PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
29149649-3	2018	In our study, Chk1 inhibitors, AZD7762 and MK-8776, had strong antitumor effects on CML cell line KBM5 and imatinib-resistant form KBM5T315I.	MK-8776	43-50	checkpoint kinase 1	Homo sapiens	14-18
28957699-0	2017	Randomized phase II trial of cytosine arabinoside with and without the CHK1 inhibitor MK-8776 in relapsed and refractory acute myeloid leukemia.	MK-8776	86-93	checkpoint kinase 1	Homo sapiens	71-75
29118324-6	2017	Furthermore, we demonstrated that FANCD2 depletion combined with CHK1 inhibitor MK-8776 significantly potentiated the cytotoxicity of gemcitabine to the two LSC cell lines, compared to individual FANCD2 depletion or MK-8776 treatment.	MK-8776	80-87	checkpoint kinase 1	Homo sapiens	65-69
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	MK-8776	186-193	checkpoint kinase 1	Homo sapiens	41-60
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	MK-8776	186-193	checkpoint kinase 1	Homo sapiens	62-66
28957699-2	2017	Incorporation of AraC into DNA activates checkpoint kinase 1 (Chk1), leading to cell-cycle arrest and diminished AraC cytotoxicity, which can be reversed by the selective Chk1 inhibitor MK-8776.	MK-8776	186-193	checkpoint kinase 1	Homo sapiens	171-175
28550769-0	2017	MK-8776, a novel Chk1 inhibitor, exhibits an improved radiosensitizing effect compared to UCN-01 by exacerbating radiation-induced aberrant mitosis.	MK-8776	0-7	checkpoint kinase 1	Mus musculus	17-21
28888100-0	2017	Chk1 Inhibitor SCH900776 Effectively Potentiates the Cytotoxic Effects of Platinum-Based Chemotherapeutic Drugs in Human Colon Cancer Cells.	MK-8776	15-24	checkpoint kinase 1	Homo sapiens	0-4
28888100-2	2017	Here we newly demonstrate the ability of one of the most specific Chk1 inhibitors, SCH900776 (MK-8776), to enhance human colon cancer cell sensitivity to the cytotoxic effects of platinum(II) cisplatin and platinum(IV)- LA-12 complexes.	MK-8776	83-92	checkpoint kinase 1	Homo sapiens	66-70
28888100-2	2017	Here we newly demonstrate the ability of one of the most specific Chk1 inhibitors, SCH900776 (MK-8776), to enhance human colon cancer cell sensitivity to the cytotoxic effects of platinum(II) cisplatin and platinum(IV)- LA-12 complexes.	MK-8776	94-101	checkpoint kinase 1	Homo sapiens	66-70
28888100-5	2017	In contrast to their wt counterparts, the p53- or p21-deficient cells treated with SCH900776 and cisplatin or LA-12 enter mitosis and become polyploid, and the senescence phenotype is strongly suppressed.	MK-8776	83-92	tumor protein p53	Homo sapiens	42-45
28888100-5	2017	In contrast to their wt counterparts, the p53- or p21-deficient cells treated with SCH900776 and cisplatin or LA-12 enter mitosis and become polyploid, and the senescence phenotype is strongly suppressed.	MK-8776	83-92	H3 histone pseudogene 16	Homo sapiens	50-53
28550769-2	2017	Here, we evaluate the radiosensitizing effects of a novel selective Chk1 inhibitor MK-8776, comparing its efficacy with a first-generation Chk1 inhibitor UCN-01, and attempt to elucidate the mechanism of radiosensitization.	MK-8776	83-90	checkpoint kinase 1	Mus musculus	68-72
28550769-7	2017	This suggests that Chk1 inhibition by MK-8776 activates a spindle assembly checkpoint and increases mitotic defects in irradiated EMT6 cells.	MK-8776	38-45	checkpoint kinase 1	Mus musculus	19-23
27690219-0	2016	MK-8776, a novel chk1 kinase inhibitor, radiosensitizes p53-defective human tumor cells.	MK-8776	0-7	checkpoint kinase 1	Homo sapiens	17-21
28978069-7	2017	The Chk1 inhibitor MK-8776 sensitized cells to gemcitabine with the greatest cell killing when added 18 h after gemcitabine.	MK-8776	19-26	checkpoint kinase 1	Homo sapiens	4-8
28978069-8	2017	In mice, the administration of MK-8776 18 h after gemcitabine elicited positivity for the DNA damage marker gammaH2AX; this also occurred at relatively low dose (40 mg/kg) gemcitabine.	MK-8776	31-38	H2A.X variant histone	Mus musculus	108-117
28042876-0	2017	The Chk1 inhibitor MK-8776 increases the radiosensitivity of human triple-negative breast cancer by inhibiting autophagy.	MK-8776	19-26	checkpoint kinase 1	Homo sapiens	4-8
27829224-10	2016	We identified two distinct classes of Chk1 inhibitors: those that induced a strong increase in gammaH2AX, pChk1 (S317) and pRPA32 (S4/S8) (including V158411, LY2603618 and ARRY-1A) and those that did not (including MK-8776 and GNE-900).	MK-8776	215-222	checkpoint kinase 1	Homo sapiens	38-42
28693160-12	2017	MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression.	MK-8776	0-7	cyclin dependent kinase 2	Homo sapiens	25-29
28693160-12	2017	MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression.	MK-8776	0-7	BCL2 associated X, apoptosis regulator	Homo sapiens	218-221
28693160-12	2017	MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression.	MK-8776	0-7	BCL2 like 11	Homo sapiens	223-226
28693160-12	2017	MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression.	MK-8776	0-7	apoptotic peptidase activating factor 1	Homo sapiens	228-234
28693160-12	2017	MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression.	MK-8776	0-7	caspase 9	Homo sapiens	236-245
28693160-12	2017	MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression.	MK-8776	0-7	caspase 3	Homo sapiens	250-259
28693160-12	2017	MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression.	MK-8776	0-7	BCL2 apoptosis regulator	Homo sapiens	277-282
28693160-12	2017	MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression.	MK-8776	136-143	cyclin dependent kinase 2	Homo sapiens	25-29
28693160-12	2017	MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression.	MK-8776	136-143	BCL2 associated X, apoptosis regulator	Homo sapiens	218-221
28693160-12	2017	MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression.	MK-8776	136-143	BCL2 like 11	Homo sapiens	223-226
28693160-12	2017	MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression.	MK-8776	136-143	apoptotic peptidase activating factor 1	Homo sapiens	228-234
28693160-12	2017	MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression.	MK-8776	136-143	caspase 9	Homo sapiens	236-245
28693160-12	2017	MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression.	MK-8776	136-143	caspase 3	Homo sapiens	250-259
28693160-12	2017	MK-8776 (an inhibitor of CDK2) antagonized the apoptosis induced by ISL, and, compared with treatment with ISL alone, pretreatment with MK-8776 inhibited the decrease in DeltaPsim, downregulated the mRNA expression of Bax, Bim, Apaf-1, caspase-9 and caspase-3, and upregulated Bcl-2 mRNA expression.	MK-8776	136-143	BCL2 apoptosis regulator	Homo sapiens	277-282
28042876-1	2017	MK-8776 is a recently described inhibitor that is highly selective for checkpoint kinase 1 (Chk1), which can weaken the DNA repair capacity in cancer cells to achieve chemo-sensitization.	MK-8776	0-7	checkpoint kinase 1	Homo sapiens	71-90
28042876-1	2017	MK-8776 is a recently described inhibitor that is highly selective for checkpoint kinase 1 (Chk1), which can weaken the DNA repair capacity in cancer cells to achieve chemo-sensitization.	MK-8776	0-7	checkpoint kinase 1	Homo sapiens	92-96
27690219-0	2016	MK-8776, a novel chk1 kinase inhibitor, radiosensitizes p53-defective human tumor cells.	MK-8776	0-7	tumor protein p53	Homo sapiens	56-59
27690219-2	2016	The aim of this study was to assess the Chk1 kinase inhibitor, MK-8776, for its ability to radiosensitize human tumor cells.	MK-8776	63-70	checkpoint kinase 1	Homo sapiens	40-44
27690219-10	2016	A comparison of MK-8776 to the wee1 inhibitor, MK-1775, suggested both similarities and differences in their activities.	MK-8776	16-23	WEE1 G2 checkpoint kinase	Homo sapiens	31-35
24179152-6	2014	The CHK1 inhibitor MK8776 sensitized acute myeloid leukemia cell lines and primary leukemia specimens to MK1775 ex vivo, whereas smaller effects were observed with the MK1775/MK8776 combination in normal myeloid progenitors.	MK-8776	19-25	checkpoint kinase 1	Homo sapiens	4-8
27625304-6	2016	Exposing the patient cells with the high abundance of CHK1 to SCH900776, an inhibitor of the kinase activity of CHK1, reduced clonogenic ability and progression of DNA replication in the presence of cytarabine.	MK-8776	62-71	checkpoint kinase 1	Homo sapiens	54-58
27625304-6	2016	Exposing the patient cells with the high abundance of CHK1 to SCH900776, an inhibitor of the kinase activity of CHK1, reduced clonogenic ability and progression of DNA replication in the presence of cytarabine.	MK-8776	62-71	checkpoint kinase 1	Homo sapiens	112-116
25372494-4	2015	With the aim of discerning the structural features that affect the inhibitory activity of triazolones, MK-8776, a Chk1 inhibitor that reached the clinical stage, was also used as a reference for simulations.	MK-8776	103-110	checkpoint kinase 1	Homo sapiens	114-118
25372494-7	2015	Moreover, introducing hydrophobic groups into triazolone inhibitors is favorable for binding to Chk1, which is corroborated by residue Leu136 with a relatively large difference in the contribution between MK-8776 and five triazolones to the total binding free energies.	MK-8776	205-212	checkpoint kinase 1	Homo sapiens	96-100
27556692-3	2016	We initially tested the potential of the highly specific Chk1 inhibitor SCH900776 to synergize with nucleoside analogs (NAs) fludarabine, cytarabine and gemcitabine in cell lines derived from B-cell malignancies.	MK-8776	72-81	checkpoint kinase 1	Mus musculus	57-61
27556692-4	2016	In p53-proficient NALM-6 cells, SCH900776 added to NAs enhanced signaling towards Chk1 (pSer317/pSer345), effectively blocked Chk1 activation (Ser296 autophosphorylation), increased replication stress (p53 and gamma-H2AX accumulation) and temporarily potentiated apoptosis.	MK-8776	32-41	tumor protein p53	Homo sapiens	3-6
27556692-4	2016	In p53-proficient NALM-6 cells, SCH900776 added to NAs enhanced signaling towards Chk1 (pSer317/pSer345), effectively blocked Chk1 activation (Ser296 autophosphorylation), increased replication stress (p53 and gamma-H2AX accumulation) and temporarily potentiated apoptosis.	MK-8776	32-41	checkpoint kinase 1	Homo sapiens	82-86
27556692-4	2016	In p53-proficient NALM-6 cells, SCH900776 added to NAs enhanced signaling towards Chk1 (pSer317/pSer345), effectively blocked Chk1 activation (Ser296 autophosphorylation), increased replication stress (p53 and gamma-H2AX accumulation) and temporarily potentiated apoptosis.	MK-8776	32-41	checkpoint kinase 1	Homo sapiens	126-130
27556692-4	2016	In p53-proficient NALM-6 cells, SCH900776 added to NAs enhanced signaling towards Chk1 (pSer317/pSer345), effectively blocked Chk1 activation (Ser296 autophosphorylation), increased replication stress (p53 and gamma-H2AX accumulation) and temporarily potentiated apoptosis.	MK-8776	32-41	tumor protein p53	Homo sapiens	202-205
27556692-8	2016	SCH900776 also increased the effect of fludarabine in a proportion of primary CLL samples treated with pro-proliferative stimuli, including those with TP53 disruption.	MK-8776	0-9	transformation related protein 53	Mus musculus	151-155
27556692-9	2016	Finally, we observed a fludarabine potentiation by SCH900776 in a T-cell leukemia 1 (TCL1)-driven mouse model of CLL.	MK-8776	51-60	T cell lymphoma breakpoint 1	Mus musculus	66-83
27556692-9	2016	Finally, we observed a fludarabine potentiation by SCH900776 in a T-cell leukemia 1 (TCL1)-driven mouse model of CLL.	MK-8776	51-60	T cell lymphoma breakpoint 1	Mus musculus	85-89
26595527-0	2016	A subset of cancer cell lines is acutely sensitive to the Chk1 inhibitor MK-8776 as monotherapy due to CDK2 activation in S phase.	MK-8776	73-80	checkpoint kinase 1	Homo sapiens	58-62
26595527-0	2016	A subset of cancer cell lines is acutely sensitive to the Chk1 inhibitor MK-8776 as monotherapy due to CDK2 activation in S phase.	MK-8776	73-80	cyclin dependent kinase 2	Homo sapiens	103-107
26595527-3	2016	From analysis of a large panel of cell lines, we demonstrate that 15% are very sensitive to the Chk1 inhibitor MK-8776.	MK-8776	111-118	checkpoint kinase 1	Homo sapiens	96-100
25605849-0	2015	Phase I dose-escalation trial of checkpoint kinase 1 inhibitor MK-8776 as monotherapy and in combination with gemcitabine in patients with advanced solid tumors.	MK-8776	63-70	checkpoint kinase 1	Homo sapiens	33-52
25605849-1	2015	PURPOSE: We determined the safety, pharmacokinetics, pharmacodynamics, and recommended phase II dose of MK-8776 (SCH 900776), a potent, selective checkpoint kinase 1 (Chk1) inhibitor, as monotherapy and in combination with gemcitabine in a first-in-human phase I clinical trial in patients with advanced solid tumor malignancies.	MK-8776	104-111	checkpoint kinase 1	Homo sapiens	146-165
25605849-1	2015	PURPOSE: We determined the safety, pharmacokinetics, pharmacodynamics, and recommended phase II dose of MK-8776 (SCH 900776), a potent, selective checkpoint kinase 1 (Chk1) inhibitor, as monotherapy and in combination with gemcitabine in a first-in-human phase I clinical trial in patients with advanced solid tumor malignancies.	MK-8776	104-111	checkpoint kinase 1	Homo sapiens	167-171
25605849-1	2015	PURPOSE: We determined the safety, pharmacokinetics, pharmacodynamics, and recommended phase II dose of MK-8776 (SCH 900776), a potent, selective checkpoint kinase 1 (Chk1) inhibitor, as monotherapy and in combination with gemcitabine in a first-in-human phase I clinical trial in patients with advanced solid tumor malignancies.	MK-8776	113-123	checkpoint kinase 1	Homo sapiens	167-171
24179152-6	2014	The CHK1 inhibitor MK8776 sensitized acute myeloid leukemia cell lines and primary leukemia specimens to MK1775 ex vivo, whereas smaller effects were observed with the MK1775/MK8776 combination in normal myeloid progenitors.	MK-8776	175-181	checkpoint kinase 1	Homo sapiens	4-8
24179152-8	2014	Further studies showed that MK8776 enhanced MK1775-mediated activation of the ATR/CHK1 pathway in acute leukemia cell lines and ex vivo.	MK-8776	28-34	ATR serine/threonine kinase	Homo sapiens	78-81
24179152-8	2014	Further studies showed that MK8776 enhanced MK1775-mediated activation of the ATR/CHK1 pathway in acute leukemia cell lines and ex vivo.	MK-8776	28-34	checkpoint kinase 1	Homo sapiens	82-86
24359526-0	2013	Sensitization of human cancer cells to gemcitabine by the Chk1 inhibitor MK-8776: cell cycle perturbation and impact of administration schedule in vitro and in vivo.	MK-8776	73-80	checkpoint kinase 1	Homo sapiens	58-62
24359526-2	2013	Here, we address the importance of appropriate drug scheduling when gemcitabine is combined with the Chk1 inhibitor MK-8776, and the mechanisms involved in the schedule dependence.	MK-8776	116-123	checkpoint kinase 1	Homo sapiens	101-105
24359526-14	2013	CONCLUSIONS: There are two reasons why delayed addition of MK-8776 enhances sensitivity to gemcitabine: first, there is an increased number of cells arrested in S phase; and second, the arrested cells have adequate time to initiate recombination and thereby become Chk1 dependent.	MK-8776	59-66	checkpoint kinase 1	Homo sapiens	265-269
23148684-5	2012	METHODS: Small molecules MK-8776 and MK-1775 were used to selectively and potently inhibit CHK1 and WEE1, respectively.	MK-8776	25-32	checkpoint kinase 1	Homo sapiens	91-95
23897988-11	2013	Microtubule-associated protein/microtubule affinity regulating kinase (MARK) inhibitors decrease blood pressure in dogs, whereas checkpoint kinase (Chk) inhibitors (AZD7762, SCH900776) exhibit dose-limiting CV toxicities in clinical trials.	MK-8776	174-183	megakaryocyte-associated tyrosine kinase	Homo sapiens	148-151
23536721-0	2013	The novel Chk1 inhibitor MK-8776 sensitizes human leukemia cells to HDAC inhibitors by targeting the intra-S checkpoint and DNA replication and repair.	MK-8776	25-32	checkpoint kinase 1	Homo sapiens	10-14
23536721-1	2013	Interactions between the novel Chk1 inhibitor MK-8776 and the histone deacetylase (HDAC) inhibitor (HDACI) vorinostat were examined in human leukemia cells harboring wild-type (wt) or deficient p53.	MK-8776	46-53	checkpoint kinase 1	Homo sapiens	31-35
23536721-2	2013	MK-8776 synergistically potentiated vorinostat-mediated apoptosis in various p53-wt or -deficient leukemia cell lines, whereas p53 knockdown by short hairpin RNA (shRNA) sensitized p53-wt cells to lethality of this regimen.	MK-8776	0-7	tumor protein p53	Homo sapiens	77-80
23536721-3	2013	Leukemia cell lines carrying FLT3-ITD were also sensitive to the MK-8776/vorinostat regimen.	MK-8776	65-72	fms related receptor tyrosine kinase 3	Homo sapiens	29-33
23536721-6	2013	Finally, the MK-8776/vorinostat regimen was active in primary acute myelogenous leukemia (AML) blasts, particularly against the CD34(+)/CD38(-)/CD123(+) population enriched for leukemia-initiating cells.	MK-8776	13-20	CD34 molecule	Homo sapiens	128-132
23536721-8	2013	Together, these findings indicate that the novel Chk1 inhibitor MK-8776 markedly potentiates HDACI lethality in leukemia cells displaying various genetic backgrounds through mechanisms involving disruption of the intra-S checkpoint, DNA replication, and DNA repair.	MK-8776	64-71	checkpoint kinase 1	Homo sapiens	49-53
23092873-2	2012	The selective Chk1 inhibitor SCH 900776 abrogates cytarabine-induced S-phase arrest and enhances cytarabine cytotoxicity in acute leukemia cell lines and leukemic blasts in vitro.	MK-8776	29-39	checkpoint kinase 1	Homo sapiens	14-18
24113549-3	2013	In this study, we evaluated the effects of a novel CHK1 inhibitor, MK-8776, in combination with pemetrexed (PMX) on cell proliferation and survival in a panel of p53 mutant non-small cell lung cancer (NSCLC) cell lines.	MK-8776	67-74	checkpoint kinase 1	Homo sapiens	51-55
24113549-3	2013	In this study, we evaluated the effects of a novel CHK1 inhibitor, MK-8776, in combination with pemetrexed (PMX) on cell proliferation and survival in a panel of p53 mutant non-small cell lung cancer (NSCLC) cell lines.	MK-8776	67-74	tumor protein p53	Homo sapiens	162-165
24113549-8	2013	We examined cell line sensitization to PMX in response to CHK1 inhibition with MK-8776 using WST-1 and clonogenic survival assays.	MK-8776	79-86	checkpoint kinase 1	Homo sapiens	58-62
24113549-11	2013	CHK1 inhibition by MK-8776 enhances sensitivity of NSCLC cell lines to PMX.	MK-8776	19-26	checkpoint kinase 1	Homo sapiens	0-4
23804422-0	2013	Sensitization of pancreatic cancer to chemoradiation by the Chk1 inhibitor MK8776.	MK-8776	75-81	checkpoint kinase 1	Homo sapiens	60-64
23804422-2	2013	To improve upon this regimen, we combined the selective Checkpoint kinase 1 (Chk1) inhibitor MK8776 with gemcitabine-based chemoradiation in preclinical pancreatic cancer models.	MK-8776	93-99	checkpoint kinase 1	Homo sapiens	56-75
23804422-2	2013	To improve upon this regimen, we combined the selective Checkpoint kinase 1 (Chk1) inhibitor MK8776 with gemcitabine-based chemoradiation in preclinical pancreatic cancer models.	MK-8776	93-99	checkpoint kinase 1	Homo sapiens	77-81
23804422-5	2013	RESULTS: We found that MK8776 significantly sensitized HRR-proficient (AsPC-1, MiaPaCa-2, BxPC-3) but not -deficient (Capan-1) pancreatic cancer cells to gemcitabine-radiation and inhibited Rad51 focus formation in HRR-proficient cells.	MK-8776	23-29	RAD51 recombinase	Homo sapiens	190-195
23804422-7	2013	We also assessed pChk1 (S345), a pharmacodynamic biomarker of DNA damage in response to Chk1 inhibition in both tumor and small intestine and found that MK8776 combined with gemcitabine or gemcitabine-radiation produced a significantly greater increase in pChk1 (S345) in tumor relative to small intestine, suggesting greater DNA damage in tumor than in normal tissue.	MK-8776	153-159	checkpoint kinase 1	Homo sapiens	18-22
23148684-5	2012	METHODS: Small molecules MK-8776 and MK-1775 were used to selectively and potently inhibit CHK1 and WEE1, respectively.	MK-8776	25-32	WEE1 G2 checkpoint kinase	Homo sapiens	100-104
21321066-0	2011	Targeting the replication checkpoint using SCH 900776, a potent and functionally selective CHK1 inhibitor identified via high content screening.	MK-8776	43-53	checkpoint kinase 1	Homo sapiens	91-95
22203733-0	2012	Preclinical development of the novel Chk1 inhibitor SCH900776 in combination with DNA-damaging agents and antimetabolites.	MK-8776	52-61	checkpoint kinase 1	Homo sapiens	37-41
22203733-4	2012	SCH900776 is a novel and more selective Chk1 inhibitor that potently inhibits Chk1 and abrogates cell-cycle arrest induced by SN38.	MK-8776	0-9	checkpoint kinase 1	Homo sapiens	40-44
22203733-4	2012	SCH900776 is a novel and more selective Chk1 inhibitor that potently inhibits Chk1 and abrogates cell-cycle arrest induced by SN38.	MK-8776	0-9	checkpoint kinase 1	Homo sapiens	78-82
22869869-2	2012	In the present study, we examined whether this checkpoint is activated in clinical acute myelogenous leukemia (AML) during cytarabine infusion in vivo and then assessed the impact of combining cytarabine with the recently described Chk1 inhibitor SCH 900776 in vitro.	MK-8776	247-257	checkpoint kinase 1	Homo sapiens	232-236
22937147-6	2012	Upon incubation with the Chk1 inhibitor MK-8776, single-stranded DNA regions (ssDNA) and double-strand breaks (DSB) begin to appear within 6 h. These DSB have been attributed to the structure-specific DNA endonuclease, Mus81.	MK-8776	40-47	checkpoint kinase 1	Homo sapiens	25-29
22937147-6	2012	Upon incubation with the Chk1 inhibitor MK-8776, single-stranded DNA regions (ssDNA) and double-strand breaks (DSB) begin to appear within 6 h. These DSB have been attributed to the structure-specific DNA endonuclease, Mus81.	MK-8776	40-47	MUS81 structure-specific endonuclease subunit	Homo sapiens	219-224
22937147-9	2012	These findings were corroborated by the discovery that Mre11-deficient ATLD1 cells are highly resistant to MK-8776 and form neither ssDNA nor DSB following treatment.	MK-8776	107-114	MRE11 homolog, double strand break repair nuclease	Homo sapiens	55-60
22937147-10	2012	However, once complimented with exogenous Mre11, the cells accumulate both ssDNA and DSB when incubated with MK-8776.	MK-8776	109-116	MRE11 homolog, double strand break repair nuclease	Homo sapiens	42-47
22937147-12	2012	The results highlight a novel role for Mre11 in the production of DSB and may help define which tumors are more sensitive to MK-8776 alone or in combination with DNA damaging agents.	MK-8776	125-132	MRE11 homolog, double strand break repair nuclease	Homo sapiens	39-44
21321066-9	2011	Using this approach, SCH 900776 was identified as a highly potent and functionally optimal CHK1 inhibitor with minimal intrinsic antagonistic properties.	MK-8776	21-31	checkpoint kinase 1	Homo sapiens	91-95
21321066-10	2011	SCH 900776 exposure phenocopies short interfering RNA-mediated CHK1 ablation and interacts synergistically with DNA antimetabolite agents in vitro and in vivo to selectively induce dsDNA breaks and cell death in tumor cell backgrounds.	MK-8776	0-10	checkpoint kinase 1	Homo sapiens	63-67
35418303-10	2022	Furthermore, CHK1 inhibition interferes with E2:ERalpha signaling to cell proliferation, and drugs approved for clinical treatment of primary and MBC (4OH-tamoxifen and the CDK4/CDK6 inhibitors abemaciclib and palbociclib) exert synergic effects with the CHK1 inhibitors in clinical trials for the treatment of solid tumors (AZD7762, MK8776, prexasertib) in preventing the proliferation of cells modeling primary and MBC.	MK-8776	334-340	checkpoint kinase 1	Homo sapiens	13-17
34508175-6	2021	Suboptimal doses of the CHK1 inhibitor MK-8776 plus the PARP inhibitor olaparib led to a MYCN-dependent accumulation of DNA damage and cell death in vitro and significantly reduced the growth of four in vivo models of MYCN-driven tumors, without major toxicities.	MK-8776	39-46	checkpoint kinase 1	Homo sapiens	24-28
34508175-6	2021	Suboptimal doses of the CHK1 inhibitor MK-8776 plus the PARP inhibitor olaparib led to a MYCN-dependent accumulation of DNA damage and cell death in vitro and significantly reduced the growth of four in vivo models of MYCN-driven tumors, without major toxicities.	MK-8776	39-46	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	89-93
34508175-6	2021	Suboptimal doses of the CHK1 inhibitor MK-8776 plus the PARP inhibitor olaparib led to a MYCN-dependent accumulation of DNA damage and cell death in vitro and significantly reduced the growth of four in vivo models of MYCN-driven tumors, without major toxicities.	MK-8776	39-46	MYCN proto-oncogene, bHLH transcription factor	Homo sapiens	218-222
35418303-10	2022	Furthermore, CHK1 inhibition interferes with E2:ERalpha signaling to cell proliferation, and drugs approved for clinical treatment of primary and MBC (4OH-tamoxifen and the CDK4/CDK6 inhibitors abemaciclib and palbociclib) exert synergic effects with the CHK1 inhibitors in clinical trials for the treatment of solid tumors (AZD7762, MK8776, prexasertib) in preventing the proliferation of cells modeling primary and MBC.	MK-8776	334-340	cyclin dependent kinase 4	Homo sapiens	173-177
33986399-3	2021	Here, we investigated the efficacy of combining gemcitabine with MK-8776, a novel CHK1 inhibitor, in four bladder cancer cell lines.	MK-8776	65-72	checkpoint kinase 1	Mus musculus	82-86
31683862-8	2019	The Chk1 inhibitor MK-8776 was most effective, reducing viral DNA amplification by 90-99% and caused DNA damage and apoptosis, preferentially in HPV infected cells.	MK-8776	19-26	checkpoint kinase 1	Homo sapiens	4-8
33860197-0	2021	Comparative Activity and Off-Target Effects in Cells of the CHK1 Inhibitors MK-8776, SRA737, and LY2606368.	MK-8776	76-83	checkpoint kinase 1	Homo sapiens	60-64
33860197-8	2021	LY2606368 was far more potent at inhibiting CHK1 and inducing growth arrest, while all three CHK1i inhibited CHK2 at concentrations 10- (MK-8776 and SRA737) to 100- (LY2606368) fold higher.	MK-8776	137-144	checkpoint kinase 1	Homo sapiens	93-98
33860197-9	2021	MK-8776 and SRA737 exhibited similar off-target effects: higher concentrations demonstrated transient protection from growth inhibition, circumvented DNA damage, and prevented checkpoint abrogation, possibly due to inhibition of CDK2.	MK-8776	0-7	cyclin dependent kinase 2	Homo sapiens	229-233
32579780-3	2020	CHK1 has been associated with prostate cancer (PCa) induction, progression, and lethality, hence CHK1 inhibitors SCH900776 (also known as MK-8776) and the more effective SCH900776 analog MU380 may have clinical applications in the therapy of PCa.	MK-8776	113-122	checkpoint kinase 1	Homo sapiens	97-101
32579780-3	2020	CHK1 has been associated with prostate cancer (PCa) induction, progression, and lethality, hence CHK1 inhibitors SCH900776 (also known as MK-8776) and the more effective SCH900776 analog MU380 may have clinical applications in the therapy of PCa.	MK-8776	138-145	checkpoint kinase 1	Homo sapiens	0-4
32579780-3	2020	CHK1 has been associated with prostate cancer (PCa) induction, progression, and lethality, hence CHK1 inhibitors SCH900776 (also known as MK-8776) and the more effective SCH900776 analog MU380 may have clinical applications in the therapy of PCa.	MK-8776	138-145	checkpoint kinase 1	Homo sapiens	97-101
32579780-3	2020	CHK1 has been associated with prostate cancer (PCa) induction, progression, and lethality, hence CHK1 inhibitors SCH900776 (also known as MK-8776) and the more effective SCH900776 analog MU380 may have clinical applications in the therapy of PCa.	MK-8776	170-179	checkpoint kinase 1	Homo sapiens	0-4
32579780-5	2020	Here we report, that such therapeutic approach may be exploited using the synergistic action of the antimetabolite gemcitabine and CHK1 inhibitors SCH900776 and MU380 in docetaxel-resistant mCRPC.	MK-8776	147-156	checkpoint kinase 1	Homo sapiens	131-135
32314919-2	2020	To elucidate the CHK1-regulated phosphorylation network, we performed a global quantitative phosphoproteomics analysis, which revealed 142 phosphosites whose phosphorylation levels were significantly different following treatment with the CHK1 inhibitor SCH 900776.	MK-8776	254-264	checkpoint kinase 1	Homo sapiens	17-21
32314919-2	2020	To elucidate the CHK1-regulated phosphorylation network, we performed a global quantitative phosphoproteomics analysis, which revealed 142 phosphosites whose phosphorylation levels were significantly different following treatment with the CHK1 inhibitor SCH 900776.	MK-8776	254-264	checkpoint kinase 1	Homo sapiens	239-243
32314919-4	2020	Furthermore, IRF3 phosphorylation at S173 and S175 was significantly reduced following treatment with SCH 900776.	MK-8776	102-112	interferon regulatory factor 3	Homo sapiens	13-17
30975911-8	2019	Moreover, in a mouse model of FLT3/ITD acute myeloid leukemia, treatment with the CHK1 inhibitor MK8776 + cytarabine extended survival over cytarabine alone.	MK-8776	97-103	FMS-like tyrosine kinase 3	Mus musculus	30-34
30975911-8	2019	Moreover, in a mouse model of FLT3/ITD acute myeloid leukemia, treatment with the CHK1 inhibitor MK8776 + cytarabine extended survival over cytarabine alone.	MK-8776	97-103	checkpoint kinase 1	Mus musculus	82-86
30837643-5	2019	Moreover, CHK1 knockdown or addition of a CHK1 inhibitor such as MK-8776, rabusertib or prexasertib enhances CPX-351-induced apoptosis in multiple TP53-null and TP53-wildtype AML cell lines.	MK-8776	65-72	checkpoint kinase 1	Homo sapiens	42-46
31443367-0	2019	Chk1 Inhibitor MK-8776 Restores the Sensitivity of Chemotherapeutics in P-glycoprotein Overexpressing Cancer Cells.	MK-8776	15-22	checkpoint kinase 1	Homo sapiens	0-4
31443367-0	2019	Chk1 Inhibitor MK-8776 Restores the Sensitivity of Chemotherapeutics in P-glycoprotein Overexpressing Cancer Cells.	MK-8776	15-22	ATP binding cassette subfamily B member 1	Homo sapiens	72-86
31443367-3	2019	Here, we report that checkpoint kinase (Chk) 1 inhibitor MK-8776, a drug candidate in clinical trial, can restore the sensitivity of chemotherapeutics that are substrates of P-gp in KB-C2, SW620/Ad300 cells and human embryonic kidney (HEK)293/ABCB1 cells that overexpress P-gp.	MK-8776	57-64	checkpoint kinase 1	Homo sapiens	21-46
31443367-3	2019	Here, we report that checkpoint kinase (Chk) 1 inhibitor MK-8776, a drug candidate in clinical trial, can restore the sensitivity of chemotherapeutics that are substrates of P-gp in KB-C2, SW620/Ad300 cells and human embryonic kidney (HEK)293/ABCB1 cells that overexpress P-gp.	MK-8776	57-64	ATP binding cassette subfamily B member 1	Homo sapiens	174-178
31443367-3	2019	Here, we report that checkpoint kinase (Chk) 1 inhibitor MK-8776, a drug candidate in clinical trial, can restore the sensitivity of chemotherapeutics that are substrates of P-gp in KB-C2, SW620/Ad300 cells and human embryonic kidney (HEK)293/ABCB1 cells that overexpress P-gp.	MK-8776	57-64	ATP binding cassette subfamily B member 1	Homo sapiens	243-248
31443367-3	2019	Here, we report that checkpoint kinase (Chk) 1 inhibitor MK-8776, a drug candidate in clinical trial, can restore the sensitivity of chemotherapeutics that are substrates of P-gp in KB-C2, SW620/Ad300 cells and human embryonic kidney (HEK)293/ABCB1 cells that overexpress P-gp.	MK-8776	57-64	ATP binding cassette subfamily B member 1	Homo sapiens	272-276
31443367-4	2019	MK-8776 remarkably enhanced the cellular [3H]-paclitaxel accumulation and suppressed the efflux function of P-gp without reducing its expression and affecting its cellular localization in cancer cells.	MK-8776	0-7	ATP binding cassette subfamily B member 1	Homo sapiens	108-112
31443367-5	2019	Furthermore, MK-8776 (0-40 muM) stimulated the activity of ATPase in P-gp, which was 4.1-fold greater than the control.	MK-8776	13-20	dynein axonemal heavy chain 8	Homo sapiens	59-65
31443367-5	2019	Furthermore, MK-8776 (0-40 muM) stimulated the activity of ATPase in P-gp, which was 4.1-fold greater than the control.	MK-8776	13-20	ATP binding cassette subfamily B member 1	Homo sapiens	69-73
31443367-6	2019	In addition, MK-8776 formed a cation-pi bond and pi-pi interaction with key residues of the substrate-binding site in P-gp, as indicated by computer-aided molecular docking study.	MK-8776	13-20	ATP binding cassette subfamily B member 1	Homo sapiens	118-122
31443367-7	2019	Our study indicated that MK-8776 may significantly enhance the sensitivity of chemotherapeutics that are substrates of P-gp, providing important information for its application in the reversal of MDR.	MK-8776	25-32	ATP binding cassette subfamily B member 1	Homo sapiens	119-123
30837643-5	2019	Moreover, CHK1 knockdown or addition of a CHK1 inhibitor such as MK-8776, rabusertib or prexasertib enhances CPX-351-induced apoptosis in multiple TP53-null and TP53-wildtype AML cell lines.	MK-8776	65-72	tumor protein p53	Homo sapiens	147-151
30837643-5	2019	Moreover, CHK1 knockdown or addition of a CHK1 inhibitor such as MK-8776, rabusertib or prexasertib enhances CPX-351-induced apoptosis in multiple TP53-null and TP53-wildtype AML cell lines.	MK-8776	65-72	tumor protein p53	Homo sapiens	161-165
30103170-0	2018	Metronomic oral doxorubicin in combination of Chk1 inhibitor MK-8776 for p53-deficient breast cancer treatment.	MK-8776	61-68	checkpoint kinase 1	Homo sapiens	46-50
30103170-0	2018	Metronomic oral doxorubicin in combination of Chk1 inhibitor MK-8776 for p53-deficient breast cancer treatment.	MK-8776	61-68	tumor protein p53	Homo sapiens	73-76
30103170-3	2018	In this light, within the limits of p53-deficient breast cancer, we demonstrate the enhanced anticancer effect of metronomic chemotherapy using doxorubicin when combined with Chk1 inhibitor MK-8776 by specifically augmenting the direct cytotoxic effect on cancer cells.	MK-8776	190-197	tumor protein p53	Homo sapiens	36-39
30103170-3	2018	In this light, within the limits of p53-deficient breast cancer, we demonstrate the enhanced anticancer effect of metronomic chemotherapy using doxorubicin when combined with Chk1 inhibitor MK-8776 by specifically augmenting the direct cytotoxic effect on cancer cells.	MK-8776	190-197	checkpoint kinase 1	Homo sapiens	175-179
30103170-5	2018	MK-8776 selectively enhanced the cytotoxic effect of low-concentration doxorubicin in p53-deficient breast cancer cells by abrogating the Chk1-dependent cell cycle arrest in vitro.	MK-8776	0-7	tumor protein p53	Homo sapiens	86-89
30103170-5	2018	MK-8776 selectively enhanced the cytotoxic effect of low-concentration doxorubicin in p53-deficient breast cancer cells by abrogating the Chk1-dependent cell cycle arrest in vitro.	MK-8776	0-7	checkpoint kinase 1	Homo sapiens	138-142
30103170-6	2018	Consistently, combining MK-8776 significantly improved the anticancer effect of the daily administered oral doxorubicin in p53-deficient breast cancer xenografts especially in a lower dose of doxorubicin without evident systemic toxicities.	MK-8776	24-31	tumor protein p53	Homo sapiens	123-126
30103170-7	2018	Combination therapy of MK-8776 and metronomic oral doxorubicin would be thus promising in the treatment of p53-deficient breast cancer benefited from the augmented direct cytotoxic effect and low risk of toxicities.	MK-8776	23-30	tumor protein p53	Homo sapiens	107-110
29895190-3	2018	The goals of this study were to directly compare the relative efficacies of the CHK1 inhibitor MK8776 and the WEE1 inhibitor AZD1775 to sensitize pancreatic cancer cell lines to gemcitabine and to identify pharmacodynamic biomarkers predictive of chemosensitization.	MK-8776	95-101	checkpoint kinase 1	Homo sapiens	80-84
29157102-0	2018	Chk1 inhibitor SCH 900776 enhances the antitumor activity of MLN4924 on pancreatic cancer.	MK-8776	15-25	checkpoint kinase 1	Mus musculus	0-4
30103203-0	2018	Targeting acute myeloid leukemia CD34+ stem/progenitor cells with small molecule inhibitor MK-8776.	MK-8776	91-98	CD34 molecule	Homo sapiens	33-37
29895190-6	2018	The abilities of either the CDK1/2 inhibitor roscovitine or exogenous nucleosides to prevent MK8776 or AZD1775-mediated chemosensitization, however, were both inhibitor-dependent and variable among cell lines.	MK-8776	93-99	cyclin dependent kinase 12	Homo sapiens	28-34
29157102-3	2018	Chk1 inhibitor SCH 900776 alone exhibited minimal cytotoxicity, and caused no DNA damage on PC cells.	MK-8776	15-25	checkpoint kinase 1	Mus musculus	0-4