthosteric Cdk2 inhibitors dinaciclib and roscovitine, which increase the affinity of ANS toward Cdk2 5-fold to 10-fold, and the relatively noncooperative effects of ATP.	dinaciclib	87-97	cyclin dependent kinase 2	Homo sapiens	157-161
32558295-3	2020	Exploring these mechanisms of resistance, we found that EML4-ALK cells parental or resistant to crizotinib, ceritinib or alectinib are remarkably sensitive to inhibition of CDK7/12 with THZ1 and CDK9 with alvocidib or dinaciclib.	dinaciclib	218-228	EMAP like 4	Homo sapiens	56-60
32558295-3	2020	Exploring these mechanisms of resistance, we found that EML4-ALK cells parental or resistant to crizotinib, ceritinib or alectinib are remarkably sensitive to inhibition of CDK7/12 with THZ1 and CDK9 with alvocidib or dinaciclib.	dinaciclib	218-228	ALK receptor tyrosine kinase	Homo sapiens	61-64
32558295-3	2020	Exploring these mechanisms of resistance, we found that EML4-ALK cells parental or resistant to crizotinib, ceritinib or alectinib are remarkably sensitive to inhibition of CDK7/12 with THZ1 and CDK9 with alvocidib or dinaciclib.	dinaciclib	218-228	cyclin dependent kinase 7	Homo sapiens	173-180
32558295-3	2020	Exploring these mechanisms of resistance, we found that EML4-ALK cells parental or resistant to crizotinib, ceritinib or alectinib are remarkably sensitive to inhibition of CDK7/12 with THZ1 and CDK9 with alvocidib or dinaciclib.	dinaciclib	218-228	cyclin dependent kinase 9	Homo sapiens	195-199
32615570-11	2021	Pharmacological inhibition of MYC mediated by the cyclin-dependent kinase inhibitor Dinaciclib strongly reduced viability of ER-BON-1.	dinaciclib	84-94	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	30-33
32397330-8	2020	Furthermore, the inhibiting effect of the Hsp90alpha gene by the combination of HAA2020 and dinaciclib was associated with increased caspase-7 and TNF-alpha, leading to apoptosis in HL60 cells.	dinaciclib	92-102	heat shock protein 90 alpha family class A member 1	Homo sapiens	42-52
32397330-8	2020	Furthermore, the inhibiting effect of the Hsp90alpha gene by the combination of HAA2020 and dinaciclib was associated with increased caspase-7 and TNF-alpha, leading to apoptosis in HL60 cells.	dinaciclib	92-102	caspase 7	Homo sapiens	133-142
32397330-8	2020	Furthermore, the inhibiting effect of the Hsp90alpha gene by the combination of HAA2020 and dinaciclib was associated with increased caspase-7 and TNF-alpha, leading to apoptosis in HL60 cells.	dinaciclib	92-102	tumor necrosis factor	Homo sapiens	147-156
32397330-10	2020	The actions of HAA2020 propagated the apoptotic and cell cycle control properties of dinaciclib, showing the importance of co-targeting Hsp90 and CDK, which could lead to the better management of leukemia.	dinaciclib	85-95	heat shock protein 90 alpha family class A member 1	Homo sapiens	136-141
32726663-0	2020	Inhibition of CD73 using folate targeted nanoparticles carrying anti-CD73 siRNA potentiates anticancer efficacy of Dinaciclib.	dinaciclib	115-125	5' nucleotidase, ecto	Mus musculus	14-18
32726663-0	2020	Inhibition of CD73 using folate targeted nanoparticles carrying anti-CD73 siRNA potentiates anticancer efficacy of Dinaciclib.	dinaciclib	115-125	5' nucleotidase, ecto	Mus musculus	69-73
33050377-10	2020	Interestingly, HAA2020 and dinaciclib showed a synergistic apoptotic and G1 cell cycle effect in MCF7 cells, which was supported by their synergistic CDK2, cyclin D1, and PCNA inhibition activities.	dinaciclib	27-37	cyclin dependent kinase 2	Homo sapiens	150-154
33050377-10	2020	Interestingly, HAA2020 and dinaciclib showed a synergistic apoptotic and G1 cell cycle effect in MCF7 cells, which was supported by their synergistic CDK2, cyclin D1, and PCNA inhibition activities.	dinaciclib	27-37	cyclin D1	Homo sapiens	156-165
33050377-10	2020	Interestingly, HAA2020 and dinaciclib showed a synergistic apoptotic and G1 cell cycle effect in MCF7 cells, which was supported by their synergistic CDK2, cyclin D1, and PCNA inhibition activities.	dinaciclib	27-37	proliferating cell nuclear antigen	Homo sapiens	171-175
32375399-4	2020	SCH727965 (dinaciclib), a potent cyclin-dependent kinase (CDK) inhibitor, was shown to synergize with other drugs to get better efficacy.	dinaciclib	0-9	cyclin dependent kinase inhibitor 3	Homo sapiens	33-72
32375399-4	2020	SCH727965 (dinaciclib), a potent cyclin-dependent kinase (CDK) inhibitor, was shown to synergize with other drugs to get better efficacy.	dinaciclib	11-21	cyclin dependent kinase inhibitor 3	Homo sapiens	33-72
32375399-8	2020	Dinaciclib was shown to drastically enhance EV-T killing effects on cancer lines that express good levels of death receptor (DR) 5, which are associated with suppression of CDK1, CDK9 and anti-apoptotic proteins.	dinaciclib	0-10	TNF receptor superfamily member 10b	Homo sapiens	109-130
32375399-8	2020	Dinaciclib was shown to drastically enhance EV-T killing effects on cancer lines that express good levels of death receptor (DR) 5, which are associated with suppression of CDK1, CDK9 and anti-apoptotic proteins.	dinaciclib	0-10	cyclin dependent kinase 1	Homo sapiens	173-177
32375399-8	2020	Dinaciclib was shown to drastically enhance EV-T killing effects on cancer lines that express good levels of death receptor (DR) 5, which are associated with suppression of CDK1, CDK9 and anti-apoptotic proteins.	dinaciclib	0-10	cyclin dependent kinase 9	Homo sapiens	179-183
32368395-1	2020	The cyclin-dependent kinase 2 (CDK2) inhibitor dinaciclib, a potential anti-cancer drug, has been tested in clinical trials and reported to suppress tumor initiating cells.	dinaciclib	47-57	cyclin dependent kinase 2	Homo sapiens	4-29
32368395-1	2020	The cyclin-dependent kinase 2 (CDK2) inhibitor dinaciclib, a potential anti-cancer drug, has been tested in clinical trials and reported to suppress tumor initiating cells.	dinaciclib	47-57	cyclin dependent kinase 2	Homo sapiens	31-35
31529315-5	2020	Cell Counting Kit (CCK-8), clone formation assay, and flow cytometry were used to test the proliferation and apoptosis of ACC-2 cells treated with dinaciclib with or without other first-line chemotherapy drugs.	dinaciclib	147-157	acetyl-CoA carboxylase beta	Homo sapiens	122-127
31529315-8	2020	As expected, CDK inhibitor dinaciclib significantly induced ACC-2 cells apoptosis.	dinaciclib	27-37	acetyl-CoA carboxylase beta	Homo sapiens	60-65
31529315-9	2020	Moreover, it sensitized cells to the chemotherapeutic agents such as cisplatin, pemetrexed, and etoposide (VP-16), and this effect by dinaciclib may induce cell cycle arrest via abrogating CDK2 activity.	dinaciclib	134-144	host cell factor C1	Homo sapiens	107-112
31529315-9	2020	Moreover, it sensitized cells to the chemotherapeutic agents such as cisplatin, pemetrexed, and etoposide (VP-16), and this effect by dinaciclib may induce cell cycle arrest via abrogating CDK2 activity.	dinaciclib	134-144	cyclin dependent kinase 2	Homo sapiens	189-193
32269732-5	2020	In vitro assays showed that dinaciclib exerted antiproliferative effects on PDAC cells by increasing surface calreticulin expression and release of ATP.	dinaciclib	28-38	calreticulin	Mus musculus	109-121
32269732-6	2020	Dinaciclib treatment inhibited proliferation and induced apoptosis in KPC tumor as assessed by Ki67 and cleaved caspase 3, respectively.	dinaciclib	0-10	antigen identified by monoclonal antibody Ki 67	Mus musculus	95-99
32269732-6	2020	Dinaciclib treatment inhibited proliferation and induced apoptosis in KPC tumor as assessed by Ki67 and cleaved caspase 3, respectively.	dinaciclib	0-10	caspase 3	Mus musculus	112-121
31590445-6	2019	In contrast, non-selective CDK inhibitors flavopiridol and dinaciclib and a CDK7/12/13 inhibitor THZ1 (but not CDK4/6 inhibitor palbociclib) suppressed luciferase induction in both WT and dKO cells, indicating a distinct role for other CDKs in the NFkappaB pathway.	dinaciclib	59-69	cyclin dependent kinase 4	Homo sapiens	27-30
31744894-0	2020	Rational combination therapy for melanoma with dinaciclib by targeting BAK-dependent cell death.	dinaciclib	47-57	BCL2 antagonist/killer 1	Homo sapiens	71-74
31744894-4	2020	We demonstrated that dinaciclib has potent anti-melanoma effects by inducing BAK-dependent apoptosis through MCL1 reduction.	dinaciclib	21-31	BCL2 antagonist/killer 1	Homo sapiens	77-80
31744894-4	2020	We demonstrated that dinaciclib has potent anti-melanoma effects by inducing BAK-dependent apoptosis through MCL1 reduction.	dinaciclib	21-31	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	109-113
31744894-5	2020	Contrary to dinaciclib, the inhibitors of BRAF / MEK / CDK4/6 induced apoptosis dominantly through a BAX-dependent mechanism.	dinaciclib	12-22	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	42-46
31744894-5	2020	Contrary to dinaciclib, the inhibitors of BRAF / MEK / CDK4/6 induced apoptosis dominantly through a BAX-dependent mechanism.	dinaciclib	12-22	mitogen-activated protein kinase kinase 7	Homo sapiens	49-52
31744894-7	2020	Collectively, our present findings suggest dinaciclib to be an effective complementary drug of BAX-dependent anti-melanoma drugs by targeting BAK-mediated apoptosis, and other such rational drug combinations can be determined by identifying complementary drugs activating either BAK or BAX.	dinaciclib	43-53	BCL2 associated X, apoptosis regulator	Homo sapiens	95-98
31744894-7	2020	Collectively, our present findings suggest dinaciclib to be an effective complementary drug of BAX-dependent anti-melanoma drugs by targeting BAK-mediated apoptosis, and other such rational drug combinations can be determined by identifying complementary drugs activating either BAK or BAX.	dinaciclib	43-53	BCL2 antagonist/killer 1	Homo sapiens	142-145
31676845-6	2019	In this study, we show that dinaciclib, a potent cyclin dependent kinase inhibitor, significantly increases the basal CYP3A4 and PXR levels in 24 hours.	dinaciclib	28-38	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	118-124
31676845-6	2019	In this study, we show that dinaciclib, a potent cyclin dependent kinase inhibitor, significantly increases the basal CYP3A4 and PXR levels in 24 hours.	dinaciclib	28-38	nuclear receptor subfamily 1 group I member 2	Homo sapiens	129-132
32395375-12	2020	The use of dinaciclib, a selective CDK inhibitor, significantly inhibited tumor growth in the PDX model.	dinaciclib	11-21	cyclin dependent kinase 2	Homo sapiens	35-38
32175313-8	2020	We reveal the ability of known CDK inhibitors, among which clinically tested SNS-032, riviciclib, flavopiridol, dinaciclib, AZD4573 and AT7519, to potently inhibit CDK10/CycM.	dinaciclib	112-122	cyclin dependent kinase 10	Homo sapiens	164-169
31439587-6	2019	Importantly, olaparib (OLA) or talazoparib (TALA) suppressed these activities, and the combination of OLA and dinaciclib (DINA), an inhibitor of CDK2 and CDK5, which also inhibits Rb1 phosphorylation, suppressed NED, and significantly improved therapeutic efficiency in neuroendocrine prostate cancer (NEPC) cells in vitro and in NEPC tumors in vivo.	dinaciclib	110-120	cyclin dependent kinase 2	Homo sapiens	145-149
31439587-6	2019	Importantly, olaparib (OLA) or talazoparib (TALA) suppressed these activities, and the combination of OLA and dinaciclib (DINA), an inhibitor of CDK2 and CDK5, which also inhibits Rb1 phosphorylation, suppressed NED, and significantly improved therapeutic efficiency in neuroendocrine prostate cancer (NEPC) cells in vitro and in NEPC tumors in vivo.	dinaciclib	110-120	cyclin dependent kinase 5	Homo sapiens	154-158
31439587-6	2019	Importantly, olaparib (OLA) or talazoparib (TALA) suppressed these activities, and the combination of OLA and dinaciclib (DINA), an inhibitor of CDK2 and CDK5, which also inhibits Rb1 phosphorylation, suppressed NED, and significantly improved therapeutic efficiency in neuroendocrine prostate cancer (NEPC) cells in vitro and in NEPC tumors in vivo.	dinaciclib	110-120	RB transcriptional corepressor 1	Homo sapiens	180-183
31496920-9	2019	Dinaciclib was added to realize the effect of CDK5 inhibition in vivo.	dinaciclib	0-10	cyclin dependent kinase 5	Homo sapiens	46-50
31300540-6	2019	We validated that inhibitors of these druggable target genes, including the CDK1/CDK2 inhibitor dinaciclib, had antiproliferative and cytotoxic effects selectively on mouse prostate cells with knockdown of Chd1 and Map3k7.	dinaciclib	96-106	cyclin-dependent kinase 1	Mus musculus	76-80
31300540-6	2019	We validated that inhibitors of these druggable target genes, including the CDK1/CDK2 inhibitor dinaciclib, had antiproliferative and cytotoxic effects selectively on mouse prostate cells with knockdown of Chd1 and Map3k7.	dinaciclib	96-106	cyclin-dependent kinase 2	Mus musculus	81-85
31300540-6	2019	We validated that inhibitors of these druggable target genes, including the CDK1/CDK2 inhibitor dinaciclib, had antiproliferative and cytotoxic effects selectively on mouse prostate cells with knockdown of Chd1 and Map3k7.	dinaciclib	96-106	chromodomain helicase DNA binding protein 1	Mus musculus	206-210
31300540-6	2019	We validated that inhibitors of these druggable target genes, including the CDK1/CDK2 inhibitor dinaciclib, had antiproliferative and cytotoxic effects selectively on mouse prostate cells with knockdown of Chd1 and Map3k7.	dinaciclib	96-106	mitogen-activated protein kinase kinase kinase 7	Mus musculus	215-221
31300540-7	2019	Dinaciclib had stronger effects on prostate cells with suppression of Map3k7 independent of Chd1 and also compared with cells without loss of Map3k7.	dinaciclib	0-10	mitogen-activated protein kinase kinase kinase 7	Mus musculus	70-76
31300540-7	2019	Dinaciclib had stronger effects on prostate cells with suppression of Map3k7 independent of Chd1 and also compared with cells without loss of Map3k7.	dinaciclib	0-10	chromodomain helicase DNA binding protein 1	Mus musculus	92-96
31300540-9	2019	Dinaciclib-induced HR disruption was also observed in human prostate cells with knockdown of MAP3K7.	dinaciclib	0-10	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	93-99
31300540-10	2019	Cotreatment of dinaciclib with DNA-damaging agents or PARP inhibitor resulted in a stronger cytotoxic effect on prostate cells with suppression of MAP3K7 compared with those without loss of MAP3K7, or to each single agent.	dinaciclib	15-25	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	147-153
31300540-10	2019	Cotreatment of dinaciclib with DNA-damaging agents or PARP inhibitor resulted in a stronger cytotoxic effect on prostate cells with suppression of MAP3K7 compared with those without loss of MAP3K7, or to each single agent.	dinaciclib	15-25	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	190-196
30178167-8	2018	METHODS: We investigated whether the CDK inhibitors flavopiridol and dinaciclib may exhibit antitumor activity in CDKN2A-defective SqCLC cells compared to control cells.	dinaciclib	69-79	cyclin dependent kinase inhibitor 2A	Homo sapiens	114-120
31207099-0	2019	Study of the mechanism by which dinaciclib induces apoptosis and cell cycle arrest of lymphoma Raji cells through a CDK1-involved pathway.	dinaciclib	32-42	cyclin dependent kinase 1	Homo sapiens	116-120
31207099-10	2019	It was revealed by cell transfection that the expression of cell cycle proteins was downregulated after treatment with dinaciclib through a CDK1-involved pathway, which eventually led to apoptosis.	dinaciclib	119-129	cyclin dependent kinase 1	Homo sapiens	140-144
31207099-13	2019	CONCLUSION: In this study, we clarified the mechanisms through which dinaciclib induces Raji cell apoptosis and blocks the cell cycle through a CDK1-involved pathway, which supported that dinaciclib had potential values in the treatment of lymphoma.	dinaciclib	69-79	cyclin dependent kinase 1	Homo sapiens	144-148
31207099-13	2019	CONCLUSION: In this study, we clarified the mechanisms through which dinaciclib induces Raji cell apoptosis and blocks the cell cycle through a CDK1-involved pathway, which supported that dinaciclib had potential values in the treatment of lymphoma.	dinaciclib	188-198	cyclin dependent kinase 1	Homo sapiens	144-148
31349793-4	2019	Conversely, down-regulation of cyclin E1 gene expression or inhibition of cyclin E1 by the cyclin-dependent kinase (CDK) inhibitors dinaciclib (DIN) or flavopiridol sensitized HCC cells to regorafenib and sorafenib by inducing apoptosis.	dinaciclib	132-142	cyclin E1	Homo sapiens	74-83
30033593-11	2019	Notably, Cdk5 is an addressable target frequently overexpressed in HCC, and with Dinaciclib, a clinically tested Cdk5 inhibitor is readily available.	dinaciclib	81-91	cyclin dependent kinase 5	Homo sapiens	9-13
30033593-11	2019	Notably, Cdk5 is an addressable target frequently overexpressed in HCC, and with Dinaciclib, a clinically tested Cdk5 inhibitor is readily available.	dinaciclib	81-91	cyclin dependent kinase 5	Homo sapiens	113-117
30178167-11	2018	RESULTS: We found that flavopiridol and dinaciclib induced cytotoxicity by enhancing apoptosis in CDKN2A-defective SqCLC cells, and that epithelial to mesenchymal transition (EMT) decreased and autophagy increased during this process.	dinaciclib	40-50	cyclin dependent kinase inhibitor 2A	Homo sapiens	98-104
29963728-0	2018	In vitro effects of FBXW7 mutation in serous endometrial cancer: Increased levels of potentially druggable proteins and sensitivity to SI-2 and dinaciclib.	dinaciclib	144-154	F-box and WD repeat domain containing 7	Homo sapiens	20-25
29963728-6	2018	Furthermore, we demonstrate that CRISPR-edited FBXW7-mutant ARK1 serous EC cells exhibit increased sensitivity to SI-2 (a SRC inhibitor) and dinaciclib (a cyclin dependent kinase (CDK) inhibitor) compared to parental ARK1 cells.	dinaciclib	141-151	F-box and WD repeat domain containing 7	Homo sapiens	47-52
29963728-6	2018	Furthermore, we demonstrate that CRISPR-edited FBXW7-mutant ARK1 serous EC cells exhibit increased sensitivity to SI-2 (a SRC inhibitor) and dinaciclib (a cyclin dependent kinase (CDK) inhibitor) compared to parental ARK1 cells.	dinaciclib	141-151	aurora kinase A	Homo sapiens	60-64
30135308-9	2018	Finally, combined inhibition of dinaciclib with a RET kinase inhibitor was synergistic.	dinaciclib	32-42	ret proto-oncogene	Homo sapiens	50-53
30405800-0	2018	Low dose dinaciclib enhances doxorubicin-induced senescence in myeloma RPMI8226 cells by transformation of the p21 and p16 pathways.	dinaciclib	9-19	H3 histone pseudogene 16	Homo sapiens	111-114
30405800-0	2018	Low dose dinaciclib enhances doxorubicin-induced senescence in myeloma RPMI8226 cells by transformation of the p21 and p16 pathways.	dinaciclib	9-19	cyclin dependent kinase inhibitor 2A	Homo sapiens	119-122
30405800-8	2018	Notably, the combination of dinaciclib and DOX inhibited cell growth and promoted senescence by transforming the suppressive effects of the ATM/Chk2/p53/p21 signaling pathway and enhancing the p16 signaling pathway.	dinaciclib	28-38	ATM serine/threonine kinase	Homo sapiens	140-143
30405800-8	2018	Notably, the combination of dinaciclib and DOX inhibited cell growth and promoted senescence by transforming the suppressive effects of the ATM/Chk2/p53/p21 signaling pathway and enhancing the p16 signaling pathway.	dinaciclib	28-38	checkpoint kinase 2	Homo sapiens	144-148
30405800-8	2018	Notably, the combination of dinaciclib and DOX inhibited cell growth and promoted senescence by transforming the suppressive effects of the ATM/Chk2/p53/p21 signaling pathway and enhancing the p16 signaling pathway.	dinaciclib	28-38	tumor protein p53	Homo sapiens	149-152
30405800-8	2018	Notably, the combination of dinaciclib and DOX inhibited cell growth and promoted senescence by transforming the suppressive effects of the ATM/Chk2/p53/p21 signaling pathway and enhancing the p16 signaling pathway.	dinaciclib	28-38	H3 histone pseudogene 16	Homo sapiens	153-156
30405800-8	2018	Notably, the combination of dinaciclib and DOX inhibited cell growth and promoted senescence by transforming the suppressive effects of the ATM/Chk2/p53/p21 signaling pathway and enhancing the p16 signaling pathway.	dinaciclib	28-38	cyclin dependent kinase inhibitor 2A	Homo sapiens	193-196
30405800-9	2018	Thus, low-dose dinaciclib enhanced anti-MM effects mediated by DOX via transformation of p21-p16 signaling pathways, leading to accelerated senescence, but not apoptosis.	dinaciclib	15-25	H3 histone pseudogene 16	Homo sapiens	89-92
30405800-9	2018	Thus, low-dose dinaciclib enhanced anti-MM effects mediated by DOX via transformation of p21-p16 signaling pathways, leading to accelerated senescence, but not apoptosis.	dinaciclib	15-25	cyclin dependent kinase inhibitor 2A	Homo sapiens	93-96
29992508-0	2018	Aldo-keto reductase 1C3 (AKR1C3): a missing piece of the puzzle in the dinaciclib interaction profile.	dinaciclib	71-81	aldo-keto reductase family 1 member C3	Homo sapiens	0-23
29992508-0	2018	Aldo-keto reductase 1C3 (AKR1C3): a missing piece of the puzzle in the dinaciclib interaction profile.	dinaciclib	71-81	aldo-keto reductase family 1 member C3	Homo sapiens	25-31
29992508-8	2018	In subsequent experiments, pretreatment with dinaciclib (0.1 microM) significantly sensitized AKR1C3-overexpressing anthracycline-resistant cancer cells to daunorubicin.	dinaciclib	45-55	aldo-keto reductase family 1 member C3	Homo sapiens	94-100
30234460-4	2018	We recently reported three iPS cell elimination strategies, including methionine-free medium, TRPV1 activation through 42 C cultivation, and dinaciclib, a cyclin-dependent kinase 1/9 inhibitor.	dinaciclib	141-151	cyclin dependent kinase 19	Homo sapiens	155-182
30234460-7	2018	After screening for suitable combinations of these strategies based on Lin28 expression in co-cultures of fibroblasts and 1 x 104 iPS cells, we found that 1 day of cultivation at 42 C in methionine-free culture medium with or without dinaciclib remarkably decreased Lin28 expression and prevented tumor formation.	dinaciclib	234-244	lin-28 homolog A	Homo sapiens	266-271
29507054-6	2018	The CDK2 inhibitor, dinaciclib, attenuated resistance to both classes of inhibitors and combinations thereof.	dinaciclib	20-30	cyclin dependent kinase 2	Homo sapiens	4-8
29968772-4	2018	Nanofluidic proteomics revealed hyper-phosphorylation of MAPKs in breast carcinoma and breast cancer cells treated with kinase inhibitors that interfere with cell cycle regulation, such as dinaciclib, an inhibitor of cyclin-dependent kinases, and rigosertib, an inhibitor of polo-like kinase 1.	dinaciclib	189-199	polo like kinase 1	Homo sapiens	275-293
29240261-3	2018	However, low nanomolar concentrations of dinaciclib showed higher cytotoxic activity against Bcl-xL silenced cells in a time- and concentration-dependent manner.	dinaciclib	41-51	BCL2 like 1	Homo sapiens	93-99
29240261-9	2018	Our results also revealed that dinaciclib, but not ribociclib or palbociclib or seliciclib or AZD5438 induced intrinsic apoptosis via upregulation of the levels of pro-apoptotic proteins (Bax and Bak), resulting in the activation of caspases and cleavage of PARP.	dinaciclib	31-41	BCL2 associated X, apoptosis regulator	Homo sapiens	188-191
29240261-9	2018	Our results also revealed that dinaciclib, but not ribociclib or palbociclib or seliciclib or AZD5438 induced intrinsic apoptosis via upregulation of the levels of pro-apoptotic proteins (Bax and Bak), resulting in the activation of caspases and cleavage of PARP.	dinaciclib	31-41	BCL2 antagonist/killer 1	Homo sapiens	196-199
29240261-9	2018	Our results also revealed that dinaciclib, but not ribociclib or palbociclib or seliciclib or AZD5438 induced intrinsic apoptosis via upregulation of the levels of pro-apoptotic proteins (Bax and Bak), resulting in the activation of caspases and cleavage of PARP.	dinaciclib	31-41	poly(ADP-ribose) polymerase 1	Homo sapiens	258-262
29240261-10	2018	We also found an additional mechanism for the dinaciclib-induced augmentation of apoptosis due to abrogation RAD51-cyclin D1 interaction, specifically proteolysis of the DNA repair proteins RAD51 and Ku80.	dinaciclib	46-56	RAD51 recombinase	Homo sapiens	109-114
29240261-10	2018	We also found an additional mechanism for the dinaciclib-induced augmentation of apoptosis due to abrogation RAD51-cyclin D1 interaction, specifically proteolysis of the DNA repair proteins RAD51 and Ku80.	dinaciclib	46-56	cyclin D1	Homo sapiens	115-124
29240261-10	2018	We also found an additional mechanism for the dinaciclib-induced augmentation of apoptosis due to abrogation RAD51-cyclin D1 interaction, specifically proteolysis of the DNA repair proteins RAD51 and Ku80.	dinaciclib	46-56	RAD51 recombinase	Homo sapiens	190-195
29240261-10	2018	We also found an additional mechanism for the dinaciclib-induced augmentation of apoptosis due to abrogation RAD51-cyclin D1 interaction, specifically proteolysis of the DNA repair proteins RAD51 and Ku80.	dinaciclib	46-56	X-ray repair cross complementing 5	Homo sapiens	200-204
29507054-7	2018	Notably, we found that MITF expression correlates with CDK2 upregulation in patients; thus, dinaciclib would warrant consideration for treatment of patients unresponsive to BRAF-MEK and/or Hsp90 inhibitors and/or harboring MITF amplification/overexpression.	dinaciclib	92-102	melanocyte inducing transcription factor	Homo sapiens	23-27
29507054-7	2018	Notably, we found that MITF expression correlates with CDK2 upregulation in patients; thus, dinaciclib would warrant consideration for treatment of patients unresponsive to BRAF-MEK and/or Hsp90 inhibitors and/or harboring MITF amplification/overexpression.	dinaciclib	92-102	cyclin dependent kinase 2	Homo sapiens	55-59
29337311-0	2018	Dinaciclib induces immunogenic cell death and enhances anti-PD1-mediated tumor suppression.	dinaciclib	0-10	programmed cell death 1	Mus musculus	60-63
29507054-7	2018	Notably, we found that MITF expression correlates with CDK2 upregulation in patients; thus, dinaciclib would warrant consideration for treatment of patients unresponsive to BRAF-MEK and/or Hsp90 inhibitors and/or harboring MITF amplification/overexpression.	dinaciclib	92-102	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	173-177
29507054-7	2018	Notably, we found that MITF expression correlates with CDK2 upregulation in patients; thus, dinaciclib would warrant consideration for treatment of patients unresponsive to BRAF-MEK and/or Hsp90 inhibitors and/or harboring MITF amplification/overexpression.	dinaciclib	92-102	mitogen-activated protein kinase kinase 7	Homo sapiens	178-181
29507054-7	2018	Notably, we found that MITF expression correlates with CDK2 upregulation in patients; thus, dinaciclib would warrant consideration for treatment of patients unresponsive to BRAF-MEK and/or Hsp90 inhibitors and/or harboring MITF amplification/overexpression.	dinaciclib	92-102	heat shock protein 90 alpha family class A member 1	Homo sapiens	189-194
29507054-7	2018	Notably, we found that MITF expression correlates with CDK2 upregulation in patients; thus, dinaciclib would warrant consideration for treatment of patients unresponsive to BRAF-MEK and/or Hsp90 inhibitors and/or harboring MITF amplification/overexpression.	dinaciclib	92-102	melanocyte inducing transcription factor	Homo sapiens	223-227
29233910-4	2018	BRAFV600E colorectal cancer cell lines expressing CDK1 were sensitized to apoptosis upon siRNA knockdown or small-molecule inhibition with RO-3306 (CDK1 inhibitor) or dinaciclib (CDK1, 2, 5, 9 inhibitors).	dinaciclib	167-177	cyclin dependent kinase 1	Homo sapiens	50-54
29233910-5	2018	Combination of RO-3306 or dinaciclib with cobimetinib (MEK inhibitor) cooperatively enhanced apoptosis and reduced clonogenic survival versus monotherapy.	dinaciclib	26-36	mitogen-activated protein kinase kinase 7	Homo sapiens	55-58
29233910-6	2018	Cells isogenic or ectopic for BRAFV600E displayed resistance to CDK1 inhibitors, as did cells with ectopic expression of constitutively active MEK CDK1 inhibitors induced a CASP8-dependent apoptosis shown by caspase-8 restoration in deficient NB7 cells that enhanced dinaciclib-induced CASP3 cleavage.	dinaciclib	267-277	mitogen-activated protein kinase kinase 7	Homo sapiens	143-146
29233910-6	2018	Cells isogenic or ectopic for BRAFV600E displayed resistance to CDK1 inhibitors, as did cells with ectopic expression of constitutively active MEK CDK1 inhibitors induced a CASP8-dependent apoptosis shown by caspase-8 restoration in deficient NB7 cells that enhanced dinaciclib-induced CASP3 cleavage.	dinaciclib	267-277	caspase 8	Homo sapiens	173-178
29180466-6	2018	Using the cyclin-dependent kinase inhibitor dinaciclib, which downregulates MYC expression, we found that combination with the PARPi niraparib increased DNA damage and downregulated homologous recombination, leading to subsequent downregulation of the epithelial-mesenchymal transition and cancer stem-like cell phenotypes.	dinaciclib	44-54	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	76-79
29337311-5	2018	Dinaciclib induced a type I IFN gene signature within the tumor, leading us to hypothesize that dinaciclib potentiates the effects of anti-PD1 by eliciting ICD.	dinaciclib	0-10	programmed cell death 1	Mus musculus	139-142
29337311-5	2018	Dinaciclib induced a type I IFN gene signature within the tumor, leading us to hypothesize that dinaciclib potentiates the effects of anti-PD1 by eliciting ICD.	dinaciclib	96-106	programmed cell death 1	Mus musculus	139-142
29337311-6	2018	Indeed, tumor cells treated with dinaciclib showed the hallmarks of ICD including surface calreticulin expression and release of high mobility group box 1 (HMGB1) and ATP.	dinaciclib	33-43	calreticulin	Mus musculus	90-102
29337311-6	2018	Indeed, tumor cells treated with dinaciclib showed the hallmarks of ICD including surface calreticulin expression and release of high mobility group box 1 (HMGB1) and ATP.	dinaciclib	33-43	high mobility group box 1	Mus musculus	129-154
29337311-6	2018	Indeed, tumor cells treated with dinaciclib showed the hallmarks of ICD including surface calreticulin expression and release of high mobility group box 1 (HMGB1) and ATP.	dinaciclib	33-43	high mobility group box 1	Mus musculus	156-161
29337311-8	2018	These findings identify a potential mechanism for the observed benefit of combining dinaciclib and anti-PD1, in which dinaciclib induces ICD, thereby converting the tumor cell into an endogenous vaccine and boosting the effects of anti-PD1.	dinaciclib	84-94	programmed cell death 1	Mus musculus	236-239
29337311-8	2018	These findings identify a potential mechanism for the observed benefit of combining dinaciclib and anti-PD1, in which dinaciclib induces ICD, thereby converting the tumor cell into an endogenous vaccine and boosting the effects of anti-PD1.	dinaciclib	118-128	programmed cell death 1	Mus musculus	104-107
29337311-8	2018	These findings identify a potential mechanism for the observed benefit of combining dinaciclib and anti-PD1, in which dinaciclib induces ICD, thereby converting the tumor cell into an endogenous vaccine and boosting the effects of anti-PD1.	dinaciclib	118-128	programmed cell death 1	Mus musculus	236-239
28756008-7	2017	Furthermore, cells treated with dinaciclib showed decreased expression of several pro-survival proteins including survivin, cyclin T1 and c-MYC.	dinaciclib	32-42	cyclin T1	Homo sapiens	124-133
28947566-7	2017	LMW-E expression overcame cell-cycle inhibition by AIs in a CDK2/Rb-dependent manner, and inhibition of CDK2 by dinaciclib reversed LMW-E-mediated resistance, whereas treatment with palbociclib, a CDK4/6 inhibitor, did not.Conclusions: Collectively, these findings suggest that cell-cycle deregulation by LMW-E mediates resistance to AIs and a combination of CDK2 inhibitors and AIs may be an effective treatment in patients with HR-positive tumors that express LMW-E. Clin Cancer Res; 23(23); 7288-300.	dinaciclib	112-122	cyclin dependent kinase 2	Homo sapiens	104-108
28947566-7	2017	LMW-E expression overcame cell-cycle inhibition by AIs in a CDK2/Rb-dependent manner, and inhibition of CDK2 by dinaciclib reversed LMW-E-mediated resistance, whereas treatment with palbociclib, a CDK4/6 inhibitor, did not.Conclusions: Collectively, these findings suggest that cell-cycle deregulation by LMW-E mediates resistance to AIs and a combination of CDK2 inhibitors and AIs may be an effective treatment in patients with HR-positive tumors that express LMW-E. Clin Cancer Res; 23(23); 7288-300.	dinaciclib	112-122	cyclin dependent kinase 2	Homo sapiens	104-108
28756008-7	2017	Furthermore, cells treated with dinaciclib showed decreased expression of several pro-survival proteins including survivin, cyclin T1 and c-MYC.	dinaciclib	32-42	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	138-143
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.	dinaciclib	19-29	BCL2 like 1	Homo sapiens	43-49
27991934-5	2017	Functional studies confirmed that inhibiting CDK5-mediated RALB activation with a clinically relevant experimental drug, dinaciclib, led to potent RALB-dependent antileukemic effects in human AML cell lines, induced apoptosis in patient-derived AML samples in vitro and led to a 2-log reduction in the leukemic burden in patient-derived xenograft mice.	dinaciclib	121-131	cyclin dependent kinase 5	Homo sapiens	45-49
27991934-5	2017	Functional studies confirmed that inhibiting CDK5-mediated RALB activation with a clinically relevant experimental drug, dinaciclib, led to potent RALB-dependent antileukemic effects in human AML cell lines, induced apoptosis in patient-derived AML samples in vitro and led to a 2-log reduction in the leukemic burden in patient-derived xenograft mice.	dinaciclib	121-131	RAS like proto-oncogene B	Homo sapiens	59-63
27991934-5	2017	Functional studies confirmed that inhibiting CDK5-mediated RALB activation with a clinically relevant experimental drug, dinaciclib, led to potent RALB-dependent antileukemic effects in human AML cell lines, induced apoptosis in patient-derived AML samples in vitro and led to a 2-log reduction in the leukemic burden in patient-derived xenograft mice.	dinaciclib	121-131	RAS like proto-oncogene B	Homo sapiens	147-151
28249908-8	2017	Treatment with GSK2334470 or the CDK2 inhibitor dinaciclib was sufficient to reverse these events and to restore the sensitivity of ribociclib-resistant cells to CDK4/6 inhibitors.	dinaciclib	48-58	cyclin dependent kinase 2	Homo sapiens	33-37
28249908-8	2017	Treatment with GSK2334470 or the CDK2 inhibitor dinaciclib was sufficient to reverse these events and to restore the sensitivity of ribociclib-resistant cells to CDK4/6 inhibitors.	dinaciclib	48-58	cyclin dependent kinase 4	Homo sapiens	162-168
28107181-4	2017	Because IBC cell lines were highly sensitive to the CDK2 inhibitors dinaciclib and meriolin 5, we developed a high-throughput survival assay (HTSA) to design novel sequential combination strategies based on the presence of cyclin E and CDK2.	dinaciclib	68-78	cyclin dependent kinase 2	Homo sapiens	52-56
27469405-3	2016	We found that dinaciclib induced apoptosis through the activation of caspases 8 and 9, which was independent of the presence of cytokines to mimic the environment of proliferation centres or IGVH mutation status.	dinaciclib	14-24	caspase 8	Homo sapiens	69-85
27469405-4	2016	Moreover, treatment with dinaciclib led to the inhibition of oncogenic pathways normally activated in stimulated CLL cells, such as STAT3, NF-kappaB, p38, PI3K/AKT and RAF/MEK/ERK.	dinaciclib	25-35	signal transducer and activator of transcription 3	Homo sapiens	132-137
27469405-4	2016	Moreover, treatment with dinaciclib led to the inhibition of oncogenic pathways normally activated in stimulated CLL cells, such as STAT3, NF-kappaB, p38, PI3K/AKT and RAF/MEK/ERK.	dinaciclib	25-35	nuclear factor kappa B subunit 1	Homo sapiens	139-148
27469405-4	2016	Moreover, treatment with dinaciclib led to the inhibition of oncogenic pathways normally activated in stimulated CLL cells, such as STAT3, NF-kappaB, p38, PI3K/AKT and RAF/MEK/ERK.	dinaciclib	25-35	mitogen-activated protein kinase 14	Homo sapiens	150-153
27469405-4	2016	Moreover, treatment with dinaciclib led to the inhibition of oncogenic pathways normally activated in stimulated CLL cells, such as STAT3, NF-kappaB, p38, PI3K/AKT and RAF/MEK/ERK.	dinaciclib	25-35	AKT serine/threonine kinase 1	Homo sapiens	160-163
27469405-4	2016	Moreover, treatment with dinaciclib led to the inhibition of oncogenic pathways normally activated in stimulated CLL cells, such as STAT3, NF-kappaB, p38, PI3K/AKT and RAF/MEK/ERK.	dinaciclib	25-35	zinc fingers and homeoboxes 2	Homo sapiens	168-171
27469405-4	2016	Moreover, treatment with dinaciclib led to the inhibition of oncogenic pathways normally activated in stimulated CLL cells, such as STAT3, NF-kappaB, p38, PI3K/AKT and RAF/MEK/ERK.	dinaciclib	25-35	mitogen-activated protein kinase kinase 7	Homo sapiens	172-175
27469405-4	2016	Moreover, treatment with dinaciclib led to the inhibition of oncogenic pathways normally activated in stimulated CLL cells, such as STAT3, NF-kappaB, p38, PI3K/AKT and RAF/MEK/ERK.	dinaciclib	25-35	mitogen-activated protein kinase 1	Homo sapiens	176-179
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.	dinaciclib	46-56	BCL2 apoptosis regulator	Homo sapiens	104-108
27550941-0	2016	Dinaciclib Induces Anaphase Catastrophe in Lung Cancer Cells via Inhibition of Cyclin-Dependent Kinases 1 and 2.	dinaciclib	0-10	cyclin dependent kinase 1	Homo sapiens	79-111
27550941-8	2016	Overexpression of CP110, which is a mediator of CDK2 inhibitor-induced anaphase catastrophe (and a CDK1 and 2 phosphorylation substrate), antagonized anaphase catastrophe and apoptosis following dinaciclib treatment.	dinaciclib	195-205	centriolar coiled-coil protein 110	Homo sapiens	18-23
27550941-8	2016	Overexpression of CP110, which is a mediator of CDK2 inhibitor-induced anaphase catastrophe (and a CDK1 and 2 phosphorylation substrate), antagonized anaphase catastrophe and apoptosis following dinaciclib treatment.	dinaciclib	195-205	cyclin dependent kinase 2	Homo sapiens	48-52
27550941-11	2016	Thus, the multi-CDK inhibitor dinaciclib causes anaphase catastrophe in lung cancer cells and should be investigated as a potential therapeutic for wild-type and KRAS-mutant lung cancer, individually or in combination with taxanes.	dinaciclib	30-40	KRAS proto-oncogene, GTPase	Homo sapiens	162-166
29137354-3	2017	Using a newly developed anti-pS294 monoclonal antibody, a combination of CDK specific siRNA knockdown studies and a broad panel of CDK selective inhibitors against ligand (E2)-stimulated MCF7 cells, we first identified CDK2 as the primary mediator of pS294 formation and showed that CDK2-selective inhibitors like Dinaciclib, but not CDK4/6 inhibitors like Palbociclib, can selectively prevent pS294 formation and repress ER-dependent gene expression.	dinaciclib	314-324	cyclin dependent kinase 2	Homo sapiens	219-223
27378523-0	2016	Multiple CDK inhibitor dinaciclib suppresses neuroblastoma growth via inhibiting CDK2 and CDK9 activity.	dinaciclib	23-33	cyclin dependent kinase 2	Homo sapiens	81-85
27378523-0	2016	Multiple CDK inhibitor dinaciclib suppresses neuroblastoma growth via inhibiting CDK2 and CDK9 activity.	dinaciclib	23-33	cyclin dependent kinase 9	Homo sapiens	90-94
27378523-4	2016	Here we show that a novel multiple-CDK inhibitor, dinaciclib (SCH727965, MK-7965), exhibits potent anti-proliferative effects on a panel of NB cell lines by blocking the activity of CDK2 and CDK9.	dinaciclib	50-60	cyclin dependent kinase 2	Homo sapiens	182-186
27378523-4	2016	Here we show that a novel multiple-CDK inhibitor, dinaciclib (SCH727965, MK-7965), exhibits potent anti-proliferative effects on a panel of NB cell lines by blocking the activity of CDK2 and CDK9.	dinaciclib	50-60	cyclin dependent kinase 9	Homo sapiens	191-195
27378523-4	2016	Here we show that a novel multiple-CDK inhibitor, dinaciclib (SCH727965, MK-7965), exhibits potent anti-proliferative effects on a panel of NB cell lines by blocking the activity of CDK2 and CDK9.	dinaciclib	62-71	cyclin dependent kinase 2	Homo sapiens	182-186
27378523-4	2016	Here we show that a novel multiple-CDK inhibitor, dinaciclib (SCH727965, MK-7965), exhibits potent anti-proliferative effects on a panel of NB cell lines by blocking the activity of CDK2 and CDK9.	dinaciclib	62-71	cyclin dependent kinase 9	Homo sapiens	191-195
27378523-4	2016	Here we show that a novel multiple-CDK inhibitor, dinaciclib (SCH727965, MK-7965), exhibits potent anti-proliferative effects on a panel of NB cell lines by blocking the activity of CDK2 and CDK9.	dinaciclib	73-80	cyclin dependent kinase 2	Homo sapiens	182-186
27378523-4	2016	Here we show that a novel multiple-CDK inhibitor, dinaciclib (SCH727965, MK-7965), exhibits potent anti-proliferative effects on a panel of NB cell lines by blocking the activity of CDK2 and CDK9.	dinaciclib	73-80	cyclin dependent kinase 9	Homo sapiens	191-195
27378523-5	2016	Dinaciclib also significantly sensitized NB cell lines to the treatment of chemotherapeutic agents such as doxorubicin (Dox) and etoposide (VP-16).	dinaciclib	0-10	host cell factor C1	Homo sapiens	140-145
27378523-6	2016	Furthermore, dinaciclib revealed in vivo antitumor efficacy in an orthotopic xenograft mouse model of two NB cell lines and blocked tumor development in the TH-MYCN transgenic NB mouse model.	dinaciclib	13-23	v-myc avian myelocytomatosis viral related oncogene, neuroblastoma derived	Mus musculus	160-164
28361959-0	2017	Dinaciclib potently suppresses MCL-1 and selectively induces the cell death in human iPS cells without affecting the viability of cardiac tissue.	dinaciclib	0-10	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	31-36
28361959-3	2017	In this report, we show that the CDKs inhibitor, Dinaciclib, selectively eliminates iPS cells without affecting the viability of cardiac cells.	dinaciclib	49-59	cyclin dependent kinase 9	Homo sapiens	33-37
28361959-7	2017	Dinaciclib also inhibited the phosphorylation of Serine 2 of the C-terminal domain of RNA Polyemrase II through CDK9 inhibition.	dinaciclib	0-10	cyclin dependent kinase 9	Homo sapiens	112-116
28361959-9	2017	Even though dinaciclib caused a slight downregulation of MCL-1 in iPS-derived cardiac cells, the viability of the cells was not significantly affected, and beating iPS-derived cardiac cell sheet could still be fabricated.	dinaciclib	12-22	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	57-62
28207834-10	2017	Dinaciclib decreased CDK1, cyclin B1, and Aurora A expression, induced cell cycle arrest in the G2/M phase, and induced accumulation of prophase mitotic cells.	dinaciclib	0-10	cyclin dependent kinase 1	Homo sapiens	21-25
28207834-10	2017	Dinaciclib decreased CDK1, cyclin B1, and Aurora A expression, induced cell cycle arrest in the G2/M phase, and induced accumulation of prophase mitotic cells.	dinaciclib	0-10	cyclin B1	Homo sapiens	27-36
28207834-10	2017	Dinaciclib decreased CDK1, cyclin B1, and Aurora A expression, induced cell cycle arrest in the G2/M phase, and induced accumulation of prophase mitotic cells.	dinaciclib	0-10	aurora kinase A	Homo sapiens	42-50
28207834-11	2017	Dinaciclib decreased Mcl-1, Bcl-xL and survivin expression, activated caspase-3 and induced apoptosis.	dinaciclib	0-10	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	21-26
28207834-11	2017	Dinaciclib decreased Mcl-1, Bcl-xL and survivin expression, activated caspase-3 and induced apoptosis.	dinaciclib	0-10	BCL2 like 1	Homo sapiens	28-34
28207834-11	2017	Dinaciclib decreased Mcl-1, Bcl-xL and survivin expression, activated caspase-3 and induced apoptosis.	dinaciclib	0-10	caspase 3	Homo sapiens	70-79
27880910-2	2016	Here, we report that dinaciclib, an inhibitor of cyclin-dependent kinases (CDKs) 1, 2, 5, and 9, additionally has potent activity against CDK12, a transcriptional regulator of HR.	dinaciclib	21-31	cyclin dependent kinase 12	Homo sapiens	75-79
27880910-2	2016	Here, we report that dinaciclib, an inhibitor of cyclin-dependent kinases (CDKs) 1, 2, 5, and 9, additionally has potent activity against CDK12, a transcriptional regulator of HR.	dinaciclib	21-31	cyclin dependent kinase 12	Homo sapiens	138-143
27880910-3	2016	In BRCA-mutated triple-negative breast cancer (TNBC) cells and patient-derived xenografts (PDXs), dinaciclib ablates restored HR and reverses PARP inhibitor resistance.	dinaciclib	98-108	BRCA1 DNA repair associated	Homo sapiens	3-7
27880910-3	2016	In BRCA-mutated triple-negative breast cancer (TNBC) cells and patient-derived xenografts (PDXs), dinaciclib ablates restored HR and reverses PARP inhibitor resistance.	dinaciclib	98-108	poly(ADP-ribose) polymerase 1	Homo sapiens	142-146
27880910-5	2016	Finally, dinaciclib augments the degree of response in a PARP-inhibitor-sensitive model, converting tumor growth inhibition to durable regression.	dinaciclib	9-19	poly(ADP-ribose) polymerase 1	Homo sapiens	57-61
27486754-0	2016	Inhibition of cyclin dependent kinase 9 by dinaciclib suppresses cyclin B1 expression and tumor growth in triple negative breast cancer.	dinaciclib	43-53	cyclin dependent kinase 9	Homo sapiens	14-39
27486754-0	2016	Inhibition of cyclin dependent kinase 9 by dinaciclib suppresses cyclin B1 expression and tumor growth in triple negative breast cancer.	dinaciclib	43-53	cyclin B1	Homo sapiens	65-74
27486754-7	2016	These data support the importance of CDK9, in addition to CDK1, in mediating the growth inhibitory effect of dinaciclib in TNBC.	dinaciclib	109-119	cyclin dependent kinase 9	Homo sapiens	37-41
27486754-7	2016	These data support the importance of CDK9, in addition to CDK1, in mediating the growth inhibitory effect of dinaciclib in TNBC.	dinaciclib	109-119	cyclin dependent kinase 1	Homo sapiens	58-62