PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
34101892-1	2022	Rivoceranib is a selective inhibitor of VEGFR-2 being developed for the treatment of solid tumor.	apatinib	0-11	kinase insert domain receptor	Homo sapiens	40-47
32795895-0	2020	Apatinib enhanced anti-PD-1 therapy for colon cancer in mice via promoting PD-L1 expression.	apatinib	0-8	programmed cell death 1	Mus musculus	23-27
32795895-0	2020	Apatinib enhanced anti-PD-1 therapy for colon cancer in mice via promoting PD-L1 expression.	apatinib	0-8	CD274 antigen	Mus musculus	75-80
32795895-2	2020	In this study, we found that an angiogenesis inhibitor apatinib enhanced anti-PD-1 therapy for colon cancer in mice via promoting PD-L1 expression.	apatinib	55-63	programmed cell death 1	Mus musculus	78-82
32795895-2	2020	In this study, we found that an angiogenesis inhibitor apatinib enhanced anti-PD-1 therapy for colon cancer in mice via promoting PD-L1 expression.	apatinib	55-63	CD274 antigen	Mus musculus	130-135
32795895-3	2020	Apatinib treatment upregulated PD-L1 expression in various colon cancer cells both at the mRNA and protein levels.	apatinib	0-8	CD274 antigen	Mus musculus	31-36
32795895-4	2020	Further, apatinib-treated cancer cells hampered activation and IFN-gamma secretion of T cells in the co-culture system, which was reversed by the anti-PD-1 antibody.	apatinib	9-17	interferon gamma	Mus musculus	63-72
32795895-4	2020	Further, apatinib-treated cancer cells hampered activation and IFN-gamma secretion of T cells in the co-culture system, which was reversed by the anti-PD-1 antibody.	apatinib	9-17	programmed cell death 1	Mus musculus	151-155
32795895-7	2020	Overall, our study here showed the enhancement of anti-PD-1 antitumor efficacy in a syngeneic mouse model (CT-26 cells in Balb/c) by the angiogenesis inhibitor apatinib via upregulating PD-L1 expression as well as angiogenesis inhibition, which may provide a rationale for the combination of apatinib and anti-PD-1 antibody for colorectal cancer treatment in the clinic.	apatinib	160-168	programmed cell death 1	Mus musculus	55-59
32795895-7	2020	Overall, our study here showed the enhancement of anti-PD-1 antitumor efficacy in a syngeneic mouse model (CT-26 cells in Balb/c) by the angiogenesis inhibitor apatinib via upregulating PD-L1 expression as well as angiogenesis inhibition, which may provide a rationale for the combination of apatinib and anti-PD-1 antibody for colorectal cancer treatment in the clinic.	apatinib	160-168	CD274 antigen	Mus musculus	186-191
32795895-7	2020	Overall, our study here showed the enhancement of anti-PD-1 antitumor efficacy in a syngeneic mouse model (CT-26 cells in Balb/c) by the angiogenesis inhibitor apatinib via upregulating PD-L1 expression as well as angiogenesis inhibition, which may provide a rationale for the combination of apatinib and anti-PD-1 antibody for colorectal cancer treatment in the clinic.	apatinib	160-168	programmed cell death 1	Mus musculus	310-314
32795895-7	2020	Overall, our study here showed the enhancement of anti-PD-1 antitumor efficacy in a syngeneic mouse model (CT-26 cells in Balb/c) by the angiogenesis inhibitor apatinib via upregulating PD-L1 expression as well as angiogenesis inhibition, which may provide a rationale for the combination of apatinib and anti-PD-1 antibody for colorectal cancer treatment in the clinic.	apatinib	292-300	programmed cell death 1	Mus musculus	55-59
32795895-7	2020	Overall, our study here showed the enhancement of anti-PD-1 antitumor efficacy in a syngeneic mouse model (CT-26 cells in Balb/c) by the angiogenesis inhibitor apatinib via upregulating PD-L1 expression as well as angiogenesis inhibition, which may provide a rationale for the combination of apatinib and anti-PD-1 antibody for colorectal cancer treatment in the clinic.	apatinib	292-300	CD274 antigen	Mus musculus	186-191
34937475-9	2022	Apatinib (a VEGFR-2 tyrosine kinase inhibitor) can reduce the incidence of camrelizumab-specific reactive cutaneous capillary endothelial proliferation (RCCEP).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	12-19
34856418-0	2022	TRIM21 improves apatinib treatment in gastric cancer through suppressing EZH1 stability.	apatinib	16-24	tripartite motif containing 21	Homo sapiens	0-6
34856418-0	2022	TRIM21 improves apatinib treatment in gastric cancer through suppressing EZH1 stability.	apatinib	16-24	enhancer of zeste 1 polycomb repressive complex 2 subunit	Homo sapiens	73-77
34856418-6	2022	We then found that apatinib (APA)-reduced GC cell proliferation was significantly abolished by TRIM21 knockdown; however, promoting TRIM21 expression further improved the sensitivity of GC cells to APA treatment, as proved by the remarkably decreased cell viability and colony formation.	apatinib	19-27	tripartite motif containing 21	Homo sapiens	95-101
34856418-6	2022	We then found that apatinib (APA)-reduced GC cell proliferation was significantly abolished by TRIM21 knockdown; however, promoting TRIM21 expression further improved the sensitivity of GC cells to APA treatment, as proved by the remarkably decreased cell viability and colony formation.	apatinib	19-27	tripartite motif containing 21	Homo sapiens	132-138
34856418-6	2022	We then found that apatinib (APA)-reduced GC cell proliferation was significantly abolished by TRIM21 knockdown; however, promoting TRIM21 expression further improved the sensitivity of GC cells to APA treatment, as proved by the remarkably decreased cell viability and colony formation.	apatinib	29-32	tripartite motif containing 21	Homo sapiens	95-101
34856418-6	2022	We then found that apatinib (APA)-reduced GC cell proliferation was significantly abolished by TRIM21 knockdown; however, promoting TRIM21 expression further improved the sensitivity of GC cells to APA treatment, as proved by the remarkably decreased cell viability and colony formation.	apatinib	29-32	tripartite motif containing 21	Homo sapiens	132-138
34856418-6	2022	We then found that apatinib (APA)-reduced GC cell proliferation was significantly abolished by TRIM21 knockdown; however, promoting TRIM21 expression further improved the sensitivity of GC cells to APA treatment, as proved by the remarkably decreased cell viability and colony formation.	apatinib	198-201	tripartite motif containing 21	Homo sapiens	132-138
34913959-2	2022	Objective: To assess the efficacy and safety of apatinib, a highly selective vascular endothelial growth factor (VEGFR-2) inhibitor, in patients with progressive locally advanced or metastatic RAIR-DTC.	apatinib	48-56	vascular endothelial growth factor A	Homo sapiens	77-111
34913959-2	2022	Objective: To assess the efficacy and safety of apatinib, a highly selective vascular endothelial growth factor (VEGFR-2) inhibitor, in patients with progressive locally advanced or metastatic RAIR-DTC.	apatinib	48-56	kinase insert domain receptor	Homo sapiens	113-120
34718369-7	2021	PAQR4 knockdown sensitized Hep3B cells to apatinib-based chemotherapy.	apatinib	42-50	progestin and adipoQ receptor family member 4	Homo sapiens	0-5
34887682-10	2021	Grade 3 or 4 adverse events were significantly more common in the apatinib plus camrelizumab combination therapy than in the apatinib or camrelizumab monotherapy, and these included increased aspartate aminotransferase and increased alanine aminotransferase levels.	apatinib	66-74	glutamic--pyruvic transaminase	Homo sapiens	233-257
34887682-10	2021	Grade 3 or 4 adverse events were significantly more common in the apatinib plus camrelizumab combination therapy than in the apatinib or camrelizumab monotherapy, and these included increased aspartate aminotransferase and increased alanine aminotransferase levels.	apatinib	125-133	glutamic--pyruvic transaminase	Homo sapiens	233-257
34970563-1	2021	Objective: Apatinib is a inhibitor of vascular endothelial growth factor receptor-2.	apatinib	11-19	kinase insert domain receptor	Homo sapiens	38-83
34868934-12	2021	High-throughput RNA sequencing showed that Apatinib downregulated the expression of TYMS and RRM2.	apatinib	43-51	thymidylate synthetase	Homo sapiens	84-88
34868934-12	2021	High-throughput RNA sequencing showed that Apatinib downregulated the expression of TYMS and RRM2.	apatinib	43-51	ribonucleotide reductase regulatory subunit M2	Homo sapiens	93-97
34868934-13	2021	Western blotting verified that Apatinib downregulated the TYMS/STAT3/PD-L1 pathway and inhibited liposarcoma proliferation by suppressing the RRM2/PI3K/AKT/mTOR pathway.	apatinib	31-39	thymidylate synthetase	Homo sapiens	58-62
34868934-13	2021	Western blotting verified that Apatinib downregulated the TYMS/STAT3/PD-L1 pathway and inhibited liposarcoma proliferation by suppressing the RRM2/PI3K/AKT/mTOR pathway.	apatinib	31-39	signal transducer and activator of transcription 3	Homo sapiens	63-68
34868934-13	2021	Western blotting verified that Apatinib downregulated the TYMS/STAT3/PD-L1 pathway and inhibited liposarcoma proliferation by suppressing the RRM2/PI3K/AKT/mTOR pathway.	apatinib	31-39	CD274 molecule	Homo sapiens	69-74
34868934-13	2021	Western blotting verified that Apatinib downregulated the TYMS/STAT3/PD-L1 pathway and inhibited liposarcoma proliferation by suppressing the RRM2/PI3K/AKT/mTOR pathway.	apatinib	31-39	ribonucleotide reductase regulatory subunit M2	Homo sapiens	142-146
34868934-13	2021	Western blotting verified that Apatinib downregulated the TYMS/STAT3/PD-L1 pathway and inhibited liposarcoma proliferation by suppressing the RRM2/PI3K/AKT/mTOR pathway.	apatinib	31-39	AKT serine/threonine kinase 1	Homo sapiens	152-155
34868934-13	2021	Western blotting verified that Apatinib downregulated the TYMS/STAT3/PD-L1 pathway and inhibited liposarcoma proliferation by suppressing the RRM2/PI3K/AKT/mTOR pathway.	apatinib	31-39	mechanistic target of rapamycin kinase	Homo sapiens	156-160
34868934-16	2021	Apatinib might inhibit liposarcoma cell proliferation through the RRM2/PI3K/AKT/mTOR signaling pathway and downregulate PD-L1 via the TYMS/STAT3 signaling pathway.	apatinib	0-8	ribonucleotide reductase regulatory subunit M2	Homo sapiens	66-70
34868934-16	2021	Apatinib might inhibit liposarcoma cell proliferation through the RRM2/PI3K/AKT/mTOR signaling pathway and downregulate PD-L1 via the TYMS/STAT3 signaling pathway.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	76-79
34868934-16	2021	Apatinib might inhibit liposarcoma cell proliferation through the RRM2/PI3K/AKT/mTOR signaling pathway and downregulate PD-L1 via the TYMS/STAT3 signaling pathway.	apatinib	0-8	mechanistic target of rapamycin kinase	Homo sapiens	80-84
34868934-16	2021	Apatinib might inhibit liposarcoma cell proliferation through the RRM2/PI3K/AKT/mTOR signaling pathway and downregulate PD-L1 via the TYMS/STAT3 signaling pathway.	apatinib	0-8	CD274 molecule	Homo sapiens	120-125
34868934-16	2021	Apatinib might inhibit liposarcoma cell proliferation through the RRM2/PI3K/AKT/mTOR signaling pathway and downregulate PD-L1 via the TYMS/STAT3 signaling pathway.	apatinib	0-8	thymidylate synthetase	Homo sapiens	134-138
34868934-16	2021	Apatinib might inhibit liposarcoma cell proliferation through the RRM2/PI3K/AKT/mTOR signaling pathway and downregulate PD-L1 via the TYMS/STAT3 signaling pathway.	apatinib	0-8	signal transducer and activator of transcription 3	Homo sapiens	139-144
34815663-2	2021	We designed a retrospective study to evaluate the efficacy and safety of anlotinib in patients with persistent, metastatic, or recurrent cervical cancer who have failed first-line therapy, and compare the efficacy of anlotinib with that of apatinib which targets only VEGFR2 and has shown efficacy in recent studies.	apatinib	240-248	kinase insert domain receptor	Homo sapiens	268-274
34742339-0	2021	Correction to: Apatinib triggers autophagic and apoptotic cell death via VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling in lung cancer.	apatinib	15-23	kinase insert domain receptor	Homo sapiens	73-79
34742339-0	2021	Correction to: Apatinib triggers autophagic and apoptotic cell death via VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling in lung cancer.	apatinib	15-23	signal transducer and activator of transcription 3	Homo sapiens	80-85
34742339-0	2021	Correction to: Apatinib triggers autophagic and apoptotic cell death via VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling in lung cancer.	apatinib	15-23	CD274 molecule	Homo sapiens	86-91
34742339-0	2021	Correction to: Apatinib triggers autophagic and apoptotic cell death via VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling in lung cancer.	apatinib	15-23	NFE2 like bZIP transcription factor 2	Homo sapiens	100-104
34742339-0	2021	Correction to: Apatinib triggers autophagic and apoptotic cell death via VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling in lung cancer.	apatinib	15-23	nucleoporin 62	Homo sapiens	105-108
34761117-5	2021	Apatinib is a novel tyrosine kinase inhibitor that inhibits angiogenesis by targeting vascular endothelial growth factor receptor-2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	86-131
34761117-5	2021	Apatinib is a novel tyrosine kinase inhibitor that inhibits angiogenesis by targeting vascular endothelial growth factor receptor-2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	133-140
34761117-7	2021	In this study, we administered apatinib in combination with anti-epidermal growth factor receptor (EGFR) targeted and systemic chemotherapy for the treatment of oral cancer and to achieve better disease outcomes.	apatinib	31-39	epidermal growth factor receptor	Homo sapiens	65-97
34365722-0	2021	Apatinib combined with Keytruda treatment induces apoptosis of gastric carcinoma cells through CES4/miR-616-5p/DUSP2 axis.	apatinib	0-8	carboxylesterase 1 pseudogene 1	Homo sapiens	95-99
34365722-0	2021	Apatinib combined with Keytruda treatment induces apoptosis of gastric carcinoma cells through CES4/miR-616-5p/DUSP2 axis.	apatinib	0-8	microRNA 616	Homo sapiens	100-107
34365722-0	2021	Apatinib combined with Keytruda treatment induces apoptosis of gastric carcinoma cells through CES4/miR-616-5p/DUSP2 axis.	apatinib	0-8	dual specificity phosphatase 2	Homo sapiens	111-116
34365722-8	2021	CES4 was highly expressed in the apatinib combined with Keytruda-treated HGC-27 and MKN-7 cells.	apatinib	33-41	carboxylesterase 1 pseudogene 1	Homo sapiens	0-4
34365722-9	2021	Apatinib combined with Keytruda treatment repressed cell viability and promoted apoptosis of HGC-27 and MKN-7 cells, which was abrogated by CES4 knockdown.	apatinib	0-8	carboxylesterase 1 pseudogene 1	Homo sapiens	140-144
34365722-12	2021	In conclusion, these data demonstrate that apatinib combined with Keytruda treatment induces apoptosis of GC cells through CES4/miR-616-5p/DUSP2 axis.	apatinib	43-51	carboxylesterase 1 pseudogene 1	Homo sapiens	123-127
34365722-12	2021	In conclusion, these data demonstrate that apatinib combined with Keytruda treatment induces apoptosis of GC cells through CES4/miR-616-5p/DUSP2 axis.	apatinib	43-51	microRNA 616	Homo sapiens	128-135
34365722-12	2021	In conclusion, these data demonstrate that apatinib combined with Keytruda treatment induces apoptosis of GC cells through CES4/miR-616-5p/DUSP2 axis.	apatinib	43-51	dual specificity phosphatase 2	Homo sapiens	139-144
34725795-11	2022	Expression of vascular endothelial VE-cadherin, ephrinA2 receptor (EPHA2), p-PI3K/phosphoinositide-3 kinase (PI3K) and phospho-AKT (p-AKT)/AKT ratios was decreased under the influence of Apatinib and a combination of Apatinib/melatonin (P <= 0.01).	apatinib	187-195	cadherin 5	Homo sapiens	35-46
34725795-11	2022	Expression of vascular endothelial VE-cadherin, ephrinA2 receptor (EPHA2), p-PI3K/phosphoinositide-3 kinase (PI3K) and phospho-AKT (p-AKT)/AKT ratios was decreased under the influence of Apatinib and a combination of Apatinib/melatonin (P <= 0.01).	apatinib	187-195	EPH receptor A2	Homo sapiens	48-65
34725795-11	2022	Expression of vascular endothelial VE-cadherin, ephrinA2 receptor (EPHA2), p-PI3K/phosphoinositide-3 kinase (PI3K) and phospho-AKT (p-AKT)/AKT ratios was decreased under the influence of Apatinib and a combination of Apatinib/melatonin (P <= 0.01).	apatinib	187-195	EPH receptor A2	Homo sapiens	67-72
34725795-11	2022	Expression of vascular endothelial VE-cadherin, ephrinA2 receptor (EPHA2), p-PI3K/phosphoinositide-3 kinase (PI3K) and phospho-AKT (p-AKT)/AKT ratios was decreased under the influence of Apatinib and a combination of Apatinib/melatonin (P <= 0.01).	apatinib	187-195	AKT serine/threonine kinase 1	Homo sapiens	127-130
34725795-11	2022	Expression of vascular endothelial VE-cadherin, ephrinA2 receptor (EPHA2), p-PI3K/phosphoinositide-3 kinase (PI3K) and phospho-AKT (p-AKT)/AKT ratios was decreased under the influence of Apatinib and a combination of Apatinib/melatonin (P <= 0.01).	apatinib	187-195	AKT serine/threonine kinase 1	Homo sapiens	134-137
34725795-11	2022	Expression of vascular endothelial VE-cadherin, ephrinA2 receptor (EPHA2), p-PI3K/phosphoinositide-3 kinase (PI3K) and phospho-AKT (p-AKT)/AKT ratios was decreased under the influence of Apatinib and a combination of Apatinib/melatonin (P <= 0.01).	apatinib	187-195	AKT serine/threonine kinase 1	Homo sapiens	139-142
34725795-11	2022	Expression of vascular endothelial VE-cadherin, ephrinA2 receptor (EPHA2), p-PI3K/phosphoinositide-3 kinase (PI3K) and phospho-AKT (p-AKT)/AKT ratios was decreased under the influence of Apatinib and a combination of Apatinib/melatonin (P <= 0.01).	apatinib	217-225	cadherin 5	Homo sapiens	35-46
34725795-11	2022	Expression of vascular endothelial VE-cadherin, ephrinA2 receptor (EPHA2), p-PI3K/phosphoinositide-3 kinase (PI3K) and phospho-AKT (p-AKT)/AKT ratios was decreased under the influence of Apatinib and a combination of Apatinib/melatonin (P <= 0.01).	apatinib	217-225	EPH receptor A2	Homo sapiens	48-65
34725795-11	2022	Expression of vascular endothelial VE-cadherin, ephrinA2 receptor (EPHA2), p-PI3K/phosphoinositide-3 kinase (PI3K) and phospho-AKT (p-AKT)/AKT ratios was decreased under the influence of Apatinib and a combination of Apatinib/melatonin (P <= 0.01).	apatinib	217-225	EPH receptor A2	Homo sapiens	67-72
34725795-11	2022	Expression of vascular endothelial VE-cadherin, ephrinA2 receptor (EPHA2), p-PI3K/phosphoinositide-3 kinase (PI3K) and phospho-AKT (p-AKT)/AKT ratios was decreased under the influence of Apatinib and a combination of Apatinib/melatonin (P <= 0.01).	apatinib	217-225	AKT serine/threonine kinase 1	Homo sapiens	127-130
34725795-11	2022	Expression of vascular endothelial VE-cadherin, ephrinA2 receptor (EPHA2), p-PI3K/phosphoinositide-3 kinase (PI3K) and phospho-AKT (p-AKT)/AKT ratios was decreased under the influence of Apatinib and a combination of Apatinib/melatonin (P <= 0.01).	apatinib	217-225	AKT serine/threonine kinase 1	Homo sapiens	134-137
34725795-11	2022	Expression of vascular endothelial VE-cadherin, ephrinA2 receptor (EPHA2), p-PI3K/phosphoinositide-3 kinase (PI3K) and phospho-AKT (p-AKT)/AKT ratios was decreased under the influence of Apatinib and a combination of Apatinib/melatonin (P <= 0.01).	apatinib	217-225	AKT serine/threonine kinase 1	Homo sapiens	139-142
34862331-3	2022	Here, we explored the role of the RhoA/Rho kinase (ROCK) signaling pathway in elevation of blood pressure (BP) induced by apatinib, a selective TKI approved in China for treatment of advanced or metastatic gastric cancer.	apatinib	122-130	ras homolog family member A	Rattus norvegicus	34-38
34862331-9	2022	Apatinib treatment mediated upregulation of RhoA and ROCK II in the mid-aorta, more significant in the high-dose group.	apatinib	0-8	ras homolog family member A	Rattus norvegicus	44-48
34862331-9	2022	Apatinib treatment mediated upregulation of RhoA and ROCK II in the mid-aorta, more significant in the high-dose group.	apatinib	0-8	Rho-associated coiled-coil containing protein kinase 2	Rattus norvegicus	53-60
34862331-12	2022	Apatinib administration was also associated with decreased levels of MLCP, and elevated endothelin-1 (ET-1) and collagen I, which were accompanied with increased mid-aortic media.	apatinib	0-8	endothelin 1	Rattus norvegicus	88-100
34862331-12	2022	Apatinib administration was also associated with decreased levels of MLCP, and elevated endothelin-1 (ET-1) and collagen I, which were accompanied with increased mid-aortic media.	apatinib	0-8	endothelin 1	Rattus norvegicus	102-106
34862331-14	2022	CONCLUSION: These findings suggest that activation of the RhoA/ROCK signaling pathway could be the underlying mechanism of apatinib-induced hypertension, while ROCK inhibitor have potential therapeutic value.	apatinib	123-131	ras homolog family member A	Rattus norvegicus	58-62
34236267-0	2021	A bivalent cyclic RGD-siRNA conjugate enhances the antitumor effect of apatinib via co-inhibiting VEGFR2 in non-small cell lung cancer xenografts.	apatinib	71-79	kinase insert domain protein receptor	Mus musculus	98-104
34880763-1	2021	Aim: Apatinib is an orally administered vascular epidermal growth factor receptor (VEGFR)-tyrosine kinase inhibitors approved for the treatment of advanced gastric adenocarcinoma or gastric esophageal junction adenocarcinoma.	apatinib	5-13	kinase insert domain receptor	Homo sapiens	40-81
34880763-1	2021	Aim: Apatinib is an orally administered vascular epidermal growth factor receptor (VEGFR)-tyrosine kinase inhibitors approved for the treatment of advanced gastric adenocarcinoma or gastric esophageal junction adenocarcinoma.	apatinib	5-13	kinase insert domain receptor	Homo sapiens	83-88
34880763-2	2021	Apatinib is predominantly metabolized by CYP3A4/5, followed by CYP2D6.	apatinib	0-8	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	41-49
34880763-9	2021	The DDI simulation showed 2-4-fold changes in apatinib exposures by moderate CYP3A4 inhibitors and CYP3A4 inducers.	apatinib	46-54	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	77-83
34880763-9	2021	The DDI simulation showed 2-4-fold changes in apatinib exposures by moderate CYP3A4 inhibitors and CYP3A4 inducers.	apatinib	46-54	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	99-105
34880763-10	2021	A moderate increase of apatinib exposure (1.25-2-fold) was found with strong CYP2D6 inhibitor.	apatinib	23-31	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	77-83
34590406-8	2021	Immunohistochemical and immunofluorescence staining revealed that VEGF, pVEGFR2, PI3K, AKT, p-ERK1/2, Ki-67 and CD31 in the tumour cells of apatinib-treated group were downregulated compared with control group.	apatinib	140-148	mitogen-activated protein kinase 3	Homo sapiens	94-100
34590406-0	2021	Apatinib inhibits the growth of small cell lung cancer via a mechanism mediated by VEGF, PI3K/Akt and Ki-67/CD31.	apatinib	0-8	vascular endothelial growth factor A	Homo sapiens	83-87
34590406-8	2021	Immunohistochemical and immunofluorescence staining revealed that VEGF, pVEGFR2, PI3K, AKT, p-ERK1/2, Ki-67 and CD31 in the tumour cells of apatinib-treated group were downregulated compared with control group.	apatinib	140-148	platelet and endothelial cell adhesion molecule 1	Homo sapiens	112-116
34590406-0	2021	Apatinib inhibits the growth of small cell lung cancer via a mechanism mediated by VEGF, PI3K/Akt and Ki-67/CD31.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	94-97
34590406-10	2021	In conclusion, apatinib inhibited the growth of SCLC cells by downregulating the expression of VEGF, pVEGFR2, p-PI3K, p-AKT, p-ERK1/2, Ki-67 and CD31.	apatinib	15-23	vascular endothelial growth factor A	Mus musculus	95-99
34590406-0	2021	Apatinib inhibits the growth of small cell lung cancer via a mechanism mediated by VEGF, PI3K/Akt and Ki-67/CD31.	apatinib	0-8	platelet and endothelial cell adhesion molecule 1	Homo sapiens	108-112
34590406-8	2021	Immunohistochemical and immunofluorescence staining revealed that VEGF, pVEGFR2, PI3K, AKT, p-ERK1/2, Ki-67 and CD31 in the tumour cells of apatinib-treated group were downregulated compared with control group.	apatinib	140-148	vascular endothelial growth factor A	Mus musculus	66-70
34590406-8	2021	Immunohistochemical and immunofluorescence staining revealed that VEGF, pVEGFR2, PI3K, AKT, p-ERK1/2, Ki-67 and CD31 in the tumour cells of apatinib-treated group were downregulated compared with control group.	apatinib	140-148	AKT serine/threonine kinase 1	Homo sapiens	87-90
34778042-4	2021	Interestingly, distinct clinical and pathological characteristics were observed that differed from those of the reported cases of severe cutaneous reactions induced by anti-PD-1 antibodies alone; thus, we speculate that it was induced by the combination of camrelizumab and apatinib.	apatinib	274-282	programmed cell death 1	Homo sapiens	173-177
34778042-7	2021	All these findings highlight the essential role of CD4+ T cells and CD8+ T cells in the TEN-like reaction induced by camrelizumab plus apatinib treatment, and we speculate that T cells, especially CD8+ T cells, attack keratinocytes.	apatinib	135-143	CD4 molecule	Homo sapiens	51-54
34778042-7	2021	All these findings highlight the essential role of CD4+ T cells and CD8+ T cells in the TEN-like reaction induced by camrelizumab plus apatinib treatment, and we speculate that T cells, especially CD8+ T cells, attack keratinocytes.	apatinib	135-143	CD8a molecule	Homo sapiens	68-71
34760374-0	2021	A novel role for apatinib in enhancing radiosensitivity in non-small cell lung cancer cells by suppressing the AKT and ERK pathways.	apatinib	17-25	AKT serine/threonine kinase 1	Homo sapiens	111-114
34760374-0	2021	A novel role for apatinib in enhancing radiosensitivity in non-small cell lung cancer cells by suppressing the AKT and ERK pathways.	apatinib	17-25	mitogen-activated protein kinase 1	Homo sapiens	119-122
34760374-2	2021	Apatinib (AP) is a highly selective inhibitor of vascular endothelial growth factor receptor 2 (VEGFR2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	49-94
34760374-2	2021	Apatinib (AP) is a highly selective inhibitor of vascular endothelial growth factor receptor 2 (VEGFR2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	96-102
34702279-1	2021	BACKGROUND: Rivoceranib, a novel tyrosine kinase inhibitor, exhibits anti-tumour effects by selectively blocking vascular endothelial growth factor receptor-2 (VEGFR2) in cancer cells.	apatinib	12-23	kinase insert domain receptor	Canis lupus familiaris	113-158
34702279-1	2021	BACKGROUND: Rivoceranib, a novel tyrosine kinase inhibitor, exhibits anti-tumour effects by selectively blocking vascular endothelial growth factor receptor-2 (VEGFR2) in cancer cells.	apatinib	12-23	kinase insert domain receptor	Canis lupus familiaris	160-166
34702279-8	2021	RESULTS: Rivoceranib treatment showed anti-proliferative effects and mediated cell cycle arrest in the canine melanoma cell line (LMeC) and the mammary gland tumour (MGT) cell line (CHMp).	apatinib	9-20	CHM Rab escort protein	Canis lupus familiaris	182-186
34786397-5	2021	The patient was diagnosed with pancreatic ductal adenocarcinoma (PDAC) with BAP1 and PIK3CA gene mutations and Raf1 fusion and achieved partial response twice after treatment with apatinib in combination with chemotherapy.	apatinib	180-188	BRCA1 associated protein 1	Homo sapiens	76-80
34786397-5	2021	The patient was diagnosed with pancreatic ductal adenocarcinoma (PDAC) with BAP1 and PIK3CA gene mutations and Raf1 fusion and achieved partial response twice after treatment with apatinib in combination with chemotherapy.	apatinib	180-188	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	85-91
34786397-5	2021	The patient was diagnosed with pancreatic ductal adenocarcinoma (PDAC) with BAP1 and PIK3CA gene mutations and Raf1 fusion and achieved partial response twice after treatment with apatinib in combination with chemotherapy.	apatinib	180-188	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	111-115
34745955-7	2021	In terms of mOS, apatinib (hazard ratio (HR) 0.61, 95% credible interval (CrI) 0.48-0.78) and nivolumab (HR 0.62, 95% CrI 0.51-0.76) were the most effective treatments compared with placebo.	apatinib	17-25	Moloney sarcoma oncogene	Mus musculus	12-15
34635636-0	2021	Apatinib inhibits glioma cell malignancy in patient-derived orthotopic xenograft mouse model by targeting thrombospondin 1/myosin heavy chain 9 axis.	apatinib	0-8	thrombospondin 1	Mus musculus	106-122
34635636-0	2021	Apatinib inhibits glioma cell malignancy in patient-derived orthotopic xenograft mouse model by targeting thrombospondin 1/myosin heavy chain 9 axis.	apatinib	0-8	myosin, heavy polypeptide 9, non-muscle	Mus musculus	123-143
34635636-8	2021	Thrombospondin 1 (THBS1) was identified as a potential target of apatinib that lead to inhibited glioma cell proliferation.	apatinib	65-73	thrombospondin 1	Mus musculus	0-16
34635636-8	2021	Thrombospondin 1 (THBS1) was identified as a potential target of apatinib that lead to inhibited glioma cell proliferation.	apatinib	65-73	thrombospondin 1	Mus musculus	18-23
34635636-9	2021	Apatinib-mediated THBS1 downregulation in glioma cells was confirmed by qPCR and western blotting.	apatinib	0-8	thrombospondin 1	Mus musculus	18-23
34635636-12	2021	These data suggest that apatinib targets THBS1 in glioma cells, potentially via MYH9, to inhibit glioma cell malignancy and may provide novel targets for glioma therapy.	apatinib	24-32	thrombospondin 1	Mus musculus	41-46
34635636-12	2021	These data suggest that apatinib targets THBS1 in glioma cells, potentially via MYH9, to inhibit glioma cell malignancy and may provide novel targets for glioma therapy.	apatinib	24-32	myosin, heavy polypeptide 9, non-muscle	Mus musculus	80-84
34590406-10	2021	In conclusion, apatinib inhibited the growth of SCLC cells by downregulating the expression of VEGF, pVEGFR2, p-PI3K, p-AKT, p-ERK1/2, Ki-67 and CD31.	apatinib	15-23	AKT serine/threonine kinase 1	Homo sapiens	120-123
34590406-10	2021	In conclusion, apatinib inhibited the growth of SCLC cells by downregulating the expression of VEGF, pVEGFR2, p-PI3K, p-AKT, p-ERK1/2, Ki-67 and CD31.	apatinib	15-23	mitogen-activated protein kinase 3	Homo sapiens	127-133
34590406-10	2021	In conclusion, apatinib inhibited the growth of SCLC cells by downregulating the expression of VEGF, pVEGFR2, p-PI3K, p-AKT, p-ERK1/2, Ki-67 and CD31.	apatinib	15-23	platelet and endothelial cell adhesion molecule 1	Homo sapiens	145-149
34343940-7	2021	We also found that the anti-angiogenic effect of apatinib increased programmed death ligand-1 (PD-L1) levels, down-regulated vascular endothelial growth factor receptor 2 (VEGFR-2) levels, and induced an increase in the extent of tumor tissue necrosis.	apatinib	49-57	CD274 antigen	Mus musculus	68-93
34343940-7	2021	We also found that the anti-angiogenic effect of apatinib increased programmed death ligand-1 (PD-L1) levels, down-regulated vascular endothelial growth factor receptor 2 (VEGFR-2) levels, and induced an increase in the extent of tumor tissue necrosis.	apatinib	49-57	CD274 antigen	Mus musculus	95-100
34343940-7	2021	We also found that the anti-angiogenic effect of apatinib increased programmed death ligand-1 (PD-L1) levels, down-regulated vascular endothelial growth factor receptor 2 (VEGFR-2) levels, and induced an increase in the extent of tumor tissue necrosis.	apatinib	49-57	kinase insert domain protein receptor	Mus musculus	125-170
34343940-7	2021	We also found that the anti-angiogenic effect of apatinib increased programmed death ligand-1 (PD-L1) levels, down-regulated vascular endothelial growth factor receptor 2 (VEGFR-2) levels, and induced an increase in the extent of tumor tissue necrosis.	apatinib	49-57	kinase insert domain protein receptor	Mus musculus	172-179
34489549-0	2021	FOXK2 transcriptionally activating VEGFA induces apatinib resistance in anaplastic thyroid cancer through VEGFA/VEGFR1 pathway.	apatinib	49-57	forkhead box K2	Homo sapiens	0-5
34489549-0	2021	FOXK2 transcriptionally activating VEGFA induces apatinib resistance in anaplastic thyroid cancer through VEGFA/VEGFR1 pathway.	apatinib	49-57	vascular endothelial growth factor A	Homo sapiens	35-40
34489549-0	2021	FOXK2 transcriptionally activating VEGFA induces apatinib resistance in anaplastic thyroid cancer through VEGFA/VEGFR1 pathway.	apatinib	49-57	vascular endothelial growth factor A	Homo sapiens	106-111
34489549-0	2021	FOXK2 transcriptionally activating VEGFA induces apatinib resistance in anaplastic thyroid cancer through VEGFA/VEGFR1 pathway.	apatinib	49-57	fms related receptor tyrosine kinase 1	Homo sapiens	112-118
34489549-5	2021	On VEGFR2 blockage by specific targeting agent, such as Apatinib, FOXK2 could rapidly trigger therapeutic resistance.	apatinib	56-64	kinase insert domain receptor	Homo sapiens	3-9
34489549-5	2021	On VEGFR2 blockage by specific targeting agent, such as Apatinib, FOXK2 could rapidly trigger therapeutic resistance.	apatinib	56-64	forkhead box K2	Homo sapiens	66-71
34683119-2	2021	Our previous study demonstrated that apatinib, an orally selective VEGFR-2 antagonist, is highly effective in T-ALL.	apatinib	37-45	kinase insert domain receptor	Homo sapiens	67-74
34409776-3	2021	Apatinib (a vascular endothelial growth factor receptor 2 tyrosine kinase inhibitor) could increase the efficacy of camrelizumab (an ICI agent).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	12-57
34524004-1	2022	Background: We conducted a trial to evaluate the efficacy and safety of apatinib, a tyrosine inhibitor against vascular endothelial growth factor receptor 2, combined with neoadjuvant chemotherapy in patients with locally advanced esophageal squamous cell carcinoma (ESCC).	apatinib	72-80	kinase insert domain receptor	Homo sapiens	111-156
34683841-3	2021	In this study, we tried to repurpose an investigational anticancer drug, rivoceranib, which is a selective inhibitor of VEGF receptor-2 (VEGFR2), and evaluate the therapeutic potential of the drug for the treatment of wet-type AMD in a laser-induced CNV mouse model using microsphere-based sustained drug release formulations.	apatinib	73-84	kinase insert domain protein receptor	Mus musculus	120-135
34683841-3	2021	In this study, we tried to repurpose an investigational anticancer drug, rivoceranib, which is a selective inhibitor of VEGF receptor-2 (VEGFR2), and evaluate the therapeutic potential of the drug for the treatment of wet-type AMD in a laser-induced CNV mouse model using microsphere-based sustained drug release formulations.	apatinib	73-84	kinase insert domain protein receptor	Mus musculus	137-143
34145174-3	2021	Apatinib, a highly selective orally administered small-molecule tyrosine kinase inhibitor that targets vascular endothelial growth factor receptor-2 (VEGFR2) has successfully been used as a second- and third-line agent in the management of ABC.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	103-148
34145174-3	2021	Apatinib, a highly selective orally administered small-molecule tyrosine kinase inhibitor that targets vascular endothelial growth factor receptor-2 (VEGFR2) has successfully been used as a second- and third-line agent in the management of ABC.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	150-156
34145174-4	2021	There are also multiple reported cases where Apatinib was miraculously effective in the management of triple-negative and HER2-positive tumors.	apatinib	45-53	erb-b2 receptor tyrosine kinase 2	Homo sapiens	122-126
34145174-6	2021	Here, we report the case of a 34-year-old woman with hormone receptor-positive and HER2-negative ABC who was successfully treated with low-dose Apatinib.	apatinib	144-152	erb-b2 receptor tyrosine kinase 2	Homo sapiens	83-87
34424120-0	2021	Apatinib inhibits cell proliferation and migration of osteosarcoma via activating LINC00261/miR-620/PTEN axis.	apatinib	0-8	long intergenic non-protein coding RNA 261	Homo sapiens	82-91
34274778-6	2021	Additionally, Apatinib is incorporated as antiangiogenic drug to downregulate the expression of vascular endothelial growth factor (VEGF), which can effectively inhibit the tumor angiogenesis after MDT.	apatinib	14-22	vascular endothelial growth factor A	Homo sapiens	96-130
34274778-6	2021	Additionally, Apatinib is incorporated as antiangiogenic drug to downregulate the expression of vascular endothelial growth factor (VEGF), which can effectively inhibit the tumor angiogenesis after MDT.	apatinib	14-22	vascular endothelial growth factor A	Homo sapiens	132-136
34424120-0	2021	Apatinib inhibits cell proliferation and migration of osteosarcoma via activating LINC00261/miR-620/PTEN axis.	apatinib	0-8	microRNA 620	Homo sapiens	92-99
34424120-0	2021	Apatinib inhibits cell proliferation and migration of osteosarcoma via activating LINC00261/miR-620/PTEN axis.	apatinib	0-8	phosphatase and tensin homolog	Homo sapiens	100-104
34424120-8	2021	LINC00261 was down-regulated in OS cells but then up-regulated after the treatment by Apatinib.	apatinib	86-94	long intergenic non-protein coding RNA 261	Homo sapiens	0-9
34424120-9	2021	Silencing LINC00261 abrogated the suppressive effect of Apatinib on OS cell proliferation and migration.	apatinib	56-64	long intergenic non-protein coding RNA 261	Homo sapiens	10-19
34424120-11	2021	Besides, miR-620 was up-regulated in OS cells and Apatinib treatment reduced miR-620 expression.	apatinib	50-58	microRNA 620	Homo sapiens	77-84
34424120-13	2021	Moreover, Apatinib hindered in vitro cell proliferation and migration as well as the in vivo tumorigenesis of OS through LINC00261/miR-620/PTEN axis.	apatinib	10-18	long intergenic non-protein coding RNA 261	Homo sapiens	121-130
34424120-13	2021	Moreover, Apatinib hindered in vitro cell proliferation and migration as well as the in vivo tumorigenesis of OS through LINC00261/miR-620/PTEN axis.	apatinib	10-18	microRNA 620	Homo sapiens	131-138
34424120-13	2021	Moreover, Apatinib hindered in vitro cell proliferation and migration as well as the in vivo tumorigenesis of OS through LINC00261/miR-620/PTEN axis.	apatinib	10-18	phosphatase and tensin homolog	Homo sapiens	139-143
34424120-14	2021	Apatinib-enhanced LINC00261 restrained OS via miR-620/PTEN axis, indicating LINC00261 might promote the efficacy of Apatinib on OS.	apatinib	0-8	long intergenic non-protein coding RNA 261	Homo sapiens	18-27
34424120-14	2021	Apatinib-enhanced LINC00261 restrained OS via miR-620/PTEN axis, indicating LINC00261 might promote the efficacy of Apatinib on OS.	apatinib	0-8	microRNA 620	Homo sapiens	46-53
34424120-14	2021	Apatinib-enhanced LINC00261 restrained OS via miR-620/PTEN axis, indicating LINC00261 might promote the efficacy of Apatinib on OS.	apatinib	0-8	phosphatase and tensin homolog	Homo sapiens	54-58
34424120-14	2021	Apatinib-enhanced LINC00261 restrained OS via miR-620/PTEN axis, indicating LINC00261 might promote the efficacy of Apatinib on OS.	apatinib	0-8	long intergenic non-protein coding RNA 261	Homo sapiens	76-85
34424120-14	2021	Apatinib-enhanced LINC00261 restrained OS via miR-620/PTEN axis, indicating LINC00261 might promote the efficacy of Apatinib on OS.	apatinib	116-124	long intergenic non-protein coding RNA 261	Homo sapiens	18-27
34424120-14	2021	Apatinib-enhanced LINC00261 restrained OS via miR-620/PTEN axis, indicating LINC00261 might promote the efficacy of Apatinib on OS.	apatinib	116-124	microRNA 620	Homo sapiens	46-53
34424120-14	2021	Apatinib-enhanced LINC00261 restrained OS via miR-620/PTEN axis, indicating LINC00261 might promote the efficacy of Apatinib on OS.	apatinib	116-124	phosphatase and tensin homolog	Homo sapiens	54-58
34424120-14	2021	Apatinib-enhanced LINC00261 restrained OS via miR-620/PTEN axis, indicating LINC00261 might promote the efficacy of Apatinib on OS.	apatinib	116-124	long intergenic non-protein coding RNA 261	Homo sapiens	76-85
34484431-2	2021	Apatinib, a VEGFR2 tyrosine kynase inhibitor, showed an activity against BTC xenografts in preclinical models.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	12-18
34459788-0	2021	Stimulator of interferon response cGAMP interactor overcomes ERBB2-mediated apatinib resistance in head and neck squamous cell carcinoma.	apatinib	76-84	stimulator of interferon response cGAMP interactor 1	Homo sapiens	0-50
34459788-0	2021	Stimulator of interferon response cGAMP interactor overcomes ERBB2-mediated apatinib resistance in head and neck squamous cell carcinoma.	apatinib	76-84	erb-b2 receptor tyrosine kinase 2	Homo sapiens	61-66
34459788-2	2021	This study aimed to evaluate the function of Erb-B2 receptor tyrosine kinase 2 (ERBB2) and stimulator of interferon response cGAMP interactor (STING) in apatinib resistance in HNSCC.	apatinib	153-161	erb-b2 receptor tyrosine kinase 2	Homo sapiens	45-51
34459788-2	2021	This study aimed to evaluate the function of Erb-B2 receptor tyrosine kinase 2 (ERBB2) and stimulator of interferon response cGAMP interactor (STING) in apatinib resistance in HNSCC.	apatinib	153-161	erb-b2 receptor tyrosine kinase 2	Homo sapiens	80-85
34459788-2	2021	This study aimed to evaluate the function of Erb-B2 receptor tyrosine kinase 2 (ERBB2) and stimulator of interferon response cGAMP interactor (STING) in apatinib resistance in HNSCC.	apatinib	153-161	stimulator of interferon response cGAMP interactor 1	Homo sapiens	91-141
34459788-2	2021	This study aimed to evaluate the function of Erb-B2 receptor tyrosine kinase 2 (ERBB2) and stimulator of interferon response cGAMP interactor (STING) in apatinib resistance in HNSCC.	apatinib	153-161	stimulator of interferon response cGAMP interactor 1	Homo sapiens	143-148
34459788-11	2021	Targeted treatment of ERBB2 using lapatinib could attenuate apatinib resistance.	apatinib	60-68	erb-b2 receptor tyrosine kinase 2	Homo sapiens	22-27
34459788-13	2021	CONCLUSION: STING could sensitize AR cells to apatinib by decreasing ERBB2 expression.	apatinib	46-54	stimulator of interferon response cGAMP interactor 1	Homo sapiens	12-17
34459788-13	2021	CONCLUSION: STING could sensitize AR cells to apatinib by decreasing ERBB2 expression.	apatinib	46-54	erb-b2 receptor tyrosine kinase 2	Homo sapiens	69-74
34459788-14	2021	The combination of lapatinib or a STING agonist with apatinib ameliorated acquired apatinib resistance in a synergistic manner.	apatinib	53-61	stimulator of interferon response cGAMP interactor 1	Homo sapiens	34-39
34459788-14	2021	The combination of lapatinib or a STING agonist with apatinib ameliorated acquired apatinib resistance in a synergistic manner.	apatinib	83-91	stimulator of interferon response cGAMP interactor 1	Homo sapiens	34-39
34453028-0	2021	Apatinib inhibits the proliferation of gastric cancer cells via the AKT/GSK signaling pathway in vivo.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	68-71
34453028-7	2021	Meanwhile, apatinib exhibited the best antitumor growth effect with dose and time dependence by suppressing AKT/GSK3alpha/beta signaling, which may be the mechanism underlying the profound antitumor clinical effect of apatinib.	apatinib	11-19	AKT serine/threonine kinase 1	Homo sapiens	108-111
34453028-7	2021	Meanwhile, apatinib exhibited the best antitumor growth effect with dose and time dependence by suppressing AKT/GSK3alpha/beta signaling, which may be the mechanism underlying the profound antitumor clinical effect of apatinib.	apatinib	11-19	glycogen synthase kinase 3 alpha	Homo sapiens	112-126
34453028-7	2021	Meanwhile, apatinib exhibited the best antitumor growth effect with dose and time dependence by suppressing AKT/GSK3alpha/beta signaling, which may be the mechanism underlying the profound antitumor clinical effect of apatinib.	apatinib	218-226	AKT serine/threonine kinase 1	Homo sapiens	108-111
34453028-7	2021	Meanwhile, apatinib exhibited the best antitumor growth effect with dose and time dependence by suppressing AKT/GSK3alpha/beta signaling, which may be the mechanism underlying the profound antitumor clinical effect of apatinib.	apatinib	218-226	glycogen synthase kinase 3 alpha	Homo sapiens	112-126
34429133-0	2021	Apatinib triggers autophagic and apoptotic cell death via VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling in lung cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	58-64
34429133-0	2021	Apatinib triggers autophagic and apoptotic cell death via VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling in lung cancer.	apatinib	0-8	signal transducer and activator of transcription 3	Homo sapiens	65-70
34429133-0	2021	Apatinib triggers autophagic and apoptotic cell death via VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling in lung cancer.	apatinib	0-8	CD274 molecule	Homo sapiens	71-76
34429133-0	2021	Apatinib triggers autophagic and apoptotic cell death via VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling in lung cancer.	apatinib	0-8	NFE2 like bZIP transcription factor 2	Homo sapiens	85-89
34429133-0	2021	Apatinib triggers autophagic and apoptotic cell death via VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling in lung cancer.	apatinib	0-8	nucleoporin 62	Homo sapiens	90-93
34429133-5	2021	The regulation of apatinib on VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling were detected.	apatinib	18-26	kinase insert domain receptor	Homo sapiens	30-36
34429133-5	2021	The regulation of apatinib on VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling were detected.	apatinib	18-26	signal transducer and activator of transcription 3	Homo sapiens	37-42
34429133-5	2021	The regulation of apatinib on VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling were detected.	apatinib	18-26	CD274 molecule	Homo sapiens	43-48
34429133-5	2021	The regulation of apatinib on VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling were detected.	apatinib	18-26	NFE2 like bZIP transcription factor 2	Homo sapiens	57-61
34429133-5	2021	The regulation of apatinib on VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling were detected.	apatinib	18-26	nucleoporin 62	Homo sapiens	62-65
34429133-6	2021	Furthermore, we collected conditioned medium (CM) from A549 and H1299 cells to stimulate phorbol myristate acetate (PMA)-activated THP-1 cells, and examined the effect of apatinib on PD-L1 expression in macrophages.	apatinib	171-179	CD274 molecule	Homo sapiens	183-188
34429133-11	2021	Apatinib induced cell cycle arrest at G1 phase and suppressed the expression of Cyclin D1 and CDK4.	apatinib	0-8	cyclin D1	Homo sapiens	80-89
34429133-11	2021	Apatinib induced cell cycle arrest at G1 phase and suppressed the expression of Cyclin D1 and CDK4.	apatinib	0-8	cyclin dependent kinase 4	Homo sapiens	94-98
34429133-12	2021	Moreover, apatinib upregulated Cleaved Caspase 3, Cleaved Caspase 9 and Bax, and downregulated Bcl-2 in NSCLC cells.	apatinib	10-18	caspase 9	Homo sapiens	58-67
34429133-12	2021	Moreover, apatinib upregulated Cleaved Caspase 3, Cleaved Caspase 9 and Bax, and downregulated Bcl-2 in NSCLC cells.	apatinib	10-18	BCL2 associated X, apoptosis regulator	Homo sapiens	72-75
34429133-12	2021	Moreover, apatinib upregulated Cleaved Caspase 3, Cleaved Caspase 9 and Bax, and downregulated Bcl-2 in NSCLC cells.	apatinib	10-18	BCL2 apoptosis regulator	Homo sapiens	95-100
34429133-13	2021	The colony formation ability and the number of CD133 positive cells were significantly decreased by apatinib, suggesting that apatinib inhibited the malignant and stem-like features of NSCLC cells.	apatinib	100-108	prominin 1	Homo sapiens	47-52
34429133-13	2021	The colony formation ability and the number of CD133 positive cells were significantly decreased by apatinib, suggesting that apatinib inhibited the malignant and stem-like features of NSCLC cells.	apatinib	126-134	prominin 1	Homo sapiens	47-52
34429133-14	2021	Mechanistically, apatinib inhibited PD-L1 and c-Myc expression by targeting VEGFR2/STAT3 signaling.	apatinib	17-25	CD274 molecule	Homo sapiens	36-41
34429133-14	2021	Mechanistically, apatinib inhibited PD-L1 and c-Myc expression by targeting VEGFR2/STAT3 signaling.	apatinib	17-25	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	46-51
34429133-14	2021	Mechanistically, apatinib inhibited PD-L1 and c-Myc expression by targeting VEGFR2/STAT3 signaling.	apatinib	17-25	kinase insert domain receptor	Homo sapiens	76-82
34429133-14	2021	Mechanistically, apatinib inhibited PD-L1 and c-Myc expression by targeting VEGFR2/STAT3 signaling.	apatinib	17-25	signal transducer and activator of transcription 3	Homo sapiens	83-88
34429133-15	2021	Apatinib also inhibited PD-L1 expression in THP-1 derived macrophages stimulated by CM from NSCLC cells.	apatinib	0-8	CD274 molecule	Homo sapiens	24-29
34429133-16	2021	Furthermore, apatinib pretreatment increased CD69 expression and IFN-gamma secretion in stimulated Jurkat T cells co-cultured with NSCLC cells.	apatinib	13-21	CD69 molecule	Homo sapiens	45-49
34429133-16	2021	Furthermore, apatinib pretreatment increased CD69 expression and IFN-gamma secretion in stimulated Jurkat T cells co-cultured with NSCLC cells.	apatinib	13-21	interferon gamma	Homo sapiens	65-74
34429133-17	2021	Apatinib also promoted ROS production and inhibited Nrf2 and p62 expression, leading to the autophagic and apoptotic cell death in NSCLC.	apatinib	0-8	NFE2 like bZIP transcription factor 2	Homo sapiens	52-56
34429133-17	2021	Apatinib also promoted ROS production and inhibited Nrf2 and p62 expression, leading to the autophagic and apoptotic cell death in NSCLC.	apatinib	0-8	nucleoporin 62	Homo sapiens	61-64
34429133-19	2021	CONCLUSION: Our data indicated that apatinib induced autophagy and apoptosis in NSCLC via regulating VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling.	apatinib	36-44	kinase insert domain receptor	Homo sapiens	101-107
34429133-19	2021	CONCLUSION: Our data indicated that apatinib induced autophagy and apoptosis in NSCLC via regulating VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling.	apatinib	36-44	signal transducer and activator of transcription 3	Homo sapiens	108-113
34429133-19	2021	CONCLUSION: Our data indicated that apatinib induced autophagy and apoptosis in NSCLC via regulating VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling.	apatinib	36-44	CD274 molecule	Homo sapiens	114-119
34429133-19	2021	CONCLUSION: Our data indicated that apatinib induced autophagy and apoptosis in NSCLC via regulating VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling.	apatinib	36-44	NFE2 like bZIP transcription factor 2	Homo sapiens	128-132
34429133-19	2021	CONCLUSION: Our data indicated that apatinib induced autophagy and apoptosis in NSCLC via regulating VEGFR2/STAT3/PD-L1 and ROS/Nrf2/p62 signaling.	apatinib	36-44	nucleoporin 62	Homo sapiens	133-136
34405891-0	2022	Apatinib weakens resistance of gastric cancer cells to paclitaxel by suppressing JAK/STAT3 signaling pathway.	apatinib	0-8	signal transducer and activator of transcription 3	Homo sapiens	85-90
34405891-10	2022	Apatinib enhanced apoptosis, diminished migration and invasion of HGC-27R cells, elevated proapoptotic protein expression, and reduced Bcl-2, vimentin, snail, MMP-3, MMP-2, and MMP-9 expressions.	apatinib	0-8	BCL2 apoptosis regulator	Homo sapiens	135-140
34405891-10	2022	Apatinib enhanced apoptosis, diminished migration and invasion of HGC-27R cells, elevated proapoptotic protein expression, and reduced Bcl-2, vimentin, snail, MMP-3, MMP-2, and MMP-9 expressions.	apatinib	0-8	vimentin	Homo sapiens	142-150
34405891-10	2022	Apatinib enhanced apoptosis, diminished migration and invasion of HGC-27R cells, elevated proapoptotic protein expression, and reduced Bcl-2, vimentin, snail, MMP-3, MMP-2, and MMP-9 expressions.	apatinib	0-8	snail family transcriptional repressor 1	Homo sapiens	152-157
34405891-10	2022	Apatinib enhanced apoptosis, diminished migration and invasion of HGC-27R cells, elevated proapoptotic protein expression, and reduced Bcl-2, vimentin, snail, MMP-3, MMP-2, and MMP-9 expressions.	apatinib	0-8	matrix metallopeptidase 3	Homo sapiens	159-164
34405891-10	2022	Apatinib enhanced apoptosis, diminished migration and invasion of HGC-27R cells, elevated proapoptotic protein expression, and reduced Bcl-2, vimentin, snail, MMP-3, MMP-2, and MMP-9 expressions.	apatinib	0-8	matrix metallopeptidase 2	Homo sapiens	166-171
34405891-10	2022	Apatinib enhanced apoptosis, diminished migration and invasion of HGC-27R cells, elevated proapoptotic protein expression, and reduced Bcl-2, vimentin, snail, MMP-3, MMP-2, and MMP-9 expressions.	apatinib	0-8	matrix metallopeptidase 9	Homo sapiens	177-182
34405891-11	2022	The phosphorylation of JAK2 and STAT3 was repressed by apatinib.	apatinib	55-63	Janus kinase 2	Homo sapiens	23-27
34405891-11	2022	The phosphorylation of JAK2 and STAT3 was repressed by apatinib.	apatinib	55-63	signal transducer and activator of transcription 3	Homo sapiens	32-37
34405891-12	2022	JAK2 partially reversed the effect of apatinib on enhancing sensitivity of GC cells to PTX.	apatinib	38-46	Janus kinase 2	Homo sapiens	0-4
34405891-13	2022	Apatinib strengthened sensitivity of GC cells to PTX by inhibiting JAK/STAT3 signaling pathway.	apatinib	0-8	signal transducer and activator of transcription 3	Homo sapiens	71-76
34333946-11	2021	All adverse reactions did not exceed grade 3 and could be controlled by symptomatic supportive treatment or reducing the dose of apatinib,and the serum aspartate aminotransferase (AST) level after treatment of 3 months((77+-33) U/L) was higher than that before treatment ((45+-26) U/L) (P<0.05).	apatinib	129-137	solute carrier family 17 member 5	Homo sapiens	152-178
34540013-0	2021	Efficacy and safety of neoadjuvant chemoradiotherapy plus apatinib for patients with locally advanced, HER2-negative, Siewert"s type II-III adenocarcinoma of esophagogastric junction: a single-arm, open-label, phase II trial.	apatinib	58-66	erb-b2 receptor tyrosine kinase 2	Homo sapiens	103-107
34540013-1	2021	This study aimed to investigate the efficacy and safety of concurrent neoadjuvant chemoradiotherapy (CRT) plus apatinib in treating locally advanced, HER2-negative, Siewert"s type II-III adenocarcinoma of esophagogastric junction (AEG) patients.	apatinib	111-119	erb-b2 receptor tyrosine kinase 2	Homo sapiens	150-154
34333946-11	2021	All adverse reactions did not exceed grade 3 and could be controlled by symptomatic supportive treatment or reducing the dose of apatinib,and the serum aspartate aminotransferase (AST) level after treatment of 3 months((77+-33) U/L) was higher than that before treatment ((45+-26) U/L) (P<0.05).	apatinib	129-137	solute carrier family 17 member 5	Homo sapiens	180-183
34141430-0	2021	Effective treatment of apatinib for chemotherapy-refractory advanced gastric carcinoma with AFP-secretion and HER2-positivity: A case report.	apatinib	23-31	alpha fetoprotein	Homo sapiens	92-95
34141430-0	2021	Effective treatment of apatinib for chemotherapy-refractory advanced gastric carcinoma with AFP-secretion and HER2-positivity: A case report.	apatinib	23-31	erb-b2 receptor tyrosine kinase 2	Homo sapiens	110-114
34141430-3	2021	To the best of our knowledge, the present report was the first to describe the use of apatinib to treat a patient with advanced GC characterized by AFP-secretion and HER2-positivity.	apatinib	86-94	alpha fetoprotein	Homo sapiens	148-151
34141430-3	2021	To the best of our knowledge, the present report was the first to describe the use of apatinib to treat a patient with advanced GC characterized by AFP-secretion and HER2-positivity.	apatinib	86-94	erb-b2 receptor tyrosine kinase 2	Homo sapiens	166-170
34141430-13	2021	Apatinib may be a promising anticancer agent in the case of advanced AFP-producing and HER2-positive GC.	apatinib	0-8	alpha fetoprotein	Homo sapiens	69-72
34141430-13	2021	Apatinib may be a promising anticancer agent in the case of advanced AFP-producing and HER2-positive GC.	apatinib	0-8	erb-b2 receptor tyrosine kinase 2	Homo sapiens	87-91
34277801-0	2021	Apatinib enhances the anti-tumor effect of paclitaxel via the PI3K/p65/Bcl-xl pathway in triple-negative breast cancer.	apatinib	0-8	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	67-70
34262864-1	2021	Apatinib is a new oral tyrosine kinase inhibitor that targets vascular endothelial growth factor receptor-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	62-107
34188525-0	2021	Association Between PDL1 Genetic Variation and Efficacy of Apatinib Monotherapy in Patients with Previously Treated Advanced NSCLC: A Real-World Retrospective Study.	apatinib	59-67	CD274 molecule	Homo sapiens	20-24
34188525-1	2021	Background: This study aimed to explore associations between PDL1 polymorphisms and efficacy of apatinib for patients with previously treated advanced non-small cell lung cancer (NSCLC) in a real-world setting.	apatinib	96-104	CD274 molecule	Homo sapiens	61-65
34188525-16	2021	Conclusion: The PDL1 polymorphism rs2297136 could be used as a potential biomarker for the prognosis of patients with NSCLC receiving apatinib monotherapy.	apatinib	134-142	CD274 molecule	Homo sapiens	16-20
34249438-1	2021	Apatinib is an oral tyrosine kinase inhibitor that targets VEGFR2 signaling and shows potent antitumor effects in various cancers.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	59-65
34249438-6	2021	Apatinib significantly induced G0/G1 phase arrest and apoptosis, inhibited cell growth and colony formation ability, and blocked autophagic flux by downregulating p-AKT and p-mTOR signaling via the VEGFR2/AKT/mTOR pathway in vitro.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	165-168
34249438-6	2021	Apatinib significantly induced G0/G1 phase arrest and apoptosis, inhibited cell growth and colony formation ability, and blocked autophagic flux by downregulating p-AKT and p-mTOR signaling via the VEGFR2/AKT/mTOR pathway in vitro.	apatinib	0-8	mechanistic target of rapamycin kinase	Homo sapiens	175-179
34249438-6	2021	Apatinib significantly induced G0/G1 phase arrest and apoptosis, inhibited cell growth and colony formation ability, and blocked autophagic flux by downregulating p-AKT and p-mTOR signaling via the VEGFR2/AKT/mTOR pathway in vitro.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	198-204
34249438-6	2021	Apatinib significantly induced G0/G1 phase arrest and apoptosis, inhibited cell growth and colony formation ability, and blocked autophagic flux by downregulating p-AKT and p-mTOR signaling via the VEGFR2/AKT/mTOR pathway in vitro.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	205-208
34249438-6	2021	Apatinib significantly induced G0/G1 phase arrest and apoptosis, inhibited cell growth and colony formation ability, and blocked autophagic flux by downregulating p-AKT and p-mTOR signaling via the VEGFR2/AKT/mTOR pathway in vitro.	apatinib	0-8	mechanistic target of rapamycin kinase	Homo sapiens	209-213
34249438-7	2021	Moreover, the inhibition of ERK phosphorylation increased apatinib-induced apoptosis in vitro and in vivo.	apatinib	58-66	EPH receptor B2	Homo sapiens	28-31
34113170-0	2021	Multiple Pulmonary Metastases of Recurrent Giant Cell Tumor of Bone with Expression of VEGFR-2 Successfully Controlled by Denosumab and Apatinib: A Case Report and Literature Review.	apatinib	136-144	kinase insert domain receptor	Homo sapiens	87-94
34113170-5	2021	Apatinib is a small-molecule tyrosine kinase inhibitor that selectively competes for the vascular endothelial growth factor receptor 2 (VEGFR-2) ATP binding site, and several studies have analyzed the effectiveness of apatinib in advanced or metastatic tumors.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	89-134
34113170-5	2021	Apatinib is a small-molecule tyrosine kinase inhibitor that selectively competes for the vascular endothelial growth factor receptor 2 (VEGFR-2) ATP binding site, and several studies have analyzed the effectiveness of apatinib in advanced or metastatic tumors.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	136-143
34350176-0	2021	Apatinib Suppresses Gastric Cancer Stem Cells Properties by Inhibiting the Sonic Hedgehog Pathway.	apatinib	0-8	sonic hedgehog signaling molecule	Homo sapiens	75-89
34350176-7	2021	Apatinib effectively suppressed GCSC traits by inhibiting tumorsphere formation and cell proliferation, suppressing GCSC markers expression and CD133+ cell number, and inducing apoptosis.	apatinib	0-8	prominin 1	Homo sapiens	144-149
34350176-8	2021	Apatinib downregulated the activation of the SHH pathway; while upregulation of the SHH pathway attenuated the inhibitory effects of apatinib on GCSCs.	apatinib	0-8	sonic hedgehog signaling molecule	Homo sapiens	45-48
34350176-8	2021	Apatinib downregulated the activation of the SHH pathway; while upregulation of the SHH pathway attenuated the inhibitory effects of apatinib on GCSCs.	apatinib	133-141	sonic hedgehog signaling molecule	Homo sapiens	45-48
34350176-8	2021	Apatinib downregulated the activation of the SHH pathway; while upregulation of the SHH pathway attenuated the inhibitory effects of apatinib on GCSCs.	apatinib	133-141	sonic hedgehog signaling molecule	Homo sapiens	84-87
34350176-10	2021	Our data suggested that apatinib exhibited inhibitory effects on GCSCs by suppressing SHH pathway both in vitro and in vivo, thus providing new insights into the therapeutic application of apatinib in GCSC suppression and advanced gastric cancer treatment.	apatinib	24-32	sonic hedgehog signaling molecule	Homo sapiens	86-89
34350176-10	2021	Our data suggested that apatinib exhibited inhibitory effects on GCSCs by suppressing SHH pathway both in vitro and in vivo, thus providing new insights into the therapeutic application of apatinib in GCSC suppression and advanced gastric cancer treatment.	apatinib	189-197	sonic hedgehog signaling molecule	Homo sapiens	86-89
34229754-0	2021	Apatinib induces endoplasmic reticulum stress-mediated apoptosis and autophagy and potentiates cell sensitivity to paclitaxel via the IRE-1alpha-AKT-mTOR pathway in esophageal squamous cell carcinoma.	apatinib	0-8	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	134-144
34229754-0	2021	Apatinib induces endoplasmic reticulum stress-mediated apoptosis and autophagy and potentiates cell sensitivity to paclitaxel via the IRE-1alpha-AKT-mTOR pathway in esophageal squamous cell carcinoma.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	145-148
34229754-0	2021	Apatinib induces endoplasmic reticulum stress-mediated apoptosis and autophagy and potentiates cell sensitivity to paclitaxel via the IRE-1alpha-AKT-mTOR pathway in esophageal squamous cell carcinoma.	apatinib	0-8	mechanistic target of rapamycin kinase	Homo sapiens	149-153
34229754-1	2021	BACKGROUND: Apatinib, a novel vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor, has been approved for the treatment of metastatic gastric cancer and other tumors.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	30-75
34229754-1	2021	BACKGROUND: Apatinib, a novel vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor, has been approved for the treatment of metastatic gastric cancer and other tumors.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	77-84
34229754-9	2021	Moreover, inhibiting autophagy by chloroquine (CQ) enhanced the apatinib-induced apoptosis of ESCC cells through the IRE-1alpha-AKT-mTOR pathway.	apatinib	64-72	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	117-127
34229754-9	2021	Moreover, inhibiting autophagy by chloroquine (CQ) enhanced the apatinib-induced apoptosis of ESCC cells through the IRE-1alpha-AKT-mTOR pathway.	apatinib	64-72	AKT serine/threonine kinase 1	Homo sapiens	128-131
34229754-9	2021	Moreover, inhibiting autophagy by chloroquine (CQ) enhanced the apatinib-induced apoptosis of ESCC cells through the IRE-1alpha-AKT-mTOR pathway.	apatinib	64-72	mechanistic target of rapamycin kinase	Homo sapiens	132-136
34229754-10	2021	In addition, we showed, for the first time, the paclitaxel combined with apatinib and CQ exhibited the best antitumor effect on ESCC both in vivo and in vitro via the IRE-1alpha-AKT-mTOR pathway.	apatinib	73-81	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	167-177
34229754-10	2021	In addition, we showed, for the first time, the paclitaxel combined with apatinib and CQ exhibited the best antitumor effect on ESCC both in vivo and in vitro via the IRE-1alpha-AKT-mTOR pathway.	apatinib	73-81	AKT serine/threonine kinase 1	Homo sapiens	178-181
34229754-10	2021	In addition, we showed, for the first time, the paclitaxel combined with apatinib and CQ exhibited the best antitumor effect on ESCC both in vivo and in vitro via the IRE-1alpha-AKT-mTOR pathway.	apatinib	73-81	mechanistic target of rapamycin kinase	Homo sapiens	182-186
34229754-13	2021	The combination of apatinib and CQ sensitized ESCC cells to paclitaxel to induce apoptosis through the IRE-1alpha-AKT-mTOR signaling pathway, thus providing the basis for its use in innovative anticancer therapeutic strategies.	apatinib	19-27	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	103-113
34229754-13	2021	The combination of apatinib and CQ sensitized ESCC cells to paclitaxel to induce apoptosis through the IRE-1alpha-AKT-mTOR signaling pathway, thus providing the basis for its use in innovative anticancer therapeutic strategies.	apatinib	19-27	AKT serine/threonine kinase 1	Homo sapiens	114-117
34229754-13	2021	The combination of apatinib and CQ sensitized ESCC cells to paclitaxel to induce apoptosis through the IRE-1alpha-AKT-mTOR signaling pathway, thus providing the basis for its use in innovative anticancer therapeutic strategies.	apatinib	19-27	mechanistic target of rapamycin kinase	Homo sapiens	118-122
34262347-1	2021	Objective: The aim of the study was to compare the efficacy and safety of drug-eluting beads TACE plus apatinib (D-TACE-A) with those of conventional TACE plus apatinib (C-TACE-A) for the treatment of unresectable HCC.	apatinib	103-111	ADAM metallopeptidase domain 17	Homo sapiens	115-119
34262347-1	2021	Objective: The aim of the study was to compare the efficacy and safety of drug-eluting beads TACE plus apatinib (D-TACE-A) with those of conventional TACE plus apatinib (C-TACE-A) for the treatment of unresectable HCC.	apatinib	160-168	ADAM metallopeptidase domain 17	Homo sapiens	172-176
34239300-4	2021	Hence, the study objective was to develop Apa-loaded bovine serum albumin nanoparticles (Apa-BSA-NPs) coated with hyaluronic acid (HA); a natural polymer possessing unique mucoadhesive and viscoelastic features with the capacity to actively target CD44 positive retinal cells, for topical administration in DR. Methods: Apa-BSA-NPs were prepared by desolvation using glutaraldehyde for cross-linking.	apatinib	42-45	albumin	Rattus norvegicus	60-73
34239300-4	2021	Hence, the study objective was to develop Apa-loaded bovine serum albumin nanoparticles (Apa-BSA-NPs) coated with hyaluronic acid (HA); a natural polymer possessing unique mucoadhesive and viscoelastic features with the capacity to actively target CD44 positive retinal cells, for topical administration in DR. Methods: Apa-BSA-NPs were prepared by desolvation using glutaraldehyde for cross-linking.	apatinib	42-45	CD44 molecule (Indian blood group)	Rattus norvegicus	248-252
34234467-6	2021	After trastuzumab resistance, the patient was treated with programmed cell death protein-1 inhibitor combined with apatinib, which selectively inhibited VEGFR2, but the effect was not satisfactory.	apatinib	115-123	kinase insert domain receptor	Homo sapiens	153-159
34277801-0	2021	Apatinib enhances the anti-tumor effect of paclitaxel via the PI3K/p65/Bcl-xl pathway in triple-negative breast cancer.	apatinib	0-8	BCL2-like 1	Mus musculus	71-77
34277801-1	2021	Background: Apatinib is a new generation of small molecule tyrosine kinase inhibitor, which can highly selectively inhibit phosphorylation of vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	12-20	kinase insert domain protein receptor	Mus musculus	142-187
34277801-1	2021	Background: Apatinib is a new generation of small molecule tyrosine kinase inhibitor, which can highly selectively inhibit phosphorylation of vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	12-20	kinase insert domain protein receptor	Mus musculus	189-196
34277801-2	2021	This study aimed to investigate the synergistic effects of apatinib and paclitaxel (PTX) on triple-negative breast cancer (TNBC) in vivo and in vitro, and to explore the molecular mechanism of the PI3K/p65/Bcl-xl pathway.	apatinib	59-67	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	202-205
34277801-2	2021	This study aimed to investigate the synergistic effects of apatinib and paclitaxel (PTX) on triple-negative breast cancer (TNBC) in vivo and in vitro, and to explore the molecular mechanism of the PI3K/p65/Bcl-xl pathway.	apatinib	59-67	BCL2-like 1	Mus musculus	206-212
34277801-4	2021	Western blot (WB) was conducted to detect protein expression levels of PI3K, p65, and Bcl-xl after the application of apatinib and PTX.	apatinib	118-126	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	77-80
34277801-4	2021	Western blot (WB) was conducted to detect protein expression levels of PI3K, p65, and Bcl-xl after the application of apatinib and PTX.	apatinib	118-126	BCL2-like 1	Mus musculus	86-92
34277801-8	2021	Apatinib could reduce the expression of p-PI3K, p65, and Bcl-xl proteins (P<0.05).	apatinib	0-8	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	48-51
34277801-8	2021	Apatinib could reduce the expression of p-PI3K, p65, and Bcl-xl proteins (P<0.05).	apatinib	0-8	BCL2-like 1	Mus musculus	57-63
34277801-10	2021	Conclusions: Apatinib could enhance the anti-tumor effect of PTX on TNBC cells through the PI3K/p65/Bcl-xl molecular pathway, and apatinib combined with PTX might be a promising option for TNBC treatment.	apatinib	13-21	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	96-99
34277801-10	2021	Conclusions: Apatinib could enhance the anti-tumor effect of PTX on TNBC cells through the PI3K/p65/Bcl-xl molecular pathway, and apatinib combined with PTX might be a promising option for TNBC treatment.	apatinib	13-21	BCL2-like 1	Mus musculus	100-106
34412054-0	2021	Apatinib Inhibits Angiogenesis in Intrahepatic Cholangiocarcinoma by Regulating the Vascular Endothelial Growth Factor Receptor-2/Signal Transducer and Activator of Transcription Factor 3/Hypoxia Inducible Factor 1 Subunit Alpha Signaling Axis.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	84-129
34158743-0	2021	Multicenter phase II study of apatinib single or combination therapy in HER2-negative breast cancer involving chest wall metastasis.	apatinib	30-38	erb-b2 receptor tyrosine kinase 2	Homo sapiens	72-76
34077013-0	2021	Apatinib strengthens the anti-tumor effect of cisplatin in thyroid carcinoma through downregulating VEGFR2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	100-106
34077013-1	2021	PURPOSE: The purpose of this study was to elucidate the influence of Apatinib combined with cisplatin on changing the phenotypes of TPC-1 cells.	apatinib	69-77	two pore segment channel 1	Homo sapiens	132-137
34077013-3	2021	Then, the viability of TPC-1 cells induced with different doses of Apatinib and cisplatin was determined by cell counting kit-8 (CCK-8).	apatinib	67-75	two pore segment channel 1	Homo sapiens	23-28
34077013-4	2021	Migratory and invasive abilities and apoptosis of TPC-1 cells induced with Apatinib combined with cisplatin were assessed.	apatinib	75-83	two pore segment channel 1	Homo sapiens	50-55
34077013-5	2021	The protein levels of p-VEGFR2, VEGFR2, p-Akt, Akt, p-mTOR and mTOR in TPC-1 cells influenced by the treatment of Apatinib combined with cisplatin were examined by Western blot.	apatinib	114-122	kinase insert domain receptor	Homo sapiens	24-30
34077013-5	2021	The protein levels of p-VEGFR2, VEGFR2, p-Akt, Akt, p-mTOR and mTOR in TPC-1 cells influenced by the treatment of Apatinib combined with cisplatin were examined by Western blot.	apatinib	114-122	kinase insert domain receptor	Homo sapiens	32-38
34077013-5	2021	The protein levels of p-VEGFR2, VEGFR2, p-Akt, Akt, p-mTOR and mTOR in TPC-1 cells influenced by the treatment of Apatinib combined with cisplatin were examined by Western blot.	apatinib	114-122	AKT serine/threonine kinase 1	Homo sapiens	42-45
34077013-5	2021	The protein levels of p-VEGFR2, VEGFR2, p-Akt, Akt, p-mTOR and mTOR in TPC-1 cells influenced by the treatment of Apatinib combined with cisplatin were examined by Western blot.	apatinib	114-122	AKT serine/threonine kinase 1	Homo sapiens	47-50
34077013-5	2021	The protein levels of p-VEGFR2, VEGFR2, p-Akt, Akt, p-mTOR and mTOR in TPC-1 cells influenced by the treatment of Apatinib combined with cisplatin were examined by Western blot.	apatinib	114-122	mechanistic target of rapamycin kinase	Homo sapiens	54-58
34077013-5	2021	The protein levels of p-VEGFR2, VEGFR2, p-Akt, Akt, p-mTOR and mTOR in TPC-1 cells influenced by the treatment of Apatinib combined with cisplatin were examined by Western blot.	apatinib	114-122	mechanistic target of rapamycin kinase	Homo sapiens	63-67
34077013-5	2021	The protein levels of p-VEGFR2, VEGFR2, p-Akt, Akt, p-mTOR and mTOR in TPC-1 cells influenced by the treatment of Apatinib combined with cisplatin were examined by Western blot.	apatinib	114-122	two pore segment channel 1	Homo sapiens	71-76
34077013-7	2021	Cisplatin treatment markedly suppressed viability, migratory and invasive abilities, and stimulated apoptosis of TPC-1 cells, which were further strengthened by combination treatment of Apatinib.	apatinib	186-194	two pore segment channel 1	Homo sapiens	113-118
34077013-8	2021	Apatinib treatment strengthened the anti-tumor influence of cisplatin on TPC-1 cells through downregulating p-VEGFR2, p-Akt and p-mTOR.	apatinib	0-8	two pore segment channel 1	Homo sapiens	73-78
34077013-8	2021	Apatinib treatment strengthened the anti-tumor influence of cisplatin on TPC-1 cells through downregulating p-VEGFR2, p-Akt and p-mTOR.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	110-116
34077013-8	2021	Apatinib treatment strengthened the anti-tumor influence of cisplatin on TPC-1 cells through downregulating p-VEGFR2, p-Akt and p-mTOR.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	120-123
34077013-8	2021	Apatinib treatment strengthened the anti-tumor influence of cisplatin on TPC-1 cells through downregulating p-VEGFR2, p-Akt and p-mTOR.	apatinib	0-8	mechanistic target of rapamycin kinase	Homo sapiens	130-134
34077013-9	2021	CONCLUSIONS: Apatinib strengthens the anti-tumor influence of cisplatin in thyroid carcinoma through VEGFR2-Akt-mTOR pathway.	apatinib	13-21	kinase insert domain receptor	Homo sapiens	101-107
34077013-9	2021	CONCLUSIONS: Apatinib strengthens the anti-tumor influence of cisplatin in thyroid carcinoma through VEGFR2-Akt-mTOR pathway.	apatinib	13-21	AKT serine/threonine kinase 1	Homo sapiens	108-111
34077013-9	2021	CONCLUSIONS: Apatinib strengthens the anti-tumor influence of cisplatin in thyroid carcinoma through VEGFR2-Akt-mTOR pathway.	apatinib	13-21	mechanistic target of rapamycin kinase	Homo sapiens	112-116
34412054-2	2021	OBJECTIVE: The study aimed to investigate the role of apatinib that targets vascular endothelial growth factor receptor-2 (VEGFR2) in ICC.	apatinib	54-62	kinase insert domain receptor	Homo sapiens	76-121
34412054-2	2021	OBJECTIVE: The study aimed to investigate the role of apatinib that targets vascular endothelial growth factor receptor-2 (VEGFR2) in ICC.	apatinib	54-62	kinase insert domain receptor	Homo sapiens	123-129
34412054-7	2021	We also proved that apatinib effectively inhibits angiogenesis in tumor cells by blocking the expression of VEGF and VEGFR2 in these cells.	apatinib	20-28	vascular endothelial growth factor A	Homo sapiens	108-112
34412054-7	2021	We also proved that apatinib effectively inhibits angiogenesis in tumor cells by blocking the expression of VEGF and VEGFR2 in these cells.	apatinib	20-28	kinase insert domain receptor	Homo sapiens	117-123
34412054-8	2021	In addition, we demonstrated that apatinib regulates the expression of STAT3 phosphorylation by inhibiting VEGFR2.	apatinib	34-42	signal transducer and activator of transcription 3	Homo sapiens	71-76
34412054-8	2021	In addition, we demonstrated that apatinib regulates the expression of STAT3 phosphorylation by inhibiting VEGFR2.	apatinib	34-42	kinase insert domain receptor	Homo sapiens	107-113
34412054-9	2021	Finally, we showed that apatinib regulates ICC angiogenesis and HIF-1alpha/VEGF expression via STAT3.	apatinib	24-32	hypoxia inducible factor 1 subunit alpha	Homo sapiens	64-74
34412054-9	2021	Finally, we showed that apatinib regulates ICC angiogenesis and HIF-1alpha/VEGF expression via STAT3.	apatinib	24-32	vascular endothelial growth factor A	Homo sapiens	75-79
34412054-9	2021	Finally, we showed that apatinib regulates ICC angiogenesis and HIF-1alpha/VEGF expression via STAT3.	apatinib	24-32	signal transducer and activator of transcription 3	Homo sapiens	95-100
34412054-10	2021	CONCLUSIONS: Based on the above findings, we conclude that apatinib inhibits HuCCT-1 and RBE cell proliferation, migration, and tumor angiogenesis by inhibiting the VEGFR2/STAT3/HIF-1alpha axis signaling pathway.	apatinib	59-67	kinase insert domain receptor	Homo sapiens	165-171
34412054-10	2021	CONCLUSIONS: Based on the above findings, we conclude that apatinib inhibits HuCCT-1 and RBE cell proliferation, migration, and tumor angiogenesis by inhibiting the VEGFR2/STAT3/HIF-1alpha axis signaling pathway.	apatinib	59-67	signal transducer and activator of transcription 3	Homo sapiens	172-177
34412054-10	2021	CONCLUSIONS: Based on the above findings, we conclude that apatinib inhibits HuCCT-1 and RBE cell proliferation, migration, and tumor angiogenesis by inhibiting the VEGFR2/STAT3/HIF-1alpha axis signaling pathway.	apatinib	59-67	hypoxia inducible factor 1 subunit alpha	Homo sapiens	178-188
35626097-6	2022	Further studies have indicated that apatinib not only promoted the degradation of MVBs via the regulation of LAMP2 but also interfered with MVB transport by inhibiting Rab11 expression.	apatinib	36-44	lysosomal associated membrane protein 2	Homo sapiens	109-114
35503144-0	2022	p53 m6A modulation sensitizes hepatocellular carcinoma to apatinib through apoptosis.	apatinib	58-66	transformation related protein 53, pseudogene	Mus musculus	0-3
35503144-4	2022	Here, we found that p53 n6-methyladenosine (m6A) played a decisive role in regulating HCC sensitivity to chemotherapy via the p53 activator RG7112 and the vascular endothelial growth factor receptor inhibitor apatinib.	apatinib	209-217	transformation related protein 53, pseudogene	Mus musculus	20-23
35626097-6	2022	Further studies have indicated that apatinib not only promoted the degradation of MVBs via the regulation of LAMP2 but also interfered with MVB transport by inhibiting Rab11 expression.	apatinib	36-44	RAB11A, member RAS oncogene family	Homo sapiens	168-173
35626097-7	2022	Moreover, apatinib inhibited MVB membrane fusion by reducing SNAP23 and VAMP2 expression.	apatinib	10-18	synaptosome associated protein 23	Homo sapiens	61-67
35626097-7	2022	Moreover, apatinib inhibited MVB membrane fusion by reducing SNAP23 and VAMP2 expression.	apatinib	10-18	vesicle associated membrane protein 2	Homo sapiens	72-77
35581670-3	2022	METHODS: Cell counting kit-8 and Annexin-V-FITC/PI assays were used to examine the interaction of chidamide and apatinib on LSC-like cell lines (CD34+CD38- KG1alpha and Kasumi-1 cells) and primary CD34+ AML cells.	apatinib	112-120	annexin A5	Homo sapiens	33-42
35581670-3	2022	METHODS: Cell counting kit-8 and Annexin-V-FITC/PI assays were used to examine the interaction of chidamide and apatinib on LSC-like cell lines (CD34+CD38- KG1alpha and Kasumi-1 cells) and primary CD34+ AML cells.	apatinib	112-120	CD34 molecule	Homo sapiens	145-149
35581670-3	2022	METHODS: Cell counting kit-8 and Annexin-V-FITC/PI assays were used to examine the interaction of chidamide and apatinib on LSC-like cell lines (CD34+CD38- KG1alpha and Kasumi-1 cells) and primary CD34+ AML cells.	apatinib	112-120	CD38 molecule	Homo sapiens	150-154
35581670-3	2022	METHODS: Cell counting kit-8 and Annexin-V-FITC/PI assays were used to examine the interaction of chidamide and apatinib on LSC-like cell lines (CD34+CD38- KG1alpha and Kasumi-1 cells) and primary CD34+ AML cells.	apatinib	112-120	CD34 molecule	Homo sapiens	197-201
35581670-6	2022	RESULTS: In this study, chidamide and apatinib were synergisitc to diminish cell viability and induce apoptosis in CD34+CD38- KG1alpha and Kasumi-1 cells and in CD34+ primary AML cells.	apatinib	38-46	CD34 molecule	Homo sapiens	115-119
35581670-6	2022	RESULTS: In this study, chidamide and apatinib were synergisitc to diminish cell viability and induce apoptosis in CD34+CD38- KG1alpha and Kasumi-1 cells and in CD34+ primary AML cells.	apatinib	38-46	CD38 molecule	Homo sapiens	120-124
35581670-6	2022	RESULTS: In this study, chidamide and apatinib were synergisitc to diminish cell viability and induce apoptosis in CD34+CD38- KG1alpha and Kasumi-1 cells and in CD34+ primary AML cells.	apatinib	38-46	CD34 molecule	Homo sapiens	161-165
35581670-10	2022	In addition, inactivating the VEGFR function and reducing the anti-apoptotic ability of the Bcl2 family contributed to the synergism of chidamide and apatinib in CD34+CD38- KG1alpha cells and CD34+ primary AML cells.	apatinib	150-158	kinase insert domain receptor	Homo sapiens	30-35
35581670-10	2022	In addition, inactivating the VEGFR function and reducing the anti-apoptotic ability of the Bcl2 family contributed to the synergism of chidamide and apatinib in CD34+CD38- KG1alpha cells and CD34+ primary AML cells.	apatinib	150-158	CD34 molecule	Homo sapiens	162-166
35581670-10	2022	In addition, inactivating the VEGFR function and reducing the anti-apoptotic ability of the Bcl2 family contributed to the synergism of chidamide and apatinib in CD34+CD38- KG1alpha cells and CD34+ primary AML cells.	apatinib	150-158	CD38 molecule	Homo sapiens	167-171
35581670-10	2022	In addition, inactivating the VEGFR function and reducing the anti-apoptotic ability of the Bcl2 family contributed to the synergism of chidamide and apatinib in CD34+CD38- KG1alpha cells and CD34+ primary AML cells.	apatinib	150-158	CD34 molecule	Homo sapiens	192-196
35549172-2	2022	Apatinib (APA), as an oral antitumor drug, which can inhibit the expression of vascular endothelial growth factor receptor-2 (VEGFR2) is loaded inside RBC, realizing the transform from oral formulation to injection preparation.	apatinib	0-8	vascular endothelial growth factor receptor 2	Oryctolagus cuniculus	79-124
35549172-2	2022	Apatinib (APA), as an oral antitumor drug, which can inhibit the expression of vascular endothelial growth factor receptor-2 (VEGFR2) is loaded inside RBC, realizing the transform from oral formulation to injection preparation.	apatinib	0-8	vascular endothelial growth factor receptor 2	Oryctolagus cuniculus	126-132
35549172-2	2022	Apatinib (APA), as an oral antitumor drug, which can inhibit the expression of vascular endothelial growth factor receptor-2 (VEGFR2) is loaded inside RBC, realizing the transform from oral formulation to injection preparation.	apatinib	10-13	vascular endothelial growth factor receptor 2	Oryctolagus cuniculus	79-124
35549172-2	2022	Apatinib (APA), as an oral antitumor drug, which can inhibit the expression of vascular endothelial growth factor receptor-2 (VEGFR2) is loaded inside RBC, realizing the transform from oral formulation to injection preparation.	apatinib	10-13	vascular endothelial growth factor receptor 2	Oryctolagus cuniculus	126-132
35602105-0	2022	Apatinib Induces Ferroptosis of Glioma Cells through Modulation of the VEGFR2/Nrf2 Pathway.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	71-77
35602105-0	2022	Apatinib Induces Ferroptosis of Glioma Cells through Modulation of the VEGFR2/Nrf2 Pathway.	apatinib	0-8	NFE2 like bZIP transcription factor 2	Homo sapiens	78-82
35602105-11	2022	It was also revealed that apatinib triggered ferroptosis of glioma cells via inhibiting the activation of nuclear factor erythroid 2-related factor 2/vascular endothelial growth factor receptor 2 (Nrf2/VEFGR2) pathway.	apatinib	26-34	NFE2 like bZIP transcription factor 2	Homo sapiens	106-149
35602105-11	2022	It was also revealed that apatinib triggered ferroptosis of glioma cells via inhibiting the activation of nuclear factor erythroid 2-related factor 2/vascular endothelial growth factor receptor 2 (Nrf2/VEFGR2) pathway.	apatinib	26-34	kinase insert domain receptor	Homo sapiens	150-195
35602105-11	2022	It was also revealed that apatinib triggered ferroptosis of glioma cells via inhibiting the activation of nuclear factor erythroid 2-related factor 2/vascular endothelial growth factor receptor 2 (Nrf2/VEFGR2) pathway.	apatinib	26-34	NFE2 like bZIP transcription factor 2	Homo sapiens	197-201
35602105-12	2022	The overexpression of Nrf2 rescued the therapeutic effects of apatinib.	apatinib	62-70	NFE2 like bZIP transcription factor 2	Homo sapiens	22-26
35602105-13	2022	Conclusion: Our study proved that treatment with apatinib could restrain proliferation of glioma cells through induction of ferroptosis via inhibiting the activation of VEGFR2/Nrf2/Keap1 pathway.	apatinib	49-57	kinase insert domain receptor	Homo sapiens	169-175
35602105-13	2022	Conclusion: Our study proved that treatment with apatinib could restrain proliferation of glioma cells through induction of ferroptosis via inhibiting the activation of VEGFR2/Nrf2/Keap1 pathway.	apatinib	49-57	NFE2 like bZIP transcription factor 2	Homo sapiens	176-180
35602105-13	2022	Conclusion: Our study proved that treatment with apatinib could restrain proliferation of glioma cells through induction of ferroptosis via inhibiting the activation of VEGFR2/Nrf2/Keap1 pathway.	apatinib	49-57	kelch like ECH associated protein 1	Homo sapiens	181-186
35602105-14	2022	Overexpression of Nrf2 could counteract the induction of ferroptosis by apatinib.	apatinib	72-80	NFE2 like bZIP transcription factor 2	Homo sapiens	18-22
35503397-0	2022	Targeting SMYD2 inhibits angiogenesis and increases the efficiency of apatinib by suppressing EGFL7 in colorectal cancer.	apatinib	70-78	SET and MYND domain containing 2	Homo sapiens	10-15
35503397-0	2022	Targeting SMYD2 inhibits angiogenesis and increases the efficiency of apatinib by suppressing EGFL7 in colorectal cancer.	apatinib	70-78	EGF like domain multiple 7	Homo sapiens	94-99
35503397-11	2022	Treatment with BAY-598, a functional inhibitor of SMYD2, can also synergize with apatinib in patient-derived xenografts.	apatinib	81-89	SET and MYND domain containing 2	Homo sapiens	50-55
35529932-5	2022	The eligible patients given S-1 therapy plus apatinib showed significantly lower levels of serum carcinoembryonic antigen (CEA), glycoantigen 199 (CA199), and glycoantigen 125 (CA125) versus those receiving S-1 therapy (P < 0.05).	apatinib	45-53	CEA cell adhesion molecule 3	Homo sapiens	97-121
35529932-5	2022	The eligible patients given S-1 therapy plus apatinib showed significantly lower levels of serum carcinoembryonic antigen (CEA), glycoantigen 199 (CA199), and glycoantigen 125 (CA125) versus those receiving S-1 therapy (P < 0.05).	apatinib	45-53	CEA cell adhesion molecule 3	Homo sapiens	123-126
35529932-5	2022	The eligible patients given S-1 therapy plus apatinib showed significantly lower levels of serum carcinoembryonic antigen (CEA), glycoantigen 199 (CA199), and glycoantigen 125 (CA125) versus those receiving S-1 therapy (P < 0.05).	apatinib	45-53	mucin 16, cell surface associated	Homo sapiens	177-182
35529932-6	2022	S-1 therapy plus apatinib outperformed the single therapy of S-1 therapy in mitigating the levels of interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin-4 (IL-4), and interleukin-10 (IL-10) (P < 0.05).	apatinib	17-25	interferon gamma	Homo sapiens	101-117
35529932-6	2022	S-1 therapy plus apatinib outperformed the single therapy of S-1 therapy in mitigating the levels of interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin-4 (IL-4), and interleukin-10 (IL-10) (P < 0.05).	apatinib	17-25	interferon gamma	Homo sapiens	119-128
35529932-6	2022	S-1 therapy plus apatinib outperformed the single therapy of S-1 therapy in mitigating the levels of interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin-4 (IL-4), and interleukin-10 (IL-10) (P < 0.05).	apatinib	17-25	tumor necrosis factor	Homo sapiens	131-158
35529932-6	2022	S-1 therapy plus apatinib outperformed the single therapy of S-1 therapy in mitigating the levels of interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin-4 (IL-4), and interleukin-10 (IL-10) (P < 0.05).	apatinib	17-25	tumor necrosis factor	Homo sapiens	160-169
35529932-6	2022	S-1 therapy plus apatinib outperformed the single therapy of S-1 therapy in mitigating the levels of interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin-4 (IL-4), and interleukin-10 (IL-10) (P < 0.05).	apatinib	17-25	interleukin 4	Homo sapiens	172-185
35529932-6	2022	S-1 therapy plus apatinib outperformed the single therapy of S-1 therapy in mitigating the levels of interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin-4 (IL-4), and interleukin-10 (IL-10) (P < 0.05).	apatinib	17-25	interleukin 4	Homo sapiens	187-191
35529932-6	2022	S-1 therapy plus apatinib outperformed the single therapy of S-1 therapy in mitigating the levels of interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin-4 (IL-4), and interleukin-10 (IL-10) (P < 0.05).	apatinib	17-25	interleukin 10	Homo sapiens	198-212
35529932-6	2022	S-1 therapy plus apatinib outperformed the single therapy of S-1 therapy in mitigating the levels of interferon-gamma (IFN-gamma), tumor necrosis factor-alpha (TNF-alpha), interleukin-4 (IL-4), and interleukin-10 (IL-10) (P < 0.05).	apatinib	17-25	interleukin 10	Homo sapiens	214-219
35432838-0	2022	Effect of Apatinib Combined with Seggio on the Expression of Serum AFP and CA724 and Long-Term Survival Rate in Patients with Advanced Gastric Cancer Undergoing Comfortable Nursing Intervention.	apatinib	10-18	alpha fetoprotein	Homo sapiens	67-70
35432838-1	2022	Objective: To study the effect of apatinib combined with seggio on the expression of serum AFP and CA724 and the long-term survival rate in advanced gastric cancer patients undergoing comfort nursing intervention.	apatinib	34-42	alpha fetoprotein	Homo sapiens	91-94
35144430-7	2022	Apatinib is a novel, oral, small-molecule tyrosine kinase inhibitor that mainly targets vascular endothelial growth factor receptor-2 (VEGFR-2) to inhibit angiogenesis.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	88-133
35620326-8	2022	When HCT-116 cells were treated with different concentrations of apatinibin combination with piperine, the synergistic effects were observed (combination index < 1).In HCT-116 cells treated with apatinib and piperine at the concentrations of 0.5xIC50 and0.2xIC50, the MDM-2 gene expression was downregulated and NO levels increased comparedto the untreated control cells and related single treatments.	apatinib	195-203	MDM2 proto-oncogene	Homo sapiens	268-273
35242497-0	2022	TWIST1-EP300 Expedites Gastric Cancer Cell Resistance to Apatinib by Activating the Expression of COL1A2.	apatinib	57-65	twist basic helix-loop-helix transcription factor 1	Mus musculus	0-6
35242497-0	2022	TWIST1-EP300 Expedites Gastric Cancer Cell Resistance to Apatinib by Activating the Expression of COL1A2.	apatinib	57-65	E1A binding protein p300	Mus musculus	7-12
35242497-0	2022	TWIST1-EP300 Expedites Gastric Cancer Cell Resistance to Apatinib by Activating the Expression of COL1A2.	apatinib	57-65	collagen, type I, alpha 2	Mus musculus	98-104
35242497-2	2022	However, the specific role of COL1A2 in gastric cancer (GC) cell resistance to apatinib, a highly selective small-molecule inhibitor of vascular endothelial growth factor receptor 2, has not been investigated before.	apatinib	79-87	collagen, type I, alpha 2	Mus musculus	30-36
35242497-2	2022	However, the specific role of COL1A2 in gastric cancer (GC) cell resistance to apatinib, a highly selective small-molecule inhibitor of vascular endothelial growth factor receptor 2, has not been investigated before.	apatinib	79-87	kinase insert domain protein receptor	Mus musculus	136-181
35242497-3	2022	The purpose of this study was to explore the potential factors associated with COL1A2 regulation on GC cell apatinib resistance in vitro.	apatinib	108-116	collagen, type I, alpha 2	Mus musculus	79-85
35242497-6	2022	In addition, overexpression of COL1A2 significantly promoted resistance to apatinib in GC cells, but knockdown of EP300 or TWIST1 remarkably inhibited COL1A2 expression and promoted sensitivity of GC cells to apatinib.	apatinib	75-83	collagen, type I, alpha 2	Mus musculus	31-37
35242497-6	2022	In addition, overexpression of COL1A2 significantly promoted resistance to apatinib in GC cells, but knockdown of EP300 or TWIST1 remarkably inhibited COL1A2 expression and promoted sensitivity of GC cells to apatinib.	apatinib	75-83	E1A binding protein p300	Mus musculus	114-119
35242497-6	2022	In addition, overexpression of COL1A2 significantly promoted resistance to apatinib in GC cells, but knockdown of EP300 or TWIST1 remarkably inhibited COL1A2 expression and promoted sensitivity of GC cells to apatinib.	apatinib	209-217	E1A binding protein p300	Mus musculus	114-119
35242497-6	2022	In addition, overexpression of COL1A2 significantly promoted resistance to apatinib in GC cells, but knockdown of EP300 or TWIST1 remarkably inhibited COL1A2 expression and promoted sensitivity of GC cells to apatinib.	apatinib	209-217	twist basic helix-loop-helix transcription factor 1	Mus musculus	123-129
35242497-7	2022	Our findings demonstrated that the combination of EP300 and TWIST1 has a synergistically regulatory effect on COL1A2 expression, thus contributing to apatinib resistance in GC cells.	apatinib	150-158	E1A binding protein p300	Mus musculus	50-55
35242497-7	2022	Our findings demonstrated that the combination of EP300 and TWIST1 has a synergistically regulatory effect on COL1A2 expression, thus contributing to apatinib resistance in GC cells.	apatinib	150-158	twist basic helix-loop-helix transcription factor 1	Mus musculus	60-66
35242497-7	2022	Our findings demonstrated that the combination of EP300 and TWIST1 has a synergistically regulatory effect on COL1A2 expression, thus contributing to apatinib resistance in GC cells.	apatinib	150-158	collagen, type I, alpha 2	Mus musculus	110-116
35184413-13	2022	The caspase-1-gasdermin D (GSDMD) axis-mediated pyroptosis was the key to extra antitumour effect of the combination of apatinib and melittin.	apatinib	120-128	caspase 1	Homo sapiens	4-13
35184413-13	2022	The caspase-1-gasdermin D (GSDMD) axis-mediated pyroptosis was the key to extra antitumour effect of the combination of apatinib and melittin.	apatinib	120-128	gasdermin D	Homo sapiens	14-25
35184413-13	2022	The caspase-1-gasdermin D (GSDMD) axis-mediated pyroptosis was the key to extra antitumour effect of the combination of apatinib and melittin.	apatinib	120-128	gasdermin D	Homo sapiens	27-32
35184413-16	2022	CONCLUSIONS: Through pyroptosis mediated by caspase-1-GSDMD and caspase-3-GSDME axes synchronically, low-dosage apatinib and melittin could synergistically achieve a comparable therapeutic potential with reduced AEs.	apatinib	112-120	caspase 1	Homo sapiens	44-53
35184413-16	2022	CONCLUSIONS: Through pyroptosis mediated by caspase-1-GSDMD and caspase-3-GSDME axes synchronically, low-dosage apatinib and melittin could synergistically achieve a comparable therapeutic potential with reduced AEs.	apatinib	112-120	gasdermin D	Homo sapiens	54-59
35184413-16	2022	CONCLUSIONS: Through pyroptosis mediated by caspase-1-GSDMD and caspase-3-GSDME axes synchronically, low-dosage apatinib and melittin could synergistically achieve a comparable therapeutic potential with reduced AEs.	apatinib	112-120	caspase 3	Homo sapiens	64-73
35173861-0	2022	Apatinib inhibits paclitaxel resistance of gastric carcinoma cells through VEGFR2 pathway.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	75-81
35173861-9	2022	After Apa intervention, PTX-resistant MGC803 cells showed decreased cell migration, invasion and proliferation, reduced MDR1, P-gp and VEGFR2 levels, and increased Bax protein level.	apatinib	6-9	ATP binding cassette subfamily B member 1	Homo sapiens	120-124
35173861-9	2022	After Apa intervention, PTX-resistant MGC803 cells showed decreased cell migration, invasion and proliferation, reduced MDR1, P-gp and VEGFR2 levels, and increased Bax protein level.	apatinib	6-9	phosphoglycolate phosphatase	Homo sapiens	126-130
35173861-9	2022	After Apa intervention, PTX-resistant MGC803 cells showed decreased cell migration, invasion and proliferation, reduced MDR1, P-gp and VEGFR2 levels, and increased Bax protein level.	apatinib	6-9	kinase insert domain receptor	Homo sapiens	135-141
35173861-9	2022	After Apa intervention, PTX-resistant MGC803 cells showed decreased cell migration, invasion and proliferation, reduced MDR1, P-gp and VEGFR2 levels, and increased Bax protein level.	apatinib	6-9	BCL2 associated X, apoptosis regulator	Homo sapiens	164-167
35069931-1	2022	Background: Apatinib is an anticancer drug known to inhibit the vascular endothelial growth factor receptor-2 (VEGFR-2) through regulating tyrosine kinases.	apatinib	12-20	kinase insert domain receptor	Rattus norvegicus	64-109
35069931-1	2022	Background: Apatinib is an anticancer drug known to inhibit the vascular endothelial growth factor receptor-2 (VEGFR-2) through regulating tyrosine kinases.	apatinib	12-20	kinase insert domain receptor	Rattus norvegicus	111-118
35378217-3	2022	Apatinib is an oral tyrosine kinase inhibitor (TKI) that selectively inhibits vascular endothelial growth factor receptor (VEGFR) 2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	123-131
35620326-0	2022	Regulatory Effects of Apatinib in Combination with Piperine on MDM-2 Gene Expression, Glutathione Peroxidase Activity and Nitric Oxide level as Mechanisms of Cytotoxicity in Colorectal Cancer Cells.	apatinib	22-30	MDM2 proto-oncogene	Homo sapiens	63-68
35234370-7	2022	Knockout of FBN1 combined with treatment of the antiangiogenic drug apatinib improved the cisplatin-sensitivity of ovarian cancer cells.	apatinib	68-76	fibrillin 1	Danio rerio	12-16
34998471-2	2022	Apatinib, a selective inhibitor of VEGFR2, has a synergistic effect with immunotherapy.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	35-41
35127498-4	2021	This study aims to evaluate the clinical value of the new score system by combining SII and PNI (SII-PNI score) as a predictor of efficacy and prognosis after neoadjuvant intraperitoneal and systemic (NIPS) paclitaxel combined with Apatinib conversion therapy for GC-CY1 patients.	apatinib	232-240	serpin family E member 2	Homo sapiens	101-104
35127498-14	2021	Conclusion: Pretreatment SII-PNI score is an important predictor for the efficacy of GC-CY1 patients after NIPS paclitaxel combined with Apatinib conversion therapy, which can help to identify high-risk groups and predict prognosis.	apatinib	137-145	serpin family E member 2	Homo sapiens	29-32
35173861-11	2022	Taken together, Apa may inhibit PTX resistance of MGC803 cells via the VEGFR2 signaling pathway.	apatinib	16-19	kinase insert domain receptor	Homo sapiens	71-77
35096582-6	2021	This case suggests that camrelizumab in combination with apatinib may be an effective treatment option for GBC patients with pMMR/MSS status, who have moderate expression of TMB and PD-L1.	apatinib	57-65	CD274 molecule	Homo sapiens	182-187
35069555-9	2021	We also demonstrated that two immune-related adverse events (irAEs) associated with camrelizumab can be managed with an anti-VEGF agent apatinib.	apatinib	136-144	vascular endothelial growth factor A	Homo sapiens	125-129
35144430-7	2022	Apatinib is a novel, oral, small-molecule tyrosine kinase inhibitor that mainly targets vascular endothelial growth factor receptor-2 (VEGFR-2) to inhibit angiogenesis.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	135-142
33098705-1	2021	Rivoceranib (known in China as apatinib) is a selective vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor which inhibits angiogenesis in solid tumors.	apatinib	0-11	kinase insert domain receptor	Homo sapiens	56-101
34037346-0	2021	Phase II study of apatinib in combination with oral vinorelbine in heavily pretreated HER2-negative metastatic breast cancer and clinical implications of monitoring ctDNA.	apatinib	18-26	erb-b2 receptor tyrosine kinase 2	Homo sapiens	86-90
34037346-1	2021	OBJECTIVE: Apatinib is an oral TKI targeting VEGFR-2.	apatinib	11-19	kinase insert domain receptor	Homo sapiens	45-52
34037346-17	2021	CONCLUSIONS: All-oral therapy with apatinib plus vinorelbine displayed objective efficacy in patients with heavily pretreated HER2-negative mBC, with acceptable and manageable toxicity profiles.	apatinib	35-43	erb-b2 receptor tyrosine kinase 2	Homo sapiens	126-130
33978839-0	2021	Autophagy inhibitor potentiates the antitumor efficacy of apatinib in uterine sarcoma by stimulating PI3K/Akt/mTOR pathway.	apatinib	58-66	AKT serine/threonine kinase 1	Homo sapiens	106-109
33978839-0	2021	Autophagy inhibitor potentiates the antitumor efficacy of apatinib in uterine sarcoma by stimulating PI3K/Akt/mTOR pathway.	apatinib	58-66	mechanistic target of rapamycin kinase	Homo sapiens	110-114
33978839-11	2021	Apatinib inhibited the PI3K/Akt/mTOR pathway, while 3-MA and the combination of 3-MA and apatinib significantly activated the PI3K/Akt/mTOR pathway and inhibited autophagy.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	28-31
33978839-11	2021	Apatinib inhibited the PI3K/Akt/mTOR pathway, while 3-MA and the combination of 3-MA and apatinib significantly activated the PI3K/Akt/mTOR pathway and inhibited autophagy.	apatinib	0-8	mechanistic target of rapamycin kinase	Homo sapiens	32-36
33978839-11	2021	Apatinib inhibited the PI3K/Akt/mTOR pathway, while 3-MA and the combination of 3-MA and apatinib significantly activated the PI3K/Akt/mTOR pathway and inhibited autophagy.	apatinib	89-97	AKT serine/threonine kinase 1	Homo sapiens	131-134
33978839-11	2021	Apatinib inhibited the PI3K/Akt/mTOR pathway, while 3-MA and the combination of 3-MA and apatinib significantly activated the PI3K/Akt/mTOR pathway and inhibited autophagy.	apatinib	89-97	mechanistic target of rapamycin kinase	Homo sapiens	135-139
33978839-15	2021	Autophagy inhibition may increase the antitumor effect of apatinib via the PI3K/Akt/mTOR pathway.	apatinib	58-66	AKT serine/threonine kinase 1	Homo sapiens	80-83
33978839-15	2021	Autophagy inhibition may increase the antitumor effect of apatinib via the PI3K/Akt/mTOR pathway.	apatinib	58-66	mechanistic target of rapamycin kinase	Homo sapiens	84-88
33994798-7	2021	This case showed that afatinib plus apatinib may be a promising therapy for patients with EGFR 19Del-T790M-cis-C797S mutant and HER2 amplified NSCLC.	apatinib	36-44	epidermal growth factor receptor	Homo sapiens	90-94
33994798-7	2021	This case showed that afatinib plus apatinib may be a promising therapy for patients with EGFR 19Del-T790M-cis-C797S mutant and HER2 amplified NSCLC.	apatinib	36-44	erb-b2 receptor tyrosine kinase 2	Homo sapiens	128-132
34026823-3	2021	This multicenter, retrospective study aimed to evaluate the efficacy of the combination treatment with apatinib and osimertinib in 39 patients with EGFR-mutant non-small cell lung carcinoma (NSCLC) who developed osimertinib resistance.	apatinib	103-111	epidermal growth factor receptor	Homo sapiens	148-152
34026823-14	2021	The combination of apatinib and osimertinib improved the ORR and the DCR of patients with osimertinib-refractory EGFR-positive NSCLC, thus making it a reasonable treatment choice after the development of osimertinib resistance.	apatinib	19-27	epidermal growth factor receptor	Homo sapiens	113-117
34012920-1	2021	Purpose: As a novel small-molecule vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor (VEGFR2-TKI), Methylsulfonic apatinib (apatinib) exhibits a specific antitumor effect in various solid tumors via inhibition of angiogenesis.	apatinib	136-144	kinase insert domain receptor	Homo sapiens	108-114
33544270-1	2021	BACKGROUND: Apatinib, a competitive inhibitor of VEGFR2, has anti-angiogenesis and anticancer activities through different mechanisms, but it still cannot fully explain the drug efficacy of apatinib.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	49-55
33544270-9	2021	Further investigation revealed that apatinib down-regulated GPX4 expression via inhibition of the transcription factors Sterol regulatory element-binding protein-1a (SREBP-1a).	apatinib	36-44	glutathione peroxidase 4	Mus musculus	60-64
33544270-9	2021	Further investigation revealed that apatinib down-regulated GPX4 expression via inhibition of the transcription factors Sterol regulatory element-binding protein-1a (SREBP-1a).	apatinib	36-44	sterol regulatory element binding transcription factor 1	Homo sapiens	166-174
33544270-10	2021	Besides, we found that multi-drug resistant GC cells were vulnerable to apatinib-induced GPX4 inhibition.	apatinib	72-80	glutathione peroxidase 4	Mus musculus	89-93
33544270-11	2021	CONCLUSIONS: In summary, we show that apatinib could induce the lipid peroxidation through GPX4 mediated by SREBP-1a, then negatively regulate the GC cell, even the multi-drug-resistant GC cell, ferroptosis.	apatinib	38-46	glutathione peroxidase 4	Mus musculus	91-95
33544270-11	2021	CONCLUSIONS: In summary, we show that apatinib could induce the lipid peroxidation through GPX4 mediated by SREBP-1a, then negatively regulate the GC cell, even the multi-drug-resistant GC cell, ferroptosis.	apatinib	38-46	sterol regulatory element binding transcription factor 1	Homo sapiens	108-116
34038201-3	2021	Apatinib mesylate, an orally administered drug, is a novel inhibitor of vascular endothelial growth factor receptor-2, a key mediator of angiogenesis, and has been shown to be safe and efficacious in the treatment of certain types of malignant tumors.	apatinib	0-17	kinase insert domain receptor	Homo sapiens	72-117
33981598-1	2021	Apatinib, an anti-tumor drug selectively targeting VEGFR2 (Vascular Endothelia Growth Factor Recpetor-2), has been proven effective in Chinese patients with liver cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	51-57
33981598-1	2021	Apatinib, an anti-tumor drug selectively targeting VEGFR2 (Vascular Endothelia Growth Factor Recpetor-2), has been proven effective in Chinese patients with liver cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	59-103
33828084-0	2021	NDUFA4L2 promotes glioblastoma progression, is associated with poor survival, and can be effectively targeted by apatinib.	apatinib	113-121	NDUFA4 mitochondrial complex associated like 2	Homo sapiens	0-8
33828084-7	2021	Apatinib was able to effectively target NDUFA4L2 in GBM, presenting an alternative to the use of lentiviruses, which currently cannot be used in humans.	apatinib	0-8	NDUFA4 mitochondrial complex associated like 2	Homo sapiens	40-48
33587347-0	2021	Successful treatment of Afatinib plus Apatinib using for a lung adenocarcinoma patient with HER-2 V659D mutation: a rare case report.	apatinib	38-46	erb-b2 receptor tyrosine kinase 2	Homo sapiens	92-97
33587347-6	2021	Apatinib is one of the small-molecule oral anti-angiogenesis-targeted agents developed firstly in China, and it"s a highly selective inhibition of the activity of VEGFR-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	163-170
33587347-7	2021	This report presents an advanced lung adenocarcinoma patient with HER2 V659D mutation who was treated with combination of Afatinib and Apatinib.	apatinib	135-143	erb-b2 receptor tyrosine kinase 2	Homo sapiens	66-70
35282086-2	2022	We sought to explore the efficacy of apatinib, an oral small-molecule vascular endothelial growth factor receptor-2 inhibitor, plus 5-fluorouracil (5-FU) as a third- or subsequent-line treatment for mCRC.	apatinib	37-45	kinase insert domain receptor	Homo sapiens	70-115
34976167-9	2022	By survival analysis, increasing NLR (P=0.003), CA125 (P<0.001) and decreasing ALB (P<0.001) predicted a shorter PFS after apatinib.	apatinib	123-131	mucin 16, cell surface associated	Homo sapiens	48-53
34976167-9	2022	By survival analysis, increasing NLR (P=0.003), CA125 (P<0.001) and decreasing ALB (P<0.001) predicted a shorter PFS after apatinib.	apatinib	123-131	albumin	Homo sapiens	79-82
34976167-11	2022	Conclusion: Increasing NLR, CA125 and decreasing ALB were associated with poorer clinical efficiency and prognosis after apatinib treatment.	apatinib	121-129	mucin 16, cell surface associated	Homo sapiens	28-33
34976167-11	2022	Conclusion: Increasing NLR, CA125 and decreasing ALB were associated with poorer clinical efficiency and prognosis after apatinib treatment.	apatinib	121-129	albumin	Homo sapiens	49-52
33968184-0	2021	Apatinib inhibits gastric carcinoma development by regulating the expression levels of IL-17 via the Bax/Bcl-2 signaling pathway.	apatinib	0-8	interleukin 17A	Homo sapiens	87-92
33968184-0	2021	Apatinib inhibits gastric carcinoma development by regulating the expression levels of IL-17 via the Bax/Bcl-2 signaling pathway.	apatinib	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	101-104
33968184-0	2021	Apatinib inhibits gastric carcinoma development by regulating the expression levels of IL-17 via the Bax/Bcl-2 signaling pathway.	apatinib	0-8	BCL2 apoptosis regulator	Homo sapiens	105-110
33968184-3	2021	The potential effect of apatinib on IL-17 expression levels in the development of gastric carcinoma has been rarely reported.	apatinib	24-32	interleukin 17A	Homo sapiens	36-41
33968184-11	2021	Conversely, apatinib treatment significantly inhibited the proliferative and invasive abilities of HGC-27 cells, but promoted cell apoptosis in the IL-17 and IL-17-apatinib groups..	apatinib	12-20	interleukin 17A	Homo sapiens	148-153
33968184-11	2021	Conversely, apatinib treatment significantly inhibited the proliferative and invasive abilities of HGC-27 cells, but promoted cell apoptosis in the IL-17 and IL-17-apatinib groups..	apatinib	12-20	interleukin 17A	Homo sapiens	158-163
33968184-11	2021	Conversely, apatinib treatment significantly inhibited the proliferative and invasive abilities of HGC-27 cells, but promoted cell apoptosis in the IL-17 and IL-17-apatinib groups..	apatinib	164-172	interleukin 17A	Homo sapiens	158-163
33968184-13	2021	The findings indicated that apatinib may inhibit gastric carcinoma development by regulating IL-17 expression via the Bax/Bcl-2 signaling pathway.	apatinib	28-36	interleukin 17A	Homo sapiens	93-98
33968184-13	2021	The findings indicated that apatinib may inhibit gastric carcinoma development by regulating IL-17 expression via the Bax/Bcl-2 signaling pathway.	apatinib	28-36	BCL2 associated X, apoptosis regulator	Homo sapiens	118-121
33968184-13	2021	The findings indicated that apatinib may inhibit gastric carcinoma development by regulating IL-17 expression via the Bax/Bcl-2 signaling pathway.	apatinib	28-36	BCL2 apoptosis regulator	Homo sapiens	122-127
33846786-0	2021	Apatinib suppresses the migration, invasion and angiogenesis of hepatocellular carcinoma cells by blocking VEGF and PI3K/AKT signaling pathways.	apatinib	0-8	vascular endothelial growth factor A	Homo sapiens	107-111
33846786-0	2021	Apatinib suppresses the migration, invasion and angiogenesis of hepatocellular carcinoma cells by blocking VEGF and PI3K/AKT signaling pathways.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	121-124
33846786-3	2021	In the present study, apatinib were used to treat HCC cells transfected with or without VEGFR2 overexpression vectors.	apatinib	22-30	kinase insert domain receptor	Homo sapiens	88-94
33846786-10	2021	In addition, apatinib inhibited the epithelial-mesenchymal transition of Hep3b cells by increasing the expression of the epithelial hallmarks E-cadherin and alpha-catenin and decreased the expression of the mesenchymal hallmarks N-cadherin and vimentin.	apatinib	13-21	cadherin 1	Homo sapiens	142-152
33846786-10	2021	In addition, apatinib inhibited the epithelial-mesenchymal transition of Hep3b cells by increasing the expression of the epithelial hallmarks E-cadherin and alpha-catenin and decreased the expression of the mesenchymal hallmarks N-cadherin and vimentin.	apatinib	13-21	cadherin 2	Homo sapiens	229-239
33846786-10	2021	In addition, apatinib inhibited the epithelial-mesenchymal transition of Hep3b cells by increasing the expression of the epithelial hallmarks E-cadherin and alpha-catenin and decreased the expression of the mesenchymal hallmarks N-cadherin and vimentin.	apatinib	13-21	vimentin	Homo sapiens	244-252
33846786-12	2021	Thus, apatinib inhibited cell migration, invasion and angiogenesis by blocking the VEGF and PI3K/AKT pathways, supporting an effective therapeutic strategy in the treatment of HCC.	apatinib	6-14	vascular endothelial growth factor A	Homo sapiens	83-87
33846786-12	2021	Thus, apatinib inhibited cell migration, invasion and angiogenesis by blocking the VEGF and PI3K/AKT pathways, supporting an effective therapeutic strategy in the treatment of HCC.	apatinib	6-14	AKT serine/threonine kinase 1	Homo sapiens	97-100
34033974-0	2021	Apatinib plus gefitinib as first-line treatment in advanced EGFR-mutant non-small cell lung cancer: the phase III ACTIVE study (CTONG1706).	apatinib	0-8	epidermal growth factor receptor	Homo sapiens	60-64
34033974-15	2021	CONCLUSIONS: Apatinib+gefitinib as first-line therapy demonstrated superior PFS in advanced EGFR-mutant NSCLC vs placebo+gefitinib.	apatinib	13-21	epidermal growth factor receptor	Homo sapiens	92-96
33980809-0	2021	Apatinib suppresses lung cancer stem-like cells by complex interplay between beta-catenin signaling and mitochondrial ROS accumulation.	apatinib	0-8	catenin beta 1	Homo sapiens	77-89
33980809-3	2021	Apatinib, a small-molecule VEGFR2-tyrosine kinase inhibitor, shows highly efficient antitumor activity in heavily treated, chemoresistant, and metastatic lung cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	27-33
33980809-4	2021	We speculated that inhibition of Wnt/beta-catenin signaling and targeting lung CSCs could be one of the anti-tumor mechanisms of apatinib.	apatinib	129-137	catenin beta 1	Homo sapiens	37-49
33980809-6	2021	Mechanistically, apatinib exerted its anti-CSC effects by inhibiting beta-catenin and its downstream targets.	apatinib	17-25	catenin beta 1	Homo sapiens	69-81
33980809-8	2021	It was found that beta-catenin regulated apatinib-induced production of ROS.	apatinib	41-49	catenin beta 1	Homo sapiens	18-30
33980809-10	2021	Collectively, our findings reveal that apatinib directly inhibits beta-catenin signaling and promotes ROS generation to suppress lung CSC-like characteristics.	apatinib	39-47	catenin beta 1	Homo sapiens	66-78
33995600-1	2021	Background: Apatinib, a vascular endothelial growth factor receptor (VEGFR) blocker, has demonstrated encouraging antitumor activities and tolerable toxicities in various cancer types.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	24-67
33995600-1	2021	Background: Apatinib, a vascular endothelial growth factor receptor (VEGFR) blocker, has demonstrated encouraging antitumor activities and tolerable toxicities in various cancer types.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	69-74
34011535-1	2021	BACKGROUND: The Camrelizumab Plus Apatinib in Patients with Advanced Cervical Cancer trial was a single-arm, phase II study that showed promising activity of the programmed death-1 (PD-1) inhibitor camrelizumab plus the vascular endothelial growth factor receptor-2 inhibitor apatinib in patients with advanced cervical cancer.	apatinib	34-42	programmed cell death 1	Homo sapiens	182-186
33205247-1	2021	Apatinib is a novel, highly selective small-molecule inhibitor of the tyrosine kinase VEGFR-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	86-93
33892656-3	2021	Apatinib, a tyrosine kinase inhibitor specifically targeting VEGFR2, has been increasingly reported as a treatment for osteosarcoma with promising outcome parameters, but there has been no systematic analysis of the treatment of osteosarcoma by apatinib.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	61-67
33845750-0	2022	Apatinib Inhibits Stem Properties and Malignant Biological Behaviors of Breast Cancer Stem Cells by Blocking Wnt/beta-catenin Signal Pathway Through Down-regulating LncRNA ROR.	apatinib	0-8	Wnt family member 3A	Homo sapiens	109-112
33845750-0	2022	Apatinib Inhibits Stem Properties and Malignant Biological Behaviors of Breast Cancer Stem Cells by Blocking Wnt/beta-catenin Signal Pathway Through Down-regulating LncRNA ROR.	apatinib	0-8	catenin beta 1	Homo sapiens	113-125
33845750-0	2022	Apatinib Inhibits Stem Properties and Malignant Biological Behaviors of Breast Cancer Stem Cells by Blocking Wnt/beta-catenin Signal Pathway Through Down-regulating LncRNA ROR.	apatinib	0-8	long intergenic non-protein coding RNA, regulator of reprogramming	Homo sapiens	172-175
33845750-7	2022	RESULTS: Apatinib decreased the viability and colony numbers of BCSCs in a concentration-dependent manner, and it also reduced sphere numbers, suppressed migration, invasion and lncRNA ROR expression, and induced apoptosis of BCSCs.	apatinib	9-17	long intergenic non-protein coding RNA, regulator of reprogramming	Homo sapiens	185-188
33845750-9	2022	Apatinib suppressed stem property, EMT process and Wnt/beta-catenin pathway in BCSCs, which was partially reversed by lncRNA ROR overexpression.	apatinib	0-8	Wnt family member 3A	Homo sapiens	51-54
33845750-9	2022	Apatinib suppressed stem property, EMT process and Wnt/beta-catenin pathway in BCSCs, which was partially reversed by lncRNA ROR overexpression.	apatinib	0-8	catenin beta 1	Homo sapiens	55-67
33845750-9	2022	Apatinib suppressed stem property, EMT process and Wnt/beta-catenin pathway in BCSCs, which was partially reversed by lncRNA ROR overexpression.	apatinib	0-8	long intergenic non-protein coding RNA, regulator of reprogramming	Homo sapiens	125-128
33845750-12	2022	CONCLUSION: Apatinib inhibited stem property and malignant biological behaviors of BCSCs by blocking Wnt/beta-catenin signal pathway through down-regulating lncRNA ROR.	apatinib	12-20	Wnt family member 3A	Homo sapiens	101-104
33845750-12	2022	CONCLUSION: Apatinib inhibited stem property and malignant biological behaviors of BCSCs by blocking Wnt/beta-catenin signal pathway through down-regulating lncRNA ROR.	apatinib	12-20	catenin beta 1	Homo sapiens	105-117
33845750-12	2022	CONCLUSION: Apatinib inhibited stem property and malignant biological behaviors of BCSCs by blocking Wnt/beta-catenin signal pathway through down-regulating lncRNA ROR.	apatinib	12-20	long intergenic non-protein coding RNA, regulator of reprogramming	Homo sapiens	164-167
33098705-1	2021	Rivoceranib (known in China as apatinib) is a selective vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor which inhibits angiogenesis in solid tumors.	apatinib	0-11	kinase insert domain receptor	Homo sapiens	103-110
33098705-1	2021	Rivoceranib (known in China as apatinib) is a selective vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor which inhibits angiogenesis in solid tumors.	apatinib	31-39	kinase insert domain receptor	Homo sapiens	56-101
33098705-1	2021	Rivoceranib (known in China as apatinib) is a selective vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor which inhibits angiogenesis in solid tumors.	apatinib	31-39	kinase insert domain receptor	Homo sapiens	103-110
33392882-0	2021	Influence of VEGFR2 gene polymorphism on the clinical outcomes of apatinib for patients with chemotherapy-refractory extensive-stage SCLC: a real-world retrospective study.	apatinib	66-74	kinase insert domain receptor	Homo sapiens	13-19
33392882-2	2021	The aim of present study was to investigate the influence of vascular endothelial growth factor receptor2 (VEGFR2) gene polymorphism on the clinical outcomes of apatinib for patients with chemotherapy-refractory extensive-stage small cell lung cancer (ES-SCLC).	apatinib	161-169	kinase insert domain receptor	Homo sapiens	61-105
33392882-2	2021	The aim of present study was to investigate the influence of vascular endothelial growth factor receptor2 (VEGFR2) gene polymorphism on the clinical outcomes of apatinib for patients with chemotherapy-refractory extensive-stage small cell lung cancer (ES-SCLC).	apatinib	161-169	kinase insert domain receptor	Homo sapiens	107-113
33392882-22	2021	The clinical outcomes of patients with ES-SCLC who were treated with apatinib could be impacted by VEGFR2 889C>T polymorphism through mediating the VEGFR2 mRNA expression.	apatinib	69-77	kinase insert domain receptor	Homo sapiens	99-105
33392882-22	2021	The clinical outcomes of patients with ES-SCLC who were treated with apatinib could be impacted by VEGFR2 889C>T polymorphism through mediating the VEGFR2 mRNA expression.	apatinib	69-77	kinase insert domain receptor	Homo sapiens	148-154
33790633-0	2021	Influence of KDR Genetic Variation on the Efficacy and Safety of Patients with Chemotherapy Refractory Metastatic CRC Who Received Apatinib Treatment.	apatinib	131-139	kinase insert domain receptor	Homo sapiens	13-16
33790633-1	2021	Background: The aim of the present study was to investigate the influence of kinase insert domain containing receptor (KDR) genetic variation on the efficacy of treatment and safety of patients with chemotherapy-refractory metastatic colorectal cancer (CRC) receiving apatinib.	apatinib	268-276	kinase insert domain receptor	Homo sapiens	77-117
33790633-1	2021	Background: The aim of the present study was to investigate the influence of kinase insert domain containing receptor (KDR) genetic variation on the efficacy of treatment and safety of patients with chemotherapy-refractory metastatic colorectal cancer (CRC) receiving apatinib.	apatinib	268-276	kinase insert domain receptor	Homo sapiens	119-122
33790633-16	2021	KDR polymorphism rs2071559 could be used as a potential biomarker for the prognosis evaluation of patients with CRC receiving apatinib therapy.	apatinib	126-134	kinase insert domain receptor	Homo sapiens	0-3
33659204-1	2020	Introduction: We performed this clinical trial to evaluate the efficacy and safety of apatinib and oral etoposide in patients with HER2-negative locally advanced or metastatic breast cancer (MBC).	apatinib	86-94	erb-b2 receptor tyrosine kinase 2	Homo sapiens	131-135
33661538-34	2021	The VEGF inhibitors apatinib and pazopanib may increase the probability of hypertension events.	apatinib	20-28	vascular endothelial growth factor A	Homo sapiens	4-8
33187916-3	2021	Apatinib, an antiangiogenic agent targeting vascular endothelial growth factor receptor-2, has shown excellent efficacy in multiple solid tumors.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	44-89
33030616-0	2021	Apatinib exhibits synergistic effect with pyrotinib and reverses acquired pyrotinib resistance in HER2-positive gastric cancer via stem cell factor/c-kit signaling and its downstream pathways.	apatinib	0-8	erb-b2 receptor tyrosine kinase 2	Homo sapiens	98-102
33030616-0	2021	Apatinib exhibits synergistic effect with pyrotinib and reverses acquired pyrotinib resistance in HER2-positive gastric cancer via stem cell factor/c-kit signaling and its downstream pathways.	apatinib	0-8	KIT ligand	Homo sapiens	131-147
33030616-0	2021	Apatinib exhibits synergistic effect with pyrotinib and reverses acquired pyrotinib resistance in HER2-positive gastric cancer via stem cell factor/c-kit signaling and its downstream pathways.	apatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	148-153
33030616-8	2021	RESULTS: Here, we reported that a combination of pyrotinib and apatinib exhibits synergistic effect in HER2-positive NCI-N87 xenografts, and showed enhanced antitumor efficacy in HER2-positive GC, both in vitro and in vivo.	apatinib	63-71	erb-b2 receptor tyrosine kinase 2	Homo sapiens	103-107
33030616-8	2021	RESULTS: Here, we reported that a combination of pyrotinib and apatinib exhibits synergistic effect in HER2-positive NCI-N87 xenografts, and showed enhanced antitumor efficacy in HER2-positive GC, both in vitro and in vivo.	apatinib	63-71	erb-b2 receptor tyrosine kinase 2	Homo sapiens	179-183
33030616-11	2021	Imatinib and apatinib augmented the sensitivity of pyrotinib-resistant cells and xenografts to pyrotinib, by blocking SCF/c-kit signaling.	apatinib	13-21	KIT ligand	Homo sapiens	118-121
33030616-11	2021	Imatinib and apatinib augmented the sensitivity of pyrotinib-resistant cells and xenografts to pyrotinib, by blocking SCF/c-kit signaling.	apatinib	13-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	122-127
33030616-12	2021	CONCLUSION: These results highlight the effectiveness of pyrotinib combined with apatinib in HER2-positive GC and acquired pyrotinib resistance, thus providing a theoretical basis for new treatment methods.	apatinib	81-89	erb-b2 receptor tyrosine kinase 2	Homo sapiens	93-97
33659204-15	2020	Conclusion: Apatinib combined with etoposide capsules is effective and tolerable in heavily pretreated, metastatic HER2-negative breast cancer patients.	apatinib	12-20	erb-b2 receptor tyrosine kinase 2	Homo sapiens	115-119
33603479-0	2021	Apatinib Promotes Ferroptosis in Colorectal Cancer Cells by Targeting ELOVL6/ACSL4 Signaling.	apatinib	0-8	ELOVL fatty acid elongase 6	Homo sapiens	70-76
33603479-0	2021	Apatinib Promotes Ferroptosis in Colorectal Cancer Cells by Targeting ELOVL6/ACSL4 Signaling.	apatinib	0-8	acyl-CoA synthetase long chain family member 4	Homo sapiens	77-82
33603479-8	2021	Elongation of very long-chain fatty acids family member 6 (ELOVL6) was one of the targets of apatinib predicted by SwissTargetPrediction.	apatinib	93-101	ELOVL fatty acid elongase 6	Homo sapiens	59-65
33603479-9	2021	Therefore, ELOVL6 expression was evaluated after treatment with apatinib.	apatinib	64-72	ELOVL fatty acid elongase 6	Homo sapiens	11-17
33603479-13	2021	Moreover, significantly upregulated ACSL4 expression was observed, accompanied by notable downregulation of GPx4 and FTH1 expression after apatinib exposure.	apatinib	139-147	acyl-CoA synthetase long chain family member 4	Homo sapiens	36-41
33603479-13	2021	Moreover, significantly upregulated ACSL4 expression was observed, accompanied by notable downregulation of GPx4 and FTH1 expression after apatinib exposure.	apatinib	139-147	glutathione peroxidase 4	Homo sapiens	108-112
33603479-13	2021	Moreover, significantly upregulated ACSL4 expression was observed, accompanied by notable downregulation of GPx4 and FTH1 expression after apatinib exposure.	apatinib	139-147	ferritin heavy chain 1	Homo sapiens	117-121
33603479-14	2021	Furthermore, ELOVL6 expression was remarkably enhanced in HCT116 cells, which was dramatically inhibited under apatinib intervention.	apatinib	111-119	ELOVL fatty acid elongase 6	Homo sapiens	13-19
33603479-15	2021	ELOVL6 overexpression reversed the effects of apatinib on cell viability and ferroptosis of HCT116 cells.	apatinib	46-54	ELOVL fatty acid elongase 6	Homo sapiens	0-6
33603479-17	2021	Conclusion: These findings demonstrated that apatinib promoted ferroptosis in CRC cells by targeting ELOVL6/ACSL4, providing a new mechanism support for apatinib application in the clinical treatment of CRC.	apatinib	45-53	ELOVL fatty acid elongase 6	Homo sapiens	101-107
33603479-17	2021	Conclusion: These findings demonstrated that apatinib promoted ferroptosis in CRC cells by targeting ELOVL6/ACSL4, providing a new mechanism support for apatinib application in the clinical treatment of CRC.	apatinib	45-53	acyl-CoA synthetase long chain family member 4	Homo sapiens	108-113
33603479-17	2021	Conclusion: These findings demonstrated that apatinib promoted ferroptosis in CRC cells by targeting ELOVL6/ACSL4, providing a new mechanism support for apatinib application in the clinical treatment of CRC.	apatinib	153-161	ELOVL fatty acid elongase 6	Homo sapiens	101-107
33416243-0	2021	Low-Dosage Apatinib in Treating Advanced Pulmonary Adenocarcinoma Patient With Kras Mutation After Osimertinib Resistance: A Case Report.	apatinib	11-19	KRAS proto-oncogene, GTPase	Homo sapiens	79-83
33393167-5	2021	BACKGROUND: The aim of this study was to evaluate the efficacy and adverse effects of the oral vascular endothelial growth factor receptor 2 (VEGFR-2) tyrosine kinase inhibitor apatinib in patients with chemotherapy-refractory esophageal squamous cell carcinoma (ESCC).	apatinib	177-185	kinase insert domain receptor	Homo sapiens	95-140
33393167-5	2021	BACKGROUND: The aim of this study was to evaluate the efficacy and adverse effects of the oral vascular endothelial growth factor receptor 2 (VEGFR-2) tyrosine kinase inhibitor apatinib in patients with chemotherapy-refractory esophageal squamous cell carcinoma (ESCC).	apatinib	177-185	kinase insert domain receptor	Homo sapiens	142-149
33545800-10	2021	This is the first reported case of the successful treatment of advanced ASPS with camrelizumab combined with apatinib.	apatinib	109-117	ASPSCR1 tether for SLC2A4, UBX domain containing	Homo sapiens	72-76
33170322-1	2021	The objective of present work is to evaluate possible interactions among four clinically-used vascular epidermal growth factor receptor (VEGFR)-tyrosine kinase inhibitors (TKIs), including apatinib, cabozantinib, sorafenib, and sunitinib, with epidermal growth factor receptor (EGFR)-TKI gefitinib.	apatinib	189-197	kinase insert domain receptor	Homo sapiens	94-135
33170322-8	2021	The docking results illustrated that binding characteristics of apatinib and gefitinib with CYP2D6 were similar, which accounts for competitive mechanism of apatinib-inhibited gefitinib metabolism.	apatinib	64-72	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	92-98
33170322-8	2021	The docking results illustrated that binding characteristics of apatinib and gefitinib with CYP2D6 were similar, which accounts for competitive mechanism of apatinib-inhibited gefitinib metabolism.	apatinib	157-165	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	92-98
33170322-9	2021	In summary, apatinib inhibited the metabolism of gefitinib in vitro and in vivo that were mediated by CYP2D6 and CYP3A4.	apatinib	12-20	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	102-108
33170322-9	2021	In summary, apatinib inhibited the metabolism of gefitinib in vitro and in vivo that were mediated by CYP2D6 and CYP3A4.	apatinib	12-20	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	113-119
32651310-0	2021	IL-17 predicts the effect of TACE combined with apatinib in hepatocellular carcinoma.	apatinib	48-56	interleukin 17A	Homo sapiens	0-5
32651310-8	2021	Compared with adjuvant TACE alone, patients with low-expression of IL-17 treated combined with apatinib have a higher 5-year overall survival.	apatinib	95-103	interleukin 17A	Homo sapiens	67-72
32651310-10	2021	CONCLUSION: IL-17 had a pivotal role in the invasion and angiogenesis of HCC and contribute to the selection of patients who may benefit from adjuvant TACE combined with apatinib.	apatinib	170-178	interleukin 17A	Homo sapiens	12-17
33225619-0	2021	Rare case of apatinib acquired resistance induced by point mutation of WRN p.V697F through activation of the PI3K/AKT apoptosis-inhibiting pathway.	apatinib	13-21	WRN RecQ like helicase	Homo sapiens	71-74
33225619-0	2021	Rare case of apatinib acquired resistance induced by point mutation of WRN p.V697F through activation of the PI3K/AKT apoptosis-inhibiting pathway.	apatinib	13-21	AKT serine/threonine kinase 1	Homo sapiens	114-117
33225619-2	2021	Apatinib is a new antiangiogenic antitumor drug developed in China which targets vascular endothelial growth factor receptor-2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	81-126
33225619-2	2021	Apatinib is a new antiangiogenic antitumor drug developed in China which targets vascular endothelial growth factor receptor-2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	128-135
33225619-13	2021	We suspected that the WRN gene mutation had led to apatinib resistance.	apatinib	51-59	WRN RecQ like helicase	Homo sapiens	22-25
32533100-0	2021	Apatinib prevents natural killer cell dysfunction to enhance the efficacy of anti-PD-1 immunotherapy in hepatocellular carcinoma.	apatinib	0-8	programmed cell death 1	Mus musculus	82-86
32533100-1	2021	Apatinib, a selective vascular endothelial growth factor receptor 2-tyrosine kinase inhibitor, has demonstrated activity against a wide range of solid tumors, including advanced hepatocellular carcinoma (HCC).	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	22-67
32533100-7	2021	Furthermore, increased interferon-gamma and decreased tumor necrosis factor-alpha and interleukin-6 levels were observed, suggesting the potential benefits of combination therapy with PD-1 blockade and apatinib in HCC.	apatinib	202-210	interferon gamma	Mus musculus	23-39
32552008-2	2021	Previous studies showed that miR-129-5p had a low expression in GC, and homeobox gene C10 (HOXC10), a carcinogenic gene, was highly expressed in GC, while the molecular mechanism of miR-129-5p involved in apatinib resistance in GC cells is still unclear.	apatinib	205-213	microRNA 1295a	Homo sapiens	29-39
32552008-2	2021	Previous studies showed that miR-129-5p had a low expression in GC, and homeobox gene C10 (HOXC10), a carcinogenic gene, was highly expressed in GC, while the molecular mechanism of miR-129-5p involved in apatinib resistance in GC cells is still unclear.	apatinib	205-213	homeobox C10	Homo sapiens	72-89
32552008-2	2021	Previous studies showed that miR-129-5p had a low expression in GC, and homeobox gene C10 (HOXC10), a carcinogenic gene, was highly expressed in GC, while the molecular mechanism of miR-129-5p involved in apatinib resistance in GC cells is still unclear.	apatinib	205-213	homeobox C10	Homo sapiens	91-97
32552008-2	2021	Previous studies showed that miR-129-5p had a low expression in GC, and homeobox gene C10 (HOXC10), a carcinogenic gene, was highly expressed in GC, while the molecular mechanism of miR-129-5p involved in apatinib resistance in GC cells is still unclear.	apatinib	205-213	microRNA 1295a	Homo sapiens	182-192
32552008-8	2021	Results: MiR-129-5p had a low expression in GC tissues and apatinib-resistant cell lines, while HOXC10 was highly expressed.	apatinib	59-67	microRNA 1295a	Homo sapiens	9-19
32552008-12	2021	The experiment in vivo also confirmed that miR-129-5p reduced apatinib resistance in GC cells by targetedly inhibiting HOXC10.	apatinib	62-70	microRNA 1295a	Homo sapiens	43-52
32552008-12	2021	The experiment in vivo also confirmed that miR-129-5p reduced apatinib resistance in GC cells by targetedly inhibiting HOXC10.	apatinib	62-70	homeobox C10	Homo sapiens	119-125
32552008-14	2021	Conclusion: miR-129-5p restrains apatinib-resistant of GC cells by regulating HOXC10.	apatinib	33-41	microRNA 1295a	Homo sapiens	12-22
32552008-14	2021	Conclusion: miR-129-5p restrains apatinib-resistant of GC cells by regulating HOXC10.	apatinib	33-41	homeobox C10	Homo sapiens	78-84
33383486-0	2021	Efficacy and safety of apatinib for the treatment of AFP-producing gastric cancer.	apatinib	23-31	alpha fetoprotein	Homo sapiens	53-56
33519240-6	2021	The small-molecular tyrosine kinase inhibitor (TKI) apatinib was initiated, which targets vascular endothelial growth factor receptor 2 (VEGFR2).	apatinib	52-60	kinase insert domain receptor	Homo sapiens	90-135
33519240-6	2021	The small-molecular tyrosine kinase inhibitor (TKI) apatinib was initiated, which targets vascular endothelial growth factor receptor 2 (VEGFR2).	apatinib	52-60	kinase insert domain receptor	Homo sapiens	137-143
33532001-2	2021	Apatinib is a tyrosine kinase inhibitor targeting VEGFR-2, which exhibited broad-spectrum antitumor activities in previous studies.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	50-57
33437808-9	2020	This is the first case describing the efficacy and safety of Camrelizumab plus Apatinib in a GBCa patient with weak PD-1 and PD-L1 expression, and low TMB and MSS.	apatinib	79-87	CD274 molecule	Homo sapiens	125-130
33365269-2	2020	In this study, we evaluated the anti-tumor activity and safety of apatinib, a vascular endothelial growth factor receptor 2 inhibitor, in MPM in vitro and in vivo.	apatinib	66-74	kinase insert domain receptor	Homo sapiens	78-123
33490189-1	2020	Background: Apatinib, a vascular endothelial growth factor receptor 2 (VEGFR-2) inhibitor, has shown promising therapeutic effect for hepatocellular carcinoma (HCC).	apatinib	12-20	kinase insert domain receptor	Homo sapiens	24-69
33490189-1	2020	Background: Apatinib, a vascular endothelial growth factor receptor 2 (VEGFR-2) inhibitor, has shown promising therapeutic effect for hepatocellular carcinoma (HCC).	apatinib	12-20	kinase insert domain receptor	Homo sapiens	71-78
33092443-3	2020	Apatinib is a selective tyrosine kinase inhibitor of vascular endothelial growth factor receptor-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	53-98
33490196-9	2020	Apatinib is orally administered at a dose of 500 mg (SOXA group) or 250 mg (SOXAP group) on days 1 to 21, and camrelizumab 200 mg is given intravenously once every 3 weeks.	apatinib	0-8	SRY-box transcription factor 21	Homo sapiens	53-57
32924634-1	2020	Apatinib mesylate is an oral antiangiogenic agent that can inhibit activation of vascular endothelial growth factor receptor-2 tyrosine kinase.	apatinib	0-17	vascular endothelial growth factor receptor 2	Oryctolagus cuniculus	81-126
32489129-5	2020	Released APA effectively inhibited the function of the P-glycoprotein (P-gp) drug pump and improved the sensitivity of MDR cells to chemotherapeutic agents, leading to the recovery of PTX chemosensitivity in MDR cells.	apatinib	9-12	ATP binding cassette subfamily B member 1	Homo sapiens	55-69
32489129-5	2020	Released APA effectively inhibited the function of the P-glycoprotein (P-gp) drug pump and improved the sensitivity of MDR cells to chemotherapeutic agents, leading to the recovery of PTX chemosensitivity in MDR cells.	apatinib	9-12	ATP binding cassette subfamily B member 1	Homo sapiens	71-75
33115264-6	2020	RESULTS: The oral treatment of apatinib in the VEGFR-2 and NF-kB positive groups was better than that in the negative groups.	apatinib	31-39	kinase insert domain receptor	Homo sapiens	47-54
33115264-13	2020	CONCLUSION: The positive expression of VEGFR-2 and NF-kB is expected to be the molecular target of oral apatinib targeted therapy for oesophageal cancer.	apatinib	104-112	kinase insert domain receptor	Homo sapiens	39-46
32363427-0	2020	Apatinib, a novel VEGFR-2 tyrosine kinase inhibitor, for relapsed and refractory nasopharyngeal carcinoma: data from an open-label, single-arm, exploratory study.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	18-25
32363427-1	2020	Purpose Apatinib, a new tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor-2, has shown promising efficacy against several solid cancers, but evidence of its efficacy against relapsed and refractory nasopharyngeal carcinoma is limited.	apatinib	8-16	kinase insert domain receptor	Homo sapiens	60-105
33052760-2	2020	We assessed the activity and safety of camrelizumab plus apatinib, a tyrosine kinase inhibitor of vascular endothelial growth factor receptor-2, in patients with advanced cervical cancer.	apatinib	57-65	kinase insert domain receptor	Homo sapiens	98-143
32864834-5	2020	Apatinib, a small molecular inhibitor, is used as a model of hydrophobic drug and loaded into CP-beta-CD to study the solubilization effect and the anti-angiogenisis activity.	apatinib	0-8	carboxypeptidase A1	Homo sapiens	94-101
32864834-7	2020	These results indicate that the apatinib can be transported into cell interior and play an excellent anti-angiogenisis activity after being loaded into CP-beta-CD drug delivery system.	apatinib	32-40	carboxypeptidase A1	Homo sapiens	152-159
33293826-0	2020	Raltitrexed Enhances the Antitumor Effect of Apatinib in Human Esophageal Squamous Carcinoma Cells via Akt and Erk Pathways.	apatinib	45-53	AKT serine/threonine kinase 1	Homo sapiens	103-106
33293826-0	2020	Raltitrexed Enhances the Antitumor Effect of Apatinib in Human Esophageal Squamous Carcinoma Cells via Akt and Erk Pathways.	apatinib	45-53	mitogen-activated protein kinase 1	Homo sapiens	111-114
33293826-8	2020	Moreover, the combination of apatinib and raltitrexed down-regulated mRNA level of the anti-apoptotic protein Bcl-2, while up-regulated pro-apoptotic protein PARP, Bax, and caspase-3 transcription.	apatinib	29-37	BCL2 apoptosis regulator	Homo sapiens	110-115
33293826-8	2020	Moreover, the combination of apatinib and raltitrexed down-regulated mRNA level of the anti-apoptotic protein Bcl-2, while up-regulated pro-apoptotic protein PARP, Bax, and caspase-3 transcription.	apatinib	29-37	collagen type XI alpha 2 chain	Homo sapiens	158-162
33293826-8	2020	Moreover, the combination of apatinib and raltitrexed down-regulated mRNA level of the anti-apoptotic protein Bcl-2, while up-regulated pro-apoptotic protein PARP, Bax, and caspase-3 transcription.	apatinib	29-37	BCL2 associated X, apoptosis regulator	Homo sapiens	164-167
33293826-8	2020	Moreover, the combination of apatinib and raltitrexed down-regulated mRNA level of the anti-apoptotic protein Bcl-2, while up-regulated pro-apoptotic protein PARP, Bax, and caspase-3 transcription.	apatinib	29-37	caspase 3	Homo sapiens	173-182
33293826-10	2020	Conclusion: Taken together, these results indicate that raltitrexed enhances the antitumor effects of apatinib on human ESCC cells by down-regulating phosphorylation of Akt and Erk, implying a combination of raltitrexed and apatinib might be an effective option for treating esophageal squamous cell carcinoma patients.	apatinib	102-110	AKT serine/threonine kinase 1	Homo sapiens	169-172
32839081-2	2020	Apatinib is an oral tyrosine kinase inhibitor that targets vascular endothelial growth factor receptor-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	59-104
33330059-0	2020	Case Report: Gastrointestinal PEComa With TFE3 Rearrangement Treated With Anti-VEGFR TKI Apatinib.	apatinib	89-97	transcription factor binding to IGHM enhancer 3	Homo sapiens	42-46
33330059-0	2020	Case Report: Gastrointestinal PEComa With TFE3 Rearrangement Treated With Anti-VEGFR TKI Apatinib.	apatinib	89-97	kinase insert domain receptor	Homo sapiens	79-84
33330059-3	2020	Here, we report the first case of malignant gastrointestinal PEComa with TFE3 rearrangement which has a response to the targeted therapy of an anti-VEGFR tyrosine kinase inhibitor (TKI), apatinib.	apatinib	187-195	transcription factor binding to IGHM enhancer 3	Homo sapiens	73-77
33330059-6	2020	The patient received the anti-VEGFR TKI apatinib to treat the hepatic metastasis.	apatinib	40-48	kinase insert domain receptor	Homo sapiens	30-35
33204107-3	2020	Apatinib, a small-molecule inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2), is beneficial in the therapy of advanced NSCLC patients.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	40-85
33204107-3	2020	Apatinib, a small-molecule inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2), is beneficial in the therapy of advanced NSCLC patients.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	87-94
32801866-3	2020	Patients and Methods: The study retrospectively reviewed recurrent or refractory advanced pediatric solid tumor patients who were treated with apatinib, an oral small-molecule tyrosine kinase inhibitor (TKI) that targets vascular endothelial growth factor receptor-2 (VEGFR2), at the Sun Yat-sen University Cancer Center (China) from January 2016 to March 2019.	apatinib	143-151	kinase insert domain receptor	Homo sapiens	221-266
33403012-1	2020	Background: Apatinib, an oral small-molecule angiogenesis inhibitor, selectively inhibits vascular endothelial growth factor receptor 2 (VEGFR-2), which inhibits vascular endothelial growth factor (VEGF) stimulated endothelial cell migration and proliferation and decreases tumour growth and metastasis.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	90-135
33403012-1	2020	Background: Apatinib, an oral small-molecule angiogenesis inhibitor, selectively inhibits vascular endothelial growth factor receptor 2 (VEGFR-2), which inhibits vascular endothelial growth factor (VEGF) stimulated endothelial cell migration and proliferation and decreases tumour growth and metastasis.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	137-144
33403012-1	2020	Background: Apatinib, an oral small-molecule angiogenesis inhibitor, selectively inhibits vascular endothelial growth factor receptor 2 (VEGFR-2), which inhibits vascular endothelial growth factor (VEGF) stimulated endothelial cell migration and proliferation and decreases tumour growth and metastasis.	apatinib	12-20	vascular endothelial growth factor A	Homo sapiens	90-124
33403012-1	2020	Background: Apatinib, an oral small-molecule angiogenesis inhibitor, selectively inhibits vascular endothelial growth factor receptor 2 (VEGFR-2), which inhibits vascular endothelial growth factor (VEGF) stimulated endothelial cell migration and proliferation and decreases tumour growth and metastasis.	apatinib	12-20	vascular endothelial growth factor A	Homo sapiens	137-141
33200015-3	2020	Apatinib, a tyrosine kinase inhibitor, can specifically inhibit vascular endothelial growth factor receptor 2, showing encouraging anti-tumor effects in a variety of tumors including advanced hepatocellular carcinoma (HCC).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	64-109
33120847-1	2020	RATIONALE: Apatinib is a novel anti-angiogenic agent that targets vascular endothelial growth factor receptor-2, thereby inhibiting tumor angiogenesis, and is effective in the treatment of brain metastases (BM) and peritumoral brain edema (PTBE).	apatinib	11-19	kinase insert domain receptor	Homo sapiens	66-111
33012286-3	2020	We aimed to evaluate the ability of distinct AT depots to predict the efficacy of apatinib, a VEGFR inhibitor, in recurrent ovarian cancers included in the AEROC trial.	apatinib	82-90	kinase insert domain receptor	Homo sapiens	94-99
33004767-3	2020	Apatinib is an oral, small-molecule, anti-tumor, angiogenesis-targeted drug, which acts mainly on the intracellular binding site of vascular endothelial growth factor receptor-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	132-177
32697395-1	2020	Apatinib (YN968D1) is a small-molecule tyrosine kinase inhibitor(TKI)which can inhibit the activity of vascular endothelial growth factor receptor-2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Rattus norvegicus	103-148
32697395-1	2020	Apatinib (YN968D1) is a small-molecule tyrosine kinase inhibitor(TKI)which can inhibit the activity of vascular endothelial growth factor receptor-2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Rattus norvegicus	150-157
32697395-1	2020	Apatinib (YN968D1) is a small-molecule tyrosine kinase inhibitor(TKI)which can inhibit the activity of vascular endothelial growth factor receptor-2 (VEGFR-2).	apatinib	10-17	kinase insert domain receptor	Rattus norvegicus	103-148
32697395-1	2020	Apatinib (YN968D1) is a small-molecule tyrosine kinase inhibitor(TKI)which can inhibit the activity of vascular endothelial growth factor receptor-2 (VEGFR-2).	apatinib	10-17	kinase insert domain receptor	Rattus norvegicus	150-157
32697395-5	2020	For in vitro experiment, apatinib administration inhibited VSMC proliferation, migration and reversed VSMC dedifferentiation with the stimulation of platelet-derived growth factor type BB (PDGF-BB).In terms of mechanism, with the preincubation of apatinib, the activations of PDGF receptor-beta (PDGFR-beta) and phosphoinositide-specific phospholipase C-gamma1 (PLC-gamma1) induced by PDGF-BB were inhibited in VSMCs.	apatinib	25-33	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	296-306
32697395-5	2020	For in vitro experiment, apatinib administration inhibited VSMC proliferation, migration and reversed VSMC dedifferentiation with the stimulation of platelet-derived growth factor type BB (PDGF-BB).In terms of mechanism, with the preincubation of apatinib, the activations of PDGF receptor-beta (PDGFR-beta) and phosphoinositide-specific phospholipase C-gamma1 (PLC-gamma1) induced by PDGF-BB were inhibited in VSMCs.	apatinib	25-33	phospholipase C, gamma 1	Rattus norvegicus	338-360
32697395-5	2020	For in vitro experiment, apatinib administration inhibited VSMC proliferation, migration and reversed VSMC dedifferentiation with the stimulation of platelet-derived growth factor type BB (PDGF-BB).In terms of mechanism, with the preincubation of apatinib, the activations of PDGF receptor-beta (PDGFR-beta) and phosphoinositide-specific phospholipase C-gamma1 (PLC-gamma1) induced by PDGF-BB were inhibited in VSMCs.	apatinib	25-33	phospholipase C, gamma 1	Rattus norvegicus	362-372
32697395-6	2020	With the preincubation of apatinib, the phosphorylation of PDGFR-beta, extracellular signal-related kinases (ERK1/2) and Jun amino-terminal kinases (JNK) induced by PDGF-BB were also inhibited in rat vascular smooth muscle cell line A7r5.	apatinib	26-34	platelet derived growth factor receptor alpha	Rattus norvegicus	59-69
32697395-6	2020	With the preincubation of apatinib, the phosphorylation of PDGFR-beta, extracellular signal-related kinases (ERK1/2) and Jun amino-terminal kinases (JNK) induced by PDGF-BB were also inhibited in rat vascular smooth muscle cell line A7r5.	apatinib	26-34	mitogen activated protein kinase 3	Rattus norvegicus	109-115
32697395-6	2020	With the preincubation of apatinib, the phosphorylation of PDGFR-beta, extracellular signal-related kinases (ERK1/2) and Jun amino-terminal kinases (JNK) induced by PDGF-BB were also inhibited in rat vascular smooth muscle cell line A7r5.	apatinib	26-34	mitogen-activated protein kinase 8	Rattus norvegicus	121-147
32697395-6	2020	With the preincubation of apatinib, the phosphorylation of PDGFR-beta, extracellular signal-related kinases (ERK1/2) and Jun amino-terminal kinases (JNK) induced by PDGF-BB were also inhibited in rat vascular smooth muscle cell line A7r5.	apatinib	26-34	mitogen-activated protein kinase 8	Rattus norvegicus	149-152
32782621-13	2020	The present study suggested that the clinical outcomes of patients with advanced EOC, who progressed after standard regimens and received apatinib treatment, might be influenced by the VEGFR2 rs2071559 polymorphism.	apatinib	138-146	kinase insert domain receptor	Homo sapiens	185-191
32872014-1	2020	INTRODUCTION: Apatinib is a novel anti-angiogenic agent that targets vascular endothelial growth factor receptor-2, and is effective in patients with advanced lung cancer who are refractory to first-line chemotherapy.	apatinib	14-22	kinase insert domain receptor	Homo sapiens	69-114
32849930-5	2020	Apatinib inhibited the expressions of ABCG2, CD24, ICAM-1, OCT4, and SOX2 and upregulated the expressions of CD44, CD13, and FOXD3.	apatinib	0-8	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	38-43
32849930-5	2020	Apatinib inhibited the expressions of ABCG2, CD24, ICAM-1, OCT4, and SOX2 and upregulated the expressions of CD44, CD13, and FOXD3.	apatinib	0-8	CD24a antigen	Mus musculus	45-49
32849930-5	2020	Apatinib inhibited the expressions of ABCG2, CD24, ICAM-1, OCT4, and SOX2 and upregulated the expressions of CD44, CD13, and FOXD3.	apatinib	0-8	intercellular adhesion molecule 1	Mus musculus	51-57
32849930-5	2020	Apatinib inhibited the expressions of ABCG2, CD24, ICAM-1, OCT4, and SOX2 and upregulated the expressions of CD44, CD13, and FOXD3.	apatinib	0-8	POU domain, class 5, transcription factor 1	Mus musculus	59-63
32849930-5	2020	Apatinib inhibited the expressions of ABCG2, CD24, ICAM-1, OCT4, and SOX2 and upregulated the expressions of CD44, CD13, and FOXD3.	apatinib	0-8	SRY (sex determining region Y)-box 2	Mus musculus	69-73
32849930-5	2020	Apatinib inhibited the expressions of ABCG2, CD24, ICAM-1, OCT4, and SOX2 and upregulated the expressions of CD44, CD13, and FOXD3.	apatinib	0-8	CD44 antigen	Mus musculus	109-113
32849930-5	2020	Apatinib inhibited the expressions of ABCG2, CD24, ICAM-1, OCT4, and SOX2 and upregulated the expressions of CD44, CD13, and FOXD3.	apatinib	0-8	alanyl (membrane) aminopeptidase	Mus musculus	115-119
32849930-5	2020	Apatinib inhibited the expressions of ABCG2, CD24, ICAM-1, OCT4, and SOX2 and upregulated the expressions of CD44, CD13, and FOXD3.	apatinib	0-8	forkhead box D3	Mus musculus	125-130
32849930-6	2020	Apatinib treatment also inhibited the Wnt/beta-catenin, Hedgehog, and Hippo signaling pathways.	apatinib	0-8	catenin (cadherin associated protein), beta 1	Mus musculus	42-54
32821164-4	2020	Apatinib, an inhibitor of targeting vascular endothelial growth factor receptor 2 (VEGFR2), has been approved for third-line treatment of advanced gastric cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	36-81
32821164-4	2020	Apatinib, an inhibitor of targeting vascular endothelial growth factor receptor 2 (VEGFR2), has been approved for third-line treatment of advanced gastric cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	83-89
32333216-7	2020	Fortunately, preclinical and clinical studies have indicated that apatinib is a novel promising VEGFR2 inhibitor showing potent anti-angiogenic and anti-neoplastic activities in advanced sarcomas.	apatinib	66-74	kinase insert domain receptor	Homo sapiens	96-102
32333216-17	2020	Fortunately, preclinical studies and clinical trials have indicated that apatinib is a novel promising VEGFR2 inhibitor showing potent anti-angiogenic and anti-neoplastic activities in advanced sarcomas.	apatinib	73-81	kinase insert domain receptor	Homo sapiens	103-109
32374627-4	2020	In vitro, we assessed the influence which Bev + Apa treatment exerts upon the proliferation as well as apoptosis of Lewis lung carcinoma (LLC) cells in virtue of the 3-(4,5-dimethyl-thiazol-2-yl)-2,5-diphenyltetrazolium bromide as assay as well as Annexin V staining, respectively.	apatinib	48-51	annexin A5	Mus musculus	248-257
32901884-10	2020	Compared with the levels prior to treatment, Beclin-1 and LC3A remained unchanged post-treatment in the Apatinib plus docetaxel group, while they were increased in the Docetaxel group.	apatinib	104-112	beclin 1	Homo sapiens	45-53
32901884-10	2020	Compared with the levels prior to treatment, Beclin-1 and LC3A remained unchanged post-treatment in the Apatinib plus docetaxel group, while they were increased in the Docetaxel group.	apatinib	104-112	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	58-62
32901884-12	2020	Moreover, apatinib repressed LC3A, Beclin-1, p-AKT expression levels and promoted the cell apoptosis rate in A549/DTX cells and docetaxel-treated A549/DTX cells.	apatinib	10-18	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	29-33
32901884-12	2020	Moreover, apatinib repressed LC3A, Beclin-1, p-AKT expression levels and promoted the cell apoptosis rate in A549/DTX cells and docetaxel-treated A549/DTX cells.	apatinib	10-18	beclin 1	Homo sapiens	35-43
32901884-12	2020	Moreover, apatinib repressed LC3A, Beclin-1, p-AKT expression levels and promoted the cell apoptosis rate in A549/DTX cells and docetaxel-treated A549/DTX cells.	apatinib	10-18	AKT serine/threonine kinase 1	Homo sapiens	47-50
33154652-0	2020	Therapeutic Potential of Apatinib Against Colorectal Cancer by Inhibiting VEGFR2-Mediated Angiogenesis and beta-Catenin Signaling.	apatinib	25-33	kinase insert domain protein receptor	Mus musculus	74-80
33154652-0	2020	Therapeutic Potential of Apatinib Against Colorectal Cancer by Inhibiting VEGFR2-Mediated Angiogenesis and beta-Catenin Signaling.	apatinib	25-33	catenin (cadherin associated protein), beta 1	Mus musculus	107-119
33154652-1	2020	Purpose: Apatinib is an inhibitor of VEGFR2 (vascular endothelial growth factor receptor 2) that has attracted a great deal of attention due to its promotion of anticancer activity.	apatinib	9-17	kinase insert domain protein receptor	Mus musculus	37-43
33154652-1	2020	Purpose: Apatinib is an inhibitor of VEGFR2 (vascular endothelial growth factor receptor 2) that has attracted a great deal of attention due to its promotion of anticancer activity.	apatinib	9-17	kinase insert domain protein receptor	Mus musculus	45-90
33154652-6	2020	An analysis of the mechanism associated with apatinib activity demonstrated that by interacting with VEGFR2, apatinib decreased p-Src, p-Akt, and p-GSK3beta levels, which further increased beta-catenin ubiquitination and reduced the nuclear translocation of beta-catenin.	apatinib	45-53	kinase insert domain protein receptor	Mus musculus	101-107
33154652-6	2020	An analysis of the mechanism associated with apatinib activity demonstrated that by interacting with VEGFR2, apatinib decreased p-Src, p-Akt, and p-GSK3beta levels, which further increased beta-catenin ubiquitination and reduced the nuclear translocation of beta-catenin.	apatinib	45-53	Rous sarcoma oncogene	Mus musculus	130-133
33154652-6	2020	An analysis of the mechanism associated with apatinib activity demonstrated that by interacting with VEGFR2, apatinib decreased p-Src, p-Akt, and p-GSK3beta levels, which further increased beta-catenin ubiquitination and reduced the nuclear translocation of beta-catenin.	apatinib	45-53	thymoma viral proto-oncogene 1	Mus musculus	137-140
33154652-6	2020	An analysis of the mechanism associated with apatinib activity demonstrated that by interacting with VEGFR2, apatinib decreased p-Src, p-Akt, and p-GSK3beta levels, which further increased beta-catenin ubiquitination and reduced the nuclear translocation of beta-catenin.	apatinib	45-53	glycogen synthase kinase 3 alpha	Mus musculus	148-156
33154652-6	2020	An analysis of the mechanism associated with apatinib activity demonstrated that by interacting with VEGFR2, apatinib decreased p-Src, p-Akt, and p-GSK3beta levels, which further increased beta-catenin ubiquitination and reduced the nuclear translocation of beta-catenin.	apatinib	45-53	catenin beta 1	Homo sapiens	189-201
33154652-6	2020	An analysis of the mechanism associated with apatinib activity demonstrated that by interacting with VEGFR2, apatinib decreased p-Src, p-Akt, and p-GSK3beta levels, which further increased beta-catenin ubiquitination and reduced the nuclear translocation of beta-catenin.	apatinib	45-53	catenin beta 1	Homo sapiens	258-270
33154652-6	2020	An analysis of the mechanism associated with apatinib activity demonstrated that by interacting with VEGFR2, apatinib decreased p-Src, p-Akt, and p-GSK3beta levels, which further increased beta-catenin ubiquitination and reduced the nuclear translocation of beta-catenin.	apatinib	109-117	kinase insert domain protein receptor	Mus musculus	101-107
33154652-6	2020	An analysis of the mechanism associated with apatinib activity demonstrated that by interacting with VEGFR2, apatinib decreased p-Src, p-Akt, and p-GSK3beta levels, which further increased beta-catenin ubiquitination and reduced the nuclear translocation of beta-catenin.	apatinib	109-117	Rous sarcoma oncogene	Mus musculus	130-133
33154652-6	2020	An analysis of the mechanism associated with apatinib activity demonstrated that by interacting with VEGFR2, apatinib decreased p-Src, p-Akt, and p-GSK3beta levels, which further increased beta-catenin ubiquitination and reduced the nuclear translocation of beta-catenin.	apatinib	109-117	thymoma viral proto-oncogene 1	Mus musculus	137-140
33154652-6	2020	An analysis of the mechanism associated with apatinib activity demonstrated that by interacting with VEGFR2, apatinib decreased p-Src, p-Akt, and p-GSK3beta levels, which further increased beta-catenin ubiquitination and reduced the nuclear translocation of beta-catenin.	apatinib	109-117	glycogen synthase kinase 3 alpha	Mus musculus	148-156
33154652-6	2020	An analysis of the mechanism associated with apatinib activity demonstrated that by interacting with VEGFR2, apatinib decreased p-Src, p-Akt, and p-GSK3beta levels, which further increased beta-catenin ubiquitination and reduced the nuclear translocation of beta-catenin.	apatinib	109-117	catenin beta 1	Homo sapiens	189-201
33154652-6	2020	An analysis of the mechanism associated with apatinib activity demonstrated that by interacting with VEGFR2, apatinib decreased p-Src, p-Akt, and p-GSK3beta levels, which further increased beta-catenin ubiquitination and reduced the nuclear translocation of beta-catenin.	apatinib	109-117	catenin beta 1	Homo sapiens	258-270
33154652-7	2020	Furthermore, apatinib strongly suppressed CT26 cell growth in mouse xenograft models by inhibiting beta-catenin signaling and angiogenesis.	apatinib	13-21	catenin (cadherin associated protein), beta 1	Mus musculus	99-111
33154652-8	2020	Conclusion: Overall, the results of the present study here indicated that by inhibiting the VEGFR2-beta-catenin-mediated malignant phenotype, apatinib significantly suppresses the growth of CRC, suggesting that the use of apatinib is a promising therapeutic strategy for CRC.	apatinib	142-150	kinase insert domain protein receptor	Mus musculus	92-98
33154652-8	2020	Conclusion: Overall, the results of the present study here indicated that by inhibiting the VEGFR2-beta-catenin-mediated malignant phenotype, apatinib significantly suppresses the growth of CRC, suggesting that the use of apatinib is a promising therapeutic strategy for CRC.	apatinib	142-150	catenin (cadherin associated protein), beta 1	Mus musculus	99-111
33154652-8	2020	Conclusion: Overall, the results of the present study here indicated that by inhibiting the VEGFR2-beta-catenin-mediated malignant phenotype, apatinib significantly suppresses the growth of CRC, suggesting that the use of apatinib is a promising therapeutic strategy for CRC.	apatinib	222-230	kinase insert domain protein receptor	Mus musculus	92-98
33154652-8	2020	Conclusion: Overall, the results of the present study here indicated that by inhibiting the VEGFR2-beta-catenin-mediated malignant phenotype, apatinib significantly suppresses the growth of CRC, suggesting that the use of apatinib is a promising therapeutic strategy for CRC.	apatinib	222-230	catenin (cadherin associated protein), beta 1	Mus musculus	99-111
32342599-4	2020	BACKGROUND: Apatinib is an inhibitor of vascular endothelial growth factor receptor-2 (VEGFR2), which is thought to play a role in esophageal cancer progression.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	40-85
32342599-4	2020	BACKGROUND: Apatinib is an inhibitor of vascular endothelial growth factor receptor-2 (VEGFR2), which is thought to play a role in esophageal cancer progression.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	87-93
32788939-0	2020	Apatinib induces apoptosis and autophagy via the PI3K/AKT/mTOR and MAPK/ERK signaling pathways in neuroblastoma.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	54-57
32788939-0	2020	Apatinib induces apoptosis and autophagy via the PI3K/AKT/mTOR and MAPK/ERK signaling pathways in neuroblastoma.	apatinib	0-8	mechanistic target of rapamycin kinase	Homo sapiens	58-62
32788939-0	2020	Apatinib induces apoptosis and autophagy via the PI3K/AKT/mTOR and MAPK/ERK signaling pathways in neuroblastoma.	apatinib	0-8	mitogen-activated protein kinase 1	Homo sapiens	67-71
32788939-0	2020	Apatinib induces apoptosis and autophagy via the PI3K/AKT/mTOR and MAPK/ERK signaling pathways in neuroblastoma.	apatinib	0-8	mitogen-activated protein kinase 1	Homo sapiens	72-75
32788939-2	2020	Apatinib, a selective inhibitor of the vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase, which was discovered to be highly associated with metastasis, has been reported to exert antitumor effects in numerous types of cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	39-84
32788939-2	2020	Apatinib, a selective inhibitor of the vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase, which was discovered to be highly associated with metastasis, has been reported to exert antitumor effects in numerous types of cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	86-93
32788939-8	2020	In addition, western blotting and immunofluorescence assays identified that the expression level of microtubule-associated protein 1A/1B-light chain 3-II, which is expressed in autophagosomes, was upregulated following apatinib treatment.	apatinib	219-227	microtubule associated protein 1A	Homo sapiens	100-136
32788939-9	2020	In conclusion, the findings of the present study suggested that apatinib may induce apoptosis and autophagy via the PI3K/AKT/mTOR and mitogen-activated protein kinase/ERK signaling pathways in NB cells.	apatinib	64-72	AKT serine/threonine kinase 1	Homo sapiens	121-124
32788939-9	2020	In conclusion, the findings of the present study suggested that apatinib may induce apoptosis and autophagy via the PI3K/AKT/mTOR and mitogen-activated protein kinase/ERK signaling pathways in NB cells.	apatinib	64-72	mechanistic target of rapamycin kinase	Homo sapiens	125-129
32788939-9	2020	In conclusion, the findings of the present study suggested that apatinib may induce apoptosis and autophagy via the PI3K/AKT/mTOR and mitogen-activated protein kinase/ERK signaling pathways in NB cells.	apatinib	64-72	mitogen-activated protein kinase 1	Homo sapiens	167-170
33014856-0	2020	Combination of Cordycepin and Apatinib Synergistically Inhibits NSCLC Cells by Down-Regulating VEGF/PI3K/Akt Signaling Pathway.	apatinib	30-38	vascular endothelial growth factor A	Homo sapiens	95-99
33014856-0	2020	Combination of Cordycepin and Apatinib Synergistically Inhibits NSCLC Cells by Down-Regulating VEGF/PI3K/Akt Signaling Pathway.	apatinib	30-38	AKT serine/threonine kinase 1	Homo sapiens	105-108
33014856-7	2020	The VEGF/PI3K/Akt pathway was inhibited after treatment with cordycepin and apatinib.	apatinib	76-84	vascular endothelial growth factor A	Homo sapiens	4-8
33014856-7	2020	The VEGF/PI3K/Akt pathway was inhibited after treatment with cordycepin and apatinib.	apatinib	76-84	AKT serine/threonine kinase 1	Homo sapiens	14-17
33014856-8	2020	Conclusion: Our findings demonstrated that the combination of cordycepin and apatinib has synergistically anticancer effect on NSCLC cells by down-regulating VEGF/PI3K/Akt signaling pathway.	apatinib	77-85	vascular endothelial growth factor A	Homo sapiens	158-162
33014856-8	2020	Conclusion: Our findings demonstrated that the combination of cordycepin and apatinib has synergistically anticancer effect on NSCLC cells by down-regulating VEGF/PI3K/Akt signaling pathway.	apatinib	77-85	AKT serine/threonine kinase 1	Homo sapiens	168-171
32347357-12	2020	However, apatinib alleviated hyperangiogenesis and hypoxia in TME and converted the immunosuppressive TME into an immunostimulatory one in VEGFA-overexpressed tumors.	apatinib	9-17	vascular endothelial growth factor A	Mus musculus	139-144
32953800-1	2020	Background: Apatinib, a selective inhibitor of vascular endothelial growth factor receptor 2 (VEGFR 2), has exhibited modest antitumor efficacy in hepatocellular carcinoma (HCC).	apatinib	12-20	kinase insert domain receptor	Homo sapiens	47-92
32953800-1	2020	Background: Apatinib, a selective inhibitor of vascular endothelial growth factor receptor 2 (VEGFR 2), has exhibited modest antitumor efficacy in hepatocellular carcinoma (HCC).	apatinib	12-20	kinase insert domain receptor	Homo sapiens	94-101
32801866-3	2020	Patients and Methods: The study retrospectively reviewed recurrent or refractory advanced pediatric solid tumor patients who were treated with apatinib, an oral small-molecule tyrosine kinase inhibitor (TKI) that targets vascular endothelial growth factor receptor-2 (VEGFR2), at the Sun Yat-sen University Cancer Center (China) from January 2016 to March 2019.	apatinib	143-151	kinase insert domain receptor	Homo sapiens	268-274
32774731-0	2020	Apatinib-induced NF-kappaB inactivation sensitizes triple-negative breast cancer cells to doxorubicin.	apatinib	0-8	nuclear factor kappa B subunit 1	Homo sapiens	17-26
32774731-7	2020	Importantly, it was found that followed by DOX treatment, apatinib could inhibit NF-kappaB signaling pathways, which have been validated to increase ROS production and reverse DOX resistance.	apatinib	58-66	nuclear factor kappa B subunit 1	Homo sapiens	81-90
32774731-9	2020	Taken together, our study suggests that apatinib sensitizes TNBC cells to DOX in vitro and in vivo through inactivation of NF-kappaB signaling pathways, providing a rationale for the combined use of apatinib and DOX in TNBC chemotherapy.	apatinib	40-48	nuclear factor kappa B subunit 1	Homo sapiens	123-132
32568635-0	2021	Evaluation of the interaction of novel tyrosine kinase inhibitor apatinib mesylate with bovine serum albumin using spectroscopies and theoretical calculation approaches.	apatinib	65-73	albumin	Homo sapiens	95-108
32664067-2	2020	Apatinib mesylate, which is a small molecule vascular endothelial growth factor receptor 2 tyrosine kinase inhibitor, could be used as antiangiogenesis therapy for gastric cancer.	apatinib	0-17	kinase insert domain receptor	Homo sapiens	45-90
32733791-1	2020	Background: Apatinib is a powerful inhibitor of vascular endothelial growth factor receptor-2.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	48-93
32212907-3	2020	Apatinib is a small-molecule antiangiogenic agent that selectively inhibits VEGFR-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	76-83
32212907-4	2020	We report three cases of recurrent AM (VEGFR-2 positive) treated with apatinib.	apatinib	70-78	kinase insert domain receptor	Homo sapiens	39-46
32212907-14	2020	Apatinib (YN968D1) is a small-molecule antiangiogenic agent that selectively inhibits VEGFR-2.Case presentation:Case #1: A 47-year-old Asian female patient with malignant meningioma underwent four operations and three radiotherapies.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	86-93
32233990-0	2020	Significant response to apatinib monotherapy in heavily pretreated advanced HER2-positive breast cancer: a case report and literature review.	apatinib	24-32	erb-b2 receptor tyrosine kinase 2	Homo sapiens	76-80
32233990-6	2020	Our case indicates that apatinib might have anti-tumor activity in patients with HER2-positive breast cancer with HER2-targeted resistance.	apatinib	24-32	erb-b2 receptor tyrosine kinase 2	Homo sapiens	81-85
32233990-6	2020	Our case indicates that apatinib might have anti-tumor activity in patients with HER2-positive breast cancer with HER2-targeted resistance.	apatinib	24-32	erb-b2 receptor tyrosine kinase 2	Homo sapiens	114-118
32026267-0	2020	The apatinib inhibits breast cancer cell line MDA-MB-231 in vitro by inducing apoptosis, cell cycle arrest, and regulating nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein kinase (MAPK) signaling pathways.	apatinib	4-12	nuclear factor kappa B subunit 1	Homo sapiens	123-144
32026267-0	2020	The apatinib inhibits breast cancer cell line MDA-MB-231 in vitro by inducing apoptosis, cell cycle arrest, and regulating nuclear factor-kappaB (NF-kappaB) and mitogen-activated protein kinase (MAPK) signaling pathways.	apatinib	4-12	nuclear factor kappa B subunit 1	Homo sapiens	146-155
32026267-8	2020	Apatinib decreased expression of p-p65 and p65 proteins in NF-kappaB signaling pathways and increased expression of p38, p-p38, JNK, and p-JNK in MAPK signaling pathways.	apatinib	0-8	RELA proto-oncogene, NF-kB subunit	Homo sapiens	35-38
32026267-8	2020	Apatinib decreased expression of p-p65 and p65 proteins in NF-kappaB signaling pathways and increased expression of p38, p-p38, JNK, and p-JNK in MAPK signaling pathways.	apatinib	0-8	nuclear factor kappa B subunit 1	Homo sapiens	59-68
32026267-8	2020	Apatinib decreased expression of p-p65 and p65 proteins in NF-kappaB signaling pathways and increased expression of p38, p-p38, JNK, and p-JNK in MAPK signaling pathways.	apatinib	0-8	mitogen-activated protein kinase 14	Homo sapiens	116-119
32026267-8	2020	Apatinib decreased expression of p-p65 and p65 proteins in NF-kappaB signaling pathways and increased expression of p38, p-p38, JNK, and p-JNK in MAPK signaling pathways.	apatinib	0-8	mitogen-activated protein kinase 8	Homo sapiens	128-131
32026267-9	2020	CONCLUSION: The results suggested that apatinib can inhibit proliferation, migration and invasion of breast cancer cell line MDA-MB-231 through inducing apoptosis, cell cycle arrest, and regulating NF-kappaB and MAPK signaling pathways.	apatinib	39-47	nuclear factor kappa B subunit 1	Homo sapiens	198-207
32266817-1	2020	Apatinib (YN968D1) is a novel and highly selective tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor-2 (VEGFR-2) and is approved as a third-line and subsequent-line treatment for advanced gastric adenocarcinoma or gastroesophageal junction adenocarcinoma in China.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	91-136
32266817-1	2020	Apatinib (YN968D1) is a novel and highly selective tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor-2 (VEGFR-2) and is approved as a third-line and subsequent-line treatment for advanced gastric adenocarcinoma or gastroesophageal junction adenocarcinoma in China.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	138-145
32655637-0	2020	An Oral Small Molecule VEGFR2 Inhibitor, Apatinib, in Patients with Recurrent or Refractory Cervical Cancer: A Real World Study.	apatinib	41-49	kinase insert domain receptor	Homo sapiens	23-29
32514243-0	2020	Apatinib suppresses tumor progression and enhances cisplatin sensitivity in esophageal cancer via the Akt/beta-catenin pathway.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	102-105
32685465-0	2020	Apatinib Inhibits the Invasion and Metastasis of Liver Cancer Cells by Downregulating MMP-Related Proteins via Regulation of the NF-kappaB Signaling Pathway.	apatinib	0-8	nuclear factor kappa B subunit 1	Homo sapiens	129-138
32685465-2	2020	Methods: The anti-invasion and antimetastasis effects of apatinib in HepG2, Hep3B,Huh7 and SMMC-7721 liver cancer cell lines were tested by the wound-healing and transwell invasion assays.	apatinib	57-65	MIR7-3 host gene	Homo sapiens	82-86
32685465-3	2020	Real-time PCR and Western blot were used to detect the influence of apatinib on the gene expression of MMPs, TIMPs, and constituents of the NF-kappaB signaling pathway in Hep3B and HepG2 liver cell lines.	apatinib	68-76	matrix metallopeptidase 1	Homo sapiens	103-107
32685465-3	2020	Real-time PCR and Western blot were used to detect the influence of apatinib on the gene expression of MMPs, TIMPs, and constituents of the NF-kappaB signaling pathway in Hep3B and HepG2 liver cell lines.	apatinib	68-76	nuclear factor kappa B subunit 1	Homo sapiens	140-149
32508029-0	2020	Dual blockade of EGFR and VEGFR pathways: Results from a pilot study evaluating apatinib plus gefitinib as a first-line treatment for advanced EGFR-mutant non-small cell lung cancer.	apatinib	80-88	epidermal growth factor receptor	Homo sapiens	17-21
32508029-0	2020	Dual blockade of EGFR and VEGFR pathways: Results from a pilot study evaluating apatinib plus gefitinib as a first-line treatment for advanced EGFR-mutant non-small cell lung cancer.	apatinib	80-88	kinase insert domain receptor	Homo sapiens	26-31
32508029-0	2020	Dual blockade of EGFR and VEGFR pathways: Results from a pilot study evaluating apatinib plus gefitinib as a first-line treatment for advanced EGFR-mutant non-small cell lung cancer.	apatinib	80-88	epidermal growth factor receptor	Homo sapiens	27-31
32508029-2	2020	Apatinib is an orally effective VEGFR-2 tyrosine kinase inhibitor (TKI).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	32-39
32508029-3	2020	This pilot study aims to evaluate the tolerability, pharmacokinetic profile, and antitumor activity of apatinib plus gefitinib as a therapy for EGFR-mutant advanced NSCLC.	apatinib	103-111	epidermal growth factor receptor	Homo sapiens	144-148
32508029-16	2020	CONCLUSION: Apatinib (500 mg) plus gefitinib (250 mg) showed a tolerable safety profile and encouraging antitumor activity for advanced EGFR-mutant NSCLC in the first-line setting.	apatinib	12-20	epidermal growth factor receptor	Homo sapiens	136-140
32215805-1	2020	OBJECTIVE: The aim of this study was to investigate the efficacy and safety of Apatinib mesylate in the treatment of metastatic osteosarcoma patients who progressed after standard therapy and the VEGFR2 gene polymorphism analysis.	apatinib	79-96	kinase insert domain receptor	Homo sapiens	196-202
32215805-16	2020	The clinical outcomes of Apatinib may be influenced by the polymorphism - 906 T > C of VEGFR2 through mediating the mRNA expression of VEGFR2.	apatinib	25-33	kinase insert domain receptor	Homo sapiens	87-93
32215805-16	2020	The clinical outcomes of Apatinib may be influenced by the polymorphism - 906 T > C of VEGFR2 through mediating the mRNA expression of VEGFR2.	apatinib	25-33	kinase insert domain receptor	Homo sapiens	135-141
32514243-0	2020	Apatinib suppresses tumor progression and enhances cisplatin sensitivity in esophageal cancer via the Akt/beta-catenin pathway.	apatinib	0-8	catenin beta 1	Homo sapiens	106-118
32514243-2	2020	Apatinib, an inhibitor of VEGFR2, has a promising antitumor effect on malignancies.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	26-32
32514243-13	2020	The effects of apatinib on esophageal cancer were partially dependent on its block of the VEGFR2/Akt/beta-catenin pathway.	apatinib	15-23	kinase insert domain receptor	Homo sapiens	90-96
32514243-13	2020	The effects of apatinib on esophageal cancer were partially dependent on its block of the VEGFR2/Akt/beta-catenin pathway.	apatinib	15-23	AKT serine/threonine kinase 1	Homo sapiens	97-100
32514243-13	2020	The effects of apatinib on esophageal cancer were partially dependent on its block of the VEGFR2/Akt/beta-catenin pathway.	apatinib	15-23	catenin beta 1	Homo sapiens	101-113
32514243-14	2020	Specifically, apatinib induced the degradation of beta-catenin and decreased its transcriptional activity through Akt/GSK-3beta repression.	apatinib	14-22	catenin beta 1	Homo sapiens	50-62
32514243-14	2020	Specifically, apatinib induced the degradation of beta-catenin and decreased its transcriptional activity through Akt/GSK-3beta repression.	apatinib	14-22	AKT serine/threonine kinase 1	Homo sapiens	114-117
32514243-14	2020	Specifically, apatinib induced the degradation of beta-catenin and decreased its transcriptional activity through Akt/GSK-3beta repression.	apatinib	14-22	glycogen synthase kinase 3 alpha	Homo sapiens	118-127
32514243-16	2020	Conclusion: Our study indicates that apatinib suppresses tumor progression and enhances cisplatin sensitivity in esophageal cancer by deactivating the Akt/beta-catenin pathway.	apatinib	37-45	AKT serine/threonine kinase 1	Homo sapiens	151-154
32514243-16	2020	Conclusion: Our study indicates that apatinib suppresses tumor progression and enhances cisplatin sensitivity in esophageal cancer by deactivating the Akt/beta-catenin pathway.	apatinib	37-45	catenin beta 1	Homo sapiens	155-167
32448335-2	2020	Apatinib mesylate, a novel, small anti-angiogenic agent, highly selectively inhibits the activity of vascular endothelial growth factor receptor-2 tyrosine kinase.	apatinib	0-17	kinase insert domain receptor	Homo sapiens	101-146
32448335-3	2020	Apatinib mesylate also blocks the signaling of vascular endothelial growth factor binding to its receptor, thereby strongly inhibiting tumor angiogenesis and exerting an anti-tumor effect.	apatinib	0-17	vascular endothelial growth factor A	Homo sapiens	47-81
32546963-2	2020	The in vitro inhibition studies suggested that apatinib exerted potent inhibition on CYP3A4 and CYP2C9.	apatinib	47-55	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	85-91
32546963-2	2020	The in vitro inhibition studies suggested that apatinib exerted potent inhibition on CYP3A4 and CYP2C9.	apatinib	47-55	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	96-102
32546963-12	2020	Owing to the risk of pharmacokinetic drug-drug interactions based on CYP3A4/CYP2C9 inhibition by apatinib, caution is advised in the concurrent use of apatinib with either CYP2C9 or CYP3A4 substrates.	apatinib	97-105	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	69-75
32546963-12	2020	Owing to the risk of pharmacokinetic drug-drug interactions based on CYP3A4/CYP2C9 inhibition by apatinib, caution is advised in the concurrent use of apatinib with either CYP2C9 or CYP3A4 substrates.	apatinib	97-105	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	76-82
32509141-0	2020	Apatinib, a Novel Tyrosine Kinase Inhibitor, Promotes ROS-Dependent Apoptosis and Autophagy via the Nrf2/HO-1 Pathway in Ovarian Cancer Cells.	apatinib	0-8	NFE2 like bZIP transcription factor 2	Homo sapiens	100-104
32509141-0	2020	Apatinib, a Novel Tyrosine Kinase Inhibitor, Promotes ROS-Dependent Apoptosis and Autophagy via the Nrf2/HO-1 Pathway in Ovarian Cancer Cells.	apatinib	0-8	heme oxygenase 1	Homo sapiens	105-109
32509141-1	2020	Apatinib, a new-generation oral tyrosine kinase inhibitor targeting the vascular endothelial growth factor receptor 2 (VEGFR2) signaling pathway, shows favorable therapeutic effects in various malignant tumors.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	72-117
32509141-1	2020	Apatinib, a new-generation oral tyrosine kinase inhibitor targeting the vascular endothelial growth factor receptor 2 (VEGFR2) signaling pathway, shows favorable therapeutic effects in various malignant tumors.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	119-125
32509141-5	2020	Mechanistically, we showed that apatinib suppressed glutathione to generate ROS via the downregulation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway and maintained an antitumor effect at a low level of VEGFR2 in ovarian cancer, suggesting that combination of apatinib with Nrf2 inhibitor may be a promising therapy strategy for patients with ovarian cancer.	apatinib	32-40	NFE2 like bZIP transcription factor 2	Homo sapiens	110-153
32509141-5	2020	Mechanistically, we showed that apatinib suppressed glutathione to generate ROS via the downregulation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway and maintained an antitumor effect at a low level of VEGFR2 in ovarian cancer, suggesting that combination of apatinib with Nrf2 inhibitor may be a promising therapy strategy for patients with ovarian cancer.	apatinib	32-40	NFE2 like bZIP transcription factor 2	Homo sapiens	155-159
32509141-5	2020	Mechanistically, we showed that apatinib suppressed glutathione to generate ROS via the downregulation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway and maintained an antitumor effect at a low level of VEGFR2 in ovarian cancer, suggesting that combination of apatinib with Nrf2 inhibitor may be a promising therapy strategy for patients with ovarian cancer.	apatinib	32-40	heme oxygenase 1	Homo sapiens	161-177
32509141-5	2020	Mechanistically, we showed that apatinib suppressed glutathione to generate ROS via the downregulation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway and maintained an antitumor effect at a low level of VEGFR2 in ovarian cancer, suggesting that combination of apatinib with Nrf2 inhibitor may be a promising therapy strategy for patients with ovarian cancer.	apatinib	32-40	heme oxygenase 1	Homo sapiens	179-183
32509141-5	2020	Mechanistically, we showed that apatinib suppressed glutathione to generate ROS via the downregulation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway and maintained an antitumor effect at a low level of VEGFR2 in ovarian cancer, suggesting that combination of apatinib with Nrf2 inhibitor may be a promising therapy strategy for patients with ovarian cancer.	apatinib	32-40	kinase insert domain receptor	Homo sapiens	246-252
32509141-5	2020	Mechanistically, we showed that apatinib suppressed glutathione to generate ROS via the downregulation of the nuclear factor erythroid 2-related factor 2 (Nrf2)/heme oxygenase 1 (HO-1) pathway and maintained an antitumor effect at a low level of VEGFR2 in ovarian cancer, suggesting that combination of apatinib with Nrf2 inhibitor may be a promising therapy strategy for patients with ovarian cancer.	apatinib	32-40	NFE2 like bZIP transcription factor 2	Homo sapiens	317-321
31610827-1	2020	Apatinib, an oral small molecular receptor tyrosine kinase inhibitor (TKI) developed first in China, exerts antiangiogenic and antineoplastic function through selectively binding and inhibiting vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	194-239
32250517-3	2020	In this prospective clinical study, we aimed to evaluate the feasibility of single-agent apatinib, a vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor, as a treatment option for patients with ES-SCLC after failure of at least two prior chemotherapy regimens.	apatinib	89-97	kinase insert domain receptor	Homo sapiens	101-146
32390940-3	2020	In this reported case, the 125I seed implantation and vascular endothelial growth factor receptor-2 (VEGFR-2) inhibitor apatinib were co-applied to treat a 49-year-old woman with anaplastic thyroid cancer.	apatinib	120-128	kinase insert domain receptor	Homo sapiens	54-99
32390940-3	2020	In this reported case, the 125I seed implantation and vascular endothelial growth factor receptor-2 (VEGFR-2) inhibitor apatinib were co-applied to treat a 49-year-old woman with anaplastic thyroid cancer.	apatinib	120-128	kinase insert domain receptor	Homo sapiens	101-108
32209188-3	2020	Apatinib is a vascular endothelial growth factor receptor 2 inhibitor independently developed in China, which has a significant inhibition in a variety of solid tumors.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	14-59
32209188-10	2020	After combined with mTOR inhibitor CCI-779, low concentration of Apatinib could inhibit the proliferation and migration of NCI-H446 small cell lung cancer cells and induce apoptosis.	apatinib	65-73	mechanistic target of rapamycin kinase	Homo sapiens	20-24
32209188-13	2020	Apatinib combined with the mTOR inhibitor CCI-779 can sensitize the NCI-H446 cells to Apatinib.	apatinib	86-94	mechanistic target of rapamycin kinase	Homo sapiens	27-31
32351894-0	2020	Clinical Response to Apatinib Combined With Brain Radiotherapy in EGFR Wild-Type and ALK-Negative Lung Adenocarcinoma With Multiple Brain Metastases.	apatinib	21-29	epidermal growth factor receptor	Homo sapiens	66-70
32351894-0	2020	Clinical Response to Apatinib Combined With Brain Radiotherapy in EGFR Wild-Type and ALK-Negative Lung Adenocarcinoma With Multiple Brain Metastases.	apatinib	21-29	ALK receptor tyrosine kinase	Homo sapiens	85-88
32351894-3	2020	Apatinib is a potent antiangiogenic compound directed at the vascular endothelial growth factor receptor-2 (VEGFR-2); however, to date, there are no investigations of apatinib concurrent with brain radiotherapy for NSCLC patients with BMs.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	61-106
32351894-3	2020	Apatinib is a potent antiangiogenic compound directed at the vascular endothelial growth factor receptor-2 (VEGFR-2); however, to date, there are no investigations of apatinib concurrent with brain radiotherapy for NSCLC patients with BMs.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	108-115
32351894-4	2020	We report a case of EGFR wild-type and ALK-negative lung adenocarcinoma patient with multiple symptomatic BMs, who received apatinib together with brain radiation therapy.	apatinib	124-132	epidermal growth factor receptor	Homo sapiens	20-24
32351894-4	2020	We report a case of EGFR wild-type and ALK-negative lung adenocarcinoma patient with multiple symptomatic BMs, who received apatinib together with brain radiation therapy.	apatinib	124-132	ALK receptor tyrosine kinase	Homo sapiens	39-42
32126236-0	2020	Apatinib exhibits cytotoxicity toward leukemia cells by targeting VEGFR2-mediated prosurvival signaling and angiogenesis.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	66-72
32126236-3	2020	The aim of this study was to evaluate the efficacy of apatinib, a novel receptor tyrosine kinase inhibitor that selectively targets VEGFR2.	apatinib	54-62	kinase insert domain receptor	Homo sapiens	132-138
32126236-12	2020	Mechanistically, apatinib-induced cytotoxicity was closely associated with inhibition of the VEGFR2-mediated Src/STAT3 and AKT/mTOR pathways and induction of mitochondria-mediated apoptosis.	apatinib	17-25	kinase insert domain receptor	Homo sapiens	93-99
32126236-12	2020	Mechanistically, apatinib-induced cytotoxicity was closely associated with inhibition of the VEGFR2-mediated Src/STAT3 and AKT/mTOR pathways and induction of mitochondria-mediated apoptosis.	apatinib	17-25	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	109-112
32126236-12	2020	Mechanistically, apatinib-induced cytotoxicity was closely associated with inhibition of the VEGFR2-mediated Src/STAT3 and AKT/mTOR pathways and induction of mitochondria-mediated apoptosis.	apatinib	17-25	signal transducer and activator of transcription 3	Homo sapiens	113-118
32126236-12	2020	Mechanistically, apatinib-induced cytotoxicity was closely associated with inhibition of the VEGFR2-mediated Src/STAT3 and AKT/mTOR pathways and induction of mitochondria-mediated apoptosis.	apatinib	17-25	AKT serine/threonine kinase 1	Homo sapiens	123-126
32126236-12	2020	Mechanistically, apatinib-induced cytotoxicity was closely associated with inhibition of the VEGFR2-mediated Src/STAT3 and AKT/mTOR pathways and induction of mitochondria-mediated apoptosis.	apatinib	17-25	mechanistic target of rapamycin kinase	Homo sapiens	127-131
32126236-13	2020	CONCLUSION: Apatinib exerts antileukemia effects by targeting VEGFR2-induced prosurvival signaling and angiogenesis, thus providing a rationale for the application of apatinib in AML.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	62-68
32126236-13	2020	CONCLUSION: Apatinib exerts antileukemia effects by targeting VEGFR2-induced prosurvival signaling and angiogenesis, thus providing a rationale for the application of apatinib in AML.	apatinib	167-175	kinase insert domain receptor	Homo sapiens	62-68
32642151-0	2020	Combination of apatinib and docetaxel in treating advanced non-squamous non-small cell lung cancer patients with wild-type EGFR: a multi-center, phase II trial.	apatinib	15-23	epidermal growth factor receptor	Homo sapiens	123-127
32642151-1	2020	Background: This trial aimed to investigate the treatment response, survival profiles and treatment-related adverse events (AEs) of apatinib plus docetaxel in advanced non-squamous non-small cell lung cancer (NSCLC) patients with wild-type epidermal growth factor receptor (EGFR).	apatinib	132-140	epidermal growth factor receptor	Homo sapiens	240-272
32642151-11	2020	Conclusions: Apatinib plus docetaxel is an effective and tolerable treatment option for advanced non-squamous NSCLC with wild-type EGFR.	apatinib	13-21	epidermal growth factor receptor	Homo sapiens	131-135
32411765-3	2020	As a novel vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor (VEGFR2-TKI), apatinib has a certain antitumor effect for a variety of solid tumors.	apatinib	97-105	kinase insert domain receptor	Homo sapiens	84-90
31889475-8	2020	DHA was observed to enhance the antitumor and antiangiogenesis effects of apatinib via further downregulation of p-Akt expression.Abbreviations: FITC: fluorescein isothiocyanate; PI: propidium iodide.	apatinib	74-82	AKT serine/threonine kinase 1	Homo sapiens	115-118
32073228-4	2020	Apatinib is a specific VEGFR-2 inhibitor that blocks the transmission of the VEGF/VEGFR-2 signaling pathway.	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	23-30
32073228-4	2020	Apatinib is a specific VEGFR-2 inhibitor that blocks the transmission of the VEGF/VEGFR-2 signaling pathway.	apatinib	0-8	vascular endothelial growth factor A	Mus musculus	23-27
32073228-4	2020	Apatinib is a specific VEGFR-2 inhibitor that blocks the transmission of the VEGF/VEGFR-2 signaling pathway.	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	82-89
31476848-1	2020	PURPOSE: This study aimed to investigate the potential systemic antitumor effects of stereotactic ablative radiotherapy (SABR) and apatinib (a novel vascular endothelial growth factor receptor 2 inhibitor) via reversing the immunosuppressive tumor microenvironment for lung carcinoma.	apatinib	131-139	kinase insert domain protein receptor	Mus musculus	149-194
31231786-0	2020	A phase I dose-reduction study of apatinib combined with pemetrexed and carboplatin in untreated EGFR and ALK negative stage IV non-squamous NSCLC.	apatinib	34-42	epidermal growth factor receptor	Homo sapiens	97-101
31231786-0	2020	A phase I dose-reduction study of apatinib combined with pemetrexed and carboplatin in untreated EGFR and ALK negative stage IV non-squamous NSCLC.	apatinib	34-42	ALK receptor tyrosine kinase	Homo sapiens	106-109
31231786-2	2020	This phase I study aimed to establish the feasible dose of apatinib in combination with pemetrexed plus carboplatin as first-line therapy for epidermal growth factor receptor (EGFR) and anaplasticlymphoma kinase (ALK) negative stage IV non-squamous non-small cell lung cancer (NSCLC).	apatinib	59-67	epidermal growth factor receptor	Homo sapiens	142-174
31231786-2	2020	This phase I study aimed to establish the feasible dose of apatinib in combination with pemetrexed plus carboplatin as first-line therapy for epidermal growth factor receptor (EGFR) and anaplasticlymphoma kinase (ALK) negative stage IV non-squamous non-small cell lung cancer (NSCLC).	apatinib	59-67	epidermal growth factor receptor	Homo sapiens	176-180
31231786-2	2020	This phase I study aimed to establish the feasible dose of apatinib in combination with pemetrexed plus carboplatin as first-line therapy for epidermal growth factor receptor (EGFR) and anaplasticlymphoma kinase (ALK) negative stage IV non-squamous non-small cell lung cancer (NSCLC).	apatinib	59-67	ALK receptor tyrosine kinase	Homo sapiens	186-211
31231786-2	2020	This phase I study aimed to establish the feasible dose of apatinib in combination with pemetrexed plus carboplatin as first-line therapy for epidermal growth factor receptor (EGFR) and anaplasticlymphoma kinase (ALK) negative stage IV non-squamous non-small cell lung cancer (NSCLC).	apatinib	59-67	ALK receptor tyrosine kinase	Homo sapiens	213-216
31610827-1	2020	Apatinib, an oral small molecular receptor tyrosine kinase inhibitor (TKI) developed first in China, exerts antiangiogenic and antineoplastic function through selectively binding and inhibiting vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	241-248
31610827-9	2020	Compared with patients who received apatinib monotherapy, patients who received apatinib combination treatment had more favorable mPFS (11.77 vs. 2.27 months, P &lt; 0.05) and mOS (24.03 vs. 6.07 months, P &lt; 0.05).	apatinib	80-88	Moloney sarcoma oncogene	Mus musculus	176-179
32219060-0	2020	Apatinib Inhibits Cell Proliferation and Induces Autophagy in Human Papillary Thyroid Carcinoma via the PI3K/Akt/mTOR Signaling Pathway.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	109-112
32219060-0	2020	Apatinib Inhibits Cell Proliferation and Induces Autophagy in Human Papillary Thyroid Carcinoma via the PI3K/Akt/mTOR Signaling Pathway.	apatinib	0-8	mechanistic target of rapamycin kinase	Homo sapiens	113-117
32219060-3	2020	Apatinib, a novel small-molecule tyrosine kinase inhibitor (TKI), is highly selective for vascular endothelial growth factor receptor-2 (VEGFR2) and exhibits antitumor effects in a variety of solid tumors.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	90-135
32219060-3	2020	Apatinib, a novel small-molecule tyrosine kinase inhibitor (TKI), is highly selective for vascular endothelial growth factor receptor-2 (VEGFR2) and exhibits antitumor effects in a variety of solid tumors.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	137-143
32219060-10	2020	Results: We found that high VEGFR2 expression is associated with tumor size, T stage, and lymph node metastasis in patients with PTC and that apatinib inhibits PTC cell growth, promotes apoptosis, and induces cell cycle arrest through the PI3K/Akt/mTOR signaling pathway.	apatinib	142-150	AKT serine/threonine kinase 1	Homo sapiens	244-247
32219060-10	2020	Results: We found that high VEGFR2 expression is associated with tumor size, T stage, and lymph node metastasis in patients with PTC and that apatinib inhibits PTC cell growth, promotes apoptosis, and induces cell cycle arrest through the PI3K/Akt/mTOR signaling pathway.	apatinib	142-150	mechanistic target of rapamycin kinase	Homo sapiens	248-252
32219060-11	2020	Moreover, apatinib induces autophagy, and pharmacological inhibition of autophagy or small interfering RNA (siRNA)-mediated targeting of autophagy-associated gene 5 (ATG5) can further increase PTC cell apoptosis.	apatinib	10-18	autophagy related 5	Homo sapiens	166-170
32219060-12	2020	Conclusion: Our data suggest that apatinib can induce apoptosis and autophagy via the PI3K/Akt/mTOR signaling pathway for the treatment of PTC and that autophagy is a potential novel target for future therapy in resistant PTC.	apatinib	34-42	AKT serine/threonine kinase 1	Homo sapiens	91-94
32219060-12	2020	Conclusion: Our data suggest that apatinib can induce apoptosis and autophagy via the PI3K/Akt/mTOR signaling pathway for the treatment of PTC and that autophagy is a potential novel target for future therapy in resistant PTC.	apatinib	34-42	mechanistic target of rapamycin kinase	Homo sapiens	95-99
32139670-4	2020	In this study, we found that apatinib promoted autophagy activation via upregulation of ATG7 expression and autophagy inhibition enhanced apatinib-induced apoptosis.	apatinib	29-37	autophagy related 7	Homo sapiens	88-92
32139670-6	2020	Silencing of circRACGAP1 inhibited apatinib-induced autophagy, which was rescued by miR-3657.	apatinib	35-43	microRNA 3657	Homo sapiens	84-92
32139670-8	2020	These findings provided the first evidence that the circRACGAP1-miR-3657-ATG7 axis mediates a novel regulatory pathway critical for the regulation of apatinib sensitivity in GC.	apatinib	150-158	microRNA 3657	Homo sapiens	64-72
32139670-8	2020	These findings provided the first evidence that the circRACGAP1-miR-3657-ATG7 axis mediates a novel regulatory pathway critical for the regulation of apatinib sensitivity in GC.	apatinib	150-158	autophagy related 7	Homo sapiens	73-77
32266105-1	2020	Apatinib, a VEGFR2 receptor tyrosine kinase inhibitor, showed survival benefits in Asian patients with heavily pretreated advanced gastric cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	12-18
31786466-0	2020	Efficacy and safety of the VEGFR2 inhibitor Apatinib for metastatic soft tissue sarcoma: Chinese cohort data from NCT03121846.	apatinib	44-52	kinase insert domain receptor	Homo sapiens	27-33
31068089-1	2020	Apatinib is an orally administered small-molecule vascular endothelial growth factor receptor-2 inhibitor that has demonstrated encouraging anticancer activity across a broad range of malignancies, including gastric cancer, non-small-cell lung cancer, breast cancer, and hepatocellular carcinoma.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	50-95
32176061-1	2020	OBJECTIVE: Apatinib mesylate is a novel vascular endothelial growth factor receptor 2 (VEGFR-2) inhibitor, which has exhibited good safety and efficacy in several types of solid tumors.	apatinib	11-28	kinase insert domain receptor	Homo sapiens	40-85
32176061-1	2020	OBJECTIVE: Apatinib mesylate is a novel vascular endothelial growth factor receptor 2 (VEGFR-2) inhibitor, which has exhibited good safety and efficacy in several types of solid tumors.	apatinib	11-28	kinase insert domain receptor	Homo sapiens	87-94
31918452-0	2020	Clinical study of apatinib combined with EGFR-TKI in the treatment of chronic progression after EGFR-TKI treatment in non-small cell lung cancer (ChiCTR1800019185).	apatinib	18-26	epidermal growth factor receptor	Homo sapiens	96-100
32158235-6	2020	Conclusion: Apatinib is a single-drug regimen that can be used in cases of recurrence of fibrosarcoma with high expression of vascular endothelial growth factor receptor-2 (VEGFR-2); its short-term efficacy is excellent, and its side effects are minimal.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	126-171
32158235-6	2020	Conclusion: Apatinib is a single-drug regimen that can be used in cases of recurrence of fibrosarcoma with high expression of vascular endothelial growth factor receptor-2 (VEGFR-2); its short-term efficacy is excellent, and its side effects are minimal.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	173-180
32076049-6	2020	Further experiments showed that Apatinib inhibited tumor microangiogenesis to achieve the aims of inhibiting tumor growth and recurrence by means of down-regulating the phosphorylation of the RAF-mek-erk, PI3K-akt and P38MAPK pathways.	apatinib	32-40	zinc fingers and homeoboxes 2	Homo sapiens	192-195
32076049-6	2020	Further experiments showed that Apatinib inhibited tumor microangiogenesis to achieve the aims of inhibiting tumor growth and recurrence by means of down-regulating the phosphorylation of the RAF-mek-erk, PI3K-akt and P38MAPK pathways.	apatinib	32-40	mitogen-activated protein kinase kinase 7	Homo sapiens	196-199
32076049-6	2020	Further experiments showed that Apatinib inhibited tumor microangiogenesis to achieve the aims of inhibiting tumor growth and recurrence by means of down-regulating the phosphorylation of the RAF-mek-erk, PI3K-akt and P38MAPK pathways.	apatinib	32-40	mitogen-activated protein kinase 1	Homo sapiens	200-203
32076049-8	2020	Taken together, we concluded that Apatinib inhibits the angiogenesis and growth of liver cancer by down-regulating the PI3K-akt, RAF-mek-erk and P38MAPK pathways, and has a stronger inhibitory effect in hypoxic environments.	apatinib	34-42	zinc fingers and homeoboxes 2	Homo sapiens	129-132
32076049-8	2020	Taken together, we concluded that Apatinib inhibits the angiogenesis and growth of liver cancer by down-regulating the PI3K-akt, RAF-mek-erk and P38MAPK pathways, and has a stronger inhibitory effect in hypoxic environments.	apatinib	34-42	mitogen-activated protein kinase kinase 7	Homo sapiens	133-136
32076049-8	2020	Taken together, we concluded that Apatinib inhibits the angiogenesis and growth of liver cancer by down-regulating the PI3K-akt, RAF-mek-erk and P38MAPK pathways, and has a stronger inhibitory effect in hypoxic environments.	apatinib	34-42	mitogen-activated protein kinase 1	Homo sapiens	137-140
31786466-2	2020	This phase II study (NCT03121846) assessed the efficacy and safety of apatinib (YN968D1), a new tyrosine kinase inhibitor that targets VEGFR-2, for patients with stage IV STS after chemotherapy failure.	apatinib	70-78	kinase insert domain receptor	Homo sapiens	135-142
32210678-9	2020	In addition, apatinib was better than the blank group when treating AFP positive GC.	apatinib	13-21	alpha fetoprotein	Homo sapiens	68-71
32210678-12	2020	It is found that apatinib"s anti infection mechanism is to prevent the phosphorylation of vascular endothelial growth factor receptor-2 (VEGFR-2) as well as stop the downstream signal pathway, so as to inhibit the tumor angiogenesis, tumor growth and metastasis, so as to achieve treatment and reduce the probability of infection.	apatinib	17-25	kinase insert domain receptor	Homo sapiens	90-135
32210678-12	2020	It is found that apatinib"s anti infection mechanism is to prevent the phosphorylation of vascular endothelial growth factor receptor-2 (VEGFR-2) as well as stop the downstream signal pathway, so as to inhibit the tumor angiogenesis, tumor growth and metastasis, so as to achieve treatment and reduce the probability of infection.	apatinib	17-25	kinase insert domain receptor	Homo sapiens	137-144
32011517-10	2020	Second-line oral apatinib (425 mg daily) plus S-1 (60 mg, twice daily for 4 weeks with a 2-week drug-free interval) for a month showed efficacy, as shown by decreased serum neuron-specific enolase and stable of the esophageal lesion.	apatinib	17-25	enolase 2	Homo sapiens	173-196
32158186-2	2020	Apatinib is a new oral tyrosine kinase inhibitor mainly targeting vascular endothelial growth factor receptor-2 (VEGFR-2) to inhibit tumour angiogenesis.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	66-111
32158186-2	2020	Apatinib is a new oral tyrosine kinase inhibitor mainly targeting vascular endothelial growth factor receptor-2 (VEGFR-2) to inhibit tumour angiogenesis.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	113-120
32021302-14	2020	Conclusion: The clinical outcomes of treatment with apatinib mesylate for advanced non-squamous NSCLC in patients who progressed after standard therapy may be influenced by the KDR 4397T>C polymorphism through mediation of the mRNA expression of KDR.	apatinib	52-69	kinase insert domain receptor	Homo sapiens	177-180
32021302-14	2020	Conclusion: The clinical outcomes of treatment with apatinib mesylate for advanced non-squamous NSCLC in patients who progressed after standard therapy may be influenced by the KDR 4397T>C polymorphism through mediation of the mRNA expression of KDR.	apatinib	52-69	kinase insert domain receptor	Homo sapiens	246-249
31786193-3	2020	In this regard, Apatinib or YN968D1, a specific inhibitor of VEGFR-2 has been suggested as a promising therapeutic agent for cancer that can prevent tumor angiogenesis and metastasis.	apatinib	16-24	kinase insert domain receptor	Homo sapiens	61-68
31668370-10	2020	The results of this study suggested that Apa/p NPs could inhibit the growth of melanoma tumors by inhibiting the phosphorylation and expression of VEGFR-2 and downstream ERK1/2, providing a theoretical basis for the clinical application of Apatinib in the treatment of melanoma.	apatinib	240-248	glutamyl aminopeptidase	Mus musculus	41-44
31668370-10	2020	The results of this study suggested that Apa/p NPs could inhibit the growth of melanoma tumors by inhibiting the phosphorylation and expression of VEGFR-2 and downstream ERK1/2, providing a theoretical basis for the clinical application of Apatinib in the treatment of melanoma.	apatinib	240-248	kinase insert domain protein receptor	Mus musculus	147-154
31668370-10	2020	The results of this study suggested that Apa/p NPs could inhibit the growth of melanoma tumors by inhibiting the phosphorylation and expression of VEGFR-2 and downstream ERK1/2, providing a theoretical basis for the clinical application of Apatinib in the treatment of melanoma.	apatinib	240-248	mitogen-activated protein kinase 3	Mus musculus	170-176
32021426-1	2020	Aim: Apatinib, a specific tyrosine kinase inhibitor (TKI) that targets mainly vascular endothelial growth factor receptor-2 (VEGFR-2) as well as Ret, c-Kit and c-Src, has been assessed in patients with advanced osteosarcoma (phase II), the primary report of which has been published in PMID 30559126.	apatinib	5-13	kinase insert domain receptor	Homo sapiens	78-123
32021426-1	2020	Aim: Apatinib, a specific tyrosine kinase inhibitor (TKI) that targets mainly vascular endothelial growth factor receptor-2 (VEGFR-2) as well as Ret, c-Kit and c-Src, has been assessed in patients with advanced osteosarcoma (phase II), the primary report of which has been published in PMID 30559126.	apatinib	5-13	kinase insert domain receptor	Homo sapiens	125-132
32129295-2	2020	The aim of this study was to evaluate apatinib, a VEGFR-2 inhibitor, as monotherapy in elderly patients with advanced metastatic NSCLC.	apatinib	38-46	kinase insert domain receptor	Homo sapiens	50-57
33045704-1	2020	PURPOSE: As a small-molecule tyrosine kinase inhibitor of vascular endothelial growth factor receptor 2 (VEGFR2), apatinib has shown a survival benefit in multiple solid tumors.	apatinib	114-122	kinase insert domain receptor	Homo sapiens	58-103
33045704-1	2020	PURPOSE: As a small-molecule tyrosine kinase inhibitor of vascular endothelial growth factor receptor 2 (VEGFR2), apatinib has shown a survival benefit in multiple solid tumors.	apatinib	114-122	kinase insert domain receptor	Homo sapiens	105-111
32924793-10	2020	Further experiments found that apatinib treatment, a potent inhibitor of KDR, resulted in profound inhibition of cell proliferation and invasion.	apatinib	31-39	kinase insert domain receptor	Homo sapiens	73-76
31884511-13	2019	The relevant SOCS genes silencing reversed the effects of miR-106a-3p inhibitor on decreasing the apatinib resistance of SGC-7901-AP cells, while the phosphorylation level of JAK and STAT reduced by miR-106a-3p inhibitor were increased.	apatinib	98-106	cytokine inducible SH2 containing protein	Homo sapiens	13-17
31884511-13	2019	The relevant SOCS genes silencing reversed the effects of miR-106a-3p inhibitor on decreasing the apatinib resistance of SGC-7901-AP cells, while the phosphorylation level of JAK and STAT reduced by miR-106a-3p inhibitor were increased.	apatinib	98-106	Janus kinase 2	Homo sapiens	175-178
31884511-15	2019	miR-106a-3p/SOCS plays a potent role in gastric cancer cell resistance to apatinib.	apatinib	74-82	cytokine inducible SH2 containing protein	Homo sapiens	12-16
31956604-4	2019	Subsequently, the patient received apatinib that selectively inhibits the VEGFR2 and obtained an evident tumor response and a PFS of 8 months.	apatinib	35-43	kinase insert domain receptor	Homo sapiens	74-80
31558974-11	2019	In phase III clinical trials, only ramucirumab (anti-VEGFR blocker) and apatinib (VEGFR-TKI blocker) have reported an improved median overall response rate and prolonged OS and progression-free survival outcomes as a 2nd-line agent combined with chemotherapy treatment in advanced GC.	apatinib	72-80	kinase insert domain receptor	Homo sapiens	82-87
31699150-0	2019	The ACTIVE study protocol: apatinib or placebo plus gefitinib as first-line treatment for patients with EGFR-mutant advanced non-small cell lung cancer (CTONG1706).	apatinib	27-35	epidermal growth factor receptor	Homo sapiens	104-108
31699150-2	2019	Apatinib (YN968D1), a potent vascular endothelial growth factor receptor (VEGFR) 2-TKI, specifically binds to VEGFR2 and leads to anti-angiogenetic and anti-neoplastic effect.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	29-72
31699150-2	2019	Apatinib (YN968D1), a potent vascular endothelial growth factor receptor (VEGFR) 2-TKI, specifically binds to VEGFR2 and leads to anti-angiogenetic and anti-neoplastic effect.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	74-79
31699150-2	2019	Apatinib (YN968D1), a potent vascular endothelial growth factor receptor (VEGFR) 2-TKI, specifically binds to VEGFR2 and leads to anti-angiogenetic and anti-neoplastic effect.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	110-116
31699150-2	2019	Apatinib (YN968D1), a potent vascular endothelial growth factor receptor (VEGFR) 2-TKI, specifically binds to VEGFR2 and leads to anti-angiogenetic and anti-neoplastic effect.	apatinib	10-17	kinase insert domain receptor	Homo sapiens	29-72
31699150-2	2019	Apatinib (YN968D1), a potent vascular endothelial growth factor receptor (VEGFR) 2-TKI, specifically binds to VEGFR2 and leads to anti-angiogenetic and anti-neoplastic effect.	apatinib	10-17	kinase insert domain receptor	Homo sapiens	74-79
31699150-2	2019	Apatinib (YN968D1), a potent vascular endothelial growth factor receptor (VEGFR) 2-TKI, specifically binds to VEGFR2 and leads to anti-angiogenetic and anti-neoplastic effect.	apatinib	10-17	kinase insert domain receptor	Homo sapiens	110-116
31699150-4	2019	This ACTIVE study aims to assess the combination of apatinib and gefitinib as a new treatment approach for EGFR-mutant NSCLC as a first-line setting.	apatinib	52-60	epidermal growth factor receptor	Homo sapiens	107-111
31699150-16	2019	ANTICIPATED OUTCOMES AND SIGNIFICANCE: The present study will be the first to evaluate the efficacy and safety profile of the combination of apatinib plus gefitinib as a first-line therapy for patients with EGFR-positive advanced non-squamous NSCLC.	apatinib	141-149	epidermal growth factor receptor	Homo sapiens	207-211
31805975-0	2019	Treatment of consistent BRAF/HRAS gene mutation and MYC amplification radiation-induced abdominal wall angiosarcoma with low-dose apatinib: a case report.	apatinib	130-138	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	24-28
31805975-0	2019	Treatment of consistent BRAF/HRAS gene mutation and MYC amplification radiation-induced abdominal wall angiosarcoma with low-dose apatinib: a case report.	apatinib	130-138	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	52-55
31819530-1	2019	Preclinical studies have demonstrated that Apatinib, major targeting vascular endothelial growth factor receptor-2 (VEGFR-2), could inhibit the proliferation of anaplastic thyroid carcinoma (ATC) cells in vitro and in vivo.	apatinib	43-51	kinase insert domain receptor	Homo sapiens	69-114
31819530-1	2019	Preclinical studies have demonstrated that Apatinib, major targeting vascular endothelial growth factor receptor-2 (VEGFR-2), could inhibit the proliferation of anaplastic thyroid carcinoma (ATC) cells in vitro and in vivo.	apatinib	43-51	kinase insert domain receptor	Homo sapiens	116-123
31861000-1	2019	RATIONALE: Apatinib is an oral tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor-2.	apatinib	11-19	kinase insert domain receptor	Homo sapiens	67-112
31876714-0	2019	Anaplastic lymphoma kinase-negative pulmonary inflammatory myofibroblastic tumor with multiple metastases and its treatment by Apatinib: A case report.	apatinib	127-135	ALK receptor tyrosine kinase	Homo sapiens	0-26
31876714-14	2019	Apatinib is effective for pulmonary IMT, and should be taken into consideration for the treatment of inoperable pulmonary IMT patients who lack ALK rearrangement.	apatinib	0-8	ALK receptor tyrosine kinase	Homo sapiens	144-147
31694662-0	2019	Apatinib potentiates irradiation effect via suppressing PI3K/AKT signaling pathway in hepatocellular carcinoma.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	61-64
31694662-2	2019	This study aimed to investigate the potential clinical utility of apatinib, a highly selective inhibitor of the vascular endothelial growth factor receptor-2 (VEGFR2) tyrosine kinase, as a radiosensitizer in the treatment of HCC.	apatinib	66-74	kinase insert domain receptor	Homo sapiens	112-157
31694662-2	2019	This study aimed to investigate the potential clinical utility of apatinib, a highly selective inhibitor of the vascular endothelial growth factor receptor-2 (VEGFR2) tyrosine kinase, as a radiosensitizer in the treatment of HCC.	apatinib	66-74	kinase insert domain receptor	Homo sapiens	159-165
31694662-10	2019	Apatinib radiosensitized HCC via suppression of radiation-induced PI3K/AKT pathway.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	71-74
31694662-12	2019	CONCLUSIONS: Our results indicate that apatinib has therapeutic potential as a radiosensitizer in HCC, and PI3K/AKT signaling pathway plays a critical role in mediating radiosensitization of apatinib.	apatinib	191-199	AKT serine/threonine kinase 1	Homo sapiens	112-115
31264262-2	2019	Apatinib is a highly selective and potent antiangiogenesis drug targeting the receptor of VEGFR2, blocking downstream signal transduction and inhibiting angiogenesis of tumor tissue.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	90-96
31570440-0	2019	Apatinib Reverses Paclitaxel-resistant Lung Cancer Cells (A549) Through Blocking the Function of ABCB1 Transporter.	apatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	97-102
31570440-2	2019	Apatinib is a novel Vascular endothelial growth factor receptor-TKI (VEGFR-TKI) which inhibits the function of ABCB1 in certain cancers.	apatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	111-116
31570440-12	2019	Apatinib-PTX combination inhibited AKT and ERK pathways.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	35-38
31570440-12	2019	Apatinib-PTX combination inhibited AKT and ERK pathways.	apatinib	0-8	mitogen-activated protein kinase 1	Homo sapiens	43-46
31570440-13	2019	CONCLUSION: Apatinib reverses the drug resistance to PTX in A549 PTX-resistant cells through inhibiting the function of ABCB1 and resumes anti-cancer effects.	apatinib	12-20	ATP binding cassette subfamily B member 1	Homo sapiens	120-125
31570442-2	2019	Rivoceranib (also known as apatinib) is a novel anti-angiogenic tyrosine kinase inhibitor that selectively binds to vascular endothelial growth factor receptor-2 (VEGFR2).	apatinib	0-11	kinase insert domain receptor	Canis lupus familiaris	116-161
31570442-2	2019	Rivoceranib (also known as apatinib) is a novel anti-angiogenic tyrosine kinase inhibitor that selectively binds to vascular endothelial growth factor receptor-2 (VEGFR2).	apatinib	0-11	kinase insert domain receptor	Canis lupus familiaris	163-169
31570442-2	2019	Rivoceranib (also known as apatinib) is a novel anti-angiogenic tyrosine kinase inhibitor that selectively binds to vascular endothelial growth factor receptor-2 (VEGFR2).	apatinib	27-35	kinase insert domain receptor	Canis lupus familiaris	116-161
31570442-2	2019	Rivoceranib (also known as apatinib) is a novel anti-angiogenic tyrosine kinase inhibitor that selectively binds to vascular endothelial growth factor receptor-2 (VEGFR2).	apatinib	27-35	kinase insert domain receptor	Canis lupus familiaris	163-169
31570442-9	2019	Rivoceranib reduced the level of phosphorylated VEGFR2.	apatinib	0-11	kinase insert domain receptor	Canis lupus familiaris	48-54
31523058-2	2019	Apatinib is a small-molecule tyrosine kinase inhibitor that selectively inhibits vascular endothelial growth factor receptor-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	81-126
31429167-0	2019	Apatinib induces 3-hydroxybutyric acid production in the liver of mice by peroxisome proliferator-activated receptor alpha activation to aid its antitumor effect.	apatinib	0-8	peroxisome proliferator activated receptor alpha	Mus musculus	74-122
31429167-7	2019	Gene expression, dual luciferase reporter gene assay and molecular docking analysis all indicated that apatinib could induce 3-HB production through the dependent activation of peroxisome proliferator-activated receptor alpha (PPARalpha) and promotion of fatty acid utilization in the liver.	apatinib	103-111	peroxisome proliferator activated receptor alpha	Mus musculus	177-225
31429167-7	2019	Gene expression, dual luciferase reporter gene assay and molecular docking analysis all indicated that apatinib could induce 3-HB production through the dependent activation of peroxisome proliferator-activated receptor alpha (PPARalpha) and promotion of fatty acid utilization in the liver.	apatinib	103-111	peroxisome proliferator activated receptor alpha	Mus musculus	227-236
31429167-8	2019	Therefore, increased content of 3-HB induced by PPARalpha activation in the liver partially contributed to the antitumor effect of apatinib.	apatinib	131-139	peroxisome proliferator activated receptor alpha	Mus musculus	48-57
31429167-9	2019	It may provide clues to another potential mechanism underlying the antitumor effect of apatinib besides its antiangiogenic effect through inhibiting vascular endothelial growth factor receptor 2.	apatinib	87-95	kinase insert domain protein receptor	Mus musculus	149-194
31325096-0	2019	Apatinib inhibits glycolysis by suppressing the VEGFR2/AKT1/SOX5/GLUT4 signaling pathway in ovarian cancer cells.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	48-54
31325096-0	2019	Apatinib inhibits glycolysis by suppressing the VEGFR2/AKT1/SOX5/GLUT4 signaling pathway in ovarian cancer cells.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	55-59
31325096-0	2019	Apatinib inhibits glycolysis by suppressing the VEGFR2/AKT1/SOX5/GLUT4 signaling pathway in ovarian cancer cells.	apatinib	0-8	SRY-box transcription factor 5	Homo sapiens	60-64
31325096-0	2019	Apatinib inhibits glycolysis by suppressing the VEGFR2/AKT1/SOX5/GLUT4 signaling pathway in ovarian cancer cells.	apatinib	0-8	solute carrier family 2 member 4	Homo sapiens	65-70
31325096-1	2019	BACKGROUND: Apatinib is a tyrosine kinase inhibitor that targets vascular endothelial growth factor receptor-2 (VEGFR2), and has shown encouraging therapeutic effects in various malignant tumors.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	65-110
31325096-1	2019	BACKGROUND: Apatinib is a tyrosine kinase inhibitor that targets vascular endothelial growth factor receptor-2 (VEGFR2), and has shown encouraging therapeutic effects in various malignant tumors.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	112-118
31325096-11	2019	We also found that apatinib effectively suppressed glucose uptake and lactate production by blocking the expression of GLUT4 in these cells.	apatinib	19-27	solute carrier family 2 member 4	Homo sapiens	119-124
31325096-12	2019	In addition, we found that SOX5 predominantly rescued the inhibitory effect of apatinib on GLUT4 expression by activating its promoter.	apatinib	79-87	SRY-box transcription factor 5	Homo sapiens	27-31
31325096-12	2019	In addition, we found that SOX5 predominantly rescued the inhibitory effect of apatinib on GLUT4 expression by activating its promoter.	apatinib	79-87	solute carrier family 2 member 4	Homo sapiens	91-96
31325096-13	2019	Finally, we found that apatinib regulated the expression of SOX5 by suppressing the VEGFR2/AKT1/GSK3beta signaling pathway.	apatinib	23-31	SRY-box transcription factor 5	Homo sapiens	60-64
31325096-13	2019	Finally, we found that apatinib regulated the expression of SOX5 by suppressing the VEGFR2/AKT1/GSK3beta signaling pathway.	apatinib	23-31	kinase insert domain receptor	Homo sapiens	84-90
31325096-13	2019	Finally, we found that apatinib regulated the expression of SOX5 by suppressing the VEGFR2/AKT1/GSK3beta signaling pathway.	apatinib	23-31	AKT serine/threonine kinase 1	Homo sapiens	91-95
31325096-13	2019	Finally, we found that apatinib regulated the expression of SOX5 by suppressing the VEGFR2/AKT1/GSK3beta signaling pathway.	apatinib	23-31	glycogen synthase kinase 3 alpha	Homo sapiens	96-104
31325096-14	2019	CONCLUSIONS: From our results, we conclude that apatinib suppresses the in vitro and in vivo viability and proliferation of ovarian cancer cells, as well as glycolysis by inhibiting the VEGFR2/AKT1/GSK3beta/SOX5/GLUT4 signaling pathway.	apatinib	48-56	kinase insert domain receptor	Homo sapiens	186-192
31325096-14	2019	CONCLUSIONS: From our results, we conclude that apatinib suppresses the in vitro and in vivo viability and proliferation of ovarian cancer cells, as well as glycolysis by inhibiting the VEGFR2/AKT1/GSK3beta/SOX5/GLUT4 signaling pathway.	apatinib	48-56	AKT serine/threonine kinase 1	Homo sapiens	193-197
31325096-14	2019	CONCLUSIONS: From our results, we conclude that apatinib suppresses the in vitro and in vivo viability and proliferation of ovarian cancer cells, as well as glycolysis by inhibiting the VEGFR2/AKT1/GSK3beta/SOX5/GLUT4 signaling pathway.	apatinib	48-56	glycogen synthase kinase 3 alpha	Homo sapiens	198-206
31325096-14	2019	CONCLUSIONS: From our results, we conclude that apatinib suppresses the in vitro and in vivo viability and proliferation of ovarian cancer cells, as well as glycolysis by inhibiting the VEGFR2/AKT1/GSK3beta/SOX5/GLUT4 signaling pathway.	apatinib	48-56	SRY-box transcription factor 5	Homo sapiens	207-211
31325096-14	2019	CONCLUSIONS: From our results, we conclude that apatinib suppresses the in vitro and in vivo viability and proliferation of ovarian cancer cells, as well as glycolysis by inhibiting the VEGFR2/AKT1/GSK3beta/SOX5/GLUT4 signaling pathway.	apatinib	48-56	solute carrier family 2 member 4	Homo sapiens	212-217
31486270-2	2019	Apatinib is a tyrosine kinase inhibitor which selectivelyacts on vascular endothelial growth factor receptor 2 (VEGFR-2) and has shown good efficacy in a variety of malignancies, but the drug resistance is fast in single drug therapy.	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	65-110
31486270-2	2019	Apatinib is a tyrosine kinase inhibitor which selectivelyacts on vascular endothelial growth factor receptor 2 (VEGFR-2) and has shown good efficacy in a variety of malignancies, but the drug resistance is fast in single drug therapy.	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	112-119
31486270-4	2019	To establish a nude mouse xenograft model, observe the inhibitory effect of apatinib combined with other drugs on lung cancer xenografts in nude mice; immunohistochemical staining of tumor microvessel density and Ki67 expression in transplanted tumor tissues; Western blot analysis of related signaling pathways expression; immunohistochemistry was used to detect tumor microvessel density in other organs and to observe its safety.	apatinib	76-84	antigen identified by monoclonal antibody Ki 67	Mus musculus	213-217
31486270-5	2019	RESULTS: In this study, we found apatinib combined with pemetrexed, the first and third generation of epidermal growth factor receptor tyrosine kinase inhibitor, could synergistically inhibit the proliferation of non-small cell lung cancer cell (NSCLC) lines, reduce the microvessel density and Ki67 protein levels of three non-small cell lung cancer xenografts, and enhance anti-tumor activity by synergistically inhibiting the MAPK-ERK and PI3K-AKT-mTOR signaling pathway.	apatinib	33-41	antigen identified by monoclonal antibody Ki 67	Mus musculus	295-299
31486270-5	2019	RESULTS: In this study, we found apatinib combined with pemetrexed, the first and third generation of epidermal growth factor receptor tyrosine kinase inhibitor, could synergistically inhibit the proliferation of non-small cell lung cancer cell (NSCLC) lines, reduce the microvessel density and Ki67 protein levels of three non-small cell lung cancer xenografts, and enhance anti-tumor activity by synergistically inhibiting the MAPK-ERK and PI3K-AKT-mTOR signaling pathway.	apatinib	33-41	mitogen-activated protein kinase 1	Mus musculus	434-437
31486270-5	2019	RESULTS: In this study, we found apatinib combined with pemetrexed, the first and third generation of epidermal growth factor receptor tyrosine kinase inhibitor, could synergistically inhibit the proliferation of non-small cell lung cancer cell (NSCLC) lines, reduce the microvessel density and Ki67 protein levels of three non-small cell lung cancer xenografts, and enhance anti-tumor activity by synergistically inhibiting the MAPK-ERK and PI3K-AKT-mTOR signaling pathway.	apatinib	33-41	thymoma viral proto-oncogene 1	Mus musculus	447-450
31486270-5	2019	RESULTS: In this study, we found apatinib combined with pemetrexed, the first and third generation of epidermal growth factor receptor tyrosine kinase inhibitor, could synergistically inhibit the proliferation of non-small cell lung cancer cell (NSCLC) lines, reduce the microvessel density and Ki67 protein levels of three non-small cell lung cancer xenografts, and enhance anti-tumor activity by synergistically inhibiting the MAPK-ERK and PI3K-AKT-mTOR signaling pathway.	apatinib	33-41	mechanistic target of rapamycin kinase	Mus musculus	451-455
31570733-0	2019	Apatinib Mesylate in the treatment of advanced progressed lung adenocarcinoma patients with EGFR-TKI resistance -A Multicenter Randomized Trial.	apatinib	0-17	epidermal growth factor receptor	Homo sapiens	92-96
31570733-1	2019	Few pieces of evidence have been published on the use of Apatinib Mesylate (AM) against EGFR-TKI resistance in lung adenocarcinoma (LA) patients.	apatinib	57-74	epidermal growth factor receptor	Homo sapiens	88-92
31451841-1	2019	BACKGROUND: The lethal effects of multiple antigen-specific cellular therapy (MASCT) may be enhanced by blocking PD-1 in vitro and vascular endothelial growth factor receptor 2 inhibitor (apatinib).	apatinib	188-196	kinase insert domain receptor	Homo sapiens	131-176
31786865-0	2019	Apatinib suppresses the Proliferation and Apoptosis of Gastric Cancer Cells via the PI3K/Akt Signaling Pathway.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	89-92
31786865-1	2019	PURPOSE: To observe the mechanism of the effects of Apatinib on the proliferation and apoptosis of human gastric cancer (HGC-27) cells via the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway through in vitro cytology experiments.	apatinib	52-60	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	143-172
31786865-1	2019	PURPOSE: To observe the mechanism of the effects of Apatinib on the proliferation and apoptosis of human gastric cancer (HGC-27) cells via the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway through in vitro cytology experiments.	apatinib	52-60	AKT serine/threonine kinase 1	Homo sapiens	198-201
31786865-3	2019	The experimental methods are as follows: (1) The proliferation of HGC-27 cells inhibited by Apatinib and LY294002 was observed by 3-(4,5)-dimethylthiahiazo-(z-y1)-3,5-diphenytetrazoli- umromide (MTT) assay; (2) flow cytometry was adopted to detect the apoptosis of cells after they were treated with drugs and the positive control; (3) different effects of varying concentrations of Apatinib on apoptosis-related genes and proteins, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and cysteine-aspartic acid protease (Caspase) 9, were detected via fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting (WB), and the effects of different concentrations of Apatinib on the protein expressions of PI3K, phosphorylated (p)-PI3K, Akt and p-Akt were detected by Western blotting.	apatinib	92-100	BCL2 apoptosis regulator	Homo sapiens	433-450
31786865-3	2019	The experimental methods are as follows: (1) The proliferation of HGC-27 cells inhibited by Apatinib and LY294002 was observed by 3-(4,5)-dimethylthiahiazo-(z-y1)-3,5-diphenytetrazoli- umromide (MTT) assay; (2) flow cytometry was adopted to detect the apoptosis of cells after they were treated with drugs and the positive control; (3) different effects of varying concentrations of Apatinib on apoptosis-related genes and proteins, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and cysteine-aspartic acid protease (Caspase) 9, were detected via fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting (WB), and the effects of different concentrations of Apatinib on the protein expressions of PI3K, phosphorylated (p)-PI3K, Akt and p-Akt were detected by Western blotting.	apatinib	92-100	BCL2 apoptosis regulator	Homo sapiens	452-457
31786865-3	2019	The experimental methods are as follows: (1) The proliferation of HGC-27 cells inhibited by Apatinib and LY294002 was observed by 3-(4,5)-dimethylthiahiazo-(z-y1)-3,5-diphenytetrazoli- umromide (MTT) assay; (2) flow cytometry was adopted to detect the apoptosis of cells after they were treated with drugs and the positive control; (3) different effects of varying concentrations of Apatinib on apoptosis-related genes and proteins, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and cysteine-aspartic acid protease (Caspase) 9, were detected via fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting (WB), and the effects of different concentrations of Apatinib on the protein expressions of PI3K, phosphorylated (p)-PI3K, Akt and p-Akt were detected by Western blotting.	apatinib	92-100	BCL2 associated X, apoptosis regulator	Homo sapiens	460-486
31786865-3	2019	The experimental methods are as follows: (1) The proliferation of HGC-27 cells inhibited by Apatinib and LY294002 was observed by 3-(4,5)-dimethylthiahiazo-(z-y1)-3,5-diphenytetrazoli- umromide (MTT) assay; (2) flow cytometry was adopted to detect the apoptosis of cells after they were treated with drugs and the positive control; (3) different effects of varying concentrations of Apatinib on apoptosis-related genes and proteins, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and cysteine-aspartic acid protease (Caspase) 9, were detected via fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting (WB), and the effects of different concentrations of Apatinib on the protein expressions of PI3K, phosphorylated (p)-PI3K, Akt and p-Akt were detected by Western blotting.	apatinib	92-100	BCL2 associated X, apoptosis regulator	Homo sapiens	488-491
31786865-3	2019	The experimental methods are as follows: (1) The proliferation of HGC-27 cells inhibited by Apatinib and LY294002 was observed by 3-(4,5)-dimethylthiahiazo-(z-y1)-3,5-diphenytetrazoli- umromide (MTT) assay; (2) flow cytometry was adopted to detect the apoptosis of cells after they were treated with drugs and the positive control; (3) different effects of varying concentrations of Apatinib on apoptosis-related genes and proteins, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and cysteine-aspartic acid protease (Caspase) 9, were detected via fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting (WB), and the effects of different concentrations of Apatinib on the protein expressions of PI3K, phosphorylated (p)-PI3K, Akt and p-Akt were detected by Western blotting.	apatinib	92-100	caspase 9	Homo sapiens	530-540
31786865-3	2019	The experimental methods are as follows: (1) The proliferation of HGC-27 cells inhibited by Apatinib and LY294002 was observed by 3-(4,5)-dimethylthiahiazo-(z-y1)-3,5-diphenytetrazoli- umromide (MTT) assay; (2) flow cytometry was adopted to detect the apoptosis of cells after they were treated with drugs and the positive control; (3) different effects of varying concentrations of Apatinib on apoptosis-related genes and proteins, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and cysteine-aspartic acid protease (Caspase) 9, were detected via fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting (WB), and the effects of different concentrations of Apatinib on the protein expressions of PI3K, phosphorylated (p)-PI3K, Akt and p-Akt were detected by Western blotting.	apatinib	92-100	AKT serine/threonine kinase 1	Homo sapiens	788-791
31786865-3	2019	The experimental methods are as follows: (1) The proliferation of HGC-27 cells inhibited by Apatinib and LY294002 was observed by 3-(4,5)-dimethylthiahiazo-(z-y1)-3,5-diphenytetrazoli- umromide (MTT) assay; (2) flow cytometry was adopted to detect the apoptosis of cells after they were treated with drugs and the positive control; (3) different effects of varying concentrations of Apatinib on apoptosis-related genes and proteins, B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X protein (Bax) and cysteine-aspartic acid protease (Caspase) 9, were detected via fluorescence quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and Western blotting (WB), and the effects of different concentrations of Apatinib on the protein expressions of PI3K, phosphorylated (p)-PI3K, Akt and p-Akt were detected by Western blotting.	apatinib	92-100	AKT serine/threonine kinase 1	Homo sapiens	798-801
31786865-6	2019	(3) The results of qRT-PCR and Western blotting demonstrated that apatinib was capable of inducing the expression of the pro-apoptotic genes, Bax and Caspase 9, and inhibit the expression of the anti-apoptotic gene Bcl-2.	apatinib	66-74	BCL2 associated X, apoptosis regulator	Homo sapiens	142-145
31786865-6	2019	(3) The results of qRT-PCR and Western blotting demonstrated that apatinib was capable of inducing the expression of the pro-apoptotic genes, Bax and Caspase 9, and inhibit the expression of the anti-apoptotic gene Bcl-2.	apatinib	66-74	caspase 9	Homo sapiens	150-159
31786865-6	2019	(3) The results of qRT-PCR and Western blotting demonstrated that apatinib was capable of inducing the expression of the pro-apoptotic genes, Bax and Caspase 9, and inhibit the expression of the anti-apoptotic gene Bcl-2.	apatinib	66-74	BCL2 apoptosis regulator	Homo sapiens	215-220
31786865-7	2019	The final results of Western blotting confirmed that Apatinib could decrease the protein expression levels of p-PI3K and p-Akt, thus inhibiting the phosphorylation of the PI3K/Akt pathway.	apatinib	53-61	AKT serine/threonine kinase 1	Homo sapiens	123-126
31786865-7	2019	The final results of Western blotting confirmed that Apatinib could decrease the protein expression levels of p-PI3K and p-Akt, thus inhibiting the phosphorylation of the PI3K/Akt pathway.	apatinib	53-61	AKT serine/threonine kinase 1	Homo sapiens	176-179
31786865-8	2019	CONCLUSIONS: The experiment proves that Apatinib can effectively suppress the proliferation and induce the apoptosis of human gastric cancer HGC-27 cells, the mechanism of which is related to the inhibition on phosphorylation of the PI3K/Akt signaling pathway.	apatinib	40-48	AKT serine/threonine kinase 1	Homo sapiens	238-241
31496821-2	2019	Several small-molecule anti-VEGFR tyrosine kinase inhibitors (TKIs), such as regorafenib, famitinib, axitinib and apatinib, have been shown to be effective in treating metastatic colorectal cancer (mCRC).	apatinib	114-122	kinase insert domain receptor	Homo sapiens	28-33
31305297-3	2019	The aim of this study was to evaluate the efficacy and safety of apatinib, an oral vascular endothelial growth factor receptor-2 inhibitor, as salvage treatment for advanced bone and soft tissue sarcomas.	apatinib	65-73	kinase insert domain receptor	Homo sapiens	83-128
32440509-0	2020	Apatinib ameliorates doxorubicin-induced migration and cancer stemness of osteosarcoma cells by inhibiting Sox2 via STAT3 signalling.	apatinib	0-8	SRY-box transcription factor 2	Homo sapiens	107-111
32440509-0	2020	Apatinib ameliorates doxorubicin-induced migration and cancer stemness of osteosarcoma cells by inhibiting Sox2 via STAT3 signalling.	apatinib	0-8	signal transducer and activator of transcription 3	Homo sapiens	116-121
32440509-16	2020	Apatinib can reduce the Doxorubicin-induced chemoresistance through STAT3/Sox2 pathway inactivation.	apatinib	0-8	signal transducer and activator of transcription 3	Homo sapiens	68-73
32440509-16	2020	Apatinib can reduce the Doxorubicin-induced chemoresistance through STAT3/Sox2 pathway inactivation.	apatinib	0-8	SRY-box transcription factor 2	Homo sapiens	74-78
31111678-3	2019	Additionally, apatinib, a selective VEGFR-2 tyrosine kinase inhibitor, prolonged survival as a third-line or later treatment option in patients with advanced gastric cancer.	apatinib	14-22	kinase insert domain receptor	Homo sapiens	36-43
31072433-4	2019	Apatinib is a novel small molecular VEGFR-2 tyrosine kinase targeted drug with poor water-solubility, showing anti-tumor ability in some solid tumors.	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	36-43
31555522-13	2019	Under hypoxic conditions, apatinib could not inhibit the protein expression of VEGFR and HIF-alpha in both cell lines; however, apatinib decreased the expression of cyclin D1 and P53 significantly.	apatinib	128-136	cyclin D1	Homo sapiens	165-174
31555522-13	2019	Under hypoxic conditions, apatinib could not inhibit the protein expression of VEGFR and HIF-alpha in both cell lines; however, apatinib decreased the expression of cyclin D1 and P53 significantly.	apatinib	128-136	tumor protein p53	Homo sapiens	179-182
30559126-2	2019	Methylsulfonic apatinib is a TKI that specifically inhibits vascular endothelial growth factor receptor-2.	apatinib	15-23	kinase insert domain receptor	Homo sapiens	60-105
30559126-18	2019	Apatinib is a TKI that specifically inhibits vascular endothelial growth factor receptor-2, which is domestically made in China.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	45-90
30877190-2	2019	BACKGROUND: Apatinib, an oral vascular endothelial growth factor (VEGF) receptor-2 inhibitor, has been approved as third-line treatment for metastatic gastric cancer in China.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	30-82
31079851-0	2019	Apatinib enhanced anti-tumor activity of cisplatin on triple-negative breast cancer through inhibition of VEGFR-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	106-113
31079851-3	2019	In addition, apatinib, a VEGFR2 inhibitor, exhibits antitumor activity in patients with TNBC.	apatinib	13-21	kinase insert domain receptor	Homo sapiens	25-31
31079851-11	2019	Moreover, apatinib increased cisplatin-induced apoptosis on MDA-MB-231 cells via increasing the level of Bax and active caspase 3 and decreasing the expression of Bcl-2.	apatinib	10-18	BCL2 associated X, apoptosis regulator	Homo sapiens	105-108
31079851-11	2019	Moreover, apatinib increased cisplatin-induced apoptosis on MDA-MB-231 cells via increasing the level of Bax and active caspase 3 and decreasing the expression of Bcl-2.	apatinib	10-18	caspase 3	Homo sapiens	120-129
31079851-11	2019	Moreover, apatinib increased cisplatin-induced apoptosis on MDA-MB-231 cells via increasing the level of Bax and active caspase 3 and decreasing the expression of Bcl-2.	apatinib	10-18	BCL2 apoptosis regulator	Homo sapiens	163-168
31079851-12	2019	Importantly, apatinib enhanced anti-tumor effect of cisplatin on MDA-MB-231 cells via inhibiting the levels of p-VEGFR2, p-Akt and p-mTOR.	apatinib	13-21	kinase insert domain receptor	Homo sapiens	113-119
31079851-12	2019	Importantly, apatinib enhanced anti-tumor effect of cisplatin on MDA-MB-231 cells via inhibiting the levels of p-VEGFR2, p-Akt and p-mTOR.	apatinib	13-21	AKT serine/threonine kinase 1	Homo sapiens	123-126
31079851-12	2019	Importantly, apatinib enhanced anti-tumor effect of cisplatin on MDA-MB-231 cells via inhibiting the levels of p-VEGFR2, p-Akt and p-mTOR.	apatinib	13-21	mechanistic target of rapamycin kinase	Homo sapiens	133-137
31079851-13	2019	CONCLUSION: Our findings indicated that apatinib enhanced the anti-tumor effects of cisplatin on MDA-MB-231 cells via inhibition of VEGFR2.	apatinib	40-48	kinase insert domain receptor	Homo sapiens	132-138
30706337-0	2019	Apatinib, a novel VEGFR inhibitor plus docetaxel in advanced lung adenocarcinoma patients with wild-type EGFR: a phase I trial.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	18-23
30706337-0	2019	Apatinib, a novel VEGFR inhibitor plus docetaxel in advanced lung adenocarcinoma patients with wild-type EGFR: a phase I trial.	apatinib	0-8	epidermal growth factor receptor	Homo sapiens	19-23
30706337-1	2019	Background This phase I trial was primarily conducted to determine the maximum tolerated dose (MTD) of apatinib combined with docetaxel in advanced lung adenocarcinoma patients with wild-type EGFR who have failed to first-line platinum-based chemotherapy, and to evaluate the safety and tolerability of apatinib plus docetaxel.	apatinib	103-111	epidermal growth factor receptor	Homo sapiens	192-196
31396349-0	2019	Apatinib suppresses breast cancer cells proliferation and invasion via angiomotin inhibition.	apatinib	0-8	angiomotin	Homo sapiens	71-81
31396349-2	2019	Apatinib is a novel tyrosine kinase inhibitor that selectively binds and inhibits vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	82-127
31396349-2	2019	Apatinib is a novel tyrosine kinase inhibitor that selectively binds and inhibits vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	129-136
31396349-9	2019	The cells were either exposed to Apatinib or vehicle and then examined for cell viabilities, migration, invasion, cell cycle distribution and the downstream signaling of VEGFR-2.	apatinib	33-41	kinase insert domain receptor	Homo sapiens	170-177
31396349-11	2019	In addition, in MCF-7 cells, Apatinib decreased AMOT expression, accompanied with the decreased expression of LATS1/2, YAP, ERK1/2 phosphorylation and cyclin D1.	apatinib	29-37	angiomotin	Homo sapiens	48-52
31396349-11	2019	In addition, in MCF-7 cells, Apatinib decreased AMOT expression, accompanied with the decreased expression of LATS1/2, YAP, ERK1/2 phosphorylation and cyclin D1.	apatinib	29-37	large tumor suppressor kinase 1	Homo sapiens	110-117
31396349-11	2019	In addition, in MCF-7 cells, Apatinib decreased AMOT expression, accompanied with the decreased expression of LATS1/2, YAP, ERK1/2 phosphorylation and cyclin D1.	apatinib	29-37	Yes1 associated transcriptional regulator	Homo sapiens	119-122
31396349-11	2019	In addition, in MCF-7 cells, Apatinib decreased AMOT expression, accompanied with the decreased expression of LATS1/2, YAP, ERK1/2 phosphorylation and cyclin D1.	apatinib	29-37	mitogen-activated protein kinase 3	Homo sapiens	124-130
31396349-11	2019	In addition, in MCF-7 cells, Apatinib decreased AMOT expression, accompanied with the decreased expression of LATS1/2, YAP, ERK1/2 phosphorylation and cyclin D1.	apatinib	29-37	cyclin D1	Homo sapiens	151-160
31396349-12	2019	The inhibitory effect of Apatinib on the cell activities and protein expressions were significantly suppressed by AMOT overexpression.	apatinib	25-33	angiomotin	Homo sapiens	114-118
31396349-13	2019	The results of this study indicated that Apatinib inhibited MCF-7 cell proliferation and invasion through AMOT/VEGFR-2 pathway.	apatinib	41-49	angiomotin	Homo sapiens	106-110
31396349-13	2019	The results of this study indicated that Apatinib inhibited MCF-7 cell proliferation and invasion through AMOT/VEGFR-2 pathway.	apatinib	41-49	kinase insert domain receptor	Homo sapiens	111-118
30985306-3	2019	Here, we report a case of Wilms tumor in a 24-year-old woman who was effectively treated with apatinib, a small-molecule inhibitor of vascular endothelial growth factor receptor-2.	apatinib	94-102	kinase insert domain receptor	Homo sapiens	134-179
31261514-1	2019	BACKGROUND: Apatinib is an oral small-molecule tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	12-20	kinase insert domain receptor	Homo sapiens	83-128
31261514-1	2019	BACKGROUND: Apatinib is an oral small-molecule tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	12-20	kinase insert domain receptor	Homo sapiens	130-137
31186764-0	2019	Clinical efficacy of apatinib in treating metastatic gastric cancer and its effect on IL-17.	apatinib	21-29	interleukin 17A	Homo sapiens	86-91
31186764-1	2019	Clinical efficacy of apatinib in treating metastatic gastric cancer and its effect on the levels of serum IL-17 were investigated.	apatinib	21-29	interleukin 17A	Homo sapiens	106-111
31186764-12	2019	In addition, apatinib can downregulate IL-17 expression, which is helpful in attenuating tumor proliferation and improving the clinical efficacy.	apatinib	13-21	interleukin 17A	Homo sapiens	39-44
30651189-9	2019	Apatinib suppressed the epithelial-mesenchymal transition in ovarian cancer cells by inhibiting the JAK/STAT3, PI3K/AKT and Notch signalling pathways.	apatinib	0-8	signal transducer and activator of transcription 3	Mus musculus	104-109
31118781-3	2019	Purpose: This study aimed to investigate the efficacy and safety of apatinib, aspecific VEGFR-2 inhibitor, in ASPS patients.	apatinib	68-76	kinase insert domain receptor	Homo sapiens	88-95
31014051-0	2019	[The inhibition effects of apatinib on cell proliferation, migration and apoptosis in esophageal carcinoma via Ras/Raf/MEK/ERK and JAK2/STAT3 pathways].	apatinib	27-35	zinc fingers and homeoboxes 2	Homo sapiens	115-118
31014051-0	2019	[The inhibition effects of apatinib on cell proliferation, migration and apoptosis in esophageal carcinoma via Ras/Raf/MEK/ERK and JAK2/STAT3 pathways].	apatinib	27-35	mitogen-activated protein kinase kinase 7	Homo sapiens	119-122
31014051-0	2019	[The inhibition effects of apatinib on cell proliferation, migration and apoptosis in esophageal carcinoma via Ras/Raf/MEK/ERK and JAK2/STAT3 pathways].	apatinib	27-35	mitogen-activated protein kinase 1	Homo sapiens	123-126
31014051-0	2019	[The inhibition effects of apatinib on cell proliferation, migration and apoptosis in esophageal carcinoma via Ras/Raf/MEK/ERK and JAK2/STAT3 pathways].	apatinib	27-35	Janus kinase 2	Homo sapiens	131-135
31014051-0	2019	[The inhibition effects of apatinib on cell proliferation, migration and apoptosis in esophageal carcinoma via Ras/Raf/MEK/ERK and JAK2/STAT3 pathways].	apatinib	27-35	signal transducer and activator of transcription 3	Homo sapiens	136-141
31014051-20	2019	In the presence of 20 mumol/L and 40 mumol/L of apatinib in KYSE-150 cells, the relative levels of VEGF mRNA were (42.57+-10.43)% and (25.69+-1.24)%, and those of VEGF-2 mRNA were (36.09+-10.82)% and (13.99+-6.54)%, which were all significantly decreased compared to control group (100.00+-0.00, P&lt;0.05 for all).	apatinib	48-56	vascular endothelial growth factor A	Homo sapiens	99-103
31014051-20	2019	In the presence of 20 mumol/L and 40 mumol/L of apatinib in KYSE-150 cells, the relative levels of VEGF mRNA were (42.57+-10.43)% and (25.69+-1.24)%, and those of VEGF-2 mRNA were (36.09+-10.82)% and (13.99+-6.54)%, which were all significantly decreased compared to control group (100.00+-0.00, P&lt;0.05 for all).	apatinib	48-56	vascular endothelial growth factor A	Homo sapiens	163-167
31014051-22	2019	Moreover, after treatment with 20 mumol/L and 40 mumol/L of apatinib in KYSE-150 cells, the VEGF concentrations were (766.48+-114.27) pg/ml and (497.40+-102.18)pg/ml, which were significantly decreased compared to control group [(967.41+-57.75) pg/ml, P&lt;0.05)].	apatinib	60-68	vascular endothelial growth factor A	Homo sapiens	92-96
31114227-0	2019	Pyrotinib treatment on HER2-positive gastric cancer cells promotes the released exosomes to enhance endothelial cell progression, which can be counteracted by apatinib.	apatinib	159-167	erb-b2 receptor tyrosine kinase 2	Homo sapiens	23-27
31114227-11	2019	Significantly, this effect was counteracted by the vascular endothelial growth factor receptor (VEGFR)-2 inhibitor apatinib which inhibits EC progression.	apatinib	115-123	kinase insert domain receptor	Homo sapiens	51-94
31114227-11	2019	Significantly, this effect was counteracted by the vascular endothelial growth factor receptor (VEGFR)-2 inhibitor apatinib which inhibits EC progression.	apatinib	115-123	kinase insert domain receptor	Homo sapiens	96-101
29977004-0	2019	Apatinib, a selective VEGFR2 inhibitor, improves the delivery of chemotherapeutic agents to tumors by normalizing tumor vessels in LoVo colon cancer xenograft mice.	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	22-28
29977004-2	2019	Apatinib (Apa), a highly selective VEGFR2 inhibitor, attracts much attentions due to its encouraging anticancer activity, especially in the clinical trials of combined treatment.	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	35-41
30773718-4	2019	A porphyrinic Zr-metal-organic framework nanoparticle is used simultaneously as the photosensitizer and the delivery vehicle of vascular endothelial growth factor receptor 2 (VEGFR2) inhibitor apatinib.	apatinib	193-201	kinase insert domain receptor	Homo sapiens	128-173
30773718-4	2019	A porphyrinic Zr-metal-organic framework nanoparticle is used simultaneously as the photosensitizer and the delivery vehicle of vascular endothelial growth factor receptor 2 (VEGFR2) inhibitor apatinib.	apatinib	193-201	kinase insert domain receptor	Homo sapiens	175-181
31157270-4	2019	Apatinib is a novel vascular endothelial growth factor receptor 2 (VEGFR-2) inhibitor and revealed potential anti-tumor efficacy in some types of sarcomas.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	20-65
31157270-4	2019	Apatinib is a novel vascular endothelial growth factor receptor 2 (VEGFR-2) inhibitor and revealed potential anti-tumor efficacy in some types of sarcomas.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	67-74
31168462-1	2019	Apatinib mesylate, a small-molecule tyrosine kinase inhibitor (TKI) of vascular endothelial growth factor receptor-2 (VEGFR-2), has been recommended as a third-line class A agent for patients with advanced gastric adenocarcinoma in China since April 2018.	apatinib	0-17	kinase insert domain receptor	Homo sapiens	71-116
31168462-1	2019	Apatinib mesylate, a small-molecule tyrosine kinase inhibitor (TKI) of vascular endothelial growth factor receptor-2 (VEGFR-2), has been recommended as a third-line class A agent for patients with advanced gastric adenocarcinoma in China since April 2018.	apatinib	0-17	kinase insert domain receptor	Homo sapiens	118-125
30755403-2	2019	Judicious dosing of antiangiogenic agents such as apatinib (VEGFR2-TKI) can modulate the tumor immunosuppressive microenvironment, which contributes to resistance to anti-PD-1/PD-L1 treatment.	apatinib	50-58	kinase insert domain receptor	Homo sapiens	60-66
30755403-2	2019	Judicious dosing of antiangiogenic agents such as apatinib (VEGFR2-TKI) can modulate the tumor immunosuppressive microenvironment, which contributes to resistance to anti-PD-1/PD-L1 treatment.	apatinib	50-58	CD274 molecule	Homo sapiens	176-181
30755403-4	2019	Here, using a syngeneic lung cancer mouse model, we demonstrated that low-dose apatinib alleviated hypoxia, increased infiltration of CD8+ T cells, reduced recruitment of tumor-associated macrophages in tumor and decreased TGFbeta amounts in both tumor and serum.	apatinib	79-87	transforming growth factor alpha	Mus musculus	223-230
31190866-3	2019	Apatinib, an oral small-molecule vascular endothelial growth factor receptor-2 inhibitor, has shown notable therapeutic effect in a wide variety of tumors.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	33-78
31073278-0	2019	Apatinib preferentially inhibits PC9 gefitinib-resistant cancer cells by inducing cell cycle arrest and inhibiting VEGFR signaling pathway.	apatinib	0-8	proprotein convertase subtilisin/kexin type 9	Homo sapiens	33-36
31073278-0	2019	Apatinib preferentially inhibits PC9 gefitinib-resistant cancer cells by inducing cell cycle arrest and inhibiting VEGFR signaling pathway.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	115-120
31073278-6	2019	Different concentrations of apatinib were used to treat PC9, PC9GR, and other two lung cancer cell lines for its anti-growth effects.	apatinib	28-36	proprotein convertase subtilisin/kexin type 9	Homo sapiens	56-59
31073278-12	2019	Apatinib demonstrated much stronger ( ~ fivefold) growth inhibition on PC9GR cells than on PC9 and other two lung cancer cell lines, A549 and H460.	apatinib	0-8	proprotein convertase subtilisin/kexin type 9	Homo sapiens	71-74
31073278-14	2019	RNA-seq revealed multiple changed pathways in PC9GR cells compared to the PC9 cells and after apatinib treatment the most changed pathways were cell cycle and DNA replication where most of gene activities were repressed.	apatinib	94-102	proprotein convertase subtilisin/kexin type 9	Homo sapiens	46-49
31073278-15	2019	Consistently, protein expression of p57, CDK2, cyclin E2, and pRb was significantly impacted by apatinib in PC9GR cells.	apatinib	96-104	cyclin dependent kinase inhibitor 1C	Homo sapiens	36-39
31073278-15	2019	Consistently, protein expression of p57, CDK2, cyclin E2, and pRb was significantly impacted by apatinib in PC9GR cells.	apatinib	96-104	cyclin dependent kinase 2	Homo sapiens	41-45
31073278-15	2019	Consistently, protein expression of p57, CDK2, cyclin E2, and pRb was significantly impacted by apatinib in PC9GR cells.	apatinib	96-104	cyclin E2	Homo sapiens	47-56
31073278-15	2019	Consistently, protein expression of p57, CDK2, cyclin E2, and pRb was significantly impacted by apatinib in PC9GR cells.	apatinib	96-104	RB transcriptional corepressor 1	Homo sapiens	62-65
31073278-16	2019	Oral intake of apatinib in mouse model significantly inhibited establishment and growth of PC9GR implanted tumors compared to PC9 established tumors.	apatinib	15-23	proprotein convertase subtilisin/kexin type 9	Mus musculus	91-94
31073278-17	2019	VEGFR2 phosphorylation in PC9GR tumors after apatinib treatment was significantly reduced along with micro-vessel formation.	apatinib	45-53	kinase insert domain receptor	Homo sapiens	0-6
31073278-20	2019	These data suggested that apatinib may provide a benefit to patients with acquired resistance to EGFR-TKI treatment.	apatinib	26-34	epidermal growth factor receptor	Homo sapiens	97-101
30651189-9	2019	Apatinib suppressed the epithelial-mesenchymal transition in ovarian cancer cells by inhibiting the JAK/STAT3, PI3K/AKT and Notch signalling pathways.	apatinib	0-8	thymoma viral proto-oncogene 1	Mus musculus	116-119
30686547-0	2019	Apatinib regulates the cell proliferation and apoptosis of liver cancer by regulation of VEGFR2/STAT3 signaling.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	89-95
30686547-0	2019	Apatinib regulates the cell proliferation and apoptosis of liver cancer by regulation of VEGFR2/STAT3 signaling.	apatinib	0-8	signal transducer and activator of transcription 3	Homo sapiens	96-101
30686547-5	2019	Apatinib significantly inhibited the mRNA levels of VEGF and VEGFR2 as well as protein levels of VEGF and p-VEGFR2 compared with those in control group.	apatinib	0-8	vascular endothelial growth factor A	Homo sapiens	52-56
30686547-5	2019	Apatinib significantly inhibited the mRNA levels of VEGF and VEGFR2 as well as protein levels of VEGF and p-VEGFR2 compared with those in control group.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	61-67
30686547-5	2019	Apatinib significantly inhibited the mRNA levels of VEGF and VEGFR2 as well as protein levels of VEGF and p-VEGFR2 compared with those in control group.	apatinib	0-8	vascular endothelial growth factor A	Homo sapiens	61-65
30686547-5	2019	Apatinib significantly inhibited the mRNA levels of VEGF and VEGFR2 as well as protein levels of VEGF and p-VEGFR2 compared with those in control group.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	108-114
30686547-8	2019	Compared with control group, Apatinib significantly induced BAX/Bcl-2 ratio elevation, reduced p-STAT3 and p-VEGFR2 expression, which were significantly augmented by the treatment of siSTAT3.	apatinib	29-37	BCL2 associated X, apoptosis regulator	Homo sapiens	60-63
30686547-8	2019	Compared with control group, Apatinib significantly induced BAX/Bcl-2 ratio elevation, reduced p-STAT3 and p-VEGFR2 expression, which were significantly augmented by the treatment of siSTAT3.	apatinib	29-37	BCL2 apoptosis regulator	Homo sapiens	64-69
30686547-8	2019	Compared with control group, Apatinib significantly induced BAX/Bcl-2 ratio elevation, reduced p-STAT3 and p-VEGFR2 expression, which were significantly augmented by the treatment of siSTAT3.	apatinib	29-37	signal transducer and activator of transcription 3	Homo sapiens	97-102
30686547-8	2019	Compared with control group, Apatinib significantly induced BAX/Bcl-2 ratio elevation, reduced p-STAT3 and p-VEGFR2 expression, which were significantly augmented by the treatment of siSTAT3.	apatinib	29-37	kinase insert domain receptor	Homo sapiens	109-115
30686547-9	2019	In conclusion, Apatinib inhibited the cell proliferation and promoted the cell apoptosis of liver cancer by inhibiting the activation of VEGFR2/STAT3.	apatinib	15-23	kinase insert domain receptor	Homo sapiens	137-143
30686547-9	2019	In conclusion, Apatinib inhibited the cell proliferation and promoted the cell apoptosis of liver cancer by inhibiting the activation of VEGFR2/STAT3.	apatinib	15-23	signal transducer and activator of transcription 3	Homo sapiens	144-149
30547193-3	2019	As a small molecule inhibitor of vascular endothelial growth factor receptor-2 tyrosine kinase, apatinib had been proved in advanced gastric cancer.	apatinib	96-104	kinase insert domain receptor	Homo sapiens	33-78
30816108-0	2019	Phase II trial of VEGFR2 inhibitor apatinib for metastatic sarcoma: focus on efficacy and safety.	apatinib	35-43	kinase insert domain receptor	Homo sapiens	18-24
30816108-1	2019	Apatinib (YN968D1) is a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	66-111
30816108-1	2019	Apatinib (YN968D1) is a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	113-120
30816108-1	2019	Apatinib (YN968D1) is a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	10-17	kinase insert domain receptor	Homo sapiens	66-111
30816108-1	2019	Apatinib (YN968D1) is a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	10-17	kinase insert domain receptor	Homo sapiens	113-120
30863099-3	2019	Apatinib, a tyrosine kinase inhibitor that selectively inhibits the vascular endothelial growth factor receptor and mildly inhibits c-Kit, PDGFR-beta, RET, and c-SRC, has been reported to show efficacy among some patients with malignant supratentorial gliomas.	apatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	132-137
30598262-10	2019	In Apatinib-Gd-PEG hydrogel group, compared with other three groups, MRI and histomorphology showed that the necrotic area of hepatocellular carcinoma model was larger, immunohistochemistry displayed minimal expression of CD34 and VEGFR2, the AOD of VEGFR2 and MVD differed markedly.	apatinib	3-11	CD34 antigen	Mus musculus	222-226
30598262-10	2019	In Apatinib-Gd-PEG hydrogel group, compared with other three groups, MRI and histomorphology showed that the necrotic area of hepatocellular carcinoma model was larger, immunohistochemistry displayed minimal expression of CD34 and VEGFR2, the AOD of VEGFR2 and MVD differed markedly.	apatinib	3-11	kinase insert domain protein receptor	Mus musculus	231-237
30598262-10	2019	In Apatinib-Gd-PEG hydrogel group, compared with other three groups, MRI and histomorphology showed that the necrotic area of hepatocellular carcinoma model was larger, immunohistochemistry displayed minimal expression of CD34 and VEGFR2, the AOD of VEGFR2 and MVD differed markedly.	apatinib	3-11	kinase insert domain protein receptor	Mus musculus	250-256
30732125-1	2019	Apatinib (Jiangsu HengRui Medicine Co. Ltd), a vascular endothelial growth factor receptor 2 (VEGFR-2) tyrosine kinase inhibitor, has been proven to be safe and to significantly prolong survival in advanced chemotherapy-refractory gastric cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	47-92
30732125-1	2019	Apatinib (Jiangsu HengRui Medicine Co. Ltd), a vascular endothelial growth factor receptor 2 (VEGFR-2) tyrosine kinase inhibitor, has been proven to be safe and to significantly prolong survival in advanced chemotherapy-refractory gastric cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	94-101
30774384-1	2019	Background: Hypertension (HTN) is a common adverse event of the vascular endothelial growth factor pathway inhibitor apatinib.	apatinib	117-125	vascular endothelial growth factor A	Homo sapiens	64-98
30774379-9	2019	When apatinib treatment was combined with S3I-201, the expression of VEGFR2, STAT3, and their downstream signaling molecules was significantly decreased (P&lt;0.01).	apatinib	5-13	kinase insert domain receptor	Homo sapiens	69-75
30774379-9	2019	When apatinib treatment was combined with S3I-201, the expression of VEGFR2, STAT3, and their downstream signaling molecules was significantly decreased (P&lt;0.01).	apatinib	5-13	signal transducer and activator of transcription 3	Homo sapiens	77-82
30423319-1	2019	Apatinib is a tyrosine kinase inhibitor that selectively targets vascular endothelial growth factor receptor-2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	65-110
30423319-1	2019	Apatinib is a tyrosine kinase inhibitor that selectively targets vascular endothelial growth factor receptor-2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	112-119
30423319-5	2019	Mechanistically, apatinib suppressed activation of VEGFR2 (manifested by reduced VEGFR2 phosphorylation), accompanied by inhibition of the Ras pathway (reflected by down-regulation Ras, Raf, pMEK1/2, pERK1/2) in OCI-ly1 (GCB subtype of DLBCL) and SU-DHL2 (ABC subtype of DLBCL) cells.	apatinib	17-25	kinase insert domain receptor	Homo sapiens	51-57
30423319-5	2019	Mechanistically, apatinib suppressed activation of VEGFR2 (manifested by reduced VEGFR2 phosphorylation), accompanied by inhibition of the Ras pathway (reflected by down-regulation Ras, Raf, pMEK1/2, pERK1/2) in OCI-ly1 (GCB subtype of DLBCL) and SU-DHL2 (ABC subtype of DLBCL) cells.	apatinib	17-25	kinase insert domain receptor	Homo sapiens	81-87
30423319-5	2019	Mechanistically, apatinib suppressed activation of VEGFR2 (manifested by reduced VEGFR2 phosphorylation), accompanied by inhibition of the Ras pathway (reflected by down-regulation Ras, Raf, pMEK1/2, pERK1/2) in OCI-ly1 (GCB subtype of DLBCL) and SU-DHL2 (ABC subtype of DLBCL) cells.	apatinib	17-25	zinc fingers and homeoboxes 2	Homo sapiens	186-189
30423319-8	2019	They also suggest that anti-NHL activity of apatinib might be associated with inhibition of tumor cell growth and induction of apoptosis as well as anti-angiogenesis by targeting VEGFR2 and its downstream Ras/Raf/MEK/ERK pathway.	apatinib	44-52	kinase insert domain receptor	Homo sapiens	179-185
30423319-8	2019	They also suggest that anti-NHL activity of apatinib might be associated with inhibition of tumor cell growth and induction of apoptosis as well as anti-angiogenesis by targeting VEGFR2 and its downstream Ras/Raf/MEK/ERK pathway.	apatinib	44-52	zinc fingers and homeoboxes 2	Homo sapiens	209-212
30423319-8	2019	They also suggest that anti-NHL activity of apatinib might be associated with inhibition of tumor cell growth and induction of apoptosis as well as anti-angiogenesis by targeting VEGFR2 and its downstream Ras/Raf/MEK/ERK pathway.	apatinib	44-52	mitogen-activated protein kinase kinase 7	Homo sapiens	213-216
30423319-8	2019	They also suggest that anti-NHL activity of apatinib might be associated with inhibition of tumor cell growth and induction of apoptosis as well as anti-angiogenesis by targeting VEGFR2 and its downstream Ras/Raf/MEK/ERK pathway.	apatinib	44-52	EPH receptor B2	Homo sapiens	217-220
30639490-5	2019	Apatinib (YN968D1) is a small-molecule antiangiogenic agent that selectively inhibits VEGFR-2 and also mildly inhibits c-Kit and c-Src tyrosine kinases, abundant in invasive pituitary adenomas.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	86-93
30639490-5	2019	Apatinib (YN968D1) is a small-molecule antiangiogenic agent that selectively inhibits VEGFR-2 and also mildly inhibits c-Kit and c-Src tyrosine kinases, abundant in invasive pituitary adenomas.	apatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	119-124
30557852-2	2019	Apatinib inhibits angiogenesis as a highly selective KDR inhibitor and has been used to treat advanced gastric cancer and malignancies in clinical settings.	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	53-56
30557852-8	2019	Although apatinib efficiently inhibited INR1G9-represented non-functional PNET liver metastasis, it led to the emergence of a hypoxic area in the INS-1-represented insulinoma and promoted liver metastasis.	apatinib	9-17	insulin I	Mus musculus	146-151
30293117-1	2019	PURPOSE: To evaluate the efficacy of maintenance apatinib after chemotherapy for extensive-stage (ED) small-cell lung cancer (SCLC).	apatinib	49-57	SCLC1	Homo sapiens	126-130
30293117-13	2019	CONCLUSION: Maintenance apatinib was safe and achieved encouraging PFS and OS in extensive-stage SCLC.	apatinib	24-32	SCLC1	Homo sapiens	97-101
30608382-0	2019	Apatinib monotherapy for advanced VEGFR-2-negative nasopharyngeal carcinoma: A case report.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	34-41
30608421-0	2019	Apatinib with EGFR-TKIs in advanced wild gene-type NSCLC: A case report.	apatinib	0-8	epidermal growth factor receptor	Homo sapiens	14-18
30863481-0	2019	Apatinib Promotes Apoptosis of Pancreatic Cancer Cells through Downregulation of Hypoxia-Inducible Factor-1alpha and Increased Levels of Reactive Oxygen Species.	apatinib	0-8	hypoxia inducible factor 1 subunit alpha	Homo sapiens	81-112
30863481-8	2019	Furthermore, we demonstrated that apatinib inhibited the expression of hypoxia-inducible factor-1alpha (HIF-1alpha), vascular endothelial growth factor, and markers of the phosphoinositide 3-kinase (PI3K)/Akt/mTOR signaling pathway, which increased the levels of reactive oxygen species in vitro.	apatinib	34-42	hypoxia inducible factor 1 subunit alpha	Homo sapiens	71-102
30863481-8	2019	Furthermore, we demonstrated that apatinib inhibited the expression of hypoxia-inducible factor-1alpha (HIF-1alpha), vascular endothelial growth factor, and markers of the phosphoinositide 3-kinase (PI3K)/Akt/mTOR signaling pathway, which increased the levels of reactive oxygen species in vitro.	apatinib	34-42	hypoxia inducible factor 1 subunit alpha	Homo sapiens	104-114
30863481-8	2019	Furthermore, we demonstrated that apatinib inhibited the expression of hypoxia-inducible factor-1alpha (HIF-1alpha), vascular endothelial growth factor, and markers of the phosphoinositide 3-kinase (PI3K)/Akt/mTOR signaling pathway, which increased the levels of reactive oxygen species in vitro.	apatinib	34-42	vascular endothelial growth factor A	Homo sapiens	117-151
30863481-8	2019	Furthermore, we demonstrated that apatinib inhibited the expression of hypoxia-inducible factor-1alpha (HIF-1alpha), vascular endothelial growth factor, and markers of the phosphoinositide 3-kinase (PI3K)/Akt/mTOR signaling pathway, which increased the levels of reactive oxygen species in vitro.	apatinib	34-42	phosphoinositide-3-kinase regulatory subunit 1	Homo sapiens	172-197
30863481-8	2019	Furthermore, we demonstrated that apatinib inhibited the expression of hypoxia-inducible factor-1alpha (HIF-1alpha), vascular endothelial growth factor, and markers of the phosphoinositide 3-kinase (PI3K)/Akt/mTOR signaling pathway, which increased the levels of reactive oxygen species in vitro.	apatinib	34-42	AKT serine/threonine kinase 1	Homo sapiens	205-208
30863481-8	2019	Furthermore, we demonstrated that apatinib inhibited the expression of hypoxia-inducible factor-1alpha (HIF-1alpha), vascular endothelial growth factor, and markers of the phosphoinositide 3-kinase (PI3K)/Akt/mTOR signaling pathway, which increased the levels of reactive oxygen species in vitro.	apatinib	34-42	mechanistic target of rapamycin kinase	Homo sapiens	209-213
30702616-0	2019	Low dose of apatinib in treating chemotherapy and EGFR-TKI refractory non-small cell lung cancer: A case report.	apatinib	12-20	epidermal growth factor receptor	Homo sapiens	50-54
30675220-2	2019	It was observed that apatinib significantly inhibited vascular endothelial growth factor (VEGF) secretion and the proliferation of KYSE-150 cells in a dose-dependent manner.	apatinib	21-29	vascular endothelial growth factor A	Homo sapiens	54-88
30675220-2	2019	It was observed that apatinib significantly inhibited vascular endothelial growth factor (VEGF) secretion and the proliferation of KYSE-150 cells in a dose-dependent manner.	apatinib	21-29	vascular endothelial growth factor A	Homo sapiens	90-94
30675220-8	2019	In conclusion, the present study suggested that apatinib increases the radiosensitivity of KYSE-150 esophageal cancer cells by inhibiting VEGF secretion and cell proliferation, and promoting apoptosis and cell cycle redistribution.	apatinib	48-56	vascular endothelial growth factor A	Homo sapiens	138-142
30669747-21	2019	VEGFR2 -906T&gt;C CC/TC genotype has a worse effect on apatinib multiline treatment in patients with advanced NSCLC.	apatinib	55-63	kinase insert domain receptor	Homo sapiens	0-6
30332553-1	2019	As a novel vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor (VEGFR2-TKI), apatinib has a certain anti-tumor effect for a variety of solid tumors.	apatinib	97-105	kinase insert domain receptor	Homo sapiens	84-90
30332553-12	2019	In conclusion, apatinib combined with TACE revealed certain survival benefits for HCC patients who experienced progression following TACE, which can provide a promising strategy for HCC treatment.	apatinib	15-23	ADAM metallopeptidase domain 17	Homo sapiens	133-137
30332959-6	2019	CONCLUSION: The results confirmed the hypothesis that apatinib nanoparticles decreased toxicity (1.36 +- 0.74 fold) and efficient VEGF inhibition (3.51 +- 0.02 fold) via VEGFR2 mediation.	apatinib	54-62	vascular endothelial growth factor A	Homo sapiens	130-134
30332959-6	2019	CONCLUSION: The results confirmed the hypothesis that apatinib nanoparticles decreased toxicity (1.36 +- 0.74 fold) and efficient VEGF inhibition (3.51 +- 0.02 fold) via VEGFR2 mediation.	apatinib	54-62	kinase insert domain receptor	Homo sapiens	170-176
31888413-7	2019	RESULT: For the apatinib group, the rate of CD4+CD25+ T cells significantly increased (P = .048).	apatinib	16-24	CD4 molecule	Homo sapiens	44-47
31888413-7	2019	RESULT: For the apatinib group, the rate of CD4+CD25+ T cells significantly increased (P = .048).	apatinib	16-24	interleukin 2 receptor subunit alpha	Homo sapiens	48-52
31888413-12	2019	CONCLUSION: The rate of CD4+CD25+ T cells is very important in patients with apatinib treatment.	apatinib	77-85	CD4 molecule	Homo sapiens	24-27
31888413-12	2019	CONCLUSION: The rate of CD4+CD25+ T cells is very important in patients with apatinib treatment.	apatinib	77-85	interleukin 2 receptor subunit alpha	Homo sapiens	28-32
31888413-13	2019	The changing number of CD4+CD25+ T cells may be a good indicator for apatinib prognosis.	apatinib	69-77	CD4 molecule	Homo sapiens	23-26
31888413-13	2019	The changing number of CD4+CD25+ T cells may be a good indicator for apatinib prognosis.	apatinib	69-77	interleukin 2 receptor subunit alpha	Homo sapiens	27-31
30863099-3	2019	Apatinib, a tyrosine kinase inhibitor that selectively inhibits the vascular endothelial growth factor receptor and mildly inhibits c-Kit, PDGFR-beta, RET, and c-SRC, has been reported to show efficacy among some patients with malignant supratentorial gliomas.	apatinib	0-8	platelet derived growth factor receptor beta	Homo sapiens	139-149
30863099-3	2019	Apatinib, a tyrosine kinase inhibitor that selectively inhibits the vascular endothelial growth factor receptor and mildly inhibits c-Kit, PDGFR-beta, RET, and c-SRC, has been reported to show efficacy among some patients with malignant supratentorial gliomas.	apatinib	0-8	ret proto-oncogene	Homo sapiens	151-154
30863099-3	2019	Apatinib, a tyrosine kinase inhibitor that selectively inhibits the vascular endothelial growth factor receptor and mildly inhibits c-Kit, PDGFR-beta, RET, and c-SRC, has been reported to show efficacy among some patients with malignant supratentorial gliomas.	apatinib	0-8	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	160-165
30863099-5	2019	Herein, a 66-year-old man with brainstem anaplastic astrocytoma isocitrate dehydrogenase (IDH) wild type was treated initially with combined radiotherapy, temozolomide, and apatinib.	apatinib	173-181	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	90-93
30863099-7	2019	To our knowledge, this is the first case report using apatinib to treat brainstem IDH wild-type anaplastic astrocytoma, displaying an excellent outcome.	apatinib	54-62	isocitrate dehydrogenase (NADP(+)) 1	Homo sapiens	82-85
30305215-3	2018	Apatinib mesylate is a novel and highly selective VEGFR-2 inhibitor, presented with an outstanding activity of anti-angiogensis, which has the potential for treating various tumors.	apatinib	0-17	kinase insert domain protein receptor	Mus musculus	50-57
30588089-4	2018	The aim of this study was to investigate the efficacy and safety of apatinib, a specific vascular endothelial growth factor receptor 2 inhibitor, in ES patients.	apatinib	68-76	kinase insert domain receptor	Homo sapiens	89-134
30573977-4	2018	Apatinib, a potent tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor 2 (VEGFR2), has been approved for the treatment of late-stage gastric or gastroesophageal junction adenocarcinoma that is resistant to at least two lines of chemotherapy.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	55-100
30573977-4	2018	Apatinib, a potent tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor 2 (VEGFR2), has been approved for the treatment of late-stage gastric or gastroesophageal junction adenocarcinoma that is resistant to at least two lines of chemotherapy.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	102-108
29573236-2	2018	As a novel vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor, apatinib has a certain antitumor effect for various solid tumors.	apatinib	84-92	kinase insert domain receptor	Homo sapiens	11-56
30305215-5	2018	In this study, Liposome and Methoxy poly(ethylene glycol)-poly(epsilon-caprolactone) (MPEG-PCL) were constructed as drug delivery system for the delivery of apatinib (Lipo-Apa) and docetaxel (DOC/M), respectively.	apatinib	157-165	glutamyl aminopeptidase	Mus musculus	172-175
30544412-3	2018	Apatinib is a new inhibitor of vascular endothelial growth factor receptor 2 tyrosine kinase, which has been reported to be effective in some solid tumors.	apatinib	0-8	vascular endothelial growth factor A	Homo sapiens	31-65
30544412-13	2018	LESSONS: Apatinib may be a substitute for the HCC patients with sorafenib resistance in the future, especially for those with high expression of VEGF.	apatinib	9-17	vascular endothelial growth factor A	Homo sapiens	145-149
30454552-4	2018	Apatinib (Hengrui Pharmaceutical Co. Ltd, Jiangsu, People"s Republic of China) is a small molecule vascular endothelial growth factor receptor 2 (VEGFR-2) inhibitor, which selectively inhibits VEGFR-2 and blocks the VEGF signal pathway, then strongly inhibiting the tumor angiogenesis.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	99-144
30454552-4	2018	Apatinib (Hengrui Pharmaceutical Co. Ltd, Jiangsu, People"s Republic of China) is a small molecule vascular endothelial growth factor receptor 2 (VEGFR-2) inhibitor, which selectively inhibits VEGFR-2 and blocks the VEGF signal pathway, then strongly inhibiting the tumor angiogenesis.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	146-153
30454552-4	2018	Apatinib (Hengrui Pharmaceutical Co. Ltd, Jiangsu, People"s Republic of China) is a small molecule vascular endothelial growth factor receptor 2 (VEGFR-2) inhibitor, which selectively inhibits VEGFR-2 and blocks the VEGF signal pathway, then strongly inhibiting the tumor angiogenesis.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	193-200
30454552-4	2018	Apatinib (Hengrui Pharmaceutical Co. Ltd, Jiangsu, People"s Republic of China) is a small molecule vascular endothelial growth factor receptor 2 (VEGFR-2) inhibitor, which selectively inhibits VEGFR-2 and blocks the VEGF signal pathway, then strongly inhibiting the tumor angiogenesis.	apatinib	0-8	vascular endothelial growth factor A	Homo sapiens	146-150
30400838-0	2018	Apatinib affect VEGF-mediated cell proliferation, migration, invasion via blocking VEGFR2/RAF/MEK/ERK and PI3K/AKT pathways in cholangiocarcinoma cell.	apatinib	0-8	vascular endothelial growth factor A	Homo sapiens	16-20
30400838-0	2018	Apatinib affect VEGF-mediated cell proliferation, migration, invasion via blocking VEGFR2/RAF/MEK/ERK and PI3K/AKT pathways in cholangiocarcinoma cell.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	83-89
30400838-0	2018	Apatinib affect VEGF-mediated cell proliferation, migration, invasion via blocking VEGFR2/RAF/MEK/ERK and PI3K/AKT pathways in cholangiocarcinoma cell.	apatinib	0-8	zinc fingers and homeoboxes 2	Homo sapiens	90-93
30400838-0	2018	Apatinib affect VEGF-mediated cell proliferation, migration, invasion via blocking VEGFR2/RAF/MEK/ERK and PI3K/AKT pathways in cholangiocarcinoma cell.	apatinib	0-8	mitogen-activated protein kinase kinase 7	Homo sapiens	94-97
30400838-0	2018	Apatinib affect VEGF-mediated cell proliferation, migration, invasion via blocking VEGFR2/RAF/MEK/ERK and PI3K/AKT pathways in cholangiocarcinoma cell.	apatinib	0-8	mitogen-activated protein kinase 1	Homo sapiens	98-101
30400838-0	2018	Apatinib affect VEGF-mediated cell proliferation, migration, invasion via blocking VEGFR2/RAF/MEK/ERK and PI3K/AKT pathways in cholangiocarcinoma cell.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	111-114
30400838-3	2018	Apatinib is a highly selective VEGFR2 antagonist which has inhibitive effect on antiapoptotic and cell growth in CCA.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	31-37
30400838-6	2018	RT-qPCR and western bloting were used to detect the mRNA and protein expression levels of VEGFR2 to investigate whether it was effectively repressed or activated with rhVEGF or apatinib treatment.	apatinib	177-185	kinase insert domain receptor	Homo sapiens	90-96
30400838-9	2018	Apatinib dramatically suppressed VEGF-mediated cell migration and invasion at the concentration of 100 nM treatment and significantly decreased the expression of metastasis-associated protein such as Slug, snail and MMP9.	apatinib	0-8	vascular endothelial growth factor A	Homo sapiens	33-37
30400838-9	2018	Apatinib dramatically suppressed VEGF-mediated cell migration and invasion at the concentration of 100 nM treatment and significantly decreased the expression of metastasis-associated protein such as Slug, snail and MMP9.	apatinib	0-8	LY6/PLAUR domain containing 5	Homo sapiens	162-191
30400838-9	2018	Apatinib dramatically suppressed VEGF-mediated cell migration and invasion at the concentration of 100 nM treatment and significantly decreased the expression of metastasis-associated protein such as Slug, snail and MMP9.	apatinib	0-8	snail family transcriptional repressor 2	Homo sapiens	200-204
30400838-9	2018	Apatinib dramatically suppressed VEGF-mediated cell migration and invasion at the concentration of 100 nM treatment and significantly decreased the expression of metastasis-associated protein such as Slug, snail and MMP9.	apatinib	0-8	snail family transcriptional repressor 1	Homo sapiens	206-211
30400838-9	2018	Apatinib dramatically suppressed VEGF-mediated cell migration and invasion at the concentration of 100 nM treatment and significantly decreased the expression of metastasis-associated protein such as Slug, snail and MMP9.	apatinib	0-8	matrix metallopeptidase 9	Homo sapiens	216-220
30400838-10	2018	Moreover, all of these inhibiting effects of apatinib depended on the VEGFR2 existence.	apatinib	45-53	kinase insert domain receptor	Homo sapiens	70-76
30400838-11	2018	In addition, VEGFR2/RAF/MEK/ERK and PI3K/AKT signal pathways were enhanced by the introduction of rhVEGF, but were dramatically suppressed after the apatinib treatment.	apatinib	149-157	kinase insert domain receptor	Homo sapiens	13-19
30400838-11	2018	In addition, VEGFR2/RAF/MEK/ERK and PI3K/AKT signal pathways were enhanced by the introduction of rhVEGF, but were dramatically suppressed after the apatinib treatment.	apatinib	149-157	zinc fingers and homeoboxes 2	Homo sapiens	20-23
30400838-11	2018	In addition, VEGFR2/RAF/MEK/ERK and PI3K/AKT signal pathways were enhanced by the introduction of rhVEGF, but were dramatically suppressed after the apatinib treatment.	apatinib	149-157	mitogen-activated protein kinase kinase 7	Homo sapiens	24-27
30400838-11	2018	In addition, VEGFR2/RAF/MEK/ERK and PI3K/AKT signal pathways were enhanced by the introduction of rhVEGF, but were dramatically suppressed after the apatinib treatment.	apatinib	149-157	mitogen-activated protein kinase 1	Homo sapiens	28-31
30400838-11	2018	In addition, VEGFR2/RAF/MEK/ERK and PI3K/AKT signal pathways were enhanced by the introduction of rhVEGF, but were dramatically suppressed after the apatinib treatment.	apatinib	149-157	AKT serine/threonine kinase 1	Homo sapiens	41-44
30400838-12	2018	CONCLUSION: Apatinib inhibit VEGF-mediated cell migration and invasion in CCA cell lines via inhibiting the VEGFR2/RAF/MEK/ERK and PI3K/AKT pathways.	apatinib	12-20	vascular endothelial growth factor A	Homo sapiens	29-33
30400838-12	2018	CONCLUSION: Apatinib inhibit VEGF-mediated cell migration and invasion in CCA cell lines via inhibiting the VEGFR2/RAF/MEK/ERK and PI3K/AKT pathways.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	108-114
30400838-12	2018	CONCLUSION: Apatinib inhibit VEGF-mediated cell migration and invasion in CCA cell lines via inhibiting the VEGFR2/RAF/MEK/ERK and PI3K/AKT pathways.	apatinib	12-20	zinc fingers and homeoboxes 2	Homo sapiens	115-118
30074936-8	2018	Taken together, our results indicate that simultaneous inhibition of ALK and vascular endothelial growth factor R2 by the combination of alectinib with apatinib may be useful for controlling progression of EML4-ALK fusion gene lung cancer by reversing ALK-TKI resistance and inhibiting angiogenesis.	apatinib	152-160	ALK receptor tyrosine kinase	Homo sapiens	69-72
30074936-8	2018	Taken together, our results indicate that simultaneous inhibition of ALK and vascular endothelial growth factor R2 by the combination of alectinib with apatinib may be useful for controlling progression of EML4-ALK fusion gene lung cancer by reversing ALK-TKI resistance and inhibiting angiogenesis.	apatinib	152-160	vascular endothelial growth factor A	Homo sapiens	77-111
30074936-8	2018	Taken together, our results indicate that simultaneous inhibition of ALK and vascular endothelial growth factor R2 by the combination of alectinib with apatinib may be useful for controlling progression of EML4-ALK fusion gene lung cancer by reversing ALK-TKI resistance and inhibiting angiogenesis.	apatinib	152-160	EMAP like 4	Homo sapiens	206-210
30074936-8	2018	Taken together, our results indicate that simultaneous inhibition of ALK and vascular endothelial growth factor R2 by the combination of alectinib with apatinib may be useful for controlling progression of EML4-ALK fusion gene lung cancer by reversing ALK-TKI resistance and inhibiting angiogenesis.	apatinib	152-160	ALK receptor tyrosine kinase	Homo sapiens	211-214
30074936-8	2018	Taken together, our results indicate that simultaneous inhibition of ALK and vascular endothelial growth factor R2 by the combination of alectinib with apatinib may be useful for controlling progression of EML4-ALK fusion gene lung cancer by reversing ALK-TKI resistance and inhibiting angiogenesis.	apatinib	152-160	ALK receptor tyrosine kinase	Homo sapiens	211-214
30324820-1	2018	INTRODUCTION: Apatinib is an orally administered small-molecule vascular endothelial growth factor receptor 2 inhibitor.	apatinib	14-22	kinase insert domain receptor	Homo sapiens	64-109
30344715-6	2018	The results demonstrate that apatinib significantly inhibited cell proliferation and colony formation through promoting cell apoptosis in p53- and EGFR-mutated and wild-type glioma cells.	apatinib	29-37	tumor protein p53	Homo sapiens	138-141
30344715-6	2018	The results demonstrate that apatinib significantly inhibited cell proliferation and colony formation through promoting cell apoptosis in p53- and EGFR-mutated and wild-type glioma cells.	apatinib	29-37	epidermal growth factor receptor	Homo sapiens	147-151
30138636-5	2018	Apatinib was a weak inhibitor of human CYP2E1 (IC50&gt;10 muM) but inhibited CYP2B6/2B1 and CYP2D6/2D1 in a competitive way (Ki = 3.84/0.59 and 5.41/0.87 muM), and inhibited CYP3A4/3A2 and rat CYP2E1 in a mixed way (Ki = 11.50/1.83 and 13.06 muM).	apatinib	0-8	latexin	Homo sapiens	154-157
30138636-5	2018	Apatinib was a weak inhibitor of human CYP2E1 (IC50&gt;10 muM) but inhibited CYP2B6/2B1 and CYP2D6/2D1 in a competitive way (Ki = 3.84/0.59 and 5.41/0.87 muM), and inhibited CYP3A4/3A2 and rat CYP2E1 in a mixed way (Ki = 11.50/1.83 and 13.06 muM).	apatinib	0-8	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	174-180
30138636-5	2018	Apatinib was a weak inhibitor of human CYP2E1 (IC50&gt;10 muM) but inhibited CYP2B6/2B1 and CYP2D6/2D1 in a competitive way (Ki = 3.84/0.59 and 5.41/0.87 muM), and inhibited CYP3A4/3A2 and rat CYP2E1 in a mixed way (Ki = 11.50/1.83 and 13.06 muM).	apatinib	0-8	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	193-199
30138636-5	2018	Apatinib was a weak inhibitor of human CYP2E1 (IC50&gt;10 muM) but inhibited CYP2B6/2B1 and CYP2D6/2D1 in a competitive way (Ki = 3.84/0.59 and 5.41/0.87 muM), and inhibited CYP3A4/3A2 and rat CYP2E1 in a mixed way (Ki = 11.50/1.83 and 13.06 muM).	apatinib	0-8	latexin	Homo sapiens	154-157
30410610-0	2018	VEGFR-2 Inhibitor Apatinib Hinders Endothelial Cells Progression Triggered by Irradiated Gastric Cancer Cells-derived Exosomes.	apatinib	18-26	kinase insert domain receptor	Homo sapiens	0-7
30410610-13	2018	Importantly, the latter is counteracted by the VEGFR-2 inhibitor Apatinib which hinders ECs progression.	apatinib	65-73	kinase insert domain receptor	Homo sapiens	47-54
30151975-8	2018	Treatment with vascular endothelial growth factor receptor 2 (VEGFR2) antagonist apatinib and VEGFR2 silencing further confirmed TP upregulation.	apatinib	81-89	kinase insert domain receptor	Homo sapiens	15-60
30151975-8	2018	Treatment with vascular endothelial growth factor receptor 2 (VEGFR2) antagonist apatinib and VEGFR2 silencing further confirmed TP upregulation.	apatinib	81-89	kinase insert domain receptor	Homo sapiens	62-68
30074936-0	2018	Apatinib reverses alectinib resistance by targeting vascular endothelial growth factor receptor 2 and attenuating the oncogenic signaling pathway in echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase fusion gene-positive lung cancer cell lines.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	52-97
30074936-0	2018	Apatinib reverses alectinib resistance by targeting vascular endothelial growth factor receptor 2 and attenuating the oncogenic signaling pathway in echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase fusion gene-positive lung cancer cell lines.	apatinib	0-8	ALK receptor tyrosine kinase	Homo sapiens	198-224
30074936-7	2018	Moreover, we found that apatinib restored sensitivity to alectinib mainly through suppression of the ALK downstream signaling pathway and antiangiogenesis signaling.	apatinib	24-32	ALK receptor tyrosine kinase	Homo sapiens	101-104
30026059-1	2018	OBJECTIVES: Apatinib exhibits broad-spectrum antitumor activities by selectively inhibiting vascular endothelial growth factor receptor-2.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	92-137
30138636-3	2018	The purpose of this study is to evaluate the inhibition effects of apatinib on human and rat cytochrome P450, including CYP3A2/4, CYP2B1/6, CYP2C9/11, CYP2D1/6, and CYP2E1.	apatinib	67-75	cytochrome P450, family 3, subfamily a, polypeptide 2	Rattus norvegicus	120-126
30138636-3	2018	The purpose of this study is to evaluate the inhibition effects of apatinib on human and rat cytochrome P450, including CYP3A2/4, CYP2B1/6, CYP2C9/11, CYP2D1/6, and CYP2E1.	apatinib	67-75	cytochrome P450, family 2, subfamily b, polypeptide 1	Rattus norvegicus	130-136
30138636-3	2018	The purpose of this study is to evaluate the inhibition effects of apatinib on human and rat cytochrome P450, including CYP3A2/4, CYP2B1/6, CYP2C9/11, CYP2D1/6, and CYP2E1.	apatinib	67-75	cytochrome P450, family 2, subfamily d, polypeptide 1	Rattus norvegicus	151-157
30138636-3	2018	The purpose of this study is to evaluate the inhibition effects of apatinib on human and rat cytochrome P450, including CYP3A2/4, CYP2B1/6, CYP2C9/11, CYP2D1/6, and CYP2E1.	apatinib	67-75	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	165-171
30138636-5	2018	Apatinib was a weak inhibitor of human CYP2E1 (IC50&gt;10 muM) but inhibited CYP2B6/2B1 and CYP2D6/2D1 in a competitive way (Ki = 3.84/0.59 and 5.41/0.87 muM), and inhibited CYP3A4/3A2 and rat CYP2E1 in a mixed way (Ki = 11.50/1.83 and 13.06 muM).	apatinib	0-8	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	39-45
30138636-5	2018	Apatinib was a weak inhibitor of human CYP2E1 (IC50&gt;10 muM) but inhibited CYP2B6/2B1 and CYP2D6/2D1 in a competitive way (Ki = 3.84/0.59 and 5.41/0.87 muM), and inhibited CYP3A4/3A2 and rat CYP2E1 in a mixed way (Ki = 11.50/1.83 and 13.06 muM).	apatinib	0-8	latexin	Homo sapiens	58-61
30138636-5	2018	Apatinib was a weak inhibitor of human CYP2E1 (IC50&gt;10 muM) but inhibited CYP2B6/2B1 and CYP2D6/2D1 in a competitive way (Ki = 3.84/0.59 and 5.41/0.87 muM), and inhibited CYP3A4/3A2 and rat CYP2E1 in a mixed way (Ki = 11.50/1.83 and 13.06 muM).	apatinib	0-8	cytochrome P450 family 2 subfamily B member 6	Homo sapiens	77-87
30138636-5	2018	Apatinib was a weak inhibitor of human CYP2E1 (IC50&gt;10 muM) but inhibited CYP2B6/2B1 and CYP2D6/2D1 in a competitive way (Ki = 3.84/0.59 and 5.41/0.87 muM), and inhibited CYP3A4/3A2 and rat CYP2E1 in a mixed way (Ki = 11.50/1.83 and 13.06 muM).	apatinib	0-8	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	92-98
30301881-0	2018	Apatinib-induced protective autophagy and apoptosis through the AKT-mTOR pathway in anaplastic thyroid cancer.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	64-67
30301881-0	2018	Apatinib-induced protective autophagy and apoptosis through the AKT-mTOR pathway in anaplastic thyroid cancer.	apatinib	0-8	mechanistic target of rapamycin kinase	Homo sapiens	68-72
30301881-1	2018	Apatinib, an inhibitor of vascular endothelial growth factor receptor-2, has been shown to promote anti-cancer action across a wide range of malignancies, including gastric, lung, and breast cancers.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	26-71
30301881-3	2018	In this study, we demonstrated that apatinib induced both autophagy and apoptosis in human ATC cells through downregulation of p-AKT and p-mTOR signals via the AKT/mTOR pathway.	apatinib	36-44	AKT serine/threonine kinase 1	Homo sapiens	129-132
30301881-3	2018	In this study, we demonstrated that apatinib induced both autophagy and apoptosis in human ATC cells through downregulation of p-AKT and p-mTOR signals via the AKT/mTOR pathway.	apatinib	36-44	mechanistic target of rapamycin kinase	Homo sapiens	139-143
30301881-3	2018	In this study, we demonstrated that apatinib induced both autophagy and apoptosis in human ATC cells through downregulation of p-AKT and p-mTOR signals via the AKT/mTOR pathway.	apatinib	36-44	AKT serine/threonine kinase 1	Homo sapiens	160-163
30301881-3	2018	In this study, we demonstrated that apatinib induced both autophagy and apoptosis in human ATC cells through downregulation of p-AKT and p-mTOR signals via the AKT/mTOR pathway.	apatinib	36-44	mechanistic target of rapamycin kinase	Homo sapiens	164-168
30301881-5	2018	These findings showed that both autophagy and AKT/mTOR signals were engaged in ATC cell death evoked by apatinib.	apatinib	104-112	AKT serine/threonine kinase 1	Homo sapiens	46-49
30301881-5	2018	These findings showed that both autophagy and AKT/mTOR signals were engaged in ATC cell death evoked by apatinib.	apatinib	104-112	mechanistic target of rapamycin kinase	Homo sapiens	50-54
30323627-1	2018	Background and purpose: Apatinib is a novel, oral, small-molecule tyrosine kinase inhibitor that targets VEGFR-2.	apatinib	24-32	kinase insert domain receptor	Homo sapiens	105-112
30323627-14	2018	Conclusion: Apatinib is a novel VEGFR-2 inhibitor with proven efficacy and safety for solid tumors.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	32-39
29770798-1	2018	Apatinib, a small-molecule inhibitor of VEGFR-2, has attracted much attention due to its encouraging anticancer activity in third-line clinical treatment for many malignancies, including non-small cell lung cancer (NSCLC).	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	40-47
29770798-5	2018	Apatinib significantly enhanced the antitumor effect of docetaxel and alleviated docetaxel-induced liver damage as well as decreased serum transaminases (ALT and AST).	apatinib	0-8	glutamic pyruvic transaminase, soluble	Mus musculus	154-157
29770798-5	2018	Apatinib significantly enhanced the antitumor effect of docetaxel and alleviated docetaxel-induced liver damage as well as decreased serum transaminases (ALT and AST).	apatinib	0-8	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	162-165
29770798-9	2018	A cellular pharmacokinetic study revealed that apatinib significantly increased cellular/subcellular accumulation (especially in the cytosol) and decreased the efflux of docetaxel in A549/DTX cells through P-gp, while apatinib exerted no significant effect on the cellular pharmacokinetics of docetaxel in A549 cells.	apatinib	47-55	phosphoglycolate phosphatase	Mus musculus	206-210
30400838-12	2018	CONCLUSION: Apatinib inhibit VEGF-mediated cell migration and invasion in CCA cell lines via inhibiting the VEGFR2/RAF/MEK/ERK and PI3K/AKT pathways.	apatinib	12-20	mitogen-activated protein kinase kinase 7	Homo sapiens	119-122
30400838-12	2018	CONCLUSION: Apatinib inhibit VEGF-mediated cell migration and invasion in CCA cell lines via inhibiting the VEGFR2/RAF/MEK/ERK and PI3K/AKT pathways.	apatinib	12-20	mitogen-activated protein kinase 1	Homo sapiens	123-126
30400838-12	2018	CONCLUSION: Apatinib inhibit VEGF-mediated cell migration and invasion in CCA cell lines via inhibiting the VEGFR2/RAF/MEK/ERK and PI3K/AKT pathways.	apatinib	12-20	AKT serine/threonine kinase 1	Homo sapiens	136-139
30126078-1	2018	BACKGROUND: Apatinib, a small-molecule inhibitor of vascular endothelial growth factor receptor 2 (VEGFR-2), has proven to be effective and safe for treating patients with advanced gastric cancer after second-line chemotherapy failure.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	52-97
30126078-1	2018	BACKGROUND: Apatinib, a small-molecule inhibitor of vascular endothelial growth factor receptor 2 (VEGFR-2), has proven to be effective and safe for treating patients with advanced gastric cancer after second-line chemotherapy failure.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	99-106
30223869-2	2018	Apatinib, a small molecule inhibitor of vascular endothelial growth factor receptor (VEGFR-2), is an orally bioavailable agent, which has shown survival benefit in multiple solid tumors.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	85-92
30271164-7	2018	Then, the patient was rechallenged with six cycles of docetaxel combined with apatinib (an oral tyrosine kinase inhibitor to vascular endothelial growth factor receptor 2 [VEGFR2]), followed by single dose of apatinib as maintenance therapy.	apatinib	78-86	kinase insert domain receptor	Homo sapiens	125-170
30271164-7	2018	Then, the patient was rechallenged with six cycles of docetaxel combined with apatinib (an oral tyrosine kinase inhibitor to vascular endothelial growth factor receptor 2 [VEGFR2]), followed by single dose of apatinib as maintenance therapy.	apatinib	78-86	kinase insert domain receptor	Homo sapiens	172-178
30104882-3	2018	This paper reported a case of RPLS induced by apatinib, a vascular endothelial growth factor receptor 2 (VEGFR-2) tyrosine kinase inhibitor.	apatinib	46-54	kinase insert domain receptor	Homo sapiens	58-103
29956792-0	2018	DUSP1 induces apatinib resistance by activating the MAPK pathway in gastric cancer.	apatinib	14-22	dual specificity phosphatase 1	Homo sapiens	0-5
29956792-2	2018	In order to investigate the potential relationship between DUSP1 and apatinib resistance in gastric cancer cells, we preformed many assays to study this problem.	apatinib	69-77	dual specificity phosphatase 1	Homo sapiens	59-64
29956792-5	2018	It was found that apatinib (Apa)-resistant gastric cancer (GC) cells showed increased expression of DUSP1, whereas the knockdown of DUSP1 in resistant cells resensitized these cells to Apa.	apatinib	18-26	dual specificity phosphatase 1	Homo sapiens	100-105
29956792-5	2018	It was found that apatinib (Apa)-resistant gastric cancer (GC) cells showed increased expression of DUSP1, whereas the knockdown of DUSP1 in resistant cells resensitized these cells to Apa.	apatinib	18-26	dual specificity phosphatase 1	Homo sapiens	132-137
29956792-5	2018	It was found that apatinib (Apa)-resistant gastric cancer (GC) cells showed increased expression of DUSP1, whereas the knockdown of DUSP1 in resistant cells resensitized these cells to Apa.	apatinib	28-31	dual specificity phosphatase 1	Homo sapiens	100-105
29956792-5	2018	It was found that apatinib (Apa)-resistant gastric cancer (GC) cells showed increased expression of DUSP1, whereas the knockdown of DUSP1 in resistant cells resensitized these cells to Apa.	apatinib	28-31	dual specificity phosphatase 1	Homo sapiens	132-137
30170427-0	2018	Efficacy and safety of apatinib in patients with advanced nonsmall cell lung cancer that failed prior chemotherapy or EGFR-TKIs: A pooled analysis.	apatinib	23-31	epidermal growth factor receptor	Homo sapiens	118-122
30170427-1	2018	BACKGROUND: Apatinib is a tyrosine kinase inhibitor (TKI) that selectively inhibits the vascular endothelial growth factor receptor-2.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	88-133
30170427-12	2018	CONCLUSION: Apatinib has promising antitumor activity and manageable toxicity profile in patients with advanced NSCLC that failed prior chemotherapy or EGFR-TKIs.	apatinib	12-20	epidermal growth factor receptor	Homo sapiens	152-156
29859300-4	2018	Moreover, activation of the IRE1alpha pathway from apatinib-induced ER stress is responsible for the induction of autophagy; however, blocking autophagy could enhance the apoptosis in apatinib-treated human CRC cell lines.	apatinib	51-59	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	28-37
29859300-4	2018	Moreover, activation of the IRE1alpha pathway from apatinib-induced ER stress is responsible for the induction of autophagy; however, blocking autophagy could enhance the apoptosis in apatinib-treated human CRC cell lines.	apatinib	184-192	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	28-37
30109780-3	2018	Apatinib, a small molecule inhibitor of VEGFR-2 tyrosine kinase, shows strong antitumor activity in various tumors.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	40-47
30109780-5	2018	Following the results in our study, apatinib inhibited phosphorylation of VEGFR-2 in HUVECs and blocked in vitro endothelial cell migration and tube formation.	apatinib	36-44	kinase insert domain receptor	Homo sapiens	74-81
30109780-6	2018	Concentration-dependent antiproliferative effects of apatinib were also observed in all 6 HCC cell lines including SK-Hep-1, HepG2, Hep3B, Huh-7, PLC/PRF/5, SMMC-7721.	apatinib	53-61	MIR7-3 host gene	Homo sapiens	139-144
30109780-7	2018	Moreover, response to apatinib of HCC cell lines was significantly correlated with VEGFR-2 expression level.	apatinib	22-30	kinase insert domain receptor	Homo sapiens	83-90
30109780-8	2018	Additionally, apatinib significantly inhibit VEGF-triggered VEGFR-2 phosphorylation and activation of downstream signaling molecules such as Akt and ERK1/2 in HCCs.	apatinib	14-22	vascular endothelial growth factor A	Homo sapiens	45-49
30109780-8	2018	Additionally, apatinib significantly inhibit VEGF-triggered VEGFR-2 phosphorylation and activation of downstream signaling molecules such as Akt and ERK1/2 in HCCs.	apatinib	14-22	kinase insert domain receptor	Homo sapiens	60-67
30109780-8	2018	Additionally, apatinib significantly inhibit VEGF-triggered VEGFR-2 phosphorylation and activation of downstream signaling molecules such as Akt and ERK1/2 in HCCs.	apatinib	14-22	AKT serine/threonine kinase 1	Homo sapiens	141-144
30109780-8	2018	Additionally, apatinib significantly inhibit VEGF-triggered VEGFR-2 phosphorylation and activation of downstream signaling molecules such as Akt and ERK1/2 in HCCs.	apatinib	14-22	mitogen-activated protein kinase 3	Homo sapiens	149-155
30109780-12	2018	The results from current study provide a clear biological rationale to evaluate apatinib as a new agent in HCC in clinical setting, especially for the VEGFR-2 overexpression ones.	apatinib	80-88	kinase insert domain receptor	Homo sapiens	151-158
29576426-3	2018	PATIENTS AND METHODS: This pilot study aimed to assess the efficacy and safety of apatinib, a novel oral inhibitor targeting vascular endothelial growth factor receptor 2, as third-line treatment for patients with mCRC refractory to standard therapies.	apatinib	82-90	kinase insert domain receptor	Homo sapiens	125-170
30127626-6	2018	GPC3, a liver tumor homing peptide, was coated onto the surface of apatinib-loaded NBs through biotin-avidin interactions to target liver cancer HepG2 cells.	apatinib	67-75	glypican 3	Homo sapiens	0-4
30127626-11	2018	Treatment with GPC3-targeted and apatinib-loaded NBs also resulted in a higher proportion of cells in the G1 phase compared with other treatment groups such as apatinib only and nontargeted apatinib-loaded NBs when US was utilized.	apatinib	160-168	glypican 3	Homo sapiens	15-19
30127626-11	2018	Treatment with GPC3-targeted and apatinib-loaded NBs also resulted in a higher proportion of cells in the G1 phase compared with other treatment groups such as apatinib only and nontargeted apatinib-loaded NBs when US was utilized.	apatinib	160-168	glypican 3	Homo sapiens	15-19
29972411-5	2018	Effects of pioglitazone and the VEGFR-2-selective inhibitor apatinib on cardiomyocyte apoptotic rate was determined using flow cytometry, and hypertrophy was evaluated using [3H]-leucine incorporation.	apatinib	60-68	kinase insert domain receptor	Rattus norvegicus	32-39
29972411-8	2018	RESULTS: Pioglitazone and VEGFR-2-selective inhibitor apatinib reduced rat cardiomyocyte viability and cardiomyocyte hypertrophy induced by angiotensin II in vitro.	apatinib	54-62	kinase insert domain receptor	Rattus norvegicus	26-33
29972411-8	2018	RESULTS: Pioglitazone and VEGFR-2-selective inhibitor apatinib reduced rat cardiomyocyte viability and cardiomyocyte hypertrophy induced by angiotensin II in vitro.	apatinib	54-62	angiotensinogen	Rattus norvegicus	140-154
29972411-9	2018	Furthermore, in the same in vitro model, pioglitazone and apatinib significantly increased the expression of Bax and phosphorylated P53 and decreased the expression of phosphorylated VEGFR-2, Akt, and mTOR, which promote cardiomyocyte hypertrophy.	apatinib	58-66	BCL2 associated X, apoptosis regulator	Rattus norvegicus	109-112
29972411-9	2018	Furthermore, in the same in vitro model, pioglitazone and apatinib significantly increased the expression of Bax and phosphorylated P53 and decreased the expression of phosphorylated VEGFR-2, Akt, and mTOR, which promote cardiomyocyte hypertrophy.	apatinib	58-66	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	132-135
29972411-9	2018	Furthermore, in the same in vitro model, pioglitazone and apatinib significantly increased the expression of Bax and phosphorylated P53 and decreased the expression of phosphorylated VEGFR-2, Akt, and mTOR, which promote cardiomyocyte hypertrophy.	apatinib	58-66	kinase insert domain receptor	Rattus norvegicus	183-190
29972411-9	2018	Furthermore, in the same in vitro model, pioglitazone and apatinib significantly increased the expression of Bax and phosphorylated P53 and decreased the expression of phosphorylated VEGFR-2, Akt, and mTOR, which promote cardiomyocyte hypertrophy.	apatinib	58-66	AKT serine/threonine kinase 1	Rattus norvegicus	192-195
29972411-9	2018	Furthermore, in the same in vitro model, pioglitazone and apatinib significantly increased the expression of Bax and phosphorylated P53 and decreased the expression of phosphorylated VEGFR-2, Akt, and mTOR, which promote cardiomyocyte hypertrophy.	apatinib	58-66	mechanistic target of rapamycin kinase	Rattus norvegicus	201-205
30104882-3	2018	This paper reported a case of RPLS induced by apatinib, a vascular endothelial growth factor receptor 2 (VEGFR-2) tyrosine kinase inhibitor.	apatinib	46-54	kinase insert domain receptor	Homo sapiens	105-112
30052652-0	2018	In vitro and in vivo apatinib inhibits vasculogenic mimicry in melanoma MUM-2B cells.	apatinib	21-29	WT1 associated protein	Homo sapiens	72-77
30052652-2	2018	MUM-2B cells cultured in three-dimensional Matrigel were treated with varying concentrations (0, 0.01, 0.05, 0.1, 0.5 mumol/L) of apatinib to test its effect on VM in vitro, followed by MTT proliferation and transwell invasion assays to determine the effect of apatinib on cell proliferation and invasion of MUM-2B cells.	apatinib	130-138	WT1 associated protein	Homo sapiens	0-5
30052652-7	2018	Mice in apatinib-treated groups showed a markedly reduced expression of VEGFR-2, ERK-1/2, PI3K, and MMP-2.	apatinib	8-16	kinase insert domain protein receptor	Mus musculus	72-79
30052652-7	2018	Mice in apatinib-treated groups showed a markedly reduced expression of VEGFR-2, ERK-1/2, PI3K, and MMP-2.	apatinib	8-16	mitogen-activated protein kinase 3	Mus musculus	81-88
30052652-7	2018	Mice in apatinib-treated groups showed a markedly reduced expression of VEGFR-2, ERK-1/2, PI3K, and MMP-2.	apatinib	8-16	matrix metallopeptidase 2	Mus musculus	100-105
30052652-8	2018	In summary, apatinib could inhibit the expression of VEGFR-2, and downregulate the ERK1/2/PI3K/MMP-2 signaling cascade, which may be one of the underlying mechanisms by which apatinib inhibits angiogenesis and the development of VM in models of melanoma cancer, and restrains the formation of VM by MUM-2B cells.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	53-60
30052652-8	2018	In summary, apatinib could inhibit the expression of VEGFR-2, and downregulate the ERK1/2/PI3K/MMP-2 signaling cascade, which may be one of the underlying mechanisms by which apatinib inhibits angiogenesis and the development of VM in models of melanoma cancer, and restrains the formation of VM by MUM-2B cells.	apatinib	12-20	mitogen-activated protein kinase 3	Homo sapiens	83-89
30052652-8	2018	In summary, apatinib could inhibit the expression of VEGFR-2, and downregulate the ERK1/2/PI3K/MMP-2 signaling cascade, which may be one of the underlying mechanisms by which apatinib inhibits angiogenesis and the development of VM in models of melanoma cancer, and restrains the formation of VM by MUM-2B cells.	apatinib	12-20	matrix metallopeptidase 2	Homo sapiens	95-100
30052652-8	2018	In summary, apatinib could inhibit the expression of VEGFR-2, and downregulate the ERK1/2/PI3K/MMP-2 signaling cascade, which may be one of the underlying mechanisms by which apatinib inhibits angiogenesis and the development of VM in models of melanoma cancer, and restrains the formation of VM by MUM-2B cells.	apatinib	175-183	mitogen-activated protein kinase 3	Homo sapiens	83-89
30052652-8	2018	In summary, apatinib could inhibit the expression of VEGFR-2, and downregulate the ERK1/2/PI3K/MMP-2 signaling cascade, which may be one of the underlying mechanisms by which apatinib inhibits angiogenesis and the development of VM in models of melanoma cancer, and restrains the formation of VM by MUM-2B cells.	apatinib	175-183	matrix metallopeptidase 2	Homo sapiens	95-100
30037379-3	2018	Apatinib, a new potent oral small-molecule tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor 2 (VEGFR-2), showed the effect of anti-angiogenesis.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	107-152
30037379-3	2018	Apatinib, a new potent oral small-molecule tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor 2 (VEGFR-2), showed the effect of anti-angiogenesis.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	154-161
30050305-4	2018	Apatinib (YN968D1) is an oral small-molecule tyrosine kinase inhibitor of VEGFR-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	74-81
30038504-2	2018	Apatinib, an oral small-molecule VEGFR-2 inhibitor, has shown good therapeutic effect and safety in chemotherapy-refractory gastric cancer, but its efficacy in lung SCC is not determined.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	33-40
30038504-3	2018	In this report, we present a 69-year-old Chinese man with locally advanced EGFR- and ALK-negative lung SCC, who received apatinib after failure of 2 treatment regimens.	apatinib	121-129	epidermal growth factor receptor	Homo sapiens	75-79
30038504-3	2018	In this report, we present a 69-year-old Chinese man with locally advanced EGFR- and ALK-negative lung SCC, who received apatinib after failure of 2 treatment regimens.	apatinib	121-129	ALK receptor tyrosine kinase	Homo sapiens	85-88
30038504-3	2018	In this report, we present a 69-year-old Chinese man with locally advanced EGFR- and ALK-negative lung SCC, who received apatinib after failure of 2 treatment regimens.	apatinib	121-129	serpin family B member 3	Homo sapiens	103-106
30038504-6	2018	Apatinib provides an additional option for salvage treatment of lung SCC without driver gene mutations, but further large-scale clinical studies are still warranted.	apatinib	0-8	serpin family B member 3	Homo sapiens	69-72
29777301-5	2018	Upon inhibition of p-VEGFR2 by apatinib in Calu-1 cells, the expression of NRP-1 protein and other related proteins in the pathway was still high.	apatinib	31-39	kinase insert domain receptor	Homo sapiens	21-27
29777301-5	2018	Upon inhibition of p-VEGFR2 by apatinib in Calu-1 cells, the expression of NRP-1 protein and other related proteins in the pathway was still high.	apatinib	31-39	neuropilin 1	Homo sapiens	75-80
29777301-8	2018	Calu-1 cells treated with NRP-1 siRNA exhibited significantly higher apoptosis and radiation sensitivity in radiation therapy compared to Calu-1 cells treated with apatinib alone (p &lt; 0.01; p &lt; 0.01).	apatinib	164-172	neuropilin 1	Homo sapiens	26-31
29552208-0	2018	Apatinib promotes apoptosis of the SMMC-7721 hepatocellular carcinoma cell line via the PI3K/Akt pathway.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	93-96
29979376-2	2018	Apatinib is a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	56-101
29928421-1	2018	As a novel vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor, Apatinib has exhibited antitumor effects in a variety of solid tumors.	apatinib	94-102	kinase insert domain receptor	Homo sapiens	11-56
29928421-1	2018	As a novel vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor, Apatinib has exhibited antitumor effects in a variety of solid tumors.	apatinib	94-102	kinase insert domain receptor	Homo sapiens	58-65
29928421-10	2018	The downregulation of p-Akt and p-ERK induced by Apatinib and Tripterine was further inhibited in the combination group (P&lt;0.05), and the expression levels of Caspase-3 and Bax were also significantly increased in the combination group (P&lt;0.05).	apatinib	49-57	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	32-37
29928421-10	2018	The downregulation of p-Akt and p-ERK induced by Apatinib and Tripterine was further inhibited in the combination group (P&lt;0.05), and the expression levels of Caspase-3 and Bax were also significantly increased in the combination group (P&lt;0.05).	apatinib	49-57	caspase 3	Homo sapiens	162-171
29928421-10	2018	The downregulation of p-Akt and p-ERK induced by Apatinib and Tripterine was further inhibited in the combination group (P&lt;0.05), and the expression levels of Caspase-3 and Bax were also significantly increased in the combination group (P&lt;0.05).	apatinib	49-57	BCL2 associated X, apoptosis regulator	Homo sapiens	176-179
29928421-11	2018	The combination of Apatinib and Tripterine significantly inhibited the proliferation, migration and invasion ability and promoted the apoptosis of Hep3B cells by downregulating the expression of p-Akt and p-ERK, and upregulating the expression of Caspase-3 and Bax.	apatinib	19-27	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	205-210
29928421-11	2018	The combination of Apatinib and Tripterine significantly inhibited the proliferation, migration and invasion ability and promoted the apoptosis of Hep3B cells by downregulating the expression of p-Akt and p-ERK, and upregulating the expression of Caspase-3 and Bax.	apatinib	19-27	caspase 3	Homo sapiens	247-256
29928421-11	2018	The combination of Apatinib and Tripterine significantly inhibited the proliferation, migration and invasion ability and promoted the apoptosis of Hep3B cells by downregulating the expression of p-Akt and p-ERK, and upregulating the expression of Caspase-3 and Bax.	apatinib	19-27	BCL2 associated X, apoptosis regulator	Homo sapiens	261-264
29384217-5	2018	Meanwhile, vitamin B2 induced activation of LSD1 may attenuate the proliferation inhibition, and anti-migration effects of apatinib in gastric cancer cells.	apatinib	123-131	lysine demethylase 1A	Homo sapiens	44-48
29924049-9	2018	Finally, only a few lesions remained LESSONS:: Apatinib alone may be a good second-line therapy for advanced HCC patients who are refractory to sorafenib.	apatinib	47-55	HCC	Homo sapiens	109-112
29855279-0	2018	Apatinib treatment for KIT- and KDR-amplified angiosarcoma: a case report.	apatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	23-27
29855279-0	2018	Apatinib treatment for KIT- and KDR-amplified angiosarcoma: a case report.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	32-35
29855279-2	2018	Apatinib, a novel tyrosine kinase inhibitor (TKI) targeting vascular endothelial growth factor receptor-2 (VEGFR2), has been approved for the treatment of advanced gastric cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	60-105
29855279-2	2018	Apatinib, a novel tyrosine kinase inhibitor (TKI) targeting vascular endothelial growth factor receptor-2 (VEGFR2), has been approved for the treatment of advanced gastric cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	107-113
29855279-3	2018	CASE PRESENTATION: Herein, we report a patient with advanced angiosarcoma, who received apatinib at a daily dose of 250 to 725 mg, resulting in a partial response for three months, which may be related to Kinase Insert Domain Receptor (KDR) gene amplification.	apatinib	88-96	kinase insert domain receptor	Homo sapiens	205-234
29855279-3	2018	CASE PRESENTATION: Herein, we report a patient with advanced angiosarcoma, who received apatinib at a daily dose of 250 to 725 mg, resulting in a partial response for three months, which may be related to Kinase Insert Domain Receptor (KDR) gene amplification.	apatinib	88-96	kinase insert domain receptor	Homo sapiens	236-239
29849960-6	2018	As a novel targeted therapy, especially with regard to angiogenesis, apatinib is a new type of small molecule tyrosine kinase inhibitor that selectively targets VEGFR-2 and has shown encouraging anticancer activity in a wide range of malignancies, including gastric cancer, non-small cell lung cancer, breast cancer, hepatocellular carcinoma, and sarcomas.	apatinib	69-77	kinase insert domain receptor	Homo sapiens	161-168
29785118-10	2018	Western blotting showed that the combination of APS and apatinib significantly enhanced the downregulation of phosphorylated protein kinase B (AKT) and extracellular signal-regulated kinase (ERK) (p-AKT and p-ERK) as well as matrix metalloproteinases-9 (MMP-9) expression.	apatinib	56-64	AKT serine/threonine kinase 1	Homo sapiens	143-146
29785118-10	2018	Western blotting showed that the combination of APS and apatinib significantly enhanced the downregulation of phosphorylated protein kinase B (AKT) and extracellular signal-regulated kinase (ERK) (p-AKT and p-ERK) as well as matrix metalloproteinases-9 (MMP-9) expression.	apatinib	56-64	mitogen-activated protein kinase 1	Homo sapiens	152-189
29785118-10	2018	Western blotting showed that the combination of APS and apatinib significantly enhanced the downregulation of phosphorylated protein kinase B (AKT) and extracellular signal-regulated kinase (ERK) (p-AKT and p-ERK) as well as matrix metalloproteinases-9 (MMP-9) expression.	apatinib	56-64	mitogen-activated protein kinase 1	Homo sapiens	191-194
29785118-10	2018	Western blotting showed that the combination of APS and apatinib significantly enhanced the downregulation of phosphorylated protein kinase B (AKT) and extracellular signal-regulated kinase (ERK) (p-AKT and p-ERK) as well as matrix metalloproteinases-9 (MMP-9) expression.	apatinib	56-64	AKT serine/threonine kinase 1	Homo sapiens	199-202
29785118-10	2018	Western blotting showed that the combination of APS and apatinib significantly enhanced the downregulation of phosphorylated protein kinase B (AKT) and extracellular signal-regulated kinase (ERK) (p-AKT and p-ERK) as well as matrix metalloproteinases-9 (MMP-9) expression.	apatinib	56-64	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	207-212
29785118-10	2018	Western blotting showed that the combination of APS and apatinib significantly enhanced the downregulation of phosphorylated protein kinase B (AKT) and extracellular signal-regulated kinase (ERK) (p-AKT and p-ERK) as well as matrix metalloproteinases-9 (MMP-9) expression.	apatinib	56-64	matrix metallopeptidase 9	Homo sapiens	225-252
29785118-10	2018	Western blotting showed that the combination of APS and apatinib significantly enhanced the downregulation of phosphorylated protein kinase B (AKT) and extracellular signal-regulated kinase (ERK) (p-AKT and p-ERK) as well as matrix metalloproteinases-9 (MMP-9) expression.	apatinib	56-64	matrix metallopeptidase 9	Homo sapiens	254-259
29785118-13	2018	Conclusion: The study first demonstrated that apatinib showed potentially inhibitory effects in pancreatic cancer cells and that APS enhanced the antitumor effects of apatinib through further downregulating the expression of phosphorylation of AKT and ERK as well as MMP-9.	apatinib	167-175	AKT serine/threonine kinase 1	Homo sapiens	244-247
29785118-13	2018	Conclusion: The study first demonstrated that apatinib showed potentially inhibitory effects in pancreatic cancer cells and that APS enhanced the antitumor effects of apatinib through further downregulating the expression of phosphorylation of AKT and ERK as well as MMP-9.	apatinib	167-175	mitogen-activated protein kinase 1	Homo sapiens	252-255
29785118-13	2018	Conclusion: The study first demonstrated that apatinib showed potentially inhibitory effects in pancreatic cancer cells and that APS enhanced the antitumor effects of apatinib through further downregulating the expression of phosphorylation of AKT and ERK as well as MMP-9.	apatinib	167-175	matrix metallopeptidase 9	Homo sapiens	267-272
29663291-1	2018	Apatinib [Aitan  (brand name in China)], also known as rivoceranib, is a novel, small molecule, selective vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor and is the second anti-angiogenic drug to be approved in China for the treatment of advanced or metastatic gastric cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	106-151
29663291-1	2018	Apatinib [Aitan  (brand name in China)], also known as rivoceranib, is a novel, small molecule, selective vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor and is the second anti-angiogenic drug to be approved in China for the treatment of advanced or metastatic gastric cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	153-160
29663291-1	2018	Apatinib [Aitan  (brand name in China)], also known as rivoceranib, is a novel, small molecule, selective vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor and is the second anti-angiogenic drug to be approved in China for the treatment of advanced or metastatic gastric cancer.	apatinib	10-15	kinase insert domain receptor	Homo sapiens	106-151
29663291-1	2018	Apatinib [Aitan  (brand name in China)], also known as rivoceranib, is a novel, small molecule, selective vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor and is the second anti-angiogenic drug to be approved in China for the treatment of advanced or metastatic gastric cancer.	apatinib	10-15	kinase insert domain receptor	Homo sapiens	153-160
29663291-1	2018	Apatinib [Aitan  (brand name in China)], also known as rivoceranib, is a novel, small molecule, selective vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor and is the second anti-angiogenic drug to be approved in China for the treatment of advanced or metastatic gastric cancer.	apatinib	55-66	kinase insert domain receptor	Homo sapiens	106-151
29663291-1	2018	Apatinib [Aitan  (brand name in China)], also known as rivoceranib, is a novel, small molecule, selective vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor and is the second anti-angiogenic drug to be approved in China for the treatment of advanced or metastatic gastric cancer.	apatinib	55-66	kinase insert domain receptor	Homo sapiens	153-160
30003733-1	2018	PURPOSE: To investigate the efficacy and safety of apatinib mesylate (AM) in treating advanced non-small cell lung cancer (aNSCLC) with wild or unknown epidermal growth factor receptor (w/nEGFR).	apatinib	51-68	epidermal growth factor receptor	Homo sapiens	152-184
29575765-6	2018	Combination therapy of apatinib with icotinib for primary acquired resistance to icotinib may be an option for patients with advanced pulmonary adenocarcinoma with EGFR mutations, but physicians must also be aware of the side effects caused by such therapy.	apatinib	23-31	epidermal growth factor receptor	Homo sapiens	164-168
29549743-1	2018	Apatinib, a highly selective small-molecule inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2), has attracted many attentions due to its anticancer activity in various malignancies containing non-small-cell lung cancer (NSCLC).	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	57-102
29549743-1	2018	Apatinib, a highly selective small-molecule inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2), has attracted many attentions due to its anticancer activity in various malignancies containing non-small-cell lung cancer (NSCLC).	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	104-111
29740957-0	2018	EGFR exon 20 insertion mutation in advanced thymic squamous cell carcinoma: Response to apatinib and clinical outcomes.	apatinib	88-96	epidermal growth factor receptor	Homo sapiens	0-4
29740957-6	2018	Herein we report a case of advanced thymic squamous cell carcinoma harboring EGFR exon 20 insertion in which apatinib was administered after multi-line chemotherapy and radiotherapy and a partial response was achieved after five months of treatment.	apatinib	109-117	epidermal growth factor receptor	Homo sapiens	77-81
29243413-1	2018	AIM: Apatinib, an oral tyrosine kinase inhibitor mainly targeting VEGFR-2, exerts both antiangiogenesis and antiproliferation effects.	apatinib	5-13	kinase insert domain receptor	Homo sapiens	66-73
29851800-5	2018	INTERVENTION: The patient received apatinib therapy for positive vascular endothelial growth factor.	apatinib	35-43	vascular endothelial growth factor A	Homo sapiens	65-99
29872316-1	2018	Introduction: Methylsulfonic apatinib (hereinafter referred to as Apatinib) is a small-molecule angiogenesis inhibitor highly and selectively targeted to vascular endothelial growth factor receptor-2.	apatinib	66-74	kinase insert domain receptor	Homo sapiens	154-199
29872316-7	2018	Apatinib combined with the aforementioned drugs, especially the combination of Apatinib and 5-FU, decreased the invasion and migration ability of the cells and increased the apoptosis ratio; expression of the anti-apoptotic protein Bcl-2 significantly decreased, and expression of the pro-apoptotic protein Bax increased.	apatinib	0-8	BCL2 apoptosis regulator	Homo sapiens	232-237
29872316-7	2018	Apatinib combined with the aforementioned drugs, especially the combination of Apatinib and 5-FU, decreased the invasion and migration ability of the cells and increased the apoptosis ratio; expression of the anti-apoptotic protein Bcl-2 significantly decreased, and expression of the pro-apoptotic protein Bax increased.	apatinib	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	307-310
29872316-7	2018	Apatinib combined with the aforementioned drugs, especially the combination of Apatinib and 5-FU, decreased the invasion and migration ability of the cells and increased the apoptosis ratio; expression of the anti-apoptotic protein Bcl-2 significantly decreased, and expression of the pro-apoptotic protein Bax increased.	apatinib	79-87	BCL2 apoptosis regulator	Homo sapiens	232-237
29765235-5	2018	Apatinib is a novel tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	84-129
29486282-7	2018	RTK pathway arrays and western blots analysis demonstrated that apatinib significantly downregulated the phosphorylation levels of several tyrosine kinase receptors, particularly PDGFR-alpha and IGF-IR, and inhibited Akt phosphorylation.	apatinib	64-72	platelet derived growth factor receptor alpha	Homo sapiens	179-190
29486282-7	2018	RTK pathway arrays and western blots analysis demonstrated that apatinib significantly downregulated the phosphorylation levels of several tyrosine kinase receptors, particularly PDGFR-alpha and IGF-IR, and inhibited Akt phosphorylation.	apatinib	64-72	insulin like growth factor 1 receptor	Homo sapiens	195-201
29486282-7	2018	RTK pathway arrays and western blots analysis demonstrated that apatinib significantly downregulated the phosphorylation levels of several tyrosine kinase receptors, particularly PDGFR-alpha and IGF-IR, and inhibited Akt phosphorylation.	apatinib	64-72	AKT serine/threonine kinase 1	Homo sapiens	217-220
29921401-1	2018	Apatinib is a novel oral, anti-tumor, angiogenic-targeting drug that can selectively target vascular endothelial growth factor receptor-2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	92-137
29921401-1	2018	Apatinib is a novel oral, anti-tumor, angiogenic-targeting drug that can selectively target vascular endothelial growth factor receptor-2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	139-146
29575765-0	2018	Combination therapy of apatinib with icotinib for primary acquired icotinib resistance in patients with advanced pulmonary adenocarcinoma with EGFR mutation.	apatinib	23-31	epidermal growth factor receptor	Homo sapiens	143-147
29575765-3	2018	The aim of this study was to explore the use of apatinib combined with icotinib therapy for primary acquired resistance to icotinib in three patients with advanced pulmonary adenocarcinoma with EGFR mutations.	apatinib	48-56	epidermal growth factor receptor	Homo sapiens	194-198
29428665-0	2018	Astragalus polysaccharide enhanced antitumor effects of Apatinib in gastric cancer AGS cells by inhibiting AKT signalling pathway.	apatinib	56-64	AKT serine/threonine kinase 1	Homo sapiens	107-110
29428665-7	2018	Western blotting showed that the combination of Apatinib and AsPs could inhibit the expression of phosphorylated AKT (p-AKT) and MMP-9 expression.	apatinib	48-56	AKT serine/threonine kinase 1	Homo sapiens	113-116
29428665-7	2018	Western blotting showed that the combination of Apatinib and AsPs could inhibit the expression of phosphorylated AKT (p-AKT) and MMP-9 expression.	apatinib	48-56	AKT serine/threonine kinase 1	Homo sapiens	120-123
29428665-7	2018	Western blotting showed that the combination of Apatinib and AsPs could inhibit the expression of phosphorylated AKT (p-AKT) and MMP-9 expression.	apatinib	48-56	matrix metallopeptidase 9	Homo sapiens	129-134
29428665-10	2018	In conclusion, the current study showed AsPs enhanced antitumor effects of Apatinib on AGS cells by the mechanism which includes inhibition of AKT signaling pathway.	apatinib	75-83	AKT serine/threonine kinase 1	Homo sapiens	143-146
29552208-4	2018	Expression of the apoptosis-related genes Bcl-2, Bax and caspase-9 after apatinib treatment was detected by reverse transcription-quantitative PCR (RT-qPCR) and western blot analysis.	apatinib	73-81	BCL2 apoptosis regulator	Homo sapiens	42-47
29552208-4	2018	Expression of the apoptosis-related genes Bcl-2, Bax and caspase-9 after apatinib treatment was detected by reverse transcription-quantitative PCR (RT-qPCR) and western blot analysis.	apatinib	73-81	BCL2 associated X, apoptosis regulator	Homo sapiens	49-52
29552208-4	2018	Expression of the apoptosis-related genes Bcl-2, Bax and caspase-9 after apatinib treatment was detected by reverse transcription-quantitative PCR (RT-qPCR) and western blot analysis.	apatinib	73-81	caspase 9	Homo sapiens	57-66
29552208-5	2018	Expression of the PI3K, p-PI3K, Akt and p-Akt proteins after apatinib treatment was detected using western blot analysis.	apatinib	61-69	AKT serine/threonine kinase 1	Homo sapiens	32-35
29552208-5	2018	Expression of the PI3K, p-PI3K, Akt and p-Akt proteins after apatinib treatment was detected using western blot analysis.	apatinib	61-69	AKT serine/threonine kinase 1	Homo sapiens	42-45
29552208-7	2018	Annexin V/PI double staining showed that apatinib induced the apoptosis of SMMC-7721 cells in a concentration-dependent manner.	apatinib	41-49	annexin A5	Homo sapiens	0-9
29552208-8	2018	Results of RT-qPCR and western blot analysis showed that apatinib was able to induce the expression of pro-apoptotic genes Bax and caspase-9 and inhibited the expression of anti-apoptotic gene Bcl-2.	apatinib	57-65	BCL2 associated X, apoptosis regulator	Homo sapiens	123-126
29552208-8	2018	Results of RT-qPCR and western blot analysis showed that apatinib was able to induce the expression of pro-apoptotic genes Bax and caspase-9 and inhibited the expression of anti-apoptotic gene Bcl-2.	apatinib	57-65	caspase 9	Homo sapiens	131-140
29552208-8	2018	Results of RT-qPCR and western blot analysis showed that apatinib was able to induce the expression of pro-apoptotic genes Bax and caspase-9 and inhibited the expression of anti-apoptotic gene Bcl-2.	apatinib	57-65	BCL2 apoptosis regulator	Homo sapiens	193-198
29552208-9	2018	In addition, the western blot analysis revealed that p-PI3K and p-Akt was significantly decreased following apatinib treatment, while no significant differences were found in the total protein levels of PI3K and Akt.	apatinib	108-116	AKT serine/threonine kinase 1	Homo sapiens	66-69
29552208-10	2018	The results of the present show that apatinib is capable of promoting the apoptosis of SMMC-7721 cells by inhibiting the PI3K/Akt signal transduction pathway, upregulating the expression of pro-apoptotic genes Bax and caspase-9, and downregulating the expression level of the anti-apoptotic gene Bcl-2.	apatinib	37-45	AKT serine/threonine kinase 1	Homo sapiens	126-129
29552208-10	2018	The results of the present show that apatinib is capable of promoting the apoptosis of SMMC-7721 cells by inhibiting the PI3K/Akt signal transduction pathway, upregulating the expression of pro-apoptotic genes Bax and caspase-9, and downregulating the expression level of the anti-apoptotic gene Bcl-2.	apatinib	37-45	BCL2 associated X, apoptosis regulator	Homo sapiens	210-213
29552208-10	2018	The results of the present show that apatinib is capable of promoting the apoptosis of SMMC-7721 cells by inhibiting the PI3K/Akt signal transduction pathway, upregulating the expression of pro-apoptotic genes Bax and caspase-9, and downregulating the expression level of the anti-apoptotic gene Bcl-2.	apatinib	37-45	caspase 9	Homo sapiens	218-227
29552208-10	2018	The results of the present show that apatinib is capable of promoting the apoptosis of SMMC-7721 cells by inhibiting the PI3K/Akt signal transduction pathway, upregulating the expression of pro-apoptotic genes Bax and caspase-9, and downregulating the expression level of the anti-apoptotic gene Bcl-2.	apatinib	37-45	BCL2 apoptosis regulator	Homo sapiens	296-301
29587657-2	2018	Apatinib is a new potent oral small-molecule tyrosine kinase inhibitor, and targets the intracellular domain of vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	112-157
29587657-2	2018	Apatinib is a new potent oral small-molecule tyrosine kinase inhibitor, and targets the intracellular domain of vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	0-8	kinase insert domain receptor	Homo sapiens	159-166
29675102-7	2018	Further analysis showed synergistic inhibition of MAPK and PI3K/Akt pathways by volitinib and apatinib.	apatinib	94-102	AKT serine/threonine kinase 1	Homo sapiens	64-67
29261000-3	2018	Apatinib is a novel tyrosine kinase inhibitor that targets vascular endothelial growth factor receptor-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	59-104
28967981-2	2018	In vitro data indicate that cytochrome P450 (CYP) 3A4 is the primary CYP isoenzyme involved in the metabolism of apatinib.	apatinib	113-121	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	28-53
28967981-6	2018	In summary, a strong CYP3A4 inducer (rifampin) had a strong effect (>5-fold) on the clinical pharmacokinetics of apatinib, whereas a strong CYP3A inhibitor (itraconazole 100 mg once a day) had a weak effect (1.25- to 2-fold).	apatinib	113-121	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	21-27
28967981-6	2018	In summary, a strong CYP3A4 inducer (rifampin) had a strong effect (>5-fold) on the clinical pharmacokinetics of apatinib, whereas a strong CYP3A inhibitor (itraconazole 100 mg once a day) had a weak effect (1.25- to 2-fold).	apatinib	113-121	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	21-26
29490645-4	2018	In this study, we investigated the effectiveness of Apatinib, a novel receptor tyrosine kinase inhibitor selectively targeting VEGFR-2 in ALL cells.	apatinib	52-60	kinase insert domain receptor	Homo sapiens	127-134
29490645-13	2018	Mechanistically, Apatinib-induced cytotoxicity was closely associated with inhibition of VEGFR2 and its downstream signaling cascades, including the PI3 K, MAPK and STAT3 pathways.	apatinib	17-25	kinase insert domain receptor	Homo sapiens	89-95
29490645-13	2018	Mechanistically, Apatinib-induced cytotoxicity was closely associated with inhibition of VEGFR2 and its downstream signaling cascades, including the PI3 K, MAPK and STAT3 pathways.	apatinib	17-25	signal transducer and activator of transcription 3	Homo sapiens	165-170
29490645-14	2018	CONCLUSION: Our study indicates that Apatinib exerts its anti-leukemia effect by inducing apoptosis through suppressing the VEGFR2 signaling pathway, supporting a potential role for Apatinib in the treatment of ALL.	apatinib	37-45	kinase insert domain receptor	Homo sapiens	124-130
29490645-14	2018	CONCLUSION: Our study indicates that Apatinib exerts its anti-leukemia effect by inducing apoptosis through suppressing the VEGFR2 signaling pathway, supporting a potential role for Apatinib in the treatment of ALL.	apatinib	182-190	kinase insert domain receptor	Homo sapiens	124-130
29502367-1	2018	Objective: To investigate the effect of triptolide, a specific inhibitor of heat shock protein 70 (HSP70), on apatinib resistance in gastric cancer cells line MKN45.	apatinib	110-118	heat shock protein family A (Hsp70) member 4	Homo sapiens	76-97
29502367-1	2018	Objective: To investigate the effect of triptolide, a specific inhibitor of heat shock protein 70 (HSP70), on apatinib resistance in gastric cancer cells line MKN45.	apatinib	110-118	heat shock protein family A (Hsp70) member 4	Homo sapiens	99-104
29502367-8	2018	When heat shock protein 70 was inhibited by triptolide, the IC(50) value of apatinib in MKN45/AR cells was reduced to 11.679 mumol/L, which was significantly lower than cells treated with apatinib alone (P&lt;0.05).	apatinib	76-84	heat shock protein family A (Hsp70) member 4	Homo sapiens	5-26
29502367-8	2018	When heat shock protein 70 was inhibited by triptolide, the IC(50) value of apatinib in MKN45/AR cells was reduced to 11.679 mumol/L, which was significantly lower than cells treated with apatinib alone (P&lt;0.05).	apatinib	188-196	heat shock protein family A (Hsp70) member 4	Homo sapiens	5-26
29248198-2	2018	Apatinib, a novel oral antiangiogenic agent targeting vascular endothelial growth factor receptor (VEGFR2), is currently being studied in different tumor types and is already used in gastric adenocarcinoma.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	99-105
29502367-9	2018	Conclusions: The apatinib-resistant MKN45 cells have high levels of heat shock protein 70.	apatinib	17-25	heat shock protein family A (Hsp70) member 4	Homo sapiens	68-89
29502367-11	2018	Therefore, inhibition of heat shock protein 70 provides a new therapy strategy for patients with apatinib resistance.	apatinib	97-105	heat shock protein family A (Hsp70) member 4	Homo sapiens	25-46
30181815-1	2018	Background: Apatinib is a novel small molecular drug targeting vascular endothelial growth factor receptor-2 (VEGFR-2), which is being studied in multiple tumor types.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	63-108
29497319-1	2018	Apatinib, a novel small molecule tyrosine kinase inhibitor that inhibits vascular endothelial growth factor receptor-2, was approved for metastatic gastric adenocarcinoma in China in Oct 2014.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	73-118
30181815-1	2018	Background: Apatinib is a novel small molecular drug targeting vascular endothelial growth factor receptor-2 (VEGFR-2), which is being studied in multiple tumor types.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	110-117
29037469-5	2018	Agents that inhibit the erb-b2 receptor tyrosine kinase 2 (ERBB2 or HER2), or vascular endothelial growth factor, including trastuzumab, ramucirumab, and apatinib, increase response and survival times.	apatinib	154-162	erb-b2 receptor tyrosine kinase 2	Homo sapiens	24-57
29225166-0	2018	Apatinib inhibits migration and invasion as well as PD-L1 expression in osteosarcoma by targeting STAT3.	apatinib	0-8	signal transducer and activator of transcription 3	Homo sapiens	98-103
29225166-13	2018	Mechanistically, we demonstrate that Apatinib attenuates migration and invasion by suppressing epithelial-mesenchymal transition (EMT) and inactivating STAT3.	apatinib	37-45	signal transducer and activator of transcription 3	Homo sapiens	152-157
29225166-14	2018	Additionally, Apatinib reduces PD-L1 expression in osteosarcoma cells.	apatinib	14-22	CD274 molecule	Homo sapiens	31-36
29662638-0	2018	An open label, single-armed, exploratory study of apatinib (a novel VEGFR-2 tyrosine kinase inhibitor) in patients with relapsed or refractory non-Hodgkin lymphoma.	apatinib	50-58	kinase insert domain receptor	Homo sapiens	68-75
29662638-1	2018	Background: Apatinib, a novel small molecule vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor, have shown remarkable efficacy in many solid cancers.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	45-90
29662638-1	2018	Background: Apatinib, a novel small molecule vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor, have shown remarkable efficacy in many solid cancers.	apatinib	12-20	kinase insert domain receptor	Homo sapiens	92-99
30081717-12	2018	Our case indicates that apatinib, a potent small-molecular TKI targeted VEGFR2 is promising for intractable VBE for satisfactory efficacy and safety.	apatinib	24-32	kinase insert domain receptor	Homo sapiens	72-78
30110192-4	2018	Apatinib is a novel and highly selective tyrosine kinase inhibitor of vascular endothelial growth factor receptor-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	70-115
29886786-1	2018	Apatinib is a novel tyrosine kinase inhibitor that targets VEGFR2 signal and exhibits potent anti-tumor effects in human cancers.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	59-65
29886786-9	2018	We also found that primary cancer tissues with higher level of VEGFR2 were much more sensitive to Apatinib.	apatinib	98-106	kinase insert domain receptor	Homo sapiens	63-69
29037469-5	2018	Agents that inhibit the erb-b2 receptor tyrosine kinase 2 (ERBB2 or HER2), or vascular endothelial growth factor, including trastuzumab, ramucirumab, and apatinib, increase response and survival times.	apatinib	154-162	vascular endothelial growth factor A	Homo sapiens	78-112
29516980-1	2018	Objectives: Apatinib, a tyrosine kinase inhibitor which selectively inhibits vascular endothelial growth factor receptor-2, has been shown to be beneficial to patients with a variety of cancers, including advanced nonsmall-cell lung cancer (NSCLC).	apatinib	12-20	kinase insert domain receptor	Homo sapiens	77-122
29467959-0	2018	Apatinib as a third- or further- line treatment in patients with advanced NSCLC harboring wild-type EGFR.	apatinib	0-8	epidermal growth factor receptor	Homo sapiens	100-104
29467959-1	2018	Objectives: This study was conducted to evaluate the efficacy and safety of apatinib in advanced NSCLC patients with EGFR wild-type who have failed more than second-line chemotherapy.	apatinib	76-84	epidermal growth factor receptor	Homo sapiens	117-121
29467959-2	2018	Materials and Methods: We retrospectively analyzed patients with EGFR wild-type advanced NSCLC who were treated with apatinib from January 2014 to August 2016.	apatinib	117-125	epidermal growth factor receptor	Homo sapiens	65-69
29467959-11	2018	Conclusions: Apatinib should be recommended as a third- or further- line therapy in advanced NSCLC patients with EGFR wild-type due to its better efficacy and tolerable toxicity.	apatinib	13-21	epidermal growth factor receptor	Homo sapiens	113-117
29340015-7	2017	In phase II study, combination apatinib with RT cohorts, AEs events increased comparing with either apatinib alone or RT alone; at the same time, combination cohorts showed PSA declines of &gt;=50% in 12 patients, and stable disease in 6 patients.	apatinib	31-39	kallikrein related peptidase 3	Homo sapiens	173-176
29243778-0	2017	Apatinib resensitizes cisplatin-resistant non-small cell lung carcinoma A549 cell through reversing multidrug resistance and suppressing ERK signaling pathway.	apatinib	0-8	mitogen-activated protein kinase 1	Homo sapiens	137-140
29243778-10	2017	In the apatinib combined with DDP group, the levels of cleaved caspase-3, cleaved caspase-9 and B-cell lymphoma-2 (Bcl-2)-associated X (BAX) proteins were significantly upregulated, while the level of Bcl-2 proteins was downregulated.	apatinib	7-15	caspase 9	Homo sapiens	82-91
29243778-10	2017	In the apatinib combined with DDP group, the levels of cleaved caspase-3, cleaved caspase-9 and B-cell lymphoma-2 (Bcl-2)-associated X (BAX) proteins were significantly upregulated, while the level of Bcl-2 proteins was downregulated.	apatinib	7-15	BCL2 apoptosis regulator	Homo sapiens	96-113
29243778-10	2017	In the apatinib combined with DDP group, the levels of cleaved caspase-3, cleaved caspase-9 and B-cell lymphoma-2 (Bcl-2)-associated X (BAX) proteins were significantly upregulated, while the level of Bcl-2 proteins was downregulated.	apatinib	7-15	BCL2 apoptosis regulator	Homo sapiens	115-120
29243778-10	2017	In the apatinib combined with DDP group, the levels of cleaved caspase-3, cleaved caspase-9 and B-cell lymphoma-2 (Bcl-2)-associated X (BAX) proteins were significantly upregulated, while the level of Bcl-2 proteins was downregulated.	apatinib	7-15	BCL2 apoptosis regulator	Homo sapiens	201-206
29243778-11	2017	Apatinib could inhibit the expression of MDR1 and the activity of the ERK signaling pathway in a dose-dependent manner.	apatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	41-45
29243778-11	2017	Apatinib could inhibit the expression of MDR1 and the activity of the ERK signaling pathway in a dose-dependent manner.	apatinib	0-8	mitogen-activated protein kinase 1	Homo sapiens	70-73
29243778-12	2017	CONCLUSIONS: Apatinib can restore the sensitivity of A549/DDP cells to DDP by down-regulating the expression level of MDR1 and inhibiting the activity of the ERK signaling pathway.	apatinib	13-21	ATP binding cassette subfamily B member 1	Homo sapiens	118-122
29243778-12	2017	CONCLUSIONS: Apatinib can restore the sensitivity of A549/DDP cells to DDP by down-regulating the expression level of MDR1 and inhibiting the activity of the ERK signaling pathway.	apatinib	13-21	mitogen-activated protein kinase 1	Homo sapiens	158-161
29245310-2	2017	This study was conducted to evaluate the efficacy and safety of apatinib, a new potent oral small-molecule tyrosine kinase inhibitor targeted vascular endothelial growth factor receptor 2, combined with irinotecan, in patients with recurrent malignant glioma.	apatinib	64-72	vascular endothelial growth factor A	Homo sapiens	142-176
29390367-4	2017	Apatinib, as a novel small-molecule tyrosine kinase inhibitor specifically targeting the vascular endothelial growth factor receptor 2 (VEGFR2), has achieved progress in treatment of a variety of cancers.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	89-134
29390367-4	2017	Apatinib, as a novel small-molecule tyrosine kinase inhibitor specifically targeting the vascular endothelial growth factor receptor 2 (VEGFR2), has achieved progress in treatment of a variety of cancers.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	136-142
29390380-4	2017	Apatinib is highly selective tyrosine kinase inhibitor of vascular endothelial growth factor receptor-2, studies have revealed that apatinib inhibit the growth of solid tumors including NSCLC.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	58-103
29390380-4	2017	Apatinib is highly selective tyrosine kinase inhibitor of vascular endothelial growth factor receptor-2, studies have revealed that apatinib inhibit the growth of solid tumors including NSCLC.	apatinib	132-140	kinase insert domain receptor	Homo sapiens	58-103
29262660-1	2017	Apatinib is a tyrosine kinase inhibitor and vascular endothelial growth factor receptor 2 (VEGFR-2) targeted drug.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	44-89
29151702-5	2017	She was then treated with apatinib, a novel and highly selective tyrosine kinase inhibitor of vascular endothelial growth factor receptor-2 and achieved a progression-free-survival of 7 mo.	apatinib	26-34	kinase insert domain receptor	Homo sapiens	94-139
29137048-3	2017	Apatinib, a new small molecule tyrosine kinase inhibitor that specifically targets VEGFR-2, has therapeutic benefits in some advanced tumors.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	83-90
28927587-1	2017	In this study, carboxymethyl chitosan-graft-poly-(epsilon-caprolactone) copolymers (CMCS-g-PCL) were synthesized and used to encapsulate apatinib to prepare apatinib-loaded CMCS-g-PCL (CPA) micelles.	apatinib	137-145	carboxypeptidase A1	Homo sapiens	185-188
29381963-4	2017	Apatinib is a novel and highly selective tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	77-122
29145238-1	2017	RATIONALE: Apatinib is a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor-2, which has observed to be effective and safe in refractory radiation-induced brain edema, like Avastin did.	apatinib	11-19	kinase insert domain receptor	Homo sapiens	67-112
29138576-3	2017	Here, we report a case of advanced ICC that was successfully treated with apatinib, a new oral tyrosine kinase inhibitor that targets the intracellular domain of vascular endothelial growth factor receptor-2.	apatinib	74-82	kinase insert domain receptor	Homo sapiens	162-207
29142602-11	2017	Treatment of MKN45 cells with aspirin reduced the levels of phosphorylated AKT by activating PPARalpha, whereas treatment with apatinib inhibited the phosphorylation of vascular endothelial growth factor receptor 2 and phosphoinositide-3 kinase in MKN45 cells.	apatinib	127-135	kinase insert domain receptor	Homo sapiens	169-214
28028915-4	2017	Apatinib mesylate, small-molecule vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor (TKI), has been approved as third-line treatment for patients with advanced gastric adenocarcinoma in China, October, 2014.	apatinib	0-17	kinase insert domain receptor	Homo sapiens	34-79
28028915-4	2017	Apatinib mesylate, small-molecule vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor (TKI), has been approved as third-line treatment for patients with advanced gastric adenocarcinoma in China, October, 2014.	apatinib	0-17	kinase insert domain receptor	Homo sapiens	81-88
28822888-0	2017	Apatinib enhances antitumour activity of EGFR-TKIs in non-small cell lung cancer with EGFR-TKI resistance.	apatinib	0-8	epidermal growth factor receptor	Homo sapiens	41-45
28822888-0	2017	Apatinib enhances antitumour activity of EGFR-TKIs in non-small cell lung cancer with EGFR-TKI resistance.	apatinib	0-8	epidermal growth factor receptor	Homo sapiens	86-90
28822888-4	2017	Furthermore, we retrospectively evaluated EGFR-TKI rechallenge with apatinib in 16 patients.	apatinib	68-76	epidermal growth factor receptor	Homo sapiens	42-46
28822888-8	2017	EGFR-TKI rechallenge with apatinib achieved a median progression-free survival of 4.60 months (95% confidence interval, 2.23-12.52 months) in the patients.	apatinib	26-34	epidermal growth factor receptor	Homo sapiens	0-4
28822888-9	2017	CONCLUSIONS: Apatinib significantly potentiated the antitumour effect of gefitinib in NSCLC with T790M-related EGFR-TKI resistance both in vivo and vitro.	apatinib	13-21	epidermal growth factor receptor	Homo sapiens	111-115
28822888-10	2017	EGFR-TKI rechallenge with apatinib might represent a new option for NSCLC with T790M or unknown resistance mechanism.	apatinib	26-34	epidermal growth factor receptor	Homo sapiens	0-4
29262660-1	2017	Apatinib is a tyrosine kinase inhibitor and vascular endothelial growth factor receptor 2 (VEGFR-2) targeted drug.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	91-98
29066909-0	2017	Case report of a KIT-mutated melanoma patient with an excellent response to apatinib and temozolomide combination therapy.	apatinib	76-84	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	17-20
29066909-4	2017	Apatinib is a novel oral small-molecule tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor 2 (VEGFR-2) and may also be effective on Ret, c-KIT, and c-src.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	104-149
29066909-4	2017	Apatinib is a novel oral small-molecule tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor 2 (VEGFR-2) and may also be effective on Ret, c-KIT, and c-src.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	151-158
29066909-4	2017	Apatinib is a novel oral small-molecule tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor 2 (VEGFR-2) and may also be effective on Ret, c-KIT, and c-src.	apatinib	0-8	ret proto-oncogene	Homo sapiens	189-192
29066909-4	2017	Apatinib is a novel oral small-molecule tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor 2 (VEGFR-2) and may also be effective on Ret, c-KIT, and c-src.	apatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	194-199
29066909-4	2017	Apatinib is a novel oral small-molecule tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor 2 (VEGFR-2) and may also be effective on Ret, c-KIT, and c-src.	apatinib	0-8	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	205-210
29066909-7	2017	This patient showed high expression of CD117, VEGFR-3, and KIT mutation in exon 11, suggesting that apatinib may induce clinical response via inhibiting VEGFR and c-KIT.	apatinib	100-108	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	39-44
28678611-6	2017	Apatinib is an oral tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor-2 (VEGFR-2), which has dual effects of anti-angiogenesis and anti-tumor cell proliferation.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	84-129
28678611-6	2017	Apatinib is an oral tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor-2 (VEGFR-2), which has dual effects of anti-angiogenesis and anti-tumor cell proliferation.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	131-138
29085592-6	2017	RESULTS: The proliferation, migration and invasion of colon cancer cells were inhibited when they were treated with different concentration of apatinib (20, 40 muM).	apatinib	143-151	latexin	Homo sapiens	160-163
29085592-7	2017	When HCT116 and SW480 cells were treated with apatinib at the concentration of 20 muM, the apoptosis percentage were 3.7% and 5.8% respectively.	apatinib	46-54	latexin	Homo sapiens	82-85
29085592-10	2017	Furthermore, apatinib inhibited the expression of AKT-mTOR signaling pathway and increased the expression of LC3-II.	apatinib	13-21	AKT serine/threonine kinase 1	Homo sapiens	50-53
29085592-10	2017	Furthermore, apatinib inhibited the expression of AKT-mTOR signaling pathway and increased the expression of LC3-II.	apatinib	13-21	mechanistic target of rapamycin kinase	Homo sapiens	54-58
29066909-7	2017	This patient showed high expression of CD117, VEGFR-3, and KIT mutation in exon 11, suggesting that apatinib may induce clinical response via inhibiting VEGFR and c-KIT.	apatinib	100-108	fms related receptor tyrosine kinase 4	Homo sapiens	46-53
29066909-7	2017	This patient showed high expression of CD117, VEGFR-3, and KIT mutation in exon 11, suggesting that apatinib may induce clinical response via inhibiting VEGFR and c-KIT.	apatinib	100-108	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	59-62
29066909-7	2017	This patient showed high expression of CD117, VEGFR-3, and KIT mutation in exon 11, suggesting that apatinib may induce clinical response via inhibiting VEGFR and c-KIT.	apatinib	100-108	kinase insert domain receptor	Homo sapiens	46-51
29066909-7	2017	This patient showed high expression of CD117, VEGFR-3, and KIT mutation in exon 11, suggesting that apatinib may induce clinical response via inhibiting VEGFR and c-KIT.	apatinib	100-108	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	163-168
29066909-8	2017	Apatinib/TMZ combination therapy could be a new option for the treatment of advanced melanoma with KIT mutation.	apatinib	0-8	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	99-102
28894382-0	2017	Apatinib in the treatment of advanced lung adenocarcinoma with KRAS mutation.	apatinib	0-8	KRAS proto-oncogene, GTPase	Homo sapiens	63-67
28894382-2	2017	As a small molecule inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase, apatinib has been proven successful in advanced gastric cancer and breast cancer.	apatinib	106-114	kinase insert domain receptor	Homo sapiens	33-78
28894382-2	2017	As a small molecule inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase, apatinib has been proven successful in advanced gastric cancer and breast cancer.	apatinib	106-114	kinase insert domain receptor	Homo sapiens	80-87
28894382-3	2017	In this study, we show the result of apatinib as salvage treatment in lung adenocarcinoma patients with KRAS mutation.	apatinib	37-45	KRAS proto-oncogene, GTPase	Homo sapiens	104-108
28894382-4	2017	Four advanced lung adenocarcinoma patients with KRAS mutation were orally administered apatinib (250 mg/d) after second-line treatment.	apatinib	87-95	KRAS proto-oncogene, GTPase	Homo sapiens	48-52
28894382-7	2017	Therefore, apatinib might be an optional choice for advanced lung adenocarcinoma patients with KRAS mutation in post second-line treatment.	apatinib	11-19	KRAS proto-oncogene, GTPase	Homo sapiens	95-99
28837148-0	2017	Apatinib promotes autophagy and apoptosis through VEGFR2/STAT3/BCL-2 signaling in osteosarcoma.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	50-56
28837148-0	2017	Apatinib promotes autophagy and apoptosis through VEGFR2/STAT3/BCL-2 signaling in osteosarcoma.	apatinib	0-8	signal transducer and activator of transcription 3	Homo sapiens	57-62
28837148-0	2017	Apatinib promotes autophagy and apoptosis through VEGFR2/STAT3/BCL-2 signaling in osteosarcoma.	apatinib	0-8	BCL2 apoptosis regulator	Homo sapiens	63-68
28837148-3	2017	Apatinib is a high selectivity inhibitor of vascular endothelial growth factor receptor-2 (VEGFR2) tyrosine kinase, exerting promising antitumoral effect in various tumors.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	44-89
28837148-3	2017	Apatinib is a high selectivity inhibitor of vascular endothelial growth factor receptor-2 (VEGFR2) tyrosine kinase, exerting promising antitumoral effect in various tumors.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	91-97
28837148-12	2017	VEGFR2 and STAT3 are inhibited by Apatinib in KHOS cells, and STAT3 act downstream of VEGFR2.	apatinib	34-42	kinase insert domain receptor	Homo sapiens	0-6
28837148-12	2017	VEGFR2 and STAT3 are inhibited by Apatinib in KHOS cells, and STAT3 act downstream of VEGFR2.	apatinib	34-42	signal transducer and activator of transcription 3	Homo sapiens	11-16
28837148-13	2017	STAT3 and BCL-2 were downregulated by Apatinib.	apatinib	38-46	signal transducer and activator of transcription 3	Homo sapiens	0-5
28837148-13	2017	STAT3 and BCL-2 were downregulated by Apatinib.	apatinib	38-46	BCL2 apoptosis regulator	Homo sapiens	10-15
28837148-14	2017	STAT3 knockdown by siRNA reinforced autophagy and apoptosis induced by Apatinib.	apatinib	71-79	signal transducer and activator of transcription 3	Homo sapiens	0-5
28837148-15	2017	BCL-2 inhibits autophagy and was apoptosis restrained by Apatinib too.	apatinib	57-65	BCL2 apoptosis regulator	Homo sapiens	0-5
28837148-16	2017	Overexpression of BCL-2 decreased Apatinib-induced apoptosis and autophagy.	apatinib	34-42	BCL2 apoptosis regulator	Homo sapiens	18-23
28837148-17	2017	Apatinib repressed the expression of STAT3 and BCL-2 and suppressed the growth of osteosarcoma in vivo.	apatinib	0-8	signal transducer and activator of transcription 3	Homo sapiens	37-42
28837148-17	2017	Apatinib repressed the expression of STAT3 and BCL-2 and suppressed the growth of osteosarcoma in vivo.	apatinib	0-8	BCL2 apoptosis regulator	Homo sapiens	47-52
28837148-18	2017	To sum up, deactivation of VEGFR2/STAT3/BCL-2 signal pathway leads to Apatinib-induced growth inhibition of osteosarcoma.	apatinib	70-78	kinase insert domain receptor	Homo sapiens	27-33
28837148-18	2017	To sum up, deactivation of VEGFR2/STAT3/BCL-2 signal pathway leads to Apatinib-induced growth inhibition of osteosarcoma.	apatinib	70-78	signal transducer and activator of transcription 3	Homo sapiens	34-39
28837148-18	2017	To sum up, deactivation of VEGFR2/STAT3/BCL-2 signal pathway leads to Apatinib-induced growth inhibition of osteosarcoma.	apatinib	70-78	BCL2 apoptosis regulator	Homo sapiens	40-45
28639910-1	2017	Apatinib is a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor 2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	56-101
29029508-3	2017	As a small molecule inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2), apatinib was suggested mainly using in advanced gastric cancer.	apatinib	90-98	kinase insert domain receptor	Homo sapiens	33-78
29029508-3	2017	As a small molecule inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2), apatinib was suggested mainly using in advanced gastric cancer.	apatinib	90-98	kinase insert domain receptor	Homo sapiens	80-87
29029508-4	2017	In this study, we showed the results of apatinib as second-line to fourth-line treatment in EGFR wild-type advanced lung adenocarcinoma patients.	apatinib	40-48	epidermal growth factor receptor	Homo sapiens	92-96
29029508-5	2017	16 EGFR wild-type advanced lung adenocarcinoma patients were administrated apatinib (250-500 mg/d) orally.	apatinib	75-83	epidermal growth factor receptor	Homo sapiens	3-7
29029508-10	2017	So, apatinib might be an optional choice for post-first-line treatment of EGFR wild-type advanced lung adenocarcinoma patients.	apatinib	4-12	epidermal growth factor receptor	Homo sapiens	74-78
28860804-2	2017	The aim of this study was to evaluate the efficacy and safety of apatinib, an oral VEGFR-2 inhibitor, as salvage treatment for advanced ESCC.	apatinib	65-73	kinase insert domain receptor	Homo sapiens	83-90
28679123-6	2017	The patient was subsequently treated with apatinib (500 mg/day), a specific VEGFR-2 inhibitor.	apatinib	42-50	kinase insert domain receptor	Homo sapiens	76-83
28740387-0	2017	Apatinib-loaded nanoparticles suppress vascular endothelial growth factor-induced angiogenesis and experimental corneal neovascularization.	apatinib	0-8	vascular endothelial growth factor A	Homo sapiens	39-73
28740387-3	2017	In this study, we aimed to investigate whether nanoparticle-based delivery of apatinib, a novel and selective inhibitor of VEGF receptor 2, inhibits VEGF-mediated angiogenesis and suppresses experimental corneal neovascularization.	apatinib	78-86	vascular endothelial growth factor A	Homo sapiens	123-127
28740387-3	2017	In this study, we aimed to investigate whether nanoparticle-based delivery of apatinib, a novel and selective inhibitor of VEGF receptor 2, inhibits VEGF-mediated angiogenesis and suppresses experimental corneal neovascularization.	apatinib	78-86	vascular endothelial growth factor A	Homo sapiens	149-153
28740387-4	2017	Water-insoluble apatinib was encapsulated in nanoparticles composed of human serum albumin (HSA)-conjugated polyethylene glycol (PEG).	apatinib	16-24	albumin	Homo sapiens	77-90
28740387-5	2017	In vitro angiogenesis assays showed that apatinib-loaded HSA-PEG (Apa-HSA-PEG) nanoparticles potently inhibited VEGF-induced tube formation, scratch wounding migration, and proliferation of human endothelial cells.	apatinib	41-49	vascular endothelial growth factor A	Homo sapiens	112-116
28715845-0	2017	Apatinib, an Inhibitor of Vascular Endothelial Growth Factor Receptor 2, Suppresses Pathologic Ocular Neovascularization in Mice.	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	26-71
28715845-2	2017	In this study, we investigated the antiangiogenic effect of apatinib, a pharmacologic inhibitor of VEGFR2 tyrosine kinase, against oxygen-induced retinopathy (OIR) and laser-induced choroidal neovascularization (CNV) in mice.	apatinib	60-68	kinase insert domain protein receptor	Mus musculus	99-105
28715845-8	2017	Results: Apatinib inhibited VEGF-mediated activation of VEGFR2 signaling and substantially reduced VEGF-induced proliferation, migration, and cord formation in HRMECs.	apatinib	9-17	vascular endothelial growth factor A	Mus musculus	28-32
28715845-8	2017	Results: Apatinib inhibited VEGF-mediated activation of VEGFR2 signaling and substantially reduced VEGF-induced proliferation, migration, and cord formation in HRMECs.	apatinib	9-17	kinase insert domain protein receptor	Mus musculus	56-62
28715845-8	2017	Results: Apatinib inhibited VEGF-mediated activation of VEGFR2 signaling and substantially reduced VEGF-induced proliferation, migration, and cord formation in HRMECs.	apatinib	9-17	vascular endothelial growth factor A	Mus musculus	56-60
28715845-10	2017	Retinal or choroidal tissues of the eyes treated with apatinib exhibited substantially lower phosphorylation of VEGFR2 than those of controls injected with vehicle.	apatinib	54-62	kinase insert domain protein receptor	Mus musculus	112-118
28490886-7	2017	The patient with unknown EGFR status benefited 5-month progressive free survival (PFS) from erlotinib, and then another 5.1-month PFS with combined treatment of apatinib, which suggested a new option for lung adenocarcinoma.	apatinib	161-169	epidermal growth factor receptor	Homo sapiens	25-29
28490886-0	2017	Apatinib to combat EGFR-TKI resistance in an advanced non-small cell lung cancer patient with unknown EGFR status: a case report.	apatinib	0-8	epidermal growth factor receptor	Homo sapiens	19-23
28881773-0	2017	Apatinib inhibits VEGFR-2 and angiogenesis in an in vivo murine model of nasopharyngeal carcinoma.	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	18-25
28490886-0	2017	Apatinib to combat EGFR-TKI resistance in an advanced non-small cell lung cancer patient with unknown EGFR status: a case report.	apatinib	0-8	epidermal growth factor receptor	Homo sapiens	102-106
28490886-6	2017	Similarly, apatinib is speculated to response by selectively inhibiting the vascular endothelial growth factor receptor-2.	apatinib	11-19	kinase insert domain receptor	Homo sapiens	76-121
28881773-3	2017	Apatinib (YN968D1) is a highly-selective inhibitor of VEGFR-2, but its effects on NPC have not been hitherto investigated.	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	54-61
28881773-7	2017	Tumors treated simultaneously with apatinib and cisplatin exhibited significantly-increased inhibition of tumor growth, prolonged survival time, decreased expression of VEGFR-2, reduced microvascular density, and frequency of apoptosis over standalone and sequential administration therapy.	apatinib	35-43	kinase insert domain protein receptor	Mus musculus	169-176
28881773-10	2017	VEGFR-2 is an important predictive marker for efficacy of apatinib treatment of NPC.	apatinib	58-66	kinase insert domain protein receptor	Mus musculus	0-7
28248891-1	2017	RATIONALE: Apatinib is a novel anti-angiogenic agent targeting vascular endothelial growth factor receptor-2, which is effective in patients with chemotherapy-refractory gastric cancer.	apatinib	11-19	kinase insert domain receptor	Homo sapiens	63-108
28383032-6	2017	Overexpression of VEGFR2 correlated with resistance to cisplatin and combination with VEGFR2-inhibitor apatinib synergistically increased cisplatin sensitivity.	apatinib	103-111	kinase insert domain receptor	Homo sapiens	18-24
28383032-6	2017	Overexpression of VEGFR2 correlated with resistance to cisplatin and combination with VEGFR2-inhibitor apatinib synergistically increased cisplatin sensitivity.	apatinib	103-111	kinase insert domain receptor	Homo sapiens	86-92
28403086-3	2017	Apatinib, a new potent oral small-molecule tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor 2 (VEGFR-2), shows survival benefits in treating advanced or metastatic gastric adenocarcinoma, non-squamous non-small cell lung cancer and metastatic breast cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	107-152
28403086-3	2017	Apatinib, a new potent oral small-molecule tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor 2 (VEGFR-2), shows survival benefits in treating advanced or metastatic gastric adenocarcinoma, non-squamous non-small cell lung cancer and metastatic breast cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	154-161
28367065-2	2017	The aim of this study was to evaluate apatinib, a VEGFR-2 inhibitor, in advanced NSCLC as salvage treatment.	apatinib	38-46	kinase insert domain receptor	Homo sapiens	50-57
28103584-1	2017	Apatinib is a novel and highly selective tyrosine kinase inhibitor of vascular endothelial growth factor receptor-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	70-115
28103584-3	2017	We report one case with advanced hepatocellular carcinoma (HCC), who received apatinib combined with transhepatic arterial chemotherapy and embolization (TACE), and chemotherapy respectively.	apatinib	78-86	ADAM metallopeptidase domain 17	Homo sapiens	154-158
28377354-4	2017	The effect of apatinib on the expressions of Akt, pAkt, Erk1/2 and pErk1/2 in HCT-116 cells was evaluated using Western blotting.	apatinib	14-22	AKT serine/threonine kinase 1	Homo sapiens	45-48
28377354-4	2017	The effect of apatinib on the expressions of Akt, pAkt, Erk1/2 and pErk1/2 in HCT-116 cells was evaluated using Western blotting.	apatinib	14-22	mitogen-activated protein kinase 3	Homo sapiens	56-62
28377354-7	2017	Apatinib induced the expression of the pro-apoptotic genes Bax and caspase-3 at both the mRNA and protein levels while inhibited the expression of the anti- apoptotic gene Bcl-2.	apatinib	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	59-62
28377354-7	2017	Apatinib induced the expression of the pro-apoptotic genes Bax and caspase-3 at both the mRNA and protein levels while inhibited the expression of the anti- apoptotic gene Bcl-2.	apatinib	0-8	caspase 3	Homo sapiens	67-76
28377354-7	2017	Apatinib induced the expression of the pro-apoptotic genes Bax and caspase-3 at both the mRNA and protein levels while inhibited the expression of the anti- apoptotic gene Bcl-2.	apatinib	0-8	BCL2 apoptosis regulator	Homo sapiens	172-177
28377354-8	2017	The expressions of p-Akt and p-Erk1/2 were decreased in HCT-116 cells after apatinib treatment, but the total protein levels did not undergo obvious changes.	apatinib	76-84	AKT serine/threonine kinase 1	Homo sapiens	21-24
28377354-8	2017	The expressions of p-Akt and p-Erk1/2 were decreased in HCT-116 cells after apatinib treatment, but the total protein levels did not undergo obvious changes.	apatinib	76-84	mitogen-activated protein kinase 3	Homo sapiens	31-37
28377354-9	2017	CONCLUSION: Apatinib inhibits the proliferation and induces apoptosis of HCT-116 cells by suppressing the phosphorylation of Erk1/2 and Akt in the MAPK/Erk and PI3K/Akt signaling pathways.	apatinib	12-20	mitogen-activated protein kinase 3	Homo sapiens	125-131
28377354-9	2017	CONCLUSION: Apatinib inhibits the proliferation and induces apoptosis of HCT-116 cells by suppressing the phosphorylation of Erk1/2 and Akt in the MAPK/Erk and PI3K/Akt signaling pathways.	apatinib	12-20	AKT serine/threonine kinase 1	Homo sapiens	136-139
28377354-9	2017	CONCLUSION: Apatinib inhibits the proliferation and induces apoptosis of HCT-116 cells by suppressing the phosphorylation of Erk1/2 and Akt in the MAPK/Erk and PI3K/Akt signaling pathways.	apatinib	12-20	mitogen-activated protein kinase 3	Homo sapiens	147-151
28377354-9	2017	CONCLUSION: Apatinib inhibits the proliferation and induces apoptosis of HCT-116 cells by suppressing the phosphorylation of Erk1/2 and Akt in the MAPK/Erk and PI3K/Akt signaling pathways.	apatinib	12-20	mitogen-activated protein kinase 1	Homo sapiens	125-128
28377354-9	2017	CONCLUSION: Apatinib inhibits the proliferation and induces apoptosis of HCT-116 cells by suppressing the phosphorylation of Erk1/2 and Akt in the MAPK/Erk and PI3K/Akt signaling pathways.	apatinib	12-20	AKT serine/threonine kinase 1	Homo sapiens	165-168
28352185-1	2017	Apatinib is a novel oral tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor-2, which has been proved by clinical trials to be effective and safe for patients with chemotherapy-refractory gastric cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	61-106
28331317-1	2017	Apatinib is an oral tyrosine kinase inhibitor, which selectively targets vascular endothelial growth factor receptor 2 and has the potential to treat many tumors therapeutically.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	73-118
28243119-3	2017	We present here two cases of refractory rMG treated using apatinib, which is a new highly selective inhibitor to VEGFR.	apatinib	58-66	kinase insert domain receptor	Homo sapiens	113-118
28061477-0	2017	Autocrine VEGF signaling promotes cell proliferation through a PLC-dependent pathway and modulates Apatinib treatment efficacy in gastric cancer.	apatinib	99-107	vascular endothelial growth factor A	Homo sapiens	10-14
28061477-2	2017	Apatinib, a highly selective VEGFR2 inhibitor, is the only effective drug for patients with terminal gastric cancer (GC) who have no other chemotherapeutic options.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	29-35
28061477-4	2017	In this study, we aimed to investigate the role of autocrine VEGF signaling in the growth of gastric cancer cells and the efficacy of Apatinib treatment.	apatinib	134-142	vascular endothelial growth factor A	Homo sapiens	61-65
28061477-11	2017	Furthermore, we demonstrated that in VEGFR2 overexpressing gastric cancer cells, Apatinib inhibited cell proliferation in vitro and delayed xenograft tumor growth in vivo.	apatinib	81-89	kinase insert domain receptor	Homo sapiens	37-43
28061477-13	2017	CONCLUSION: These results suggested that autocrine VEGF signaling promotes gastric cancer cell proliferation and enhances Apatinib treatment outcome in VEGFR2 overexpression gastric cancer cells both in vitro and in vivo.	apatinib	122-130	vascular endothelial growth factor A	Homo sapiens	51-55
28061477-13	2017	CONCLUSION: These results suggested that autocrine VEGF signaling promotes gastric cancer cell proliferation and enhances Apatinib treatment outcome in VEGFR2 overexpression gastric cancer cells both in vitro and in vivo.	apatinib	122-130	kinase insert domain receptor	Homo sapiens	152-158
28176910-0	2017	Apatinib as post second-line therapy in EGFR wild-type and ALK-negative advanced lung adenocarcinoma.	apatinib	0-8	epidermal growth factor receptor	Homo sapiens	40-44
28176910-3	2017	Apatinib, a small molecule vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor, is a first-generation oral antiangiogenesis drug approved in the People"s Republic of China for use as a subsequent line of treatment for advanced gastric cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	27-72
28176910-3	2017	Apatinib, a small molecule vascular endothelial growth factor receptor-2 (VEGFR-2) tyrosine kinase inhibitor, is a first-generation oral antiangiogenesis drug approved in the People"s Republic of China for use as a subsequent line of treatment for advanced gastric cancer.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	74-81
28176910-4	2017	Herein, we report three cases of advanced NSCLC with epidermal growth factor receptor wild-type and anaplastic lymphoma kinase-negative status, wherein the patients showed partial response to apatinib.	apatinib	192-200	epidermal growth factor receptor	Homo sapiens	53-85
29190616-0	2017	Apatinib Inhibits Angiogenesis Via Suppressing Akt/GSK3beta/ANG Signaling Pathway in Anaplastic Thyroid Cancer.	apatinib	0-8	AKT serine/threonine kinase 1	Homo sapiens	47-50
29190616-0	2017	Apatinib Inhibits Angiogenesis Via Suppressing Akt/GSK3beta/ANG Signaling Pathway in Anaplastic Thyroid Cancer.	apatinib	0-8	glycogen synthase kinase 3 beta	Homo sapiens	51-59
29190616-0	2017	Apatinib Inhibits Angiogenesis Via Suppressing Akt/GSK3beta/ANG Signaling Pathway in Anaplastic Thyroid Cancer.	apatinib	0-8	angiogenin	Homo sapiens	60-63
29190616-8	2017	Moreover, Apatinib treatment decreased the expression of angiogenin (ANG) and inhibited angiogenesis of ATC cells in vitro and in vitro.	apatinib	10-18	angiogenin	Homo sapiens	57-67
29190616-8	2017	Moreover, Apatinib treatment decreased the expression of angiogenin (ANG) and inhibited angiogenesis of ATC cells in vitro and in vitro.	apatinib	10-18	angiogenin	Homo sapiens	69-72
29190616-9	2017	We further confirmed that recombinant human ANG (rhANG) significantly abrogated Apatinib-mediated anti-angiogenic ability in ATC cells.	apatinib	80-88	angiogenin	Homo sapiens	44-47
29190616-10	2017	Additionally, Apatinib treatment decreased the level of p-Akt and p-GSK3beta.	apatinib	14-22	AKT serine/threonine kinase 1	Homo sapiens	58-61
29190616-13	2017	CONCLUSION: Our results demonstrated that Apatinib treatment inhibited tumor growth, and Apatinib-induced suppression of Akt/GSK3beta/ANG signaling pathway may play an important role in the inhibition of angiogenesis in ATC, supporting a potential therapeutic approach for using Apatinib in the treatment of ATC.	apatinib	89-97	glycogen synthase kinase 3 beta	Homo sapiens	125-133
29190616-13	2017	CONCLUSION: Our results demonstrated that Apatinib treatment inhibited tumor growth, and Apatinib-induced suppression of Akt/GSK3beta/ANG signaling pathway may play an important role in the inhibition of angiogenesis in ATC, supporting a potential therapeutic approach for using Apatinib in the treatment of ATC.	apatinib	89-97	angiogenin	Homo sapiens	134-137
29190616-10	2017	Additionally, Apatinib treatment decreased the level of p-Akt and p-GSK3beta.	apatinib	14-22	glycogen synthase kinase 3 beta	Homo sapiens	68-76
29190616-11	2017	Moreover, the Apatinib-mediated decrease of ANG and anti-angiogenic ability were partly reversed when an Akt activator, SC79, was administered.	apatinib	14-22	angiogenin	Homo sapiens	44-47
29190616-11	2017	Moreover, the Apatinib-mediated decrease of ANG and anti-angiogenic ability were partly reversed when an Akt activator, SC79, was administered.	apatinib	14-22	AKT serine/threonine kinase 1	Homo sapiens	105-108
29190616-12	2017	Furthermore, the anti-angiogenic ability of Apatinib can be enhanced in the presence of Akt inhibitor, and the inhibition of GSK3beta attenuated the anti-angiogenic ability of Apatinib.	apatinib	44-52	AKT serine/threonine kinase 1	Homo sapiens	88-91
29190616-12	2017	Furthermore, the anti-angiogenic ability of Apatinib can be enhanced in the presence of Akt inhibitor, and the inhibition of GSK3beta attenuated the anti-angiogenic ability of Apatinib.	apatinib	176-184	glycogen synthase kinase 3 beta	Homo sapiens	125-133
29190616-13	2017	CONCLUSION: Our results demonstrated that Apatinib treatment inhibited tumor growth, and Apatinib-induced suppression of Akt/GSK3beta/ANG signaling pathway may play an important role in the inhibition of angiogenesis in ATC, supporting a potential therapeutic approach for using Apatinib in the treatment of ATC.	apatinib	89-97	AKT serine/threonine kinase 1	Homo sapiens	121-124
29190616-13	2017	CONCLUSION: Our results demonstrated that Apatinib treatment inhibited tumor growth, and Apatinib-induced suppression of Akt/GSK3beta/ANG signaling pathway may play an important role in the inhibition of angiogenesis in ATC, supporting a potential therapeutic approach for using Apatinib in the treatment of ATC.	apatinib	89-97	glycogen synthase kinase 3 beta	Homo sapiens	125-133
29190616-13	2017	CONCLUSION: Our results demonstrated that Apatinib treatment inhibited tumor growth, and Apatinib-induced suppression of Akt/GSK3beta/ANG signaling pathway may play an important role in the inhibition of angiogenesis in ATC, supporting a potential therapeutic approach for using Apatinib in the treatment of ATC.	apatinib	89-97	angiogenin	Homo sapiens	134-137
29190616-13	2017	CONCLUSION: Our results demonstrated that Apatinib treatment inhibited tumor growth, and Apatinib-induced suppression of Akt/GSK3beta/ANG signaling pathway may play an important role in the inhibition of angiogenesis in ATC, supporting a potential therapeutic approach for using Apatinib in the treatment of ATC.	apatinib	89-97	AKT serine/threonine kinase 1	Homo sapiens	121-124
27738308-6	2016	After disease progressed with therapy of Bevacizumab combined with Albumin-bound Paclitaxel and Cisplatin, we treated the patient with Apatinib according to her VEGFR expression, which showed nearly complete response and controllable and tolerated side effects.	apatinib	135-143	kinase insert domain receptor	Homo sapiens	161-166
27462154-1	2016	Apatinib, a novel and selective inhibitor of vascular endothelial growth factor (VEGF) receptor 2, has been demonstrated recently to exhibit anticancer efficacy by inhibiting the VEGF signaling pathway.	apatinib	0-8	kinase insert domain protein receptor	Mus musculus	45-97
27531538-10	2016	Apatinib, a novel oral vascular endothelial growth factor receptor 2 tyrosine kinase inhibitor, improved the median overall survival of patients with advanced GC and progressive disease after two or more lines of prior chemotherapy of nearly 3 months.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	23-68
27631210-0	2016	A case report of targeted therapy with apatinib in a patient with advanced gastric cancer and high serum level of alpha-fetoprotein.	apatinib	39-47	alpha fetoprotein	Homo sapiens	114-131
27631210-9	2016	CONCLUSION: So, we speculate that maybe we can focus apatinib on serum AFP elevated GC patients.	apatinib	53-61	alpha fetoprotein	Homo sapiens	71-74
27376400-1	2016	INTRODUCTION: Apatinib, a small-molecule inhibitor of vascular endothelial growth factor receptor 2, has demonstrated encouraging anti-cancer activity in gastric cancer within both in vitro and in vivo models.	apatinib	14-22	kinase insert domain receptor	Homo sapiens	54-99
27494860-0	2016	Apatinib inhibits cellular invasion and migration by fusion kinase KIF5B-RET via suppressing RET/Src signaling pathway.	apatinib	0-8	kinesin family member 5B	Homo sapiens	67-72
27494860-0	2016	Apatinib inhibits cellular invasion and migration by fusion kinase KIF5B-RET via suppressing RET/Src signaling pathway.	apatinib	0-8	ret proto-oncogene	Homo sapiens	73-76
27494860-0	2016	Apatinib inhibits cellular invasion and migration by fusion kinase KIF5B-RET via suppressing RET/Src signaling pathway.	apatinib	0-8	ret proto-oncogene	Homo sapiens	93-96
27494860-0	2016	Apatinib inhibits cellular invasion and migration by fusion kinase KIF5B-RET via suppressing RET/Src signaling pathway.	apatinib	0-8	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	97-100
27494860-3	2016	We also investigate the anti-tumor activity of Apatinib, a potent inhibitor of VEGFR-2, PDGFR-beta, c-Src and RET, in RET-rearranged lung adenocarcinoma, together with the mechanisms underlying.	apatinib	47-55	kinase insert domain receptor	Homo sapiens	79-86
27494860-3	2016	We also investigate the anti-tumor activity of Apatinib, a potent inhibitor of VEGFR-2, PDGFR-beta, c-Src and RET, in RET-rearranged lung adenocarcinoma, together with the mechanisms underlying.	apatinib	47-55	platelet derived growth factor receptor beta	Homo sapiens	88-98
27494860-3	2016	We also investigate the anti-tumor activity of Apatinib, a potent inhibitor of VEGFR-2, PDGFR-beta, c-Src and RET, in RET-rearranged lung adenocarcinoma, together with the mechanisms underlying.	apatinib	47-55	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	100-105
27494860-3	2016	We also investigate the anti-tumor activity of Apatinib, a potent inhibitor of VEGFR-2, PDGFR-beta, c-Src and RET, in RET-rearranged lung adenocarcinoma, together with the mechanisms underlying.	apatinib	47-55	ret proto-oncogene	Homo sapiens	110-113
27494860-5	2016	Apatinib exerted its anti-cancer effect not only via cytotoxicity, but also via inhibition of migration and invasion by suppressing RET/Src signaling pathway, supporting a potential role for Apatinib in the treatment of KIF5B-RET driven tumors.	apatinib	0-8	ret proto-oncogene	Homo sapiens	132-135
27494860-5	2016	Apatinib exerted its anti-cancer effect not only via cytotoxicity, but also via inhibition of migration and invasion by suppressing RET/Src signaling pathway, supporting a potential role for Apatinib in the treatment of KIF5B-RET driven tumors.	apatinib	0-8	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	136-139
27494860-5	2016	Apatinib exerted its anti-cancer effect not only via cytotoxicity, but also via inhibition of migration and invasion by suppressing RET/Src signaling pathway, supporting a potential role for Apatinib in the treatment of KIF5B-RET driven tumors.	apatinib	0-8	kinesin family member 5B	Homo sapiens	220-225
27494860-5	2016	Apatinib exerted its anti-cancer effect not only via cytotoxicity, but also via inhibition of migration and invasion by suppressing RET/Src signaling pathway, supporting a potential role for Apatinib in the treatment of KIF5B-RET driven tumors.	apatinib	0-8	ret proto-oncogene	Homo sapiens	226-229
27494860-5	2016	Apatinib exerted its anti-cancer effect not only via cytotoxicity, but also via inhibition of migration and invasion by suppressing RET/Src signaling pathway, supporting a potential role for Apatinib in the treatment of KIF5B-RET driven tumors.	apatinib	191-199	kinesin family member 5B	Homo sapiens	220-225
27563253-3	2016	Here, we report a case of advanced angiosarcoma that was successfully treated with apatinib, an oral tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor-2 (VEGFR-2).	apatinib	83-91	kinase insert domain receptor	Homo sapiens	165-210
27563253-3	2016	Here, we report a case of advanced angiosarcoma that was successfully treated with apatinib, an oral tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor-2 (VEGFR-2).	apatinib	83-91	kinase insert domain receptor	Homo sapiens	212-219
27563253-6	2016	Quantitative polymerase chain reaction analysis revealed high expression of VEGFR-2 mRNA, suggesting that apatinib leads to clinical response by inhibiting VEGFR-2 tyrosine kinase activity and that VEGFR-2 plays a crucial role for angiosarcoma.	apatinib	106-114	kinase insert domain receptor	Homo sapiens	76-83
27563253-6	2016	Quantitative polymerase chain reaction analysis revealed high expression of VEGFR-2 mRNA, suggesting that apatinib leads to clinical response by inhibiting VEGFR-2 tyrosine kinase activity and that VEGFR-2 plays a crucial role for angiosarcoma.	apatinib	106-114	kinase insert domain receptor	Homo sapiens	156-163
27563253-6	2016	Quantitative polymerase chain reaction analysis revealed high expression of VEGFR-2 mRNA, suggesting that apatinib leads to clinical response by inhibiting VEGFR-2 tyrosine kinase activity and that VEGFR-2 plays a crucial role for angiosarcoma.	apatinib	106-114	kinase insert domain receptor	Homo sapiens	156-163
27495042-0	2016	Significant partial response of metastatic intra-abdominal and pelvic round cell liposarcoma to a small-molecule VEGFR-2 tyrosine kinase inhibitor apatinib: A case report.	apatinib	147-155	kinase insert domain receptor	Homo sapiens	113-120
27462154-1	2016	Apatinib, a novel and selective inhibitor of vascular endothelial growth factor (VEGF) receptor 2, has been demonstrated recently to exhibit anticancer efficacy by inhibiting the VEGF signaling pathway.	apatinib	0-8	vascular endothelial growth factor A	Mus musculus	81-85
27462154-2	2016	Given the importance of VEGF in retinal vascular leakage, the present study was designed to investigate whether apatinib-loaded polymeric nanoparticles inhibit VEGF-mediated retinal vascular hyperpermeability and block diabetes-induced retinal vascular leakage.	apatinib	112-120	vascular endothelial growth factor A	Mus musculus	24-28
27462154-2	2016	Given the importance of VEGF in retinal vascular leakage, the present study was designed to investigate whether apatinib-loaded polymeric nanoparticles inhibit VEGF-mediated retinal vascular hyperpermeability and block diabetes-induced retinal vascular leakage.	apatinib	112-120	vascular endothelial growth factor A	Mus musculus	160-164
27462154-4	2016	In vitro paracellular permeability and transendothelial electric resistance assays showed that apatinib-loaded HSA-PEG (Apa-HSA-PEG) nanoparticles significantly inhibited VEGF-induced endothelial hyperpermeability in human retinal microvascular endothelial cells.	apatinib	95-103	vascular endothelial growth factor A	Homo sapiens	171-175
26884585-2	2016	We assessed the efficacy and safety of apatinib, a novel vascular endothelial growth factor receptor 2 tyrosine kinase inhibitor, in patients with advanced gastric or gastroesophageal junction adenocarcinoma for whom at least two lines of prior chemotherapy had failed.	apatinib	39-47	kinase insert domain receptor	Homo sapiens	57-102
27196461-1	2016	Apatinib is a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor-2, which has been proved to be effective and safe in treating heavily pretreated patients with gastric cancer.The aim of the study was to explore the use of apatinib in treatment of nonsmall cell lung cancer and its side effects.We report 2 patients presented with advanced nonsmall-cell lung cancer, who received apatinib after failure in the first- or third-line chemotherapy.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	56-101
27196461-1	2016	Apatinib is a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor-2, which has been proved to be effective and safe in treating heavily pretreated patients with gastric cancer.The aim of the study was to explore the use of apatinib in treatment of nonsmall cell lung cancer and its side effects.We report 2 patients presented with advanced nonsmall-cell lung cancer, who received apatinib after failure in the first- or third-line chemotherapy.	apatinib	257-265	kinase insert domain receptor	Homo sapiens	56-101
26797419-5	2016	In the scenario of possible new target therapies with particular regard to angiogenesis, apatinib is a novel receptor tyrosine kinase inhibitor selectively targeting VEGFR-2.	apatinib	89-97	kinase insert domain receptor	Homo sapiens	166-173
26805764-0	2016	Intracellular autocrine VEGF signaling promotes EBDC cell proliferation, which can be inhibited by Apatinib.	apatinib	99-107	vascular endothelial growth factor A	Homo sapiens	24-28
26805764-2	2016	We aimed to investigate the role of extracellular/intracellular autocrine VEGF signaling and Apatinib, a highly selective VEGFR2 inhibitor, in extrahepatic bile duct cancer (EBDC).	apatinib	93-101	kinase insert domain receptor	Homo sapiens	122-128
26805764-6	2016	Internal VEGFR2 inhibitor Apatinib significantly inhibited intracellular VEGF signaling, suppressed cell proliferation in vitro and delayed xenograft tumor growth in vivo, while anti-VEGF antibody Bevacizumab showed no effect.	apatinib	26-34	kinase insert domain receptor	Homo sapiens	9-15
26805764-6	2016	Internal VEGFR2 inhibitor Apatinib significantly inhibited intracellular VEGF signaling, suppressed cell proliferation in vitro and delayed xenograft tumor growth in vivo, while anti-VEGF antibody Bevacizumab showed no effect.	apatinib	26-34	vascular endothelial growth factor A	Homo sapiens	9-13
26805764-6	2016	Internal VEGFR2 inhibitor Apatinib significantly inhibited intracellular VEGF signaling, suppressed cell proliferation in vitro and delayed xenograft tumor growth in vivo, while anti-VEGF antibody Bevacizumab showed no effect.	apatinib	26-34	vascular endothelial growth factor A	Homo sapiens	73-77
26805764-9	2016	Apatinib is an effective intracellular VEGF pathway blocker that presents a great therapeutic potential in EBDC.	apatinib	0-8	vascular endothelial growth factor A	Homo sapiens	39-43
26967384-0	2016	Apatinib inhibits VEGF signaling and promotes apoptosis in intrahepatic cholangiocarcinoma.	apatinib	0-8	vascular endothelial growth factor A	Homo sapiens	18-22
26967384-3	2016	Apatinib is a highly selective VEGFR2 inhibitor, but its effects on ICC have not been investigated.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	31-37
26967384-6	2016	Apatinib inhibited the anti-apoptosis induced by VEGF signaling, and promoted cell death in vitro.	apatinib	0-8	vascular endothelial growth factor A	Homo sapiens	49-53
26967384-9	2016	Apatinib inhibits anti-apoptotic cell growth through suppressing the autocrine VEGF signaling, supporting a potential role for using Apatinib in the treatment of ICC.	apatinib	0-8	vascular endothelial growth factor A	Homo sapiens	79-83
26967384-9	2016	Apatinib inhibits anti-apoptotic cell growth through suppressing the autocrine VEGF signaling, supporting a potential role for using Apatinib in the treatment of ICC.	apatinib	133-141	vascular endothelial growth factor A	Homo sapiens	79-83
26917971-3	2016	We present here a case of advanced MFH with partial response to apatinib, a new potent oral small-molecule tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	64-72	kinase insert domain receptor	Homo sapiens	171-216
26917971-3	2016	We present here a case of advanced MFH with partial response to apatinib, a new potent oral small-molecule tyrosine kinase inhibitor targeting the intracellular domain of vascular endothelial growth factor receptor 2 (VEGFR-2).	apatinib	64-72	kinase insert domain receptor	Homo sapiens	218-225
26917971-5	2016	Quantitative polymerase chain reaction analysis revealed high expression of VEGFR-2 mRNA, suggesting that apatinib leads to clinical response by inhibiting VEGFR-2 tyrosine kinase activity and the crucial role of VEGFR-2 for MFH.	apatinib	106-114	kinase insert domain receptor	Homo sapiens	76-83
26917971-5	2016	Quantitative polymerase chain reaction analysis revealed high expression of VEGFR-2 mRNA, suggesting that apatinib leads to clinical response by inhibiting VEGFR-2 tyrosine kinase activity and the crucial role of VEGFR-2 for MFH.	apatinib	106-114	kinase insert domain receptor	Homo sapiens	156-163
26917971-5	2016	Quantitative polymerase chain reaction analysis revealed high expression of VEGFR-2 mRNA, suggesting that apatinib leads to clinical response by inhibiting VEGFR-2 tyrosine kinase activity and the crucial role of VEGFR-2 for MFH.	apatinib	106-114	kinase insert domain receptor	Homo sapiens	156-163
26622168-2	2015	Apatinib, a small-molecule inhibitor of vascular endothelial growth factor receptor-2, has demonstrated encouraging anticancer activity across a broad range of malignancies, including gastric cancer, non-small-cell lung cancer, breast cancer, and hepatocellular carcinoma.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	40-85
26880889-7	2016	The VEGFR-2 tyrosine kinase inhibitor, apatinib, can improve the survival of advanced gastric cancer patients after second-line chemotherapy failure.	apatinib	39-47	kinase insert domain receptor	Homo sapiens	4-11
26426663-1	2015	Apatinib is a novel tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor-2, which shows good efficacy and safety in clinical trials for chemotherapy-refractory gastric cancer patients.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	56-101
26483065-7	2015	Apatinib, a small molecule tyrosine kinase inhibitor targeting VEGF, has demonstrated activity in Asian populations whose disease has progressed on 2 lines of therapy.	apatinib	0-8	vascular endothelial growth factor A	Homo sapiens	63-67
26451083-3	2015	A better understanding of angiogenesis has led to the investigation of drugs that inhibit the vascular endothelial growth factor (VEGF) pathway including anti-VEGF antibody therapy (eg, bevacizumab), inhibitors of angiogenic receptor tyrosine kinases (eg, sunitinib, sorafenib, apatinib, regorafenib), and inhibitors of vascular endothelial growth factor receptors (VEGFRs) (eg, ramucirumab).	apatinib	278-286	vascular endothelial growth factor A	Homo sapiens	94-128
26451083-3	2015	A better understanding of angiogenesis has led to the investigation of drugs that inhibit the vascular endothelial growth factor (VEGF) pathway including anti-VEGF antibody therapy (eg, bevacizumab), inhibitors of angiogenic receptor tyrosine kinases (eg, sunitinib, sorafenib, apatinib, regorafenib), and inhibitors of vascular endothelial growth factor receptors (VEGFRs) (eg, ramucirumab).	apatinib	278-286	vascular endothelial growth factor A	Homo sapiens	130-134
25464097-3	2014	The purpose of the study was to investigate the effect of apatinib on these cytochrome P450 enzymes in vivo with co-administration of these probes.	apatinib	58-66	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	76-91
25464097-0	2014	Evaluation of the effect of apatinib (YN968D1) on cytochrome P450 enzymes with cocktail probe drugs in rats by UPLC-MS/MS.	apatinib	28-36	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	50-65
26020064-3	2015	Apatinib, a small-molecule inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2), is an orally bioavailable agent currently being studied in multiple tumor types.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	40-85
26020064-3	2015	Apatinib, a small-molecule inhibitor of vascular endothelial growth factor receptor-2 (VEGFR-2), is an orally bioavailable agent currently being studied in multiple tumor types.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	87-94
25464097-10	2014	This method was successfully applied to evaluate the effects of apatinib on the cytochrome P450 enzymes in rats.	apatinib	64-72	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	80-95
22503745-3	2012	Apatinib is extensively metabolized in humans, and its major metabolites in circulation include cis-3-hydroxy-apatinib (M1-1), trans-3-hydroxy-apatinib (M1-2), apatinib-25-N-oxide (M1-6), and cis-3-hydroxy-apatinib-O-glucuronide (M9-2).	apatinib	0-8	cholinergic receptor muscarinic 1	Homo sapiens	153-157
25376790-1	2014	BACKGROUND: Apatinib is a tyrosine kinase inhibitor targeting vascular endothelial growth factor receptor 2(VEGFR-2).	apatinib	12-20	kinase insert domain receptor	Homo sapiens	108-115
24604288-0	2014	Multicenter phase II study of apatinib, a novel VEGFR inhibitor in heavily pretreated patients with metastatic triple-negative breast cancer.	apatinib	30-38	kinase insert domain receptor	Homo sapiens	48-53
24604288-1	2014	Apatinib is an oral, highly potent tyrosine-kinase inhibitor targeting VEGFR2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	71-77
24292957-2	2014	Apatinib, a specific tyrosine kinase inhibitor that targets VEGF receptor 2, was assessed in patients with advanced breast cancer (ABC) (ClinicalTrials.gov NCT01176669 and NCT01653561).	apatinib	0-8	vascular endothelial growth factor A	Homo sapiens	60-64
24292957-3	2014	This substudy was to explore the potential biomarkers for VEGF-dependency in apatinib-treated breast cancer.	apatinib	77-85	vascular endothelial growth factor A	Homo sapiens	58-62
25152762-2	2014	In an in vivo experiment, we found that apatinib, a tyrosine kinase inhibitor that selectively inhibits VEGFR2, combined with elemene injection (Ele) for the treatment of H22 solid tumor in mice resulted in worse effectiveness than apatinib alone.	apatinib	40-48	kinase insert domain protein receptor	Mus musculus	104-110
23509226-0	2013	Metabolism and pharmacokinetics of novel selective vascular endothelial growth factor receptor-2 inhibitor apatinib in humans.	apatinib	107-115	kinase insert domain receptor	Homo sapiens	51-96
23509226-1	2013	Apatinib is a new oral antiangiogenic molecule that inhibits vascular endothelial growth factor receptor-2.	apatinib	0-8	kinase insert domain receptor	Homo sapiens	61-106
23509226-8	2013	The major circulating metabolite was the pharmacologically inactive E-3-hydroxy-apatinib-O-glucuronide (M9-2), the steady-state exposure of which was 125% that of the apatinib.	apatinib	80-88	ATPase H+ transporting V0 subunit e1	Homo sapiens	104-108
23509226-13	2013	Apatinib was metabolized primarily by CYP3A4/5 and, to a lesser extent, by CYP2D6, CYP2C9, and CYP2E1.	apatinib	0-8	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	38-44
23509226-13	2013	Apatinib was metabolized primarily by CYP3A4/5 and, to a lesser extent, by CYP2D6, CYP2C9, and CYP2E1.	apatinib	0-8	cytochrome P450 family 2 subfamily D member 6	Homo sapiens	75-81
23509226-13	2013	Apatinib was metabolized primarily by CYP3A4/5 and, to a lesser extent, by CYP2D6, CYP2C9, and CYP2E1.	apatinib	0-8	cytochrome P450 family 2 subfamily C member 9	Homo sapiens	83-89
23509226-13	2013	Apatinib was metabolized primarily by CYP3A4/5 and, to a lesser extent, by CYP2D6, CYP2C9, and CYP2E1.	apatinib	0-8	cytochrome P450 family 2 subfamily E member 1	Homo sapiens	95-101
22503745-3	2012	Apatinib is extensively metabolized in humans, and its major metabolites in circulation include cis-3-hydroxy-apatinib (M1-1), trans-3-hydroxy-apatinib (M1-2), apatinib-25-N-oxide (M1-6), and cis-3-hydroxy-apatinib-O-glucuronide (M9-2).	apatinib	0-8	cholinergic receptor muscarinic 1	Homo sapiens	181-185
22503745-3	2012	Apatinib is extensively metabolized in humans, and its major metabolites in circulation include cis-3-hydroxy-apatinib (M1-1), trans-3-hydroxy-apatinib (M1-2), apatinib-25-N-oxide (M1-6), and cis-3-hydroxy-apatinib-O-glucuronide (M9-2).	apatinib	0-8	ATPase H+ transporting V0 subunit e1	Homo sapiens	230-234
20876799-2	2010	In this study, we determined the effect of apatinib on the interaction of specific antineoplastic compounds with P-glycoprotein (ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), and breast cancer resistance protein (BCRP, ABCG2).	apatinib	43-51	ATP binding cassette subfamily B member 1	Homo sapiens	129-134
22212563-0	2012	Apatinib (YN968D1) enhances the efficacy of conventional chemotherapeutical drugs in side population cells and ABCB1-overexpressing leukemia cells.	apatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	111-116
22212563-4	2012	Furthermore, apatinib also strongly reversed multidrug resistance (MDR) in K562/ADR cells, and the primary leukemia blasts overexpressing ABCB1 while showed no synergistic interactions with chemotherapeutic agents in MRP1-, MRP4-, MRP7- and LRP-overexpressing cells.	apatinib	13-21	MDM4 regulator of p53	Homo sapiens	217-221
22212563-4	2012	Furthermore, apatinib also strongly reversed multidrug resistance (MDR) in K562/ADR cells, and the primary leukemia blasts overexpressing ABCB1 while showed no synergistic interactions with chemotherapeutic agents in MRP1-, MRP4-, MRP7- and LRP-overexpressing cells.	apatinib	13-21	ATP binding cassette subfamily C member 4	Homo sapiens	224-228
22212563-4	2012	Furthermore, apatinib also strongly reversed multidrug resistance (MDR) in K562/ADR cells, and the primary leukemia blasts overexpressing ABCB1 while showed no synergistic interactions with chemotherapeutic agents in MRP1-, MRP4-, MRP7- and LRP-overexpressing cells.	apatinib	13-21	ATP binding cassette subfamily C member 10	Homo sapiens	231-235
22212563-4	2012	Furthermore, apatinib also strongly reversed multidrug resistance (MDR) in K562/ADR cells, and the primary leukemia blasts overexpressing ABCB1 while showed no synergistic interactions with chemotherapeutic agents in MRP1-, MRP4-, MRP7- and LRP-overexpressing cells.	apatinib	13-21	protein tyrosine phosphatase receptor type A	Homo sapiens	241-244
22212563-5	2012	Apatinib treatment markedly increased the intracellular accumulation of doxorubicin and rhodamine 123 in K562/ADR cells and the accumulation of rhodamine 123 in the primary leukemia blasts with ABCB1 overexpression.	apatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	194-199
22212563-6	2012	Apatinib stimulated the ATPase activity of P-gp in a dose-dependent manner but did not alter the expression of ABCB1 at both mRNA and protein levels.	apatinib	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	43-47
22212563-9	2012	Taken together, our results suggest that apatinib could target to SP cells and ABCB1-overexpressing leukemia cells to enhance the efficacy of chemotherapeutic drugs.	apatinib	41-49	ATP binding cassette subfamily B member 1	Homo sapiens	79-84
21602146-1	2011	OBJECTIVE: To investigate the effect of apatinib, a small-molecule vascular endothelial growth factor receptor-2 tyrosine kinase inhibitor, on the proliferation of human acute myeloid leukemia HL-60 cells and explore the possible mechanism.	apatinib	40-48	kinase insert domain receptor	Homo sapiens	67-112
21602146-6	2011	Western blotting showed that the expressions of P-Akt and P-Erk1/2 decreased in HL-60 cells after a 48-h apatinib treatment.	apatinib	105-113	AKT serine/threonine kinase 1	Homo sapiens	50-53
21602146-6	2011	Western blotting showed that the expressions of P-Akt and P-Erk1/2 decreased in HL-60 cells after a 48-h apatinib treatment.	apatinib	105-113	mitogen-activated protein kinase 3	Homo sapiens	60-66
21602146-7	2011	CONCLUSION: Apatinib inhibits the proliferation of HL-60 cells by inducing cell apoptosis probably through the mechanism of inhibiting the expressions of the Akt/Erk1/2 signal transduction pathway.	apatinib	12-20	AKT serine/threonine kinase 1	Homo sapiens	158-161
21602146-7	2011	CONCLUSION: Apatinib inhibits the proliferation of HL-60 cells by inducing cell apoptosis probably through the mechanism of inhibiting the expressions of the Akt/Erk1/2 signal transduction pathway.	apatinib	12-20	mitogen-activated protein kinase 3	Homo sapiens	162-168
20876799-2	2010	In this study, we determined the effect of apatinib on the interaction of specific antineoplastic compounds with P-glycoprotein (ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), and breast cancer resistance protein (BCRP, ABCG2).	apatinib	43-51	ATP binding cassette subfamily B member 1	Homo sapiens	137-167
20876799-2	2010	In this study, we determined the effect of apatinib on the interaction of specific antineoplastic compounds with P-glycoprotein (ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), and breast cancer resistance protein (BCRP, ABCG2).	apatinib	43-51	ATP binding cassette subfamily B member 1	Homo sapiens	169-173
20876799-2	2010	In this study, we determined the effect of apatinib on the interaction of specific antineoplastic compounds with P-glycoprotein (ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), and breast cancer resistance protein (BCRP, ABCG2).	apatinib	43-51	ATP binding cassette subfamily C member 1	Homo sapiens	175-180
20876799-2	2010	In this study, we determined the effect of apatinib on the interaction of specific antineoplastic compounds with P-glycoprotein (ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), and breast cancer resistance protein (BCRP, ABCG2).	apatinib	43-51	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	187-219
20876799-2	2010	In this study, we determined the effect of apatinib on the interaction of specific antineoplastic compounds with P-glycoprotein (ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), and breast cancer resistance protein (BCRP, ABCG2).	apatinib	43-51	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	221-225
20876799-2	2010	In this study, we determined the effect of apatinib on the interaction of specific antineoplastic compounds with P-glycoprotein (ABCB1), multidrug resistance protein 1 (MRP1, ABCC1), and breast cancer resistance protein (BCRP, ABCG2).	apatinib	43-51	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	227-232
20876799-3	2010	Our results showed that apatinib significantly enhanced the cytotoxicity of ABCB1 or ABCG2 substrate drugs in KBv200, MCF-7/adr, and HEK293/ABCB1 cells overexpressing ABCB1 and in S1-M1-80, MCF-7/FLV1000, and HEK293/ABCG2-R2 cells overexpressing ABCG2 (wild-type).	apatinib	24-32	ATP binding cassette subfamily B member 1	Homo sapiens	76-81
20876799-3	2010	Our results showed that apatinib significantly enhanced the cytotoxicity of ABCB1 or ABCG2 substrate drugs in KBv200, MCF-7/adr, and HEK293/ABCB1 cells overexpressing ABCB1 and in S1-M1-80, MCF-7/FLV1000, and HEK293/ABCG2-R2 cells overexpressing ABCG2 (wild-type).	apatinib	24-32	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	85-90
20876799-3	2010	Our results showed that apatinib significantly enhanced the cytotoxicity of ABCB1 or ABCG2 substrate drugs in KBv200, MCF-7/adr, and HEK293/ABCB1 cells overexpressing ABCB1 and in S1-M1-80, MCF-7/FLV1000, and HEK293/ABCG2-R2 cells overexpressing ABCG2 (wild-type).	apatinib	24-32	ATP binding cassette subfamily B member 1	Homo sapiens	140-145
20923544-0	2010	Safety and pharmacokinetics of novel selective vascular endothelial growth factor receptor-2 inhibitor YN968D1 in patients with advanced malignancies.	apatinib	103-110	kinase insert domain receptor	Homo sapiens	47-92
20923544-1	2010	BACKGROUND: YN968D1 (Apatinib) selectively inhibits phosphorylation of VEGFR-2 and tumor angiogenesis in mice model.	apatinib	21-29	kinase insert domain protein receptor	Mus musculus	71-78
20876799-3	2010	Our results showed that apatinib significantly enhanced the cytotoxicity of ABCB1 or ABCG2 substrate drugs in KBv200, MCF-7/adr, and HEK293/ABCB1 cells overexpressing ABCB1 and in S1-M1-80, MCF-7/FLV1000, and HEK293/ABCG2-R2 cells overexpressing ABCG2 (wild-type).	apatinib	24-32	ATP binding cassette subfamily B member 1	Homo sapiens	140-145
20876799-3	2010	Our results showed that apatinib significantly enhanced the cytotoxicity of ABCB1 or ABCG2 substrate drugs in KBv200, MCF-7/adr, and HEK293/ABCB1 cells overexpressing ABCB1 and in S1-M1-80, MCF-7/FLV1000, and HEK293/ABCG2-R2 cells overexpressing ABCG2 (wild-type).	apatinib	24-32	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	216-221
20876799-3	2010	Our results showed that apatinib significantly enhanced the cytotoxicity of ABCB1 or ABCG2 substrate drugs in KBv200, MCF-7/adr, and HEK293/ABCB1 cells overexpressing ABCB1 and in S1-M1-80, MCF-7/FLV1000, and HEK293/ABCG2-R2 cells overexpressing ABCG2 (wild-type).	apatinib	24-32	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	216-221
20876799-6	2010	Furthermore, apatinib significantly inhibited the photoaffinity labeling of both ABCB1 and ABCG2 with [(125)I]iodoarylazidoprazosin in a concentration-dependent manner.	apatinib	13-21	ATP binding cassette subfamily B member 1	Homo sapiens	81-86
20876799-6	2010	Furthermore, apatinib significantly inhibited the photoaffinity labeling of both ABCB1 and ABCG2 with [(125)I]iodoarylazidoprazosin in a concentration-dependent manner.	apatinib	13-21	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	91-96
20876799-7	2010	The ATPase activity of both ABCB1 and ABCG2 was significantly increased by apatinib.	apatinib	75-83	ATP binding cassette subfamily B member 1	Homo sapiens	28-33
20876799-7	2010	The ATPase activity of both ABCB1 and ABCG2 was significantly increased by apatinib.	apatinib	75-83	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	38-43
20876799-9	2010	Importantly, apatinib significantly enhanced the effect of paclitaxel against the ABCB1-resistant KBv200 cancer cell xenografts in nude mice.	apatinib	13-21	ATP binding cassette subfamily B member 1	Homo sapiens	82-87
20876799-10	2010	In conclusion, apatinib reverses ABCB1- and ABCG2-mediated MDR by inhibiting their transport function, but not by blocking the AKT or ERK1/2 pathway or downregulating ABCB1 or ABCG2 expression.	apatinib	15-23	ATP binding cassette subfamily B member 1	Homo sapiens	33-38
20876799-10	2010	In conclusion, apatinib reverses ABCB1- and ABCG2-mediated MDR by inhibiting their transport function, but not by blocking the AKT or ERK1/2 pathway or downregulating ABCB1 or ABCG2 expression.	apatinib	15-23	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	44-49