PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
33907977-4	2021	Ponatinib is a third generation TKI that demonstrates higher binding affinity for ABL1 than first/second generation TKIs.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-86
33955652-0	2022	Repurposing the FDA-approved anticancer agent ponatinib as a fluconazole potentiator by suppression of multidrug efflux and Pma1 expression in a broad spectrum of yeast species.	ponatinib	46-55	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	124-128
33955652-5	2022	Mechanistic insights into the mode of action unravelled that ponatinib reduced the efflux of fluconazole via Pdr5 and suppressed the expression of the proton pump, Pma1.	ponatinib	61-70	ATP-binding cassette multidrug transporter PDR5	Saccharomyces cerevisiae S288C	109-113
33955652-5	2022	Mechanistic insights into the mode of action unravelled that ponatinib reduced the efflux of fluconazole via Pdr5 and suppressed the expression of the proton pump, Pma1.	ponatinib	61-70	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	164-168
33390067-4	2021	RANBP2-ABL1 Ba/F3 cells developed the clinically relevant ABL1 p.T315I mutation and upon secondary resistance to ponatinib, developed compound mutations, including a novel ABL1 p.L302H mutation.	ponatinib	113-122	RAN binding protein 2	Mus musculus	0-6
33390067-4	2021	RANBP2-ABL1 Ba/F3 cells developed the clinically relevant ABL1 p.T315I mutation and upon secondary resistance to ponatinib, developed compound mutations, including a novel ABL1 p.L302H mutation.	ponatinib	113-122	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	7-11
33836003-7	2021	By analysing dose-response profiles to 397 anti-cancer drugs of 612 well-characterised human cancer cell lines, we discover that cell lines that expressed high ELF4 mRNA transcript are significantly less responsive to 129 anti-cancer drugs, and only significantly more response to three drugs: dasatinib, WH-4-023, and Ponatinib, all of which remarkably target the proto-oncogene tyrosine-protein kinase SRC and tyrosine-protein kinase ABL1.	ponatinib	319-328	E74 like ETS transcription factor 4	Homo sapiens	160-164
33732370-9	2021	Therefore, it is proposed that PDGFR inhibitors, including sunitinib and ponatinib, should be applied effectively to treat ER-alpha+ breast cancer.	ponatinib	73-82	platelet derived growth factor receptor beta	Homo sapiens	31-36
33732370-9	2021	Therefore, it is proposed that PDGFR inhibitors, including sunitinib and ponatinib, should be applied effectively to treat ER-alpha+ breast cancer.	ponatinib	73-82	estrogen receptor 1	Homo sapiens	123-131
33796468-2	2021	Ponatinib is a 3rd generation TKI that binds BCR-ABL1 with high affinity and inhibits most BCR-ABL1 mutants, including the T315I mutation.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-53
33796468-2	2021	Ponatinib is a 3rd generation TKI that binds BCR-ABL1 with high affinity and inhibits most BCR-ABL1 mutants, including the T315I mutation.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-99
33389067-14	2021	Ponatinib (FGFR1 inhibitor) reversed the suppressive effects of miR-214 inhibition on lung injury and inflammation of VILI mice.	ponatinib	0-9	fibroblast growth factor receptor 1	Mus musculus	11-16
33748144-3	2021	Although the use of the BCR-ABL tyrosine kinase inhibitors (TKIs), such as imatinib, nilotinib, dasatinib, bosutinib, and ponatinib have increased the overall survival of CML patients, their use is limited by drug resistance and severe adverse effects.	ponatinib	122-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	24-31
33531202-10	2021	Ponatinib, a Src inhibitor, significantly enhanced romidepsin-induced apoptosis not only in HH, MJ, and Hut78 cells, but also in Myla and SeAx CTCL cell lines.	ponatinib	0-9	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	13-16
33593493-0	2021	Evaluation of ponatinib in vitro effect in three canine mast cell tumor cell lines expressing FGFR-1, PDGFR-alpha, and VEGFR-2.	ponatinib	14-23	fibroblast growth factor receptor 1 (fms-related tyrosine kinase 2, Pfeiffer syndrome)	Canis lupus familiaris	94-100
33593493-1	2021	Ponatinib is a broad-spectrum tyrosine kinase inhibitor that targets numerous receptor tyrosine kinases (RTKs), including but not limited to fibroblast growth factor receptor (FGFR)-1, platelet derived growth factor receptor (PDGFR)-alpha, and vascular endothelial growth factor receptor (VEGFR)-2.	ponatinib	0-9	fibroblast growth factor receptor 1 (fms-related tyrosine kinase 2, Pfeiffer syndrome)	Canis lupus familiaris	141-183
33593493-1	2021	Ponatinib is a broad-spectrum tyrosine kinase inhibitor that targets numerous receptor tyrosine kinases (RTKs), including but not limited to fibroblast growth factor receptor (FGFR)-1, platelet derived growth factor receptor (PDGFR)-alpha, and vascular endothelial growth factor receptor (VEGFR)-2.	ponatinib	0-9	platelet derived growth factor receptor alpha	Canis lupus familiaris	185-238
33593493-6	2021	Significantly increased apoptosis in each cell line was seen between 12 and 18 h after treatment with IC50 of ponatinib via Annexin-V and Caspase-3/7 assays.	ponatinib	110-119	caspase 3	Canis lupus familiaris	138-149
33732370-4	2021	To block the PDGF-BB signaling pathway, PDGFR inhibitors (sunitinib or ponatinib) were employed.	ponatinib	71-80	platelet derived growth factor receptor beta	Homo sapiens	40-45
32898857-8	2021	However, the addition of dasatinib or ponatinib inhibited T-cell proliferation and IFN-gamma production.	ponatinib	38-47	interferon gamma	Homo sapiens	83-92
33107354-5	2021	In this study, we sought to determine ponatinib"s potential utility, a clinically approved and potent cAbl inhibitor, in MPM treatment.	ponatinib	38-47	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-106
33107354-12	2021	Western blot analysis showed that the activation of Abl signaling was blocked in the ponatinib-treated MMP lines.	ponatinib	85-94	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	52-55
33107354-16	2021	CONCLUSION: Ponatinib may offer a new therapeutic strategy for MPM patients based on cAbl signaling pathway inhibition.	ponatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	85-89
33389067-14	2021	Ponatinib (FGFR1 inhibitor) reversed the suppressive effects of miR-214 inhibition on lung injury and inflammation of VILI mice.	ponatinib	0-9	microRNA 214	Mus musculus	64-71
33452624-9	2021	Even in Imatinib, Nilotinib, and Ponatinib-resistant CML cells, a dual PI3K/mTOR inhibitor, BEZ235, showed antiproliferative activity.	ponatinib	33-42	mechanistic target of rapamycin kinase	Homo sapiens	76-80
33118510-0	2020	[Ponatinib inhibits growth of patient-derived xenograft of cholangiocarcinoma expressing FGFR2-CCDC6 fusion protein in nude mice].	ponatinib	1-10	fibroblast growth factor receptor 2	Homo sapiens	89-94
33460055-0	2020	Dynamic evolution of ponatinib-resistant mutations in BCR-ABL1-positive leukaemias revealed by next-generation sequencing.	ponatinib	21-30	BCR activator of RhoGEF and GTPase	Homo sapiens	54-57
33460055-0	2020	Dynamic evolution of ponatinib-resistant mutations in BCR-ABL1-positive leukaemias revealed by next-generation sequencing.	ponatinib	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-62
32801162-7	2020	Fixed-ratio combination cytotoxicity assays using the tyrosine kinase inhibitors BMS-754807 and ponatinib that target IGF1R and FGFR1, respectively, revealed strong synergy against both cell line and patient-derived xenograft (PDX) models of CRLF2r Ph-like ALL.	ponatinib	96-105	insulin like growth factor 1 receptor	Homo sapiens	118-123
32801162-7	2020	Fixed-ratio combination cytotoxicity assays using the tyrosine kinase inhibitors BMS-754807 and ponatinib that target IGF1R and FGFR1, respectively, revealed strong synergy against both cell line and patient-derived xenograft (PDX) models of CRLF2r Ph-like ALL.	ponatinib	96-105	fibroblast growth factor receptor 1	Homo sapiens	128-133
32801162-7	2020	Fixed-ratio combination cytotoxicity assays using the tyrosine kinase inhibitors BMS-754807 and ponatinib that target IGF1R and FGFR1, respectively, revealed strong synergy against both cell line and patient-derived xenograft (PDX) models of CRLF2r Ph-like ALL.	ponatinib	96-105	cytokine receptor like factor 2	Homo sapiens	242-247
32910995-5	2020	On the other hand, the third-generation BCR-ABL1 TKI ponatinib is not well studied in terms of its efficacy on CML LSCs.	ponatinib	53-62	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	44-48
32910995-6	2020	Here, we evaluate the efficacy of ponatinib against CML LSC-containing lin-Sca-1+c-Kit+ (LSK) cells using a mouse CML-like model.	ponatinib	34-43	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	81-86
32470534-7	2020	We have summarized our recent findings with transgenic zebrafish line harboring BNP luciferase activity to demonstrate the cardiotoxic potential of ponatinib.	ponatinib	148-157	basonuclin 2	Danio rerio	80-83
32470534-8	2020	Additionally, we will review the recent discoveries reported by our and other laboratories that ponatinib primarily exerts its cardiotoxicity via an off-target effect on cardiomyocyte prosurvival signaling pathways, AKT and ERK.	ponatinib	96-105	AKT serine/threonine kinase 1	Homo sapiens	216-219
32470534-8	2020	Additionally, we will review the recent discoveries reported by our and other laboratories that ponatinib primarily exerts its cardiotoxicity via an off-target effect on cardiomyocyte prosurvival signaling pathways, AKT and ERK.	ponatinib	96-105	mitogen-activated protein kinase 1	Homo sapiens	224-227
32780298-11	2020	Furthermore, ponatinib was more effective than imatinib in reducing the percentage of CD26-expressing cells in primary CML cells, whereas imatinib and ponatinib showed similar efficacy on KCL22 cells.	ponatinib	13-22	dipeptidyl peptidase 4	Homo sapiens	86-90
33419251-4	2020	Here, we presented a 77-year-old male with a diagnosis of Ph positive ALL resistant to ponatinib and carrying a rare threonine to leucine (T315L) mutation on BCR-ABL1 gene.	ponatinib	87-96	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	162-166
33118510-0	2020	[Ponatinib inhibits growth of patient-derived xenograft of cholangiocarcinoma expressing FGFR2-CCDC6 fusion protein in nude mice].	ponatinib	1-10	coiled-coil domain containing 6	Homo sapiens	95-100
33118510-1	2020	OBJECTIVE: To investigate the antitumor effect of ponatinib on the growth of cholangiocarcinoma xenograft derived from a clinical patient in a mouse model expressing FGFR2-CCDC6 fusion protein.	ponatinib	50-59	fibroblast growth factor receptor 2	Mus musculus	166-171
33118510-8	2020	Western blotting and immunohistochemistry revealed obviously lowered phosphorylation level of FGFR and its downstream signal markers FRS2, AKT and ERK in the xenografts from ponatinib-treated mice.	ponatinib	174-183	fibroblast growth factor receptor substrate 2	Mus musculus	133-137
33118510-8	2020	Western blotting and immunohistochemistry revealed obviously lowered phosphorylation level of FGFR and its downstream signal markers FRS2, AKT and ERK in the xenografts from ponatinib-treated mice.	ponatinib	174-183	thymoma viral proto-oncogene 1	Mus musculus	139-142
33118510-8	2020	Western blotting and immunohistochemistry revealed obviously lowered phosphorylation level of FGFR and its downstream signal markers FRS2, AKT and ERK in the xenografts from ponatinib-treated mice.	ponatinib	174-183	mitogen-activated protein kinase 1	Mus musculus	147-150
33118510-10	2020	CONCLUSIONS: Ponatinib can regulate FGFR signaling to inhibit the proliferation and induce apoptosis of tumor cells in mice bearing patient-derived cholangiocarcinoma xenograft with FGFR2 fusion.	ponatinib	13-22	fibroblast growth factor receptor 2	Homo sapiens	182-187
33194747-6	2020	Patients 2 and 3 showed some response to combined FLT3-inhibitor and BCR-ABL targeted therapy (gilteritinib and ponatinib).	ponatinib	112-121	fms related receptor tyrosine kinase 3	Homo sapiens	50-54
32086952-9	2020	As CDK7 inhibitors are currently under clinical evaluation in patients, our data suggestion the addition of the TKI ponatinib or lapatinib in CDK7 inhibitor clinical trials in patients.	ponatinib	116-125	cyclin dependent kinase 7	Homo sapiens	142-146
32064608-4	2020	Cell/molecular biological and analytical chemistry methods were applied to investigate uptake kinetics/subcellular distribution, the role of lipid droplets (LDs) and lipoid microenvironment compartments in responsiveness of FGFR1-driven lung cancer cells towards ponatinib.	ponatinib	263-272	fibroblast growth factor receptor 1	Mus musculus	224-229
32873792-4	2020	We found that Ponatinib, an FDA-approved drug, is an effective inhibitor of BRAF monomers and dimers.	ponatinib	14-23	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	76-80
32873792-5	2020	Ponatinib binds the BRAF dimer and stabilizes a distinct alphaC-helix conformation through interaction with a previously unrevealed allosteric site.	ponatinib	0-9	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	20-24
32112427-3	2020	Ponatinib was incubated with human liver microsomes in the presence of NADPH and trapping agents (glutathione or potassium cyanide).	ponatinib	0-9	2,4-dienoyl-CoA reductase 1	Homo sapiens	71-76
32112427-8	2020	In addition, two reactive metabolites (cyano adducts) were detected in human liver microsomes in the presence of potassium cyanide and NADPH, suggesting that ponatinib underwent CYP450-mediated metabolic activation, which could be one of the causative mechanisms for its hepatotoxicity.	ponatinib	158-167	2,4-dienoyl-CoA reductase 1	Homo sapiens	135-140
32184020-0	2020	Involvement of MCL1, c-myc, and cyclin D2 protein degradation in ponatinib-induced cytotoxicity against T315I(+) Ph+leukemia cells.	ponatinib	65-74	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	15-19
32184020-0	2020	Involvement of MCL1, c-myc, and cyclin D2 protein degradation in ponatinib-induced cytotoxicity against T315I(+) Ph+leukemia cells.	ponatinib	65-74	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	21-26
32184020-0	2020	Involvement of MCL1, c-myc, and cyclin D2 protein degradation in ponatinib-induced cytotoxicity against T315I(+) Ph+leukemia cells.	ponatinib	65-74	cyclin D2	Homo sapiens	32-41
32184020-4	2020	PNT induced apoptosis (increased sub G1 cells, and cleaved caspase3 and PARP), and suppressed protein expression of MCL1, cyclin D2 and c-myc, which were reversed by a proteasome inhibitor, MG132, suggesting enhanced proteasomal degradation by PNT.	ponatinib	0-3	caspase 3	Homo sapiens	59-67
32184020-4	2020	PNT induced apoptosis (increased sub G1 cells, and cleaved caspase3 and PARP), and suppressed protein expression of MCL1, cyclin D2 and c-myc, which were reversed by a proteasome inhibitor, MG132, suggesting enhanced proteasomal degradation by PNT.	ponatinib	0-3	collagen type XI alpha 2 chain	Homo sapiens	72-76
32184020-4	2020	PNT induced apoptosis (increased sub G1 cells, and cleaved caspase3 and PARP), and suppressed protein expression of MCL1, cyclin D2 and c-myc, which were reversed by a proteasome inhibitor, MG132, suggesting enhanced proteasomal degradation by PNT.	ponatinib	0-3	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	116-120
32184020-4	2020	PNT induced apoptosis (increased sub G1 cells, and cleaved caspase3 and PARP), and suppressed protein expression of MCL1, cyclin D2 and c-myc, which were reversed by a proteasome inhibitor, MG132, suggesting enhanced proteasomal degradation by PNT.	ponatinib	0-3	cyclin D2	Homo sapiens	122-131
32184020-4	2020	PNT induced apoptosis (increased sub G1 cells, and cleaved caspase3 and PARP), and suppressed protein expression of MCL1, cyclin D2 and c-myc, which were reversed by a proteasome inhibitor, MG132, suggesting enhanced proteasomal degradation by PNT.	ponatinib	0-3	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	136-141
32360510-7	2020	In in vitro analyses, two genes that were predicted to undergo similar regulation using pseudotime analysis (ALOX5 and FGFR) were found to be similarly inhibited by ponatinib, an FGFR inhibitor.	ponatinib	165-174	arachidonate 5-lipoxygenase	Homo sapiens	109-114
32215194-5	2020	Furthermore, the incorporation of novel monoclonal antibodies or potent BCR-ABL1 tyrosine kinase inhibitors, such as ponatinib into frontline treatment may have the advantage of achieving higher rates of MRD negativity while minimizing chemotherapy-related toxicities.	ponatinib	117-126	BCR activator of RhoGEF and GTPase	Homo sapiens	72-80
31937621-0	2020	A combinatorial strategy for targeting BRAF V600E mutant cancers with BRAF V600E inhibitor (PLX4720) and tyrosine kinase inhibitor (ponatinib).	ponatinib	132-141	Braf transforming gene	Mus musculus	39-43
31937621-11	2020	CONCLUSIONS: Combination treatment with ponatinib and PLX4720 exhibited significant synergistic anticancer activity in preclinical models of BRAF V600E thyroid cancer, in addition to overcoming PLX4720 resistance.	ponatinib	40-49	Braf transforming gene	Mus musculus	141-145
31980503-7	2020	Additionally, we observed that that primary leukemia cells from Case 1 demonstrated sensitivity to the tyrosine kinase inhibitors Ponatinib and Dovitinib that can target FGFR1 kinase activity, while primary cells from Case 2 were resistant to both drugs.	ponatinib	130-139	fibroblast growth factor receptor 1	Homo sapiens	170-175
31990987-0	2020	Ponatinib treatment in chronic myeloid leukemia cell lines targets aurora kinase A/FOXM1 axis.	ponatinib	0-9	forkhead box M1	Homo sapiens	83-88
32175644-0	2020	Renovascular hypertension from the BCR-ABL tyrosine kinase inhibitor ponatinib.	ponatinib	69-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-42
32197359-0	2020	Ponatinib Induces Vascular Toxicity through the Notch-1 Signaling Pathway.	ponatinib	0-9	notch receptor 1	Homo sapiens	48-55
32197359-2	2020	Specific activation of Notch signaling in CML cells by ponatinib can be considered as the "on-target effect" on the tumor and represents a therapeutic approach for CML.	ponatinib	55-64	notch receptor 1	Homo sapiens	23-28
32197359-7	2020	We delineated the signaling of ponatinib-induced vascular toxicity, demonstrating that ponatinib inhibits endothelial survival, reduces angiogenesis and induces endothelial senescence and apoptosis via the Notch-1 pathway.	ponatinib	31-40	notch receptor 1	Homo sapiens	206-213
32197359-7	2020	We delineated the signaling of ponatinib-induced vascular toxicity, demonstrating that ponatinib inhibits endothelial survival, reduces angiogenesis and induces endothelial senescence and apoptosis via the Notch-1 pathway.	ponatinib	87-96	notch receptor 1	Homo sapiens	206-213
32197359-10	2020	By hyperactivating Notch-1 in the vessels, ponatinib exerts an "on-target off tumor effect", which leads to deleterious effects and may explain the drug"s vasculotoxicity.	ponatinib	43-52	notch receptor 1	Homo sapiens	19-26
32197359-11	2020	Selective blockade of Notch-1 prevented ponatinib-induced vascular toxicity.	ponatinib	40-49	notch receptor 1	Homo sapiens	22-29
32292555-7	2020	Our best compound exhibited a hERG IC50 of 12.1 muM (compared to nilotinib with an IC50 of 0.45 muM and ponatinib with IC50 of 0.767 muM).	ponatinib	104-113	ETS transcription factor ERG	Homo sapiens	30-34
31664678-8	2020	Moreover, inhibiting Smad2/3 phosphorylation with ponatinib or SIS3 also significantly reduced seizure severity, alongside reducing GFAP/CS56 immunoreactivity.	ponatinib	50-59	SMAD family member 2	Rattus norvegicus	21-28
32095692-1	2020	Ponatinib is a multikinase inhibitor that is used to treat chronic myeloid leukemia patients harboring mutated ABL1(T315I) kinase.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	111-115
32095692-6	2020	A nicotinamide analogue of ponatinib, HSN748, retains activity against FLT3, ABL1, RET, and PDGFRalpha/beta but loses activity against c-Src and P38alpha.	ponatinib	27-36	fms related receptor tyrosine kinase 3	Homo sapiens	71-75
32095692-6	2020	A nicotinamide analogue of ponatinib, HSN748, retains activity against FLT3, ABL1, RET, and PDGFRalpha/beta but loses activity against c-Src and P38alpha.	ponatinib	27-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	77-81
32095692-6	2020	A nicotinamide analogue of ponatinib, HSN748, retains activity against FLT3, ABL1, RET, and PDGFRalpha/beta but loses activity against c-Src and P38alpha.	ponatinib	27-36	ret proto-oncogene	Homo sapiens	83-86
32095692-6	2020	A nicotinamide analogue of ponatinib, HSN748, retains activity against FLT3, ABL1, RET, and PDGFRalpha/beta but loses activity against c-Src and P38alpha.	ponatinib	27-36	platelet derived growth factor receptor alpha	Homo sapiens	92-107
32095692-6	2020	A nicotinamide analogue of ponatinib, HSN748, retains activity against FLT3, ABL1, RET, and PDGFRalpha/beta but loses activity against c-Src and P38alpha.	ponatinib	27-36	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	135-140
32095692-6	2020	A nicotinamide analogue of ponatinib, HSN748, retains activity against FLT3, ABL1, RET, and PDGFRalpha/beta but loses activity against c-Src and P38alpha.	ponatinib	27-36	mitogen-activated protein kinase 14	Homo sapiens	145-153
31925328-3	2020	Using BCR-ABL as a case study, we successfully recaptured the clinically observed mutations that confer resistance imatinib, nilotinib, dasatinib, bosutinib, and ponatinib.	ponatinib	162-171	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-13
31101753-8	2020	Treatment of BCR-ABL1p210 expressing flies with potent kinase inhibitors (dasatinib and ponatinib) resulted in the rescue of ommatidial loss and restoration of normal development.	ponatinib	88-97	BCR activator of RhoGEF and GTPase	Homo sapiens	13-16
32829325-1	2020	INTRODUCTION: Ponatinib (PNT) is a tyrosine kinase inhibitor approved for treating patients with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph + ALL), or chronic myeloid leukemia, resistant or intolerant to other tyrosine kinase inhibitor or showing T315I mutation of BCR-ABL.	ponatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	288-295
31770593-14	2020	Ponatinib binds to FGFR4 in a DFG-Dout conformation and is classified as a type II inhibitor.	ponatinib	0-9	fibroblast growth factor receptor 4	Homo sapiens	19-24
31600013-7	2020	Accordingly, simultaneous inhibition of these RTKs using a multi-kinase inhibitor ponatinib has a superior effect at eliminating the CSC population and reduces metastasis of PIK3CA-overexpressing HNSCC cells.	ponatinib	82-91	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	174-180
30661457-0	2020	How does the novel T315L mutation of breakpoint cluster region-abelson (BCR-ABL) kinase confer resistance to ponatinib: a comparative molecular dynamics simulation study.	ponatinib	109-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-70
30661457-0	2020	How does the novel T315L mutation of breakpoint cluster region-abelson (BCR-ABL) kinase confer resistance to ponatinib: a comparative molecular dynamics simulation study.	ponatinib	109-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
30661457-5	2020	The latest third-generation TKIs, ponatinib, can tackle most abnormal BCR-ABL kinases, including the T315I mutant that is resistant to first- and second-generations TKIs such as imatinib.	ponatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	70-77
30661457-7	2020	Here, using molecular dynamics (MD) simulations, we explored into the detailed interactions between ponatinib and BCR-ABL in the wild-type (WT), T315I, and T315L systems.	ponatinib	100-109	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
30661457-9	2020	Binding free energy analysis unveiled that the affinity of ponatinib to BCR-ABL decreased upon T315L mutation, which resulted in its unfavorable binding and drug resistance.	ponatinib	59-68	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	72-79
31810968-7	2019	CONCLUSION: Treatment with second- (nilotinib) and third-generation (ponatinib) TKIs was effective in suppressing leukemic clones exhibiting the atypical e12a2 Ins/Del BCR-ABL1.	ponatinib	69-78	BCR activator of RhoGEF and GTPase	Homo sapiens	168-176
31371345-8	2019	Furthermore, the FGFR2 N549H secondary mutation displayed cross-resistance to other selective FGFR inhibitors, but remained sensitive to the nonselective inhibitor, ponatinib.	ponatinib	165-174	fibroblast growth factor receptor 2	Homo sapiens	17-22
31043681-8	2019	The KLK2-FGFR2 fusion protein was determined to be highly sensitive to the selective FGFR inhibitors AZD-4547, BGJ398, JNJ-42756943, the irreversible inhibitor TAS-120, and the non-selective inhibitor Ponatinib.	ponatinib	201-210	kallikrein related peptidase 2	Homo sapiens	4-8
31043681-8	2019	The KLK2-FGFR2 fusion protein was determined to be highly sensitive to the selective FGFR inhibitors AZD-4547, BGJ398, JNJ-42756943, the irreversible inhibitor TAS-120, and the non-selective inhibitor Ponatinib.	ponatinib	201-210	fibroblast growth factor receptor 2	Mus musculus	9-14
30580670-2	2019	Ponatinib, an oral drug, was discovered as an efficient BCR-ABL inhibitor by addressing imatinib drug resistance arising due to the point mutations at its active sites.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	56-63
30580670-3	2019	In this study, 44 BCR-ABL kinase inhibitors, which are derivatives of ponatinib, were used to develop a robust two-dimensional quantitative structure-activity relationship (2D-QSAR) and 3D-Pharmacophore models by dividing dataset into 32 training sets and 12 test set molecules.	ponatinib	70-79	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-25
31510844-0	2019	Ponatinib use in two pediatric patients with relapsed Ph + ALL with ABL1 kinase domain mutations.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-72
31543464-0	2019	Combining the Allosteric Inhibitor Asciminib with Ponatinib Suppresses Emergence of and Restores Efficacy against Highly Resistant BCR-ABL1 Mutants.	ponatinib	50-59	BCR activator of RhoGEF and GTPase	Homo sapiens	131-139
31543464-1	2019	BCR-ABL1 point mutation-mediated resistance to tyrosine kinase inhibitor (TKI) therapy in Philadelphia chromosome-positive (Ph+) leukemia is effectively managed with several approved drugs, including ponatinib for BCR-ABL1T315I-mutant disease.	ponatinib	200-209	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
31543464-1	2019	BCR-ABL1 point mutation-mediated resistance to tyrosine kinase inhibitor (TKI) therapy in Philadelphia chromosome-positive (Ph+) leukemia is effectively managed with several approved drugs, including ponatinib for BCR-ABL1T315I-mutant disease.	ponatinib	200-209	BCR activator of RhoGEF and GTPase	Homo sapiens	0-3
31444999-3	2019	By targeting vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor, Src, and FGF receptor pathways, ponatinib may potentially help to overcome some of the putative mechanisms of adaptive resistance.	ponatinib	139-148	kinase insert domain receptor	Homo sapiens	13-56
31444999-3	2019	By targeting vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor, Src, and FGF receptor pathways, ponatinib may potentially help to overcome some of the putative mechanisms of adaptive resistance.	ponatinib	139-148	kinase insert domain receptor	Homo sapiens	58-63
31444999-3	2019	By targeting vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor, Src, and FGF receptor pathways, ponatinib may potentially help to overcome some of the putative mechanisms of adaptive resistance.	ponatinib	139-148	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	107-110
31444999-14	2019	Ponatinib treatment significantly increased plasma VEGF, soluble (s)VEGFR1, sVEGFR2, sTIE2, interferon gamma (IFNgamma), tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-6, IL-8, and IL-10 and decreased sVEGFR2.	ponatinib	0-9	vascular endothelial growth factor A	Homo sapiens	51-55
31444999-14	2019	Ponatinib treatment significantly increased plasma VEGF, soluble (s)VEGFR1, sVEGFR2, sTIE2, interferon gamma (IFNgamma), tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-6, IL-8, and IL-10 and decreased sVEGFR2.	ponatinib	0-9	fms related receptor tyrosine kinase 1	Homo sapiens	68-74
31444999-14	2019	Ponatinib treatment significantly increased plasma VEGF, soluble (s)VEGFR1, sVEGFR2, sTIE2, interferon gamma (IFNgamma), tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-6, IL-8, and IL-10 and decreased sVEGFR2.	ponatinib	0-9	interferon gamma	Homo sapiens	92-108
31444999-14	2019	Ponatinib treatment significantly increased plasma VEGF, soluble (s)VEGFR1, sVEGFR2, sTIE2, interferon gamma (IFNgamma), tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-6, IL-8, and IL-10 and decreased sVEGFR2.	ponatinib	0-9	interferon gamma	Homo sapiens	110-118
31444999-14	2019	Ponatinib treatment significantly increased plasma VEGF, soluble (s)VEGFR1, sVEGFR2, sTIE2, interferon gamma (IFNgamma), tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-6, IL-8, and IL-10 and decreased sVEGFR2.	ponatinib	0-9	tumor necrosis factor	Homo sapiens	121-148
31444999-14	2019	Ponatinib treatment significantly increased plasma VEGF, soluble (s)VEGFR1, sVEGFR2, sTIE2, interferon gamma (IFNgamma), tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-6, IL-8, and IL-10 and decreased sVEGFR2.	ponatinib	0-9	tumor necrosis factor	Homo sapiens	150-159
31444999-14	2019	Ponatinib treatment significantly increased plasma VEGF, soluble (s)VEGFR1, sVEGFR2, sTIE2, interferon gamma (IFNgamma), tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-6, IL-8, and IL-10 and decreased sVEGFR2.	ponatinib	0-9	interleukin 6	Homo sapiens	162-180
31444999-14	2019	Ponatinib treatment significantly increased plasma VEGF, soluble (s)VEGFR1, sVEGFR2, sTIE2, interferon gamma (IFNgamma), tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-6, IL-8, and IL-10 and decreased sVEGFR2.	ponatinib	0-9	C-X-C motif chemokine ligand 8	Homo sapiens	182-186
31444999-14	2019	Ponatinib treatment significantly increased plasma VEGF, soluble (s)VEGFR1, sVEGFR2, sTIE2, interferon gamma (IFNgamma), tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-6, IL-8, and IL-10 and decreased sVEGFR2.	ponatinib	0-9	interleukin 10	Homo sapiens	192-197
31128178-0	2019	Insight into ponatinib resistance mechanisms in rhabdomyosarcoma caused by the mutations in FGFR4 tyrosine kinase using molecular modeling strategies.	ponatinib	13-22	fibroblast growth factor receptor 4	Homo sapiens	92-97
31079415-5	2019	Treatment of wild-type C57BL/6 mice with ponatinib and nilotinib but not imatinib, dasatinib or vehicle control for 4 hours significantly increased thrombus growth following ex vivo perfusion on collagen and FeCl3-induced vascular injury of mesenteric arterioles and carotid artery in vivo and increased plasma levels of soluble P-selectin, tumour necrosis factor-alpha, interleukin-6, interferon-gamma and thromboxane B2 (TxB2).	ponatinib	41-50	interleukin 6	Mus musculus	371-384
30943283-6	2019	Further, pharmacological inhibition of FGFR and PP2A signaling through ponatinib and LB-100 treatment, respectively, exhibited strong tumor-specific anti-proliferative and apoptotic activity in cultured DIPG cells.	ponatinib	71-80	protein phosphatase 2 phosphatase activator	Homo sapiens	48-52
31115499-3	2019	PF-114, a derivative of the third generation BCR-ABL inhibitor ponatinib, demonstrated a high inhibitory activity against wild-type and mutant BCR-ABL forms, such as the clinically important T315I.	ponatinib	63-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	45-52
31115499-3	2019	PF-114, a derivative of the third generation BCR-ABL inhibitor ponatinib, demonstrated a high inhibitory activity against wild-type and mutant BCR-ABL forms, such as the clinically important T315I.	ponatinib	63-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-150
31079415-5	2019	Treatment of wild-type C57BL/6 mice with ponatinib and nilotinib but not imatinib, dasatinib or vehicle control for 4 hours significantly increased thrombus growth following ex vivo perfusion on collagen and FeCl3-induced vascular injury of mesenteric arterioles and carotid artery in vivo and increased plasma levels of soluble P-selectin, tumour necrosis factor-alpha, interleukin-6, interferon-gamma and thromboxane B2 (TxB2).	ponatinib	41-50	interferon gamma	Mus musculus	386-402
31037149-0	2019	Repurposing Ponatinib as a Potent Agent against KIT Mutant Melanomas.	ponatinib	12-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	48-51
30679311-6	2019	The ability of unphosphorylated IRAK4 to take on variable conformations prompted us to screen for small-molecule inhibitors that bind preferentially to unphosphorylated IRAK4, leading to the identification of ponatinib and HG-12-6.	ponatinib	209-218	interleukin 1 receptor associated kinase 4	Homo sapiens	32-37
30679311-6	2019	The ability of unphosphorylated IRAK4 to take on variable conformations prompted us to screen for small-molecule inhibitors that bind preferentially to unphosphorylated IRAK4, leading to the identification of ponatinib and HG-12-6.	ponatinib	209-218	interleukin 1 receptor associated kinase 4	Homo sapiens	169-174
30780089-0	2019	Molecular interaction study of an anticancer drug, ponatinib with human serum albumin using spectroscopic and molecular docking methods.	ponatinib	51-60	albumin	Homo sapiens	72-85
30780089-1	2019	Binding of a potent anticancer agent, ponatinib (PTB) to human serum albumin (HSA), main ligand transporter in blood plasma was analyzed with several spectral techniques such as fluorescence, absorption and circular dichroism along with molecular docking studies.	ponatinib	38-47	albumin	Homo sapiens	63-76
30780089-1	2019	Binding of a potent anticancer agent, ponatinib (PTB) to human serum albumin (HSA), main ligand transporter in blood plasma was analyzed with several spectral techniques such as fluorescence, absorption and circular dichroism along with molecular docking studies.	ponatinib	49-52	albumin	Homo sapiens	63-76
30629146-8	2019	Then using a combination of zebrafish and isolated neonatal rat cardiomyocytes, we delineated the signalling mechanism of ponatinib-induced cardiotoxicity by demonstrating that ponatinib inhibits cardiac prosurvival signalling pathways AKT and extra-cellular-signal-regulated kinase (ERK), and induces cardiomyocyte apoptosis.	ponatinib	122-131	AKT serine/threonine kinase 1	Rattus norvegicus	236-239
30629146-8	2019	Then using a combination of zebrafish and isolated neonatal rat cardiomyocytes, we delineated the signalling mechanism of ponatinib-induced cardiotoxicity by demonstrating that ponatinib inhibits cardiac prosurvival signalling pathways AKT and extra-cellular-signal-regulated kinase (ERK), and induces cardiomyocyte apoptosis.	ponatinib	122-131	Eph receptor B1	Rattus norvegicus	244-282
30629146-8	2019	Then using a combination of zebrafish and isolated neonatal rat cardiomyocytes, we delineated the signalling mechanism of ponatinib-induced cardiotoxicity by demonstrating that ponatinib inhibits cardiac prosurvival signalling pathways AKT and extra-cellular-signal-regulated kinase (ERK), and induces cardiomyocyte apoptosis.	ponatinib	122-131	Eph receptor B1	Rattus norvegicus	284-287
30629146-8	2019	Then using a combination of zebrafish and isolated neonatal rat cardiomyocytes, we delineated the signalling mechanism of ponatinib-induced cardiotoxicity by demonstrating that ponatinib inhibits cardiac prosurvival signalling pathways AKT and extra-cellular-signal-regulated kinase (ERK), and induces cardiomyocyte apoptosis.	ponatinib	177-186	AKT serine/threonine kinase 1	Rattus norvegicus	236-239
30629146-8	2019	Then using a combination of zebrafish and isolated neonatal rat cardiomyocytes, we delineated the signalling mechanism of ponatinib-induced cardiotoxicity by demonstrating that ponatinib inhibits cardiac prosurvival signalling pathways AKT and extra-cellular-signal-regulated kinase (ERK), and induces cardiomyocyte apoptosis.	ponatinib	177-186	Eph receptor B1	Rattus norvegicus	244-282
30629146-8	2019	Then using a combination of zebrafish and isolated neonatal rat cardiomyocytes, we delineated the signalling mechanism of ponatinib-induced cardiotoxicity by demonstrating that ponatinib inhibits cardiac prosurvival signalling pathways AKT and extra-cellular-signal-regulated kinase (ERK), and induces cardiomyocyte apoptosis.	ponatinib	177-186	Eph receptor B1	Rattus norvegicus	284-287
30629146-9	2019	As a proof of concept, we augmented AKT and ERK signalling by administration of Neuregulin-1beta (NRG-1beta), and this prevented ponatinib-induced cardiomyocyte apoptosis.	ponatinib	129-138	AKT serine/threonine kinase 1	Rattus norvegicus	36-39
30629146-9	2019	As a proof of concept, we augmented AKT and ERK signalling by administration of Neuregulin-1beta (NRG-1beta), and this prevented ponatinib-induced cardiomyocyte apoptosis.	ponatinib	129-138	Eph receptor B1	Rattus norvegicus	44-47
30959969-0	2019	Ponatinib Inhibits Proliferation and Induces Apoptosis of Liver Cancer Cells, but Its Efficacy Is Compromised by Its Activation on PDK1/Akt/mTOR Signaling.	ponatinib	0-9	AKT serine/threonine kinase 1	Homo sapiens	136-139
30959969-0	2019	Ponatinib Inhibits Proliferation and Induces Apoptosis of Liver Cancer Cells, but Its Efficacy Is Compromised by Its Activation on PDK1/Akt/mTOR Signaling.	ponatinib	0-9	mechanistic target of rapamycin kinase	Homo sapiens	140-144
30959969-3	2019	Toward SK-Hep-1 and SNU-423 cells, ponatinib induces apoptosis by upregulation of cleaved caspase-3 and -7 and promotes cell cycle arrest in the G1 phase by inhibiting CDK4/6/CyclinD1 complex and phosphorylation of retinoblastoma protein.	ponatinib	35-44	cyclin dependent kinase 4	Homo sapiens	168-174
30959969-3	2019	Toward SK-Hep-1 and SNU-423 cells, ponatinib induces apoptosis by upregulation of cleaved caspase-3 and -7 and promotes cell cycle arrest in the G1 phase by inhibiting CDK4/6/CyclinD1 complex and phosphorylation of retinoblastoma protein.	ponatinib	35-44	cyclin D1	Homo sapiens	175-183
30959969-6	2019	Blocking mTOR signaling strongly sensitizes cells to inhibition by ponatinib and makes ponatinib a much more potent inhibitor of hepatocellular carcinoma cell proliferation.	ponatinib	67-76	mechanistic target of rapamycin kinase	Homo sapiens	9-13
30959969-6	2019	Blocking mTOR signaling strongly sensitizes cells to inhibition by ponatinib and makes ponatinib a much more potent inhibitor of hepatocellular carcinoma cell proliferation.	ponatinib	87-96	mechanistic target of rapamycin kinase	Homo sapiens	9-13
30692122-3	2019	We hypothesized that ponatinib produces an endothelial angiopathy involving excessive endothelial-associated von Willebrand factor (VWF) and secondary platelet adhesion.	ponatinib	21-30	Von Willebrand factor	Mus musculus	132-135
30692122-5	2019	After treatment of wild-type mice for 7 days, aortic molecular signal for endothelial-associated VWF and platelet adhesion were five- to sixfold higher in ponatinib vs sham therapy (P < .001), whereas dasatinib had no effect.	ponatinib	155-164	Von Willebrand factor	Mus musculus	97-100
30692122-6	2019	In ApoE-/- mice, aortic VWF and platelet signals were two- to fourfold higher for ponatinib-treated compared with sham-treated mice (P < .05) and were significantly higher than in treated wild-type mice (P < .05).	ponatinib	82-91	apolipoprotein E	Mus musculus	3-7
30692122-7	2019	Platelet and VWF signals in ponatinib-treated mice were significantly reduced by N-acetylcysteine and completely eliminated by recombinant ADAMTS13.	ponatinib	28-37	Von Willebrand factor	Mus musculus	13-16
30692122-7	2019	Platelet and VWF signals in ponatinib-treated mice were significantly reduced by N-acetylcysteine and completely eliminated by recombinant ADAMTS13.	ponatinib	28-37	a disintegrin-like and metallopeptidase (reprolysin type) with thrombospondin type 1 motif, 13	Mus musculus	139-147
30692122-8	2019	Ponatinib produced segmental left ventricular wall motion abnormalities in 33% of wild-type and 45% of ApoE-/- mice and corresponding patchy perfusion defects, yet coronary arteries were normal on angiography.	ponatinib	0-9	apolipoprotein E	Mus musculus	103-107
30692122-10	2019	Our findings reveal a new form of vascular toxicity for the TKI ponatinib that involves VWF-mediated platelet adhesion and a secondary microvascular angiopathy that produces ischemic wall motion abnormalities.	ponatinib	64-73	Von Willebrand factor	Mus musculus	88-91
31037149-6	2019	Results: Ponatinib was more potent than imatinib against cells bearing KIT mutations.	ponatinib	9-18	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	71-74
31037149-7	2019	In vivo drug efficacy evaluation experiments showed that ponatinib treatment caused much stronger inhibition of KIT-mutation-bearing melanomas than did imatinib.	ponatinib	57-66	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	112-115
31037149-8	2019	Mechanistically, molecular dynamics (MD) simulations revealed a plausible atomic-level explanation for the observation that ponatinib has a higher affinity for the KIT D816V mutant protein than does imatinib.	ponatinib	124-133	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	164-167
31037149-9	2019	Conclusions: Our study of KIT-mutation-and KIT WT-bearing melanomas demonstrates that ponatinib is a far more potent inhibitor than is imatinib for KIT-mutation-bearing melanomas and thus underscores that ponatinib should be given priority consideration for the design of precision treatments for melanoma patients triaged to have KIT mutations.	ponatinib	86-95	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	26-29
31037149-9	2019	Conclusions: Our study of KIT-mutation-and KIT WT-bearing melanomas demonstrates that ponatinib is a far more potent inhibitor than is imatinib for KIT-mutation-bearing melanomas and thus underscores that ponatinib should be given priority consideration for the design of precision treatments for melanoma patients triaged to have KIT mutations.	ponatinib	86-95	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	43-46
31037149-9	2019	Conclusions: Our study of KIT-mutation-and KIT WT-bearing melanomas demonstrates that ponatinib is a far more potent inhibitor than is imatinib for KIT-mutation-bearing melanomas and thus underscores that ponatinib should be given priority consideration for the design of precision treatments for melanoma patients triaged to have KIT mutations.	ponatinib	86-95	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	43-46
31037149-9	2019	Conclusions: Our study of KIT-mutation-and KIT WT-bearing melanomas demonstrates that ponatinib is a far more potent inhibitor than is imatinib for KIT-mutation-bearing melanomas and thus underscores that ponatinib should be given priority consideration for the design of precision treatments for melanoma patients triaged to have KIT mutations.	ponatinib	86-95	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	43-46
30854182-2	2019	Oral ponatinib (Iclusig ) is a third-generation TKI structurally designed to inhibit native BCR-ABL1 tyrosine kinase and several BCR-ABL1 mutants, including T315I.	ponatinib	5-14	BCR activator of RhoGEF and GTPase	Homo sapiens	92-100
29667003-0	2019	Chemical genomics reveals inhibition of breast cancer lung metastasis by Ponatinib via c-Jun.	ponatinib	73-82	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	87-92
29667003-6	2019	Mechanistically, Ponatinib represses the expression of BCLM-associated genes mainly through the ERK/c-Jun signaling pathway by inhibiting the transcription of JUN and accelerating the degradation of c-Jun protein.	ponatinib	17-26	mitogen-activated protein kinase 1	Homo sapiens	96-99
29667003-6	2019	Mechanistically, Ponatinib represses the expression of BCLM-associated genes mainly through the ERK/c-Jun signaling pathway by inhibiting the transcription of JUN and accelerating the degradation of c-Jun protein.	ponatinib	17-26	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	100-105
29667003-6	2019	Mechanistically, Ponatinib represses the expression of BCLM-associated genes mainly through the ERK/c-Jun signaling pathway by inhibiting the transcription of JUN and accelerating the degradation of c-Jun protein.	ponatinib	17-26	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	199-204
30854182-2	2019	Oral ponatinib (Iclusig ) is a third-generation TKI structurally designed to inhibit native BCR-ABL1 tyrosine kinase and several BCR-ABL1 mutants, including T315I.	ponatinib	5-14	BCR activator of RhoGEF and GTPase	Homo sapiens	129-137
30854182-2	2019	Oral ponatinib (Iclusig ) is a third-generation TKI structurally designed to inhibit native BCR-ABL1 tyrosine kinase and several BCR-ABL1 mutants, including T315I.	ponatinib	16-23	BCR activator of RhoGEF and GTPase	Homo sapiens	92-100
30854182-2	2019	Oral ponatinib (Iclusig ) is a third-generation TKI structurally designed to inhibit native BCR-ABL1 tyrosine kinase and several BCR-ABL1 mutants, including T315I.	ponatinib	16-23	BCR activator of RhoGEF and GTPase	Homo sapiens	129-137
31723821-0	2019	FIP1L1-PDGFRalpha p.T674I-D842L: A Novel and Ponatinib Resistant Compound Mutation in FIP1L1-PDGFRalpha Positive Leukemia.	ponatinib	45-54	factor interacting with PAPOLA and CPSF1	Homo sapiens	0-6
31723821-0	2019	FIP1L1-PDGFRalpha p.T674I-D842L: A Novel and Ponatinib Resistant Compound Mutation in FIP1L1-PDGFRalpha Positive Leukemia.	ponatinib	45-54	factor interacting with PAPOLA and CPSF1	Homo sapiens	86-92
30705592-3	2019	Iclusig  (ponatinib, previously known as AP24534) is an orally active multi-tyrosine kinase inhibitor and is currently approved by the US Food and Drug Administration for patients with chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia, specifically targeting the BCR-ABL gene mutation, T315I.	ponatinib	0-7	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	304-311
30705592-4	2019	Due to ponatinib"s unique multi-targeted characteristics, further studies have demonstrated its ability to target other important tyrosine kinases (FGFR, PDGFR, SRC, RET, KIT, and FLT1) in other human malignancies.	ponatinib	7-16	fms related receptor tyrosine kinase 1	Homo sapiens	180-184
30695783-0	2019	Relapsed Philadelphia Chromosome-Positive Pre-B-ALL after CD19-Directed CAR-T Cell Therapy Successfully Treated with Combination of Blinatumomab and Ponatinib.	ponatinib	149-158	CD19 molecule	Homo sapiens	58-62
30297175-4	2019	Patients with positive findings were offered ponatinib, a multi-kinase inhibitor of FGFR1-4.	ponatinib	45-54	fibroblast growth factor receptor 1	Homo sapiens	84-89
30297175-15	2019	Ponatinib"s poor tolerance suggests further fibroblast growth factor receptor exploration in ISH+ cases should utilize more selective FGFR1 inhibitors.	ponatinib	0-9	fibroblast growth factor receptor 1	Homo sapiens	134-139
30705592-3	2019	Iclusig  (ponatinib, previously known as AP24534) is an orally active multi-tyrosine kinase inhibitor and is currently approved by the US Food and Drug Administration for patients with chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia, specifically targeting the BCR-ABL gene mutation, T315I.	ponatinib	10-19	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	304-311
30705592-3	2019	Iclusig  (ponatinib, previously known as AP24534) is an orally active multi-tyrosine kinase inhibitor and is currently approved by the US Food and Drug Administration for patients with chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia, specifically targeting the BCR-ABL gene mutation, T315I.	ponatinib	41-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	304-311
30705592-4	2019	Due to ponatinib"s unique multi-targeted characteristics, further studies have demonstrated its ability to target other important tyrosine kinases (FGFR, PDGFR, SRC, RET, KIT, and FLT1) in other human malignancies.	ponatinib	7-16	platelet derived growth factor receptor beta	Homo sapiens	154-159
30705592-4	2019	Due to ponatinib"s unique multi-targeted characteristics, further studies have demonstrated its ability to target other important tyrosine kinases (FGFR, PDGFR, SRC, RET, KIT, and FLT1) in other human malignancies.	ponatinib	7-16	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	161-164
30705592-4	2019	Due to ponatinib"s unique multi-targeted characteristics, further studies have demonstrated its ability to target other important tyrosine kinases (FGFR, PDGFR, SRC, RET, KIT, and FLT1) in other human malignancies.	ponatinib	7-16	ret proto-oncogene	Homo sapiens	166-169
30705592-4	2019	Due to ponatinib"s unique multi-targeted characteristics, further studies have demonstrated its ability to target other important tyrosine kinases (FGFR, PDGFR, SRC, RET, KIT, and FLT1) in other human malignancies.	ponatinib	7-16	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	171-174
31597839-6	2019	Other types of TKI, i.e., PKC412, sorafenib, ponatinib, dasatinib, and dovitinib, show growth-inhibitory effects against the cells harboring several types of FGFR-1 fusion genes in in vitro studies; however, the usefulness of either drug has not been confirmed by clinical trials.	ponatinib	45-54	fibroblast growth factor receptor 1	Homo sapiens	158-164
30217442-4	2018	Treatment of CML-derived K562 cells with BCR-ABL tyrosine kinase inhibitors, including imatinib, dasatinib, nilotinib and ponatinib, prevented activation of eIF2alpha kinases, protein kinase-like endoplasmic reticulum kinase (PERK) and general control nonderepressible 2, and downstream ATF4 induction during metabolic stress.	ponatinib	122-131	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
30572654-0	2018	Ponatinib Inhibits Multiple Signaling Pathways Involved in STAT3 Signaling and Attenuates Colorectal Tumor Growth.	ponatinib	0-9	signal transducer and activator of transcription 3	Homo sapiens	59-64
30572654-2	2018	Here, we performed an extensive screen for STAT3 inhibitors among a library of 1167 FDA-approved agents, identifying Ponatinib as a lead candidate.	ponatinib	117-126	signal transducer and activator of transcription 3	Homo sapiens	43-48
30572654-3	2018	We found that Ponatinib inhibits STAT3 activity driven by EGF/EGFR, IL-6/IL-6R and IL-11/IL-11R, three major ligand/receptor systems involved in CRC development and progression.	ponatinib	14-23	signal transducer and activator of transcription 3	Homo sapiens	33-38
30572654-3	2018	We found that Ponatinib inhibits STAT3 activity driven by EGF/EGFR, IL-6/IL-6R and IL-11/IL-11R, three major ligand/receptor systems involved in CRC development and progression.	ponatinib	14-23	epidermal growth factor	Homo sapiens	58-61
30572654-3	2018	We found that Ponatinib inhibits STAT3 activity driven by EGF/EGFR, IL-6/IL-6R and IL-11/IL-11R, three major ligand/receptor systems involved in CRC development and progression.	ponatinib	14-23	epidermal growth factor receptor	Homo sapiens	62-66
30572654-3	2018	We found that Ponatinib inhibits STAT3 activity driven by EGF/EGFR, IL-6/IL-6R and IL-11/IL-11R, three major ligand/receptor systems involved in CRC development and progression.	ponatinib	14-23	interleukin 6	Homo sapiens	68-72
30572654-3	2018	We found that Ponatinib inhibits STAT3 activity driven by EGF/EGFR, IL-6/IL-6R and IL-11/IL-11R, three major ligand/receptor systems involved in CRC development and progression.	ponatinib	14-23	interleukin 6 receptor	Homo sapiens	73-78
30572654-3	2018	We found that Ponatinib inhibits STAT3 activity driven by EGF/EGFR, IL-6/IL-6R and IL-11/IL-11R, three major ligand/receptor systems involved in CRC development and progression.	ponatinib	14-23	interleukin 11	Homo sapiens	83-88
30572654-5	2018	In addition, Ponatinib displayed a greater ability to inhibit STAT3 activity and mediated superior anti-proliferative efficacy compared to five FDA approved SRC and Janus Kinase (JAK) inhibitors.	ponatinib	13-22	signal transducer and activator of transcription 3	Homo sapiens	62-67
30572654-5	2018	In addition, Ponatinib displayed a greater ability to inhibit STAT3 activity and mediated superior anti-proliferative efficacy compared to five FDA approved SRC and Janus Kinase (JAK) inhibitors.	ponatinib	13-22	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	157-160
30572654-8	2018	Overall, our results identify a novel anti-STAT3 property of Ponatinib and thus, Ponatinib offers a potential therapeutic strategy for CRC.	ponatinib	61-70	signal transducer and activator of transcription 3	Homo sapiens	43-48
30572654-8	2018	Overall, our results identify a novel anti-STAT3 property of Ponatinib and thus, Ponatinib offers a potential therapeutic strategy for CRC.	ponatinib	81-90	signal transducer and activator of transcription 3	Homo sapiens	43-48
30417093-0	2018	Ponatinib (AP24534) inhibits MEKK3-KLF signaling and prevents formation and progression of cerebral cavernous malformations.	ponatinib	0-9	mitogen-activated protein kinase kinase kinase 3	Mus musculus	29-34
30417093-0	2018	Ponatinib (AP24534) inhibits MEKK3-KLF signaling and prevents formation and progression of cerebral cavernous malformations.	ponatinib	11-18	mitogen-activated protein kinase kinase kinase 3	Mus musculus	29-34
30417093-6	2018	Using a U.S. Food and Drug Administration-approved kinase inhibitor library combined with virtual modeling and biochemical and cellular assays, we have identified a clinically approved small compound, ponatinib, that is capable of inhibiting MEKK3 activity and normalizing expression of downstream kruppel-like factor (KLF) target genes.	ponatinib	201-210	mitogen-activated protein kinase kinase kinase 3	Mus musculus	242-247
30417093-9	2018	Collectively, our study demonstrates ponatinib as a novel compound that may prevent CCM initiation and progression in mouse models through inhibition of MEKK3-KLF signaling.	ponatinib	37-46	mitogen-activated protein kinase kinase kinase 3	Mus musculus	153-158
30217442-4	2018	Treatment of CML-derived K562 cells with BCR-ABL tyrosine kinase inhibitors, including imatinib, dasatinib, nilotinib and ponatinib, prevented activation of eIF2alpha kinases, protein kinase-like endoplasmic reticulum kinase (PERK) and general control nonderepressible 2, and downstream ATF4 induction during metabolic stress.	ponatinib	122-131	eukaryotic translation initiation factor 2A	Homo sapiens	157-166
30217442-4	2018	Treatment of CML-derived K562 cells with BCR-ABL tyrosine kinase inhibitors, including imatinib, dasatinib, nilotinib and ponatinib, prevented activation of eIF2alpha kinases, protein kinase-like endoplasmic reticulum kinase (PERK) and general control nonderepressible 2, and downstream ATF4 induction during metabolic stress.	ponatinib	122-131	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	176-224
30217442-4	2018	Treatment of CML-derived K562 cells with BCR-ABL tyrosine kinase inhibitors, including imatinib, dasatinib, nilotinib and ponatinib, prevented activation of eIF2alpha kinases, protein kinase-like endoplasmic reticulum kinase (PERK) and general control nonderepressible 2, and downstream ATF4 induction during metabolic stress.	ponatinib	122-131	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	226-230
30217442-4	2018	Treatment of CML-derived K562 cells with BCR-ABL tyrosine kinase inhibitors, including imatinib, dasatinib, nilotinib and ponatinib, prevented activation of eIF2alpha kinases, protein kinase-like endoplasmic reticulum kinase (PERK) and general control nonderepressible 2, and downstream ATF4 induction during metabolic stress.	ponatinib	122-131	eukaryotic translation initiation factor 2 alpha kinase 4	Homo sapiens	236-270
30217442-4	2018	Treatment of CML-derived K562 cells with BCR-ABL tyrosine kinase inhibitors, including imatinib, dasatinib, nilotinib and ponatinib, prevented activation of eIF2alpha kinases, protein kinase-like endoplasmic reticulum kinase (PERK) and general control nonderepressible 2, and downstream ATF4 induction during metabolic stress.	ponatinib	122-131	activating transcription factor 4	Homo sapiens	287-291
29675611-9	2018	Ponatinib seems a valid second-line treatment option for chronic phase CML, in particular for patients who failed a front-line second-generation TKI due to BCR-ABL-independent mechanisms of resistance.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	156-163
30410673-0	2018	Modelling ponatinib resistance in tyrosine kinase inhibitor-naive and dasatinib resistant BCR-ABL1+ cell lines.	ponatinib	10-19	BCR activator of RhoGEF and GTPase	Homo sapiens	90-98
30410673-2	2018	In this study, we investigated the emerging modes of ponatinib resistance in TKI-naive and dasatinib resistant BCR-ABL1+ cell lines.	ponatinib	53-62	BCR activator of RhoGEF and GTPase	Homo sapiens	111-119
30410673-3	2018	To investigate potential resistance mechanisms, ponatinib resistance was generated in BCR-ABL1+ cell-lines by long-term exposure to increasing concentrations of ponatinib.	ponatinib	48-57	BCR activator of RhoGEF and GTPase	Homo sapiens	86-94
30410673-4	2018	Two cell lines with prior dasatinib resistance demonstrated BCR-ABL1 kinase domain (KD) mutation(s) upon exposure to ponatinib.	ponatinib	117-126	BCR activator of RhoGEF and GTPase	Homo sapiens	60-68
30410673-6	2018	When further cultured with ponatinib, the T315I mutation level and BCR-ABL1 mRNA expression level were increased.	ponatinib	27-36	BCR activator of RhoGEF and GTPase	Homo sapiens	67-75
30410673-11	2018	Ponatinib sensitivity was restored following Axl inhibition or shRNA-mediated-knockdown of Axl, suggesting that Axl was the primary driver of resistance and a potential target for therapy in this setting.	ponatinib	0-9	AXL receptor tyrosine kinase	Homo sapiens	45-48
30410673-11	2018	Ponatinib sensitivity was restored following Axl inhibition or shRNA-mediated-knockdown of Axl, suggesting that Axl was the primary driver of resistance and a potential target for therapy in this setting.	ponatinib	0-9	AXL receptor tyrosine kinase	Homo sapiens	91-94
30410673-11	2018	Ponatinib sensitivity was restored following Axl inhibition or shRNA-mediated-knockdown of Axl, suggesting that Axl was the primary driver of resistance and a potential target for therapy in this setting.	ponatinib	0-9	AXL receptor tyrosine kinase	Homo sapiens	91-94
30238007-0	2018	Ponatinib Activates an Inflammatory Response in Endothelial Cells via ERK5 SUMOylation.	ponatinib	0-9	mitogen-activated protein kinase 7	Homo sapiens	70-74
30238007-1	2018	Ponatinib is a multi-targeted third generation tyrosine kinase inhibitor (TKI) used in the treatment of chronic myeloid leukemia (CML) patients harboring the Abelson (Abl)-breakpoint cluster region (Bcr) T315I mutation.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	158-165
30238007-1	2018	Ponatinib is a multi-targeted third generation tyrosine kinase inhibitor (TKI) used in the treatment of chronic myeloid leukemia (CML) patients harboring the Abelson (Abl)-breakpoint cluster region (Bcr) T315I mutation.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	167-170
29103102-2	2018	Emricasan is an inhibitor of caspases in clinical trials for liver diseases while ponatinib could be a potential inhibitor for RIPK1/3.	ponatinib	82-91	receptor interacting serine/threonine kinase 1	Rattus norvegicus	127-132
30238007-4	2018	Furthermore, ponatinib-mediated anti-angiogenic effect has been suggested to play a partial role in systemic and pulmonary hypertension via inhibition of vascular endothelial growth factor receptor 2 (VEGFR2).	ponatinib	13-22	kinase insert domain receptor	Homo sapiens	154-199
30238007-4	2018	Furthermore, ponatinib-mediated anti-angiogenic effect has been suggested to play a partial role in systemic and pulmonary hypertension via inhibition of vascular endothelial growth factor receptor 2 (VEGFR2).	ponatinib	13-22	kinase insert domain receptor	Homo sapiens	201-207
30238007-7	2018	In cultured human aortic ECs (HAECs) treated with ponatinib, we found an increase in nuclear factor NF-kB/p65 phosphorylation and NF-kB activity, inflammatory gene expression, cell permeability, and cell apoptosis.	ponatinib	50-59	RELA proto-oncogene, NF-kB subunit	Homo sapiens	106-109
30238007-8	2018	Mechanistically, ponatinib abolished extracellular signal-regulated kinase 5 (ERK5) transcriptional activity even under activation by its upstream kinase mitogen-activated protein kinase kinase 5alpha (CA-MEK5alpha).	ponatinib	17-26	mitogen-activated protein kinase 7	Homo sapiens	37-76
30238007-8	2018	Mechanistically, ponatinib abolished extracellular signal-regulated kinase 5 (ERK5) transcriptional activity even under activation by its upstream kinase mitogen-activated protein kinase kinase 5alpha (CA-MEK5alpha).	ponatinib	17-26	mitogen-activated protein kinase 7	Homo sapiens	78-82
30238007-9	2018	Ponatinib also diminished expression of ERK5 responsive genes such as Kruppel-like Factor 2/4 (klf2/4) and eNOS.	ponatinib	0-9	mitogen-activated protein kinase 7	Homo sapiens	40-44
30238007-10	2018	Because ERK5 SUMOylation counteracts its transcriptional activity, we examined the effect of ponatinib on ERK5 SUMOylation, and found that ERK5 SUMOylation is increased by ponatinib.	ponatinib	93-102	mitogen-activated protein kinase 7	Homo sapiens	8-12
30238007-10	2018	Because ERK5 SUMOylation counteracts its transcriptional activity, we examined the effect of ponatinib on ERK5 SUMOylation, and found that ERK5 SUMOylation is increased by ponatinib.	ponatinib	93-102	mitogen-activated protein kinase 7	Homo sapiens	106-110
30238007-10	2018	Because ERK5 SUMOylation counteracts its transcriptional activity, we examined the effect of ponatinib on ERK5 SUMOylation, and found that ERK5 SUMOylation is increased by ponatinib.	ponatinib	93-102	mitogen-activated protein kinase 7	Homo sapiens	106-110
30238007-10	2018	Because ERK5 SUMOylation counteracts its transcriptional activity, we examined the effect of ponatinib on ERK5 SUMOylation, and found that ERK5 SUMOylation is increased by ponatinib.	ponatinib	172-181	mitogen-activated protein kinase 7	Homo sapiens	8-12
30238007-12	2018	Overall, we propose a novel mechanism by which ponatinib up-regulates endothelial ERK5 SUMOylation and shifts ECs to an inflammatory phenotype, disrupting vascular homeostasis.	ponatinib	47-56	mitogen-activated protein kinase 7	Homo sapiens	82-86
30146263-6	2018	A predictive panel of 3 miRNAs (let-7c, miRNA155, and miRNA218) was developed that had an area under the curve (AUC) of 0.886 with a sensitivity of 71.4% and specificity of 77.3% to predict response to ponatinib.	ponatinib	202-211	microRNA let-7c	Homo sapiens	32-38
30146263-9	2018	CONCLUSION: The developed miRNA panel (let-7c, miRNA155, and miRNA218) may be useful in predicting response to FGFR tyrosine kinase inhibitors, either ponatinib or AZD4547 in lung cancer cell lines, and warrants further validation in the clinical setting.	ponatinib	151-160	microRNA let-7c	Homo sapiens	39-45
30024740-6	2018	Moreover, the inactivation of both Abl and Src by the inhibitor imatinib, dasatinib, and ponatinib was simultaneously traced, giving a whole picture of the competition behavior between the kinases for binding therapeutic molecules.	ponatinib	89-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-38
30024740-6	2018	Moreover, the inactivation of both Abl and Src by the inhibitor imatinib, dasatinib, and ponatinib was simultaneously traced, giving a whole picture of the competition behavior between the kinases for binding therapeutic molecules.	ponatinib	89-98	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	43-46
30038711-0	2018	RET fusions observed in lung and colorectal cancers are sensitive to ponatinib.	ponatinib	69-78	ret proto-oncogene	Homo sapiens	0-3
30038711-4	2018	Identifying ponatinib as the most potent RET inhibitor tested, we used ponatinib to gauge therapeutic responsiveness in RET fusion-positive patient-derived xenograft (PDX) models.	ponatinib	12-21	ret proto-oncogene	Homo sapiens	41-44
30038711-6	2018	By comparing ponatinib activity in RET fusion-positive and RET fusion-negative PDX models alongside a standard of care chemotherapeutic agent, we show that RET fusions in colorectal tumors are therapeutically responsive to RET inhibition.	ponatinib	13-22	ret proto-oncogene	Homo sapiens	35-38
29704617-10	2018	Based upon the X-ray crystallographic structures, imatinib, sunitinib, and ponatinib are Type II Kit inhibitors.	ponatinib	75-84	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	97-100
29608815-5	2018	Ponatinib (AP24534) is currently the only approved CML drug that is active against the ABL1(T315I) mutation.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	87-91
29608815-6	2018	However, ponatinib has severe cardiovascular toxicities; hence, there have been efforts to find safer CML drugs that work against ABL1 secondary mutations.	ponatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-134
29899872-2	2018	Ponatinib blocks a variety of tyrosine kinases including ABL and fibroblast growth factor receptor (FGFR), and the BET bromodomain (BRD) antagonists JQ1 and dBET1 impede MYC oncogene expression.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	57-60
29946549-8	2018	In line with this, ponatinib enhanced plasma levels of FVII, whereas nilotinib increased plasma FVIIa activity.	ponatinib	19-28	coagulation factor VII	Mus musculus	55-59
29675955-7	2018	Consistently, primary cells from BCR/ABL1-like cases responded in vitro to ponatinib.	ponatinib	75-84	BCR activator of RhoGEF and GTPase	Homo sapiens	33-36
29675955-7	2018	Consistently, primary cells from BCR/ABL1-like cases responded in vitro to ponatinib.	ponatinib	75-84	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-41
29845876-6	2018	Ponatinib is active against all BCR-ABL1 mutants, including T315I, and is widely used to treat patients who developed resistance to other TKIs in any CML phase; however, only limited data is available on the possible role of ponatinib for intolerant patients.	ponatinib	0-9	BCR activator of RhoGEF and GTPase	Homo sapiens	32-40
29899872-9	2018	Phospho-FGFR and MYC, major targets of ponatinib and BET inhibitors, were downregulated after treatment with single drugs.	ponatinib	39-48	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	17-20
29899872-10	2018	Remarkably, ponatinib was found to sensitize cells to BET antagonists by enhancing apoptotic cell death, and this effect was associated with downregulation of MYC.	ponatinib	12-21	delta/notch like EGF repeat containing	Homo sapiens	54-57
29899872-10	2018	Remarkably, ponatinib was found to sensitize cells to BET antagonists by enhancing apoptotic cell death, and this effect was associated with downregulation of MYC.	ponatinib	12-21	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	159-162
29899872-11	2018	In summary, our data shows that ponatinib sensitizes colon, breast, and ovarian cancer cells to BET bromodomain inhibitors.	ponatinib	32-41	delta/notch like EGF repeat containing	Homo sapiens	96-99
29434033-4	2018	Further genomic profiling of longitudinally collected samples during treatment revealed the emergence of a mutation, PDGFRBC843G , which directly conferred resistance to all generations of ABL TKIs, including imatinib, dasatinib, nilotinib, and ponatinib.	ponatinib	245-254	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	189-192
29440450-2	2018	In vivo pharmacokinetic studies in wild-type and transporter knockout mice showed that two major BBB efflux transporters, P-glycoprotein (P-gp) and breast cancer resistance protein (Bcrp), cooperate to modulate the brain exposure of ponatinib.	ponatinib	233-242	phosphoglycolate phosphatase	Mus musculus	122-136
29165716-2	2018	Although ponatinib, a third-generation TKI, improves outcomes for patients with BCR-ABL-dependent mechanisms of resistance, including the T315I mutation, a proportion of patients may have or develop BCR-ABL-independent resistance and fail ponatinib treatment.	ponatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
29165716-2	2018	Although ponatinib, a third-generation TKI, improves outcomes for patients with BCR-ABL-dependent mechanisms of resistance, including the T315I mutation, a proportion of patients may have or develop BCR-ABL-independent resistance and fail ponatinib treatment.	ponatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	199-206
29165716-4	2018	Methods: Two CML cell lines with acquired BCR-ABL-independent resistance were generated following culture in ponatinib.	ponatinib	109-118	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	42-49
29165716-9	2018	Results: We show that ponatinib-resistant CML cells can acquire BCR-ABL-independent resistance mediated through alternative activation of mTOR.	ponatinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
29165716-9	2018	Results: We show that ponatinib-resistant CML cells can acquire BCR-ABL-independent resistance mediated through alternative activation of mTOR.	ponatinib	22-31	mechanistic target of rapamycin kinase	Homo sapiens	138-142
29440450-2	2018	In vivo pharmacokinetic studies in wild-type and transporter knockout mice showed that two major BBB efflux transporters, P-glycoprotein (P-gp) and breast cancer resistance protein (Bcrp), cooperate to modulate the brain exposure of ponatinib.	ponatinib	233-242	phosphoglycolate phosphatase	Mus musculus	138-142
29440450-2	2018	In vivo pharmacokinetic studies in wild-type and transporter knockout mice showed that two major BBB efflux transporters, P-glycoprotein (P-gp) and breast cancer resistance protein (Bcrp), cooperate to modulate the brain exposure of ponatinib.	ponatinib	233-242	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	182-186
29440450-4	2018	The triple knockout mice had a greater than an additive increase in the brain exposure of ponatinib when compared with single knockout mice [Bcrp1(-/-) or Mdr1a/b(-/-)], suggesting functional compensation of transporter-mediated drug efflux.	ponatinib	90-99	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	141-151
29358661-3	2018	The third generation TKI ponatinib is the only effective TKI to treat CML patients harboring T315I-BCR-ABL mutation, but with high rate of major arterial thrombotic events.	ponatinib	25-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	99-106
29440177-4	2018	Ponatinib was tested for efficacy in two patient-derived xenograft (PDX) models and one cell-line xenograft model of SCCOHT.Results: The receptor tyrosine kinase (RTK) family was enriched in siRNA screen hits, with FGFRs and PDGFRs being overlapping hits between drug and siRNA screens.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	137-161
29440177-4	2018	Ponatinib was tested for efficacy in two patient-derived xenograft (PDX) models and one cell-line xenograft model of SCCOHT.Results: The receptor tyrosine kinase (RTK) family was enriched in siRNA screen hits, with FGFRs and PDGFRs being overlapping hits between drug and siRNA screens.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	163-166
29440177-6	2018	We further identified ponatinib as the most effective clinically approved RTK inhibitor.	ponatinib	22-31	ret proto-oncogene	Homo sapiens	74-77
29440177-7	2018	Reexpression of SMARCA4 was shown to confer a 1.7-fold increase in resistance to ponatinib.	ponatinib	81-90	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4	Homo sapiens	16-23
29440177-9	2018	Finally, ponatinib delayed tumor doubling time 4-fold in SCCOHT-1 xenografts while reducing final tumor volumes in SCCOHT PDX models by 58.6% and 42.5%.Conclusions: Ponatinib is an effective agent for SMARCA4-mutant SCCOHT in both in vitro and in vivo preclinical models through its inhibition of multiple kinases.	ponatinib	165-174	SWI/SNF related, matrix associated, actin dependent regulator of chromatin, subfamily a, member 4	Homo sapiens	201-208
29463017-3	2018	In this study, a pharmacophoric model based on the crystallographic pose of ponatinib, a potent RIPK2 inhibitor, and 30 other ones selected from the BindingDB repository database, was built.	ponatinib	76-85	receptor interacting serine/threonine kinase 2	Homo sapiens	96-101
31249931-2	2018	Second- (dasatinib, nilotinib, and bosutinib) and third-generation (ponatinib) TKIs have been developed to be effective against BCR-ABL mutations making imatinib less effective.	ponatinib	68-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	128-135
28983061-0	2018	BCR-ABL1 compound mutants display differential and dose-dependent responses to ponatinib.	ponatinib	79-88	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
30174789-0	2018	Ponatinib exerts anti-angiogenic effects in the zebrafish and human umbilical vein endothelial cells via blocking VEGFR signaling pathway.	ponatinib	0-9	kinase insert domain receptor	Homo sapiens	114-119
30174789-9	2018	Further experiments showed that Ponatinib inhibited VEGF-induced VEGFR2 phosphorylation and its downstream signaling pathways including Akt/eNOS/NO pathway and MAPK pathways (ERK and p38MAPK).	ponatinib	32-41	vascular endothelial growth factor Aa	Danio rerio	52-56
30174789-9	2018	Further experiments showed that Ponatinib inhibited VEGF-induced VEGFR2 phosphorylation and its downstream signaling pathways including Akt/eNOS/NO pathway and MAPK pathways (ERK and p38MAPK).	ponatinib	32-41	kinase insert domain receptor like	Danio rerio	65-71
30174789-10	2018	Taken together, these results suggest that inhibition of VEGF signaling at its receptor level and downstream pathways may likely be responsible for the antiangiogenic activity of Ponatinib.	ponatinib	179-188	vascular endothelial growth factor Aa	Danio rerio	57-61
30184522-9	2018	That ponatinib briefly induced remission in our patient with acute myeloid leukemia arising from a myeloproliferative neoplasm with eosinophilia and FIP1L1-PDGFRalpha fusion may merit exploration of ponatinib as a potential second-line treatment option for this patient population.	ponatinib	5-14	factor interacting with PAPOLA and CPSF1	Homo sapiens	149-155
30184522-9	2018	That ponatinib briefly induced remission in our patient with acute myeloid leukemia arising from a myeloproliferative neoplasm with eosinophilia and FIP1L1-PDGFRalpha fusion may merit exploration of ponatinib as a potential second-line treatment option for this patient population.	ponatinib	5-14	platelet derived growth factor receptor alpha	Homo sapiens	156-166
30372691-5	2018	We report on a young patient affected by Ph"+-ALL, who relapsed after the second HSCT and who reached molecular remission and long-term disease control by treatment with the anti-CD22 monoclonal antibody inotuzumab ozogamicin, DLI, and the 3rd generation TKI ponatinib.	ponatinib	259-268	CD22 molecule	Homo sapiens	179-183
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	ponatinib	29-38	microRNA 214	Homo sapiens	118-125
30069627-10	2018	In conclusion, ponatinib has proved to be a powerful BCR-ABL inhibitor, which exhibits clinical activity both in BCR-ABL wild-type and mutant CML, including the pan-resistant T315I mutation.	ponatinib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
30069627-10	2018	In conclusion, ponatinib has proved to be a powerful BCR-ABL inhibitor, which exhibits clinical activity both in BCR-ABL wild-type and mutant CML, including the pan-resistant T315I mutation.	ponatinib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
28881484-0	2017	Primary cells in BCR/FGFR1-positive 8p11 myeloproliferative syndrome are sensitive to dovitinib, ponatinib, and dasatinib.	ponatinib	97-106	fibroblast growth factor receptor 1	Homo sapiens	21-26
29132397-8	2017	In vitro assays showed that ponatinib inhibited the clonogenic proliferation of liposarcoma, and this anti-growth effect was associated with apoptosis and cell cycle arrest at the G0/G1 phase as well as a decrease in the KIT signaling pathway.	ponatinib	28-37	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	221-224
28646488-3	2017	Since resistance to targeted therapies is a major reason for relapse, we developed FGFR1-overexpressing mouse and human cell lines that are resistant to the specific FGFR inhibitors AZD4547 and BGJ398, as well as non-specific inhibitors, such as ponatinib, TKI258 and E3810.	ponatinib	246-255	fibroblast growth factor receptor 1	Mus musculus	83-88
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	ponatinib	29-38	membrane associated ring-CH-type finger 8	Homo sapiens	58-61
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	ponatinib	29-38	membrane associated ring-CH-type finger 8	Homo sapiens	118-121
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	ponatinib	29-38	membrane associated ring-CH-type finger 8	Homo sapiens	118-121
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	ponatinib	29-38	microRNA 27b	Homo sapiens	166-173
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	ponatinib	29-38	microRNA 23b	Homo sapiens	179-186
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	ponatinib	29-38	microRNA 320e	Homo sapiens	192-200
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	ponatinib	29-38	membrane associated ring-CH-type finger 8	Homo sapiens	118-121
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	ponatinib	29-38	membrane associated ring-CH-type finger 8	Homo sapiens	118-121
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	ponatinib	29-38	microRNA 33a	Homo sapiens	228-234
28942039-8	2017	We pointed that imatinib and ponatinib caused significant miRNA profile alterations, especially in the expressions of miR-214-pre, miR-218, miR-19a-5p, miR-19b-1-5p, miR-27b-pre, miR-23b-pre, miR-320e, miR-200a-pre, miR-508-3p, miR-33-pre and miR-766.	ponatinib	29-38	microRNA 766	Homo sapiens	243-250
28882992-0	2017	Novel Pathways of Ponatinib Disposition Catalyzed By CYP1A1 Involving Generation of Potentially Toxic Metabolites.	ponatinib	18-27	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	53-59
28751539-9	2017	As a result, we found that ponatinib and nintedanib effectively inhibited the survival of TPM3-NTRK1-G667C but not G595R mutants, both of which showed resistance to entrectinib or larotrectinib (LOXO-101).	ponatinib	27-36	tropomyosin 3	Homo sapiens	90-94
28751539-9	2017	As a result, we found that ponatinib and nintedanib effectively inhibited the survival of TPM3-NTRK1-G667C but not G595R mutants, both of which showed resistance to entrectinib or larotrectinib (LOXO-101).	ponatinib	27-36	neurotrophic receptor tyrosine kinase 1	Homo sapiens	95-100
28880088-0	2017	Brain Accumulation of Ponatinib and Its Active Metabolite, N-Desmethyl Ponatinib, Is Limited by P-Glycoprotein (P-GP/ABCB1) and Breast Cancer Resistance Protein (BCRP/ABCG2).	ponatinib	22-31	phosphoglycolate phosphatase	Mus musculus	112-116
28880088-0	2017	Brain Accumulation of Ponatinib and Its Active Metabolite, N-Desmethyl Ponatinib, Is Limited by P-Glycoprotein (P-GP/ABCB1) and Breast Cancer Resistance Protein (BCRP/ABCG2).	ponatinib	22-31	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	117-122
28880088-0	2017	Brain Accumulation of Ponatinib and Its Active Metabolite, N-Desmethyl Ponatinib, Is Limited by P-Glycoprotein (P-GP/ABCB1) and Breast Cancer Resistance Protein (BCRP/ABCG2).	ponatinib	22-31	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	162-166
28880088-0	2017	Brain Accumulation of Ponatinib and Its Active Metabolite, N-Desmethyl Ponatinib, Is Limited by P-Glycoprotein (P-GP/ABCB1) and Breast Cancer Resistance Protein (BCRP/ABCG2).	ponatinib	22-31	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	167-172
28880088-1	2017	Ponatinib is an oral BCR-ABL1 inhibitor for treatment of advanced leukemic diseases that carry the Philadelphia chromosome, specifically containing the T315I mutation yielding resistance to previously approved BCR-ABL1 inhibitors.	ponatinib	0-9	BCR activator of RhoGEF and GTPase	Mus musculus	21-29
28880088-1	2017	Ponatinib is an oral BCR-ABL1 inhibitor for treatment of advanced leukemic diseases that carry the Philadelphia chromosome, specifically containing the T315I mutation yielding resistance to previously approved BCR-ABL1 inhibitors.	ponatinib	0-9	BCR activator of RhoGEF and GTPase	Mus musculus	210-218
28880088-2	2017	Using in vitro transport assays and knockout mouse models, we investigated whether the multidrug efflux transporters ABCB1 and ABCG2 transport ponatinib and whether they, or the drug-metabolizing enzyme CYP3A, affect the oral availability and brain accumulation of ponatinib and its active N-desmethyl metabolite (DMP).	ponatinib	143-152	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	127-132
28880088-3	2017	In vitro, mouse Abcg2 and human ABCB1 modestly transported ponatinib.	ponatinib	59-68	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	16-21
28880088-3	2017	In vitro, mouse Abcg2 and human ABCB1 modestly transported ponatinib.	ponatinib	59-68	ATP binding cassette subfamily B member 1	Homo sapiens	32-37
28880088-4	2017	In mice, both Abcb1 and Abcg2 markedly restricted brain accumulation of ponatinib and DMP, but not ponatinib oral availability.	ponatinib	72-81	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	14-19
28880088-4	2017	In mice, both Abcb1 and Abcg2 markedly restricted brain accumulation of ponatinib and DMP, but not ponatinib oral availability.	ponatinib	72-81	ATP binding cassette subfamily G member 2 (Junior blood group)	Mus musculus	24-29
28880088-6	2017	Cyp3a deficiency increased the ponatinib plasma AUC 1.4-fold.	ponatinib	31-40	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	0-5
28880088-7	2017	Our results suggest that pharmacological inhibition of ABCG2 and ABCB1 during ponatinib therapy might benefit patients with brain (micro)metastases positioned behind an intact blood-brain barrier, or with substantial expression of these transporters in the malignant cells.	ponatinib	78-87	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	55-60
28880088-7	2017	Our results suggest that pharmacological inhibition of ABCG2 and ABCB1 during ponatinib therapy might benefit patients with brain (micro)metastases positioned behind an intact blood-brain barrier, or with substantial expression of these transporters in the malignant cells.	ponatinib	78-87	ATP binding cassette subfamily B member 1	Homo sapiens	65-70
28880088-8	2017	CYP3A inhibitors might increase ponatinib oral availability, enhancing efficacy but possibly also toxicity of this drug.	ponatinib	32-41	cytochrome P450, family 3, subfamily a, polypeptide 11	Mus musculus	0-5
28882992-8	2017	Ponatinib exposure was significantly decreased in treated mice compared with controls (7.7- and 2.2-fold for WT and humanized CYP1A1/2, respectively).	ponatinib	0-9	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	126-132
28882992-11	2017	These results indicate that not only could CYP1A1 be involved in ponatinib disposition, which has not been previously reported, but also that electrophilic intermediates resulting from CYP1A1 metabolism in normal tissues may contribute to ponatinib toxicity.	ponatinib	65-74	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	43-49
28619758-5	2017	Combination treatment with an MEK inhibitor and the multikinase inhibitor ponatinib was effective in targeting pancreatic cancer cells both in monolayer and spheroids by effectively blocking signaling via the PDGFRalpha and MEK kinases, while also preventing the activation of STAT3- and S6-mediated compensatory feedback loops in cancer cells.	ponatinib	74-83	platelet derived growth factor receptor alpha	Homo sapiens	209-219
28882992-11	2017	These results indicate that not only could CYP1A1 be involved in ponatinib disposition, which has not been previously reported, but also that electrophilic intermediates resulting from CYP1A1 metabolism in normal tissues may contribute to ponatinib toxicity.	ponatinib	239-248	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	43-49
28882992-11	2017	These results indicate that not only could CYP1A1 be involved in ponatinib disposition, which has not been previously reported, but also that electrophilic intermediates resulting from CYP1A1 metabolism in normal tissues may contribute to ponatinib toxicity.	ponatinib	239-248	cytochrome P450, family 1, subfamily a, polypeptide 1	Mus musculus	185-191
29050692-3	2017	In particular, ponatinib, a potent pan-BCR-ABL TKI capable of overcoming the T315I mutation, holds significant promise in the treatment of Ph+ ALL, although the potential cardiovascular toxicity of this agent remains a concern.	ponatinib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	39-46
28619758-5	2017	Combination treatment with an MEK inhibitor and the multikinase inhibitor ponatinib was effective in targeting pancreatic cancer cells both in monolayer and spheroids by effectively blocking signaling via the PDGFRalpha and MEK kinases, while also preventing the activation of STAT3- and S6-mediated compensatory feedback loops in cancer cells.	ponatinib	74-83	mitogen-activated protein kinase kinase 7	Homo sapiens	224-227
28619758-5	2017	Combination treatment with an MEK inhibitor and the multikinase inhibitor ponatinib was effective in targeting pancreatic cancer cells both in monolayer and spheroids by effectively blocking signaling via the PDGFRalpha and MEK kinases, while also preventing the activation of STAT3- and S6-mediated compensatory feedback loops in cancer cells.	ponatinib	74-83	signal transducer and activator of transcription 3	Homo sapiens	277-282
28500237-3	2017	Here, we demonstrate that ponatinib exhibits potent antiproliferative activity in RET fusion-positive LC-2/ad lung adenocarcinoma cells and inhibits phosphorylation of the RET fusion protein and signaling through ERK1/2 and AKT.	ponatinib	26-35	mitogen-activated protein kinase 3	Homo sapiens	213-219
28500237-2	2017	Ponatinib is a multi-kinase inhibitor with low-nanomolar potency against the RET kinase domain.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	77-80
28500237-3	2017	Here, we demonstrate that ponatinib exhibits potent antiproliferative activity in RET fusion-positive LC-2/ad lung adenocarcinoma cells and inhibits phosphorylation of the RET fusion protein and signaling through ERK1/2 and AKT.	ponatinib	26-35	ret proto-oncogene	Homo sapiens	82-85
28500237-3	2017	Here, we demonstrate that ponatinib exhibits potent antiproliferative activity in RET fusion-positive LC-2/ad lung adenocarcinoma cells and inhibits phosphorylation of the RET fusion protein and signaling through ERK1/2 and AKT.	ponatinib	26-35	ret proto-oncogene	Homo sapiens	172-175
28500237-3	2017	Here, we demonstrate that ponatinib exhibits potent antiproliferative activity in RET fusion-positive LC-2/ad lung adenocarcinoma cells and inhibits phosphorylation of the RET fusion protein and signaling through ERK1/2 and AKT.	ponatinib	26-35	AKT serine/threonine kinase 1	Homo sapiens	224-227
28500237-4	2017	Using distinct dose escalation strategies, two ponatinib-resistant LC-2/ad cell lines, PR1 and PR2, were derived.	ponatinib	47-56	transmembrane protein 37	Homo sapiens	87-90
28500237-9	2017	Expression of NRAS p.Q61K in RET fusion expressing TPC1 cells conferred resistance to ponatinib.	ponatinib	86-95	neuroblastoma RAS viral oncogene homolog	Gallus gallus	14-18
28500237-9	2017	Expression of NRAS p.Q61K in RET fusion expressing TPC1 cells conferred resistance to ponatinib.	ponatinib	86-95	ret proto-oncogene	Gallus gallus	29-32
28500237-14	2017	Collectively, these findings demonstrate that resistance to ponatinib in RET-rearranged lung adenocarcinoma is mediated by bypass signaling mechanisms that result in restored RAS/MAPK activation.	ponatinib	60-69	ret proto-oncogene	Gallus gallus	73-76
28500237-14	2017	Collectively, these findings demonstrate that resistance to ponatinib in RET-rearranged lung adenocarcinoma is mediated by bypass signaling mechanisms that result in restored RAS/MAPK activation.	ponatinib	60-69	mitogen-activated protein kinase 3	Homo sapiens	179-183
27696211-1	2017	Five clinically approved BCR-ABL1-targeted tyrosine kinase inhibitors (bosutinib, dasatinib, imatinib, nilotinib, and ponatinib) used for treating chronic myelogenous leukemia have been studied in a neonatal rat myocyte model for their relative ability to induce myocyte damage.	ponatinib	118-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-33
28427224-0	2017	Ponatinib promotes a G1 cell-cycle arrest of merlin/NF2-deficient human schwann cells.	ponatinib	0-9	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	45-51
28520795-10	2017	RNAi-mediated knockdown or inhibition of Lyn (dasatinib/ponatinib) reduced BIRC6 protein stability and increased caspase activation.	ponatinib	56-65	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	41-44
28520795-10	2017	RNAi-mediated knockdown or inhibition of Lyn (dasatinib/ponatinib) reduced BIRC6 protein stability and increased caspase activation.	ponatinib	56-65	baculoviral IAP repeat containing 6	Homo sapiens	75-80
28615362-4	2017	We report that potent inhibitors, such as AD80 or ponatinib, that stably bind in the DFG-out conformation of RET may overcome these limitations and selectively kill RET-rearranged tumors.	ponatinib	50-59	ret proto-oncogene	Homo sapiens	109-112
28615362-4	2017	We report that potent inhibitors, such as AD80 or ponatinib, that stably bind in the DFG-out conformation of RET may overcome these limitations and selectively kill RET-rearranged tumors.	ponatinib	50-59	ret proto-oncogene	Homo sapiens	165-168
27733071-6	2017	Furthermore, in HUVECs transfected with VEGF receptor 2 (VEGFR2), the effect of ponatinib on tube formation and on all parameters representing normal endothelial cell function was less prominent than in control cells.	ponatinib	80-89	kinase insert domain receptor	Homo sapiens	40-55
27733071-6	2017	Furthermore, in HUVECs transfected with VEGF receptor 2 (VEGFR2), the effect of ponatinib on tube formation and on all parameters representing normal endothelial cell function was less prominent than in control cells.	ponatinib	80-89	kinase insert domain receptor	Homo sapiens	57-63
27733071-8	2017	The antiangiogenic effect of ponatinib, possibly mediated by VEGFR2 inhibition, as shown in our study, is another piece in the intricate puzzle of TKI-associated VAEs.	ponatinib	29-38	kinase insert domain receptor	Homo sapiens	61-67
28427224-0	2017	Ponatinib promotes a G1 cell-cycle arrest of merlin/NF2-deficient human schwann cells.	ponatinib	0-9	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	52-55
28427224-4	2017	The goal of this study was to determine whether ponatinib, an FDA-approved ABL/SRC inhibitor, reduced proliferation and/or survival of merlin-deficient human Schwann cells (HSC).	ponatinib	48-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	75-78
28427224-4	2017	The goal of this study was to determine whether ponatinib, an FDA-approved ABL/SRC inhibitor, reduced proliferation and/or survival of merlin-deficient human Schwann cells (HSC).	ponatinib	48-57	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	79-82
28427224-4	2017	The goal of this study was to determine whether ponatinib, an FDA-approved ABL/SRC inhibitor, reduced proliferation and/or survival of merlin-deficient human Schwann cells (HSC).	ponatinib	48-57	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	135-141
28427224-4	2017	The goal of this study was to determine whether ponatinib, an FDA-approved ABL/SRC inhibitor, reduced proliferation and/or survival of merlin-deficient human Schwann cells (HSC).	ponatinib	48-57	fucosyltransferase 1 (H blood group)	Homo sapiens	173-176
28427224-7	2017	Ponatinib reduced merlin-deficient HSC viability in a dose-dependent manner by decreasing phosphorylation of PDGFRalpha/beta, AKT, p70S6K, MEK1/2, ERK1/2 and STAT3.	ponatinib	0-9	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	18-24
28427224-7	2017	Ponatinib reduced merlin-deficient HSC viability in a dose-dependent manner by decreasing phosphorylation of PDGFRalpha/beta, AKT, p70S6K, MEK1/2, ERK1/2 and STAT3.	ponatinib	0-9	fucosyltransferase 1 (H blood group)	Homo sapiens	35-38
28427224-7	2017	Ponatinib reduced merlin-deficient HSC viability in a dose-dependent manner by decreasing phosphorylation of PDGFRalpha/beta, AKT, p70S6K, MEK1/2, ERK1/2 and STAT3.	ponatinib	0-9	AKT serine/threonine kinase 1	Homo sapiens	126-129
28427224-7	2017	Ponatinib reduced merlin-deficient HSC viability in a dose-dependent manner by decreasing phosphorylation of PDGFRalpha/beta, AKT, p70S6K, MEK1/2, ERK1/2 and STAT3.	ponatinib	0-9	ribosomal protein S6 kinase B1	Homo sapiens	131-137
28427224-7	2017	Ponatinib reduced merlin-deficient HSC viability in a dose-dependent manner by decreasing phosphorylation of PDGFRalpha/beta, AKT, p70S6K, MEK1/2, ERK1/2 and STAT3.	ponatinib	0-9	mitogen-activated protein kinase kinase 1	Homo sapiens	139-145
28427224-7	2017	Ponatinib reduced merlin-deficient HSC viability in a dose-dependent manner by decreasing phosphorylation of PDGFRalpha/beta, AKT, p70S6K, MEK1/2, ERK1/2 and STAT3.	ponatinib	0-9	mitogen-activated protein kinase 3	Homo sapiens	147-153
28427224-7	2017	Ponatinib reduced merlin-deficient HSC viability in a dose-dependent manner by decreasing phosphorylation of PDGFRalpha/beta, AKT, p70S6K, MEK1/2, ERK1/2 and STAT3.	ponatinib	0-9	signal transducer and activator of transcription 3	Homo sapiens	158-163
28427224-10	2017	These results suggest that ponatinib is a potential therapeutic agent for NF2-associated schwannomas and warrants further in vivo investigation.	ponatinib	27-36	NF2, moesin-ezrin-radixin like (MERLIN) tumor suppressor	Homo sapiens	74-77
28184964-1	2017	PURPOSE: Ponatinib is a novel tyrosine kinase inhibitor (TKI) specifically designed to inhibit native and mutated BCR-ABL.	ponatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	114-121
28415816-6	2017	To block these pathways, Ponatinib, a broadly active tyrosine kinase inhibitor (TKI) used to treat chronic myelogenous leukemia, was added to this PIM-inhibitor regimen.	ponatinib	25-34	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	147-150
28415816-7	2017	The combination of Ponatinib with a PIM inhibitor resulted in synergistic T-ALL growth inhibition and marked apoptotic cell death.	ponatinib	19-28	Pim-1 proto-oncogene, serine/threonine kinase	Homo sapiens	36-39
27856601-4	2017	We investigated the therapeutic potential of Axl inhibition in CML.Experimental Design: We used primary cells from patients with CML and TKI-sensitive and -resistant BCR-ABL1+ CML cell lines and a novel ponatinib-resistant cell line KCL-22 PonR.	ponatinib	203-212	AXL receptor tyrosine kinase	Homo sapiens	45-48
28416739-4	2017	Treatment with ponatinib resulted in blast cell clearance, decrease in fibrosis, and disappearance of BCR-ABL1, but also in severe thrombocytopenia with bleedings requiring platelet transfusions.	ponatinib	15-24	BCR activator of RhoGEF and GTPase	Homo sapiens	102-110
28416739-8	2017	Therefore, we  switched back  to ponatinib, and this was again followed by disappearance of BCR-ABL1 and a decrease in platelets.	ponatinib	33-42	BCR activator of RhoGEF and GTPase	Homo sapiens	92-100
28278078-2	2017	In recent years, compound BCR-ABL mutations have emerged as a new threat to CML patients by causing higher degrees of resistance involving multiple TKIs, including ponatinib.	ponatinib	164-173	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	26-33
27761606-0	2017	BCR-ABL-positive acute myeloid leukemia: About one case treated with ponatinib.	ponatinib	69-78	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
28138694-0	2017	Activity of fibroblast growth factor receptor inhibitors TKI258, ponatinib and AZD4547 against TPR-FGFR1 fusion.	ponatinib	65-74	translocated promoter region, nuclear basket protein	Mus musculus	95-98
28138694-0	2017	Activity of fibroblast growth factor receptor inhibitors TKI258, ponatinib and AZD4547 against TPR-FGFR1 fusion.	ponatinib	65-74	fibroblast growth factor receptor 1	Mus musculus	99-104
28138694-4	2017	To identify the most promising drug for EMS, the activities and associated mechanism of three tyrosine kinase inhibitors (TKIs), TKI258, ponatinib and AZD4547, against TPR-FGFR1 were tested by MTT assay, flow cytometry and western blot.	ponatinib	137-146	translocated promoter region, nuclear basket protein	Mus musculus	168-171
28138694-4	2017	To identify the most promising drug for EMS, the activities and associated mechanism of three tyrosine kinase inhibitors (TKIs), TKI258, ponatinib and AZD4547, against TPR-FGFR1 were tested by MTT assay, flow cytometry and western blot.	ponatinib	137-146	fibroblast growth factor receptor 1	Mus musculus	172-177
27864605-0	2017	Erratum to: BCR-ABL-positive acute myeloid leukemia: About one case treated with ponatinib.	ponatinib	81-90	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	12-19
27564113-0	2017	Novel multiple tyrosine kinase inhibitor ponatinib inhibits bFGF-activated signaling in neuroblastoma cells and suppresses neuroblastoma growth in vivo.	ponatinib	41-50	fibroblast growth factor 2	Homo sapiens	60-64
28094372-5	2017	Ponatinib, a type II inhibitor, has high affinity towards FGFR1/4 isoforms, but AZD4547, a type I inhibitor of FGFR1, displays much reduced inhibition toward FGFR4.	ponatinib	0-9	fibroblast growth factor receptor 1	Homo sapiens	58-63
28094372-6	2017	In this study, conventional molecular dynamics (MD) simulations, molecular mechanics/generalized Born surface area (MM/GBSA) free energy calculations and umbrella sampling (US) simulations were carried out to reveal the principle of the binding preference of ponatinib and AZD4547 towards FGFR4/FGFR1.	ponatinib	259-268	fibroblast growth factor receptor 4	Homo sapiens	289-294
28094372-6	2017	In this study, conventional molecular dynamics (MD) simulations, molecular mechanics/generalized Born surface area (MM/GBSA) free energy calculations and umbrella sampling (US) simulations were carried out to reveal the principle of the binding preference of ponatinib and AZD4547 towards FGFR4/FGFR1.	ponatinib	259-268	fibroblast growth factor receptor 1	Homo sapiens	295-300
28094372-7	2017	The results provided by MM/GBSA illustrate that ponatinib has similar binding affinities to FGFR4 and FGFR1, while AZD4547 has much stronger binding affinity to FGFR1 than to FGFR4.	ponatinib	48-57	fibroblast growth factor receptor 4	Homo sapiens	92-97
28094372-7	2017	The results provided by MM/GBSA illustrate that ponatinib has similar binding affinities to FGFR4 and FGFR1, while AZD4547 has much stronger binding affinity to FGFR1 than to FGFR4.	ponatinib	48-57	fibroblast growth factor receptor 1	Homo sapiens	102-107
27750146-0	2017	Discovery of novel Ponatinib analogues for reducing KDR activity as potent FGFRs inhibitors.	ponatinib	19-28	kinase insert domain receptor	Homo sapiens	52-55
27750146-5	2017	The results of the current investigation, show that novel Ponatinib analogues are highly active as FGFR inhibitors and that they possess reduced kinase insert domain receptor (KDR) activities.	ponatinib	58-67	kinase insert domain receptor	Homo sapiens	145-174
27750146-5	2017	The results of the current investigation, show that novel Ponatinib analogues are highly active as FGFR inhibitors and that they possess reduced kinase insert domain receptor (KDR) activities.	ponatinib	58-67	kinase insert domain receptor	Homo sapiens	176-179
27564113-6	2017	Mechanistically, ponatinib effectively inhibited the FGFR1-activated signaling pathway.	ponatinib	17-26	fibroblast growth factor receptor 1	Homo sapiens	53-58
27957861-3	2017	SAR302503 prevented cytokine-dependent resistance to ponatinib via inhibition of JAK2/STAT5 phosphorylation.	ponatinib	53-62	Janus kinase 2	Mus musculus	81-85
28069043-11	2017	Importantly, targeting FGF19/FGFR4 axis by ponatinib, a third-generation inhibitor of chronic myeloid leukemia, overcomes HCC resistance of sorafenib by enhancing ROS-associated apoptosis in sorafenib-treated HCC.	ponatinib	43-52	fibroblast growth factor 19	Homo sapiens	23-28
28069043-11	2017	Importantly, targeting FGF19/FGFR4 axis by ponatinib, a third-generation inhibitor of chronic myeloid leukemia, overcomes HCC resistance of sorafenib by enhancing ROS-associated apoptosis in sorafenib-treated HCC.	ponatinib	43-52	fibroblast growth factor receptor 4	Homo sapiens	29-34
27957861-3	2017	SAR302503 prevented cytokine-dependent resistance to ponatinib via inhibition of JAK2/STAT5 phosphorylation.	ponatinib	53-62	signal transducer and activator of transcription 5A	Mus musculus	86-91
27852118-1	2017	BACKGROUND: A previous meta-analysis demonstrated that 3 of the new-generation BCR-ABL tyrosine kinase inhibitors (TKIs) (dasatinib, nilotinib and ponatinib) are associated with an increased risk of vascular occlusive events in patients with Ph+ chronic myeloid leukemia compared with imatinib.	ponatinib	147-156	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-86
27901368-4	2017	Ponatinib, active against all BCR-ABL1 mutants including T315I, became widely used for resistant patients in all phases of disease after previous therapies.	ponatinib	0-9	BCR activator of RhoGEF and GTPase	Homo sapiens	30-38
27562641-1	2016	With BCR-ABL1 tyrosine kinase inhibitors (TKIs), such as imatinib, nilotinib, dasatinib, bosutinib, and ponatinib, many patients with chronic myeloid leukemia in chronic phase (CML-CP) can expect to live near-normal life spans.	ponatinib	104-113	BCR activator of RhoGEF and GTPase	Homo sapiens	5-13
27432881-4	2016	Imatinib inhibited hCNT2 with an IC50 value of 2.3 mum Ponatinib inhibited all five hNTs with the greatest effect seen for hENT1 (IC50 value, 9 mum).	ponatinib	55-64	solute carrier family 29 member 1 (Augustine blood group)	Homo sapiens	123-128
27783942-4	2016	Inhibitor combinations targeting both receptors and the dual inhibitor ponatinib suppress the AKT and ERK1/2 pathways leading to apoptosis.	ponatinib	71-80	AKT serine/threonine kinase 1	Homo sapiens	94-97
27783942-4	2016	Inhibitor combinations targeting both receptors and the dual inhibitor ponatinib suppress the AKT and ERK1/2 pathways leading to apoptosis.	ponatinib	71-80	mitogen-activated protein kinase 3	Homo sapiens	102-108
26479578-6	2016	Baustinib, Nilotinib, Dasatinib, Ponatinib, Bafetinib, etc., which can able to combat against mutated domain of ABL tyrosine kinase protein.	ponatinib	33-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	112-115
27496134-6	2016	Among cabozantinib, lenvatinib, ponatinib, and vandetanib, ponatinib was identified as the most potent inhibitor against KIF5B-RET and its drug-resistant mutants.	ponatinib	59-68	kinesin family member 5B	Mus musculus	121-126
27496134-6	2016	Among cabozantinib, lenvatinib, ponatinib, and vandetanib, ponatinib was identified as the most potent inhibitor against KIF5B-RET and its drug-resistant mutants.	ponatinib	59-68	ret proto-oncogene	Mus musculus	127-130
27496134-7	2016	Interestingly, the vandetanib-resistant KIF5B-RETG810A mutant displayed gain-of-sensitivity (GOS) to ponatinib and lenvatinib.	ponatinib	101-110	kinesin family member 5B	Mus musculus	40-45
27496134-8	2016	Treatment of doxycycline-induced CCSP-rtTA/tetO-KIF5B-RET bitransgenic mice with ponatinib effectively induced tumor regression.	ponatinib	81-90	kinesin family member 5B	Mus musculus	48-53
27496134-8	2016	Treatment of doxycycline-induced CCSP-rtTA/tetO-KIF5B-RET bitransgenic mice with ponatinib effectively induced tumor regression.	ponatinib	81-90	ret proto-oncogene	Mus musculus	54-57
27496134-9	2016	These results indicate that KIF5B-RET-associated lung tumors are addicted to the fusion oncogene and ponatinib is the most effective inhibitor for targeting KIF5B-RET in lung adenocarcinoma.	ponatinib	101-110	kinesin family member 5B	Mus musculus	28-33
27496134-9	2016	These results indicate that KIF5B-RET-associated lung tumors are addicted to the fusion oncogene and ponatinib is the most effective inhibitor for targeting KIF5B-RET in lung adenocarcinoma.	ponatinib	101-110	ret proto-oncogene	Mus musculus	34-37
27496134-9	2016	These results indicate that KIF5B-RET-associated lung tumors are addicted to the fusion oncogene and ponatinib is the most effective inhibitor for targeting KIF5B-RET in lung adenocarcinoma.	ponatinib	101-110	kinesin family member 5B	Mus musculus	157-162
27496134-9	2016	These results indicate that KIF5B-RET-associated lung tumors are addicted to the fusion oncogene and ponatinib is the most effective inhibitor for targeting KIF5B-RET in lung adenocarcinoma.	ponatinib	101-110	ret proto-oncogene	Mus musculus	163-166
27216979-5	2016	Using this PDX model, we confirmed the ability of the FGFR inhibitors, ponatinib, dovitinib and BGJ398, to modulate FGFR signaling, inhibit cell proliferation and induce cell apoptosis in cholangiocarcinoma tumors harboring FGFR2 fusions.	ponatinib	71-80	fibroblast growth factor receptor 2	Homo sapiens	224-229
27505637-1	2016	Ponatinib is approved for adults with refractory chronic myeloid leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia, including those with the T315I BCR-ABL1 mutation.	ponatinib	0-9	BCR activator of RhoGEF and GTPase	Homo sapiens	171-179
27582059-7	2016	Furthermore, the multikinase inhibitors dasatinib and ponatinib appear to have the added advantage of inducing Lck/Yes novel tyrosine kinase (LYN)-mediated proapoptotic BCL-2-like protein 11 (BIM) expression and inhibiting up-regulation of antiapoptotic myeloid cell leukemia 1 (MCL-1), thereby potentially overcoming the development of venetoclax resistance.	ponatinib	54-63	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	111-114
27582059-7	2016	Furthermore, the multikinase inhibitors dasatinib and ponatinib appear to have the added advantage of inducing Lck/Yes novel tyrosine kinase (LYN)-mediated proapoptotic BCL-2-like protein 11 (BIM) expression and inhibiting up-regulation of antiapoptotic myeloid cell leukemia 1 (MCL-1), thereby potentially overcoming the development of venetoclax resistance.	ponatinib	54-63	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	142-145
27582059-7	2016	Furthermore, the multikinase inhibitors dasatinib and ponatinib appear to have the added advantage of inducing Lck/Yes novel tyrosine kinase (LYN)-mediated proapoptotic BCL-2-like protein 11 (BIM) expression and inhibiting up-regulation of antiapoptotic myeloid cell leukemia 1 (MCL-1), thereby potentially overcoming the development of venetoclax resistance.	ponatinib	54-63	BCL2 like 11	Homo sapiens	169-190
27582059-7	2016	Furthermore, the multikinase inhibitors dasatinib and ponatinib appear to have the added advantage of inducing Lck/Yes novel tyrosine kinase (LYN)-mediated proapoptotic BCL-2-like protein 11 (BIM) expression and inhibiting up-regulation of antiapoptotic myeloid cell leukemia 1 (MCL-1), thereby potentially overcoming the development of venetoclax resistance.	ponatinib	54-63	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	254-277
27582059-7	2016	Furthermore, the multikinase inhibitors dasatinib and ponatinib appear to have the added advantage of inducing Lck/Yes novel tyrosine kinase (LYN)-mediated proapoptotic BCL-2-like protein 11 (BIM) expression and inhibiting up-regulation of antiapoptotic myeloid cell leukemia 1 (MCL-1), thereby potentially overcoming the development of venetoclax resistance.	ponatinib	54-63	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	279-284
26864341-5	2016	Conversely, allosteric stimulation of ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias expressing BCR-ABL1, TEL-ABL1, and NUP214-ABL1.	ponatinib	141-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	38-42
27245147-5	2016	AZD4547, dovitinib and ponatinib are multi-kinase inhibitors targeting FGFRs, colony stimulating factor 1 receptor (CSF1R), vascular endothelial growth factor (VEGF)R2, and others.	ponatinib	23-32	colony stimulating factor 1 receptor	Homo sapiens	78-114
27245147-5	2016	AZD4547, dovitinib and ponatinib are multi-kinase inhibitors targeting FGFRs, colony stimulating factor 1 receptor (CSF1R), vascular endothelial growth factor (VEGF)R2, and others.	ponatinib	23-32	colony stimulating factor 1 receptor	Homo sapiens	116-121
27245147-5	2016	AZD4547, dovitinib and ponatinib are multi-kinase inhibitors targeting FGFRs, colony stimulating factor 1 receptor (CSF1R), vascular endothelial growth factor (VEGF)R2, and others.	ponatinib	23-32	vascular endothelial growth factor A	Homo sapiens	124-158
27245147-5	2016	AZD4547, dovitinib and ponatinib are multi-kinase inhibitors targeting FGFRs, colony stimulating factor 1 receptor (CSF1R), vascular endothelial growth factor (VEGF)R2, and others.	ponatinib	23-32	vascular endothelial growth factor A	Homo sapiens	160-164
27044711-1	2016	Chronic myeloid leukemia (CML) patients who relapse on imatinib due to acquired ABL1 kinase domain mutations are successfully treated with second-generation ABL1-tyrosine kinase inhibitors (ABL-TKIs) such as dasatinib, nilotinib or ponatinib.	ponatinib	232-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-84
27044711-1	2016	Chronic myeloid leukemia (CML) patients who relapse on imatinib due to acquired ABL1 kinase domain mutations are successfully treated with second-generation ABL1-tyrosine kinase inhibitors (ABL-TKIs) such as dasatinib, nilotinib or ponatinib.	ponatinib	232-241	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	157-161
27015352-5	2016	The expression of MT-1G messenger RNA and protein is remarkably induced by sorafenib but not other clinically relevant kinase inhibitors (e.g., erlotinib, gefitinib, tivantinib, vemurafenib, selumetinib, imatinib, masitinib, and ponatinib).	ponatinib	229-238	metallothionein 1G	Homo sapiens	18-23
27068398-8	2016	Expression of the KIT(D816G) rendered the HCC78 and CUTO2 cell lines resistant to crizotinib, and only dual inhibition of ROS1 and KIT with crizotinib and ponatinib could resensitize the cells to inhibition of proliferation.	ponatinib	155-164	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-23
27068398-8	2016	Expression of the KIT(D816G) rendered the HCC78 and CUTO2 cell lines resistant to crizotinib, and only dual inhibition of ROS1 and KIT with crizotinib and ponatinib could resensitize the cells to inhibition of proliferation.	ponatinib	155-164	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	18-21
27405085-7	2016	By contrast, ABCB1 polymorphisms influenced the activity of nilotinib, dasatinib and ponatinib to a much lesser extent.	ponatinib	85-94	ATP binding cassette subfamily B member 1	Homo sapiens	13-18
27405085-9	2016	Our results also point to a weaker impact of ABCB1 polymorphisms on the activity of nilotinib, dasatinib and ponatinib.	ponatinib	109-118	ATP binding cassette subfamily B member 1	Homo sapiens	45-50
27166836-10	2016	Ponatinib inhibited phosphorylation not only of BCR-ABL but also of downstream signal transducer and activator of transcription 5, protein kinase B, and ERK1/2 in both K562/IM-R1 and Ba/F3/T315I, and the addition of panobinostat to ponatinib further inhibited these phosphorylations.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	48-55
27166836-10	2016	Ponatinib inhibited phosphorylation not only of BCR-ABL but also of downstream signal transducer and activator of transcription 5, protein kinase B, and ERK1/2 in both K562/IM-R1 and Ba/F3/T315I, and the addition of panobinostat to ponatinib further inhibited these phosphorylations.	ponatinib	0-9	mitogen-activated protein kinase 3	Homo sapiens	153-159
27166836-11	2016	In conclusion, panobinostat enhanced the cytotoxicity of ponatinib towards IM-resistant CML cells including those with T315I-mutated BCR-ABL.	ponatinib	57-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	133-140
27179188-1	2016	Ponatinib is a multi-targeted third generation BCR-ABL1 tyrosine-kinase inhibitor approved for specific types of leukemia.	ponatinib	0-9	BCR activator of RhoGEF and GTPase	Mus musculus	47-55
26864341-5	2016	Conversely, allosteric stimulation of ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias expressing BCR-ABL1, TEL-ABL1, and NUP214-ABL1.	ponatinib	141-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	95-99
26864341-5	2016	Conversely, allosteric stimulation of ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias expressing BCR-ABL1, TEL-ABL1, and NUP214-ABL1.	ponatinib	141-150	BCR activator of RhoGEF and GTPase	Mus musculus	193-201
26864341-5	2016	Conversely, allosteric stimulation of ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias expressing BCR-ABL1, TEL-ABL1, and NUP214-ABL1.	ponatinib	141-150	ets variant 6	Mus musculus	203-211
26864341-5	2016	Conversely, allosteric stimulation of ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias expressing BCR-ABL1, TEL-ABL1, and NUP214-ABL1.	ponatinib	141-150	nucleoporin 214	Mus musculus	217-223
26864341-5	2016	Conversely, allosteric stimulation of ABL1 kinase activity enhanced the antileukemia effect of ABL1 tyrosine kinase inhibitors (imatinib and ponatinib) in human and murine leukemias expressing BCR-ABL1, TEL-ABL1, and NUP214-ABL1.	ponatinib	141-150	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	95-99
26607600-9	2016	Moreover, the BCR/ABL1 inhibitors nilotinib and ponatinib were found to decrease STAT5 activity and CD25 expression in KU812 cells and primary CML LSCs.	ponatinib	48-57	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	18-22
26607600-9	2016	Moreover, the BCR/ABL1 inhibitors nilotinib and ponatinib were found to decrease STAT5 activity and CD25 expression in KU812 cells and primary CML LSCs.	ponatinib	48-57	signal transducer and activator of transcription 5A	Homo sapiens	81-86
26607600-9	2016	Moreover, the BCR/ABL1 inhibitors nilotinib and ponatinib were found to decrease STAT5 activity and CD25 expression in KU812 cells and primary CML LSCs.	ponatinib	48-57	interleukin 2 receptor subunit alpha	Homo sapiens	100-104
26773037-0	2016	The impact of multiple low-level BCR-ABL1 mutations on response to ponatinib.	ponatinib	67-76	BCR activator of RhoGEF and GTPase	Homo sapiens	33-41
26773037-1	2016	The third-generation tyrosine kinase inhibitor (TKI) ponatinib shows activity against all common BCR-ABL1 single mutants, including the highly resistant BCR-ABL1-T315I mutant, improving outcome for patients with refractory chronic myeloid leukemia (CML).	ponatinib	53-62	BCR activator of RhoGEF and GTPase	Homo sapiens	97-105
26773037-1	2016	The third-generation tyrosine kinase inhibitor (TKI) ponatinib shows activity against all common BCR-ABL1 single mutants, including the highly resistant BCR-ABL1-T315I mutant, improving outcome for patients with refractory chronic myeloid leukemia (CML).	ponatinib	53-62	BCR activator of RhoGEF and GTPase	Homo sapiens	153-161
26574622-0	2016	Antitumor effects and molecular mechanisms of ponatinib on endometrial cancer cells harboring activating FGFR2 mutations.	ponatinib	46-55	fibroblast growth factor receptor 2	Homo sapiens	105-110
26860892-0	2016	Ponatinib attenuates experimental pulmonary arterial hypertension by modulating Wnt signaling and vasohibin-2/vasohibin-1.	ponatinib	0-9	vasohibin 1	Homo sapiens	110-121
26603839-2	2016	In preclinical studies, clinically achievable concentrations of the third-generation BCR-ABL1 TKI ponatinib inhibit T315I and all other single BCR-ABL1 mutants except T315M, which generates a single amino acid exchange, but requires 2 sequential nucleotide exchanges.	ponatinib	98-107	BCR activator of RhoGEF and GTPase	Homo sapiens	85-93
26603839-2	2016	In preclinical studies, clinically achievable concentrations of the third-generation BCR-ABL1 TKI ponatinib inhibit T315I and all other single BCR-ABL1 mutants except T315M, which generates a single amino acid exchange, but requires 2 sequential nucleotide exchanges.	ponatinib	98-107	BCR activator of RhoGEF and GTPase	Homo sapiens	143-151
26603839-4	2016	Initial analyses based largely on conventional Sanger sequencing (SS) have suggested that the preclinical relationship between BCR-ABL1 mutation status and ponatinib efficacy is generally recapitulated in patients receiving therapy.	ponatinib	156-165	BCR activator of RhoGEF and GTPase	Homo sapiens	127-135
26055304-0	2016	Clinical activity of ponatinib in a patient with FGFR1-rearranged mixed-phenotype acute leukemia.	ponatinib	21-30	fibroblast growth factor receptor 1	Homo sapiens	49-54
27161743-11	2016	Thrombin generation was not significantly affected by therapeutic levels of TKIs, whereas higher doses of dasatinib, bosutinib, ponatinib and imatinib significantly changed one or several of the thrombin generation parameters (n=7-8).	ponatinib	128-137	coagulation factor II, thrombin	Homo sapiens	195-203
26860892-0	2016	Ponatinib attenuates experimental pulmonary arterial hypertension by modulating Wnt signaling and vasohibin-2/vasohibin-1.	ponatinib	0-9	Wnt family member 5A	Homo sapiens	80-83
26860892-0	2016	Ponatinib attenuates experimental pulmonary arterial hypertension by modulating Wnt signaling and vasohibin-2/vasohibin-1.	ponatinib	0-9	vasohibin 2	Homo sapiens	98-109
26869304-0	2016	BCR-ABL1 mutation   ponatinib resistance.	ponatinib	20-29	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
26574622-3	2016	Our biochemical kinase assay showed that AP24534 is potent against wild-type FGFR1-4 and 5 mutant FGFRs (V561M-FGFR1, N549H-FGFR2, K650E-FGFR3, G697C-FGFR3, N535K-FGFR4) and possesses the strongest kinase-inhibitory activity on N549H-FGFR2 (IC50 of 0.5 nM) among all FGFRs tested.	ponatinib	41-48	fibroblast growth factor receptor 1	Homo sapiens	77-82
26574622-3	2016	Our biochemical kinase assay showed that AP24534 is potent against wild-type FGFR1-4 and 5 mutant FGFRs (V561M-FGFR1, N549H-FGFR2, K650E-FGFR3, G697C-FGFR3, N535K-FGFR4) and possesses the strongest kinase-inhibitory activity on N549H-FGFR2 (IC50 of 0.5 nM) among all FGFRs tested.	ponatinib	41-48	fibroblast growth factor receptor 1	Homo sapiens	111-116
26574622-3	2016	Our biochemical kinase assay showed that AP24534 is potent against wild-type FGFR1-4 and 5 mutant FGFRs (V561M-FGFR1, N549H-FGFR2, K650E-FGFR3, G697C-FGFR3, N535K-FGFR4) and possesses the strongest kinase-inhibitory activity on N549H-FGFR2 (IC50 of 0.5 nM) among all FGFRs tested.	ponatinib	41-48	fibroblast growth factor receptor 2	Homo sapiens	124-129
26574622-3	2016	Our biochemical kinase assay showed that AP24534 is potent against wild-type FGFR1-4 and 5 mutant FGFRs (V561M-FGFR1, N549H-FGFR2, K650E-FGFR3, G697C-FGFR3, N535K-FGFR4) and possesses the strongest kinase-inhibitory activity on N549H-FGFR2 (IC50 of 0.5 nM) among all FGFRs tested.	ponatinib	41-48	fibroblast growth factor receptor 3	Homo sapiens	137-142
26574622-3	2016	Our biochemical kinase assay showed that AP24534 is potent against wild-type FGFR1-4 and 5 mutant FGFRs (V561M-FGFR1, N549H-FGFR2, K650E-FGFR3, G697C-FGFR3, N535K-FGFR4) and possesses the strongest kinase-inhibitory activity on N549H-FGFR2 (IC50 of 0.5 nM) among all FGFRs tested.	ponatinib	41-48	fibroblast growth factor receptor 3	Homo sapiens	150-155
26574622-3	2016	Our biochemical kinase assay showed that AP24534 is potent against wild-type FGFR1-4 and 5 mutant FGFRs (V561M-FGFR1, N549H-FGFR2, K650E-FGFR3, G697C-FGFR3, N535K-FGFR4) and possesses the strongest kinase-inhibitory activity on N549H-FGFR2 (IC50 of 0.5 nM) among all FGFRs tested.	ponatinib	41-48	fibroblast growth factor receptor 4	Homo sapiens	163-168
26574622-3	2016	Our biochemical kinase assay showed that AP24534 is potent against wild-type FGFR1-4 and 5 mutant FGFRs (V561M-FGFR1, N549H-FGFR2, K650E-FGFR3, G697C-FGFR3, N535K-FGFR4) and possesses the strongest kinase-inhibitory activity on N549H-FGFR2 (IC50 of 0.5 nM) among all FGFRs tested.	ponatinib	41-48	fibroblast growth factor receptor 2	Homo sapiens	234-239
26574622-7	2016	AP24534 caused substantial reductions in ERK phosphorylation, PLCgamma signaling and STAT5 signal transduction on ECs bearing FGFR2 activating mutations.	ponatinib	0-7	EPH receptor B2	Homo sapiens	41-44
26574622-7	2016	AP24534 caused substantial reductions in ERK phosphorylation, PLCgamma signaling and STAT5 signal transduction on ECs bearing FGFR2 activating mutations.	ponatinib	0-7	signal transducer and activator of transcription 5A	Homo sapiens	85-90
26574622-7	2016	AP24534 caused substantial reductions in ERK phosphorylation, PLCgamma signaling and STAT5 signal transduction on ECs bearing FGFR2 activating mutations.	ponatinib	0-7	fibroblast growth factor receptor 2	Homo sapiens	126-131
26574622-9	2016	AP24534 causes the chemotherapeutic effect through mainly the blockade of ERK, PLCgamma and STAT5 signal transduction on ECs.	ponatinib	0-7	EPH receptor B2	Homo sapiens	74-77
26574622-9	2016	AP24534 causes the chemotherapeutic effect through mainly the blockade of ERK, PLCgamma and STAT5 signal transduction on ECs.	ponatinib	0-7	signal transducer and activator of transcription 5A	Homo sapiens	92-97
26391436-7	2016	Ponatinib, a multitargeted tyrosine kinase inhibitor, is already shown to be effective against several FGFR1-fusion kinases.	ponatinib	0-9	fibroblast growth factor receptor 1	Homo sapiens	103-108
27014420-1	2016	Targeting BCR/ABL with Tyrosine kinase inhibitors (TKIs) is a proven concept for the treatment of Philadelphia chromosome-positive (Ph+) leukemias but the "gatekeeper" mutation T315I confers resistance against all approved TKIs, with the only exception of ponatinib, a multi-targeted kinase inhibitor.	ponatinib	256-265	BCR activator of RhoGEF and GTPase	Mus musculus	10-13
27014420-1	2016	Targeting BCR/ABL with Tyrosine kinase inhibitors (TKIs) is a proven concept for the treatment of Philadelphia chromosome-positive (Ph+) leukemias but the "gatekeeper" mutation T315I confers resistance against all approved TKIs, with the only exception of ponatinib, a multi-targeted kinase inhibitor.	ponatinib	256-265	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	14-17
26320862-3	2015	The most potent RIPK2 inhibitors were the US Food and Drug Administration-approved drugs ponatinib and regorafenib.	ponatinib	89-98	receptor interacting serine/threonine kinase 2	Homo sapiens	16-21
26373734-9	2016	Our results revealed that ponatinib inhibited cell proliferation and induced apoptosis as determined by loss of mitochondrial membrane potential, increased caspase-3 enzyme activity, and transfer of phosphatidylserine to the plasma membrane in both K562 and K562/IMA-3 cells.	ponatinib	26-35	caspase 3	Homo sapiens	156-165
26562217-3	2015	Inspired by the successful development of ponatinib to curb drug resistance, we hypothesize that the incorporation of an alkyne linker in other heterocyclic scaffolds can also achieve potent inhibition of Bcr-Abl(T315I) by allowing for simultaneous occupancy of both the active site and the allosteric pocket in the Abl kinase domain.	ponatinib	42-51	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	205-212
26377589-3	2015	Several related clinical trials for non-small cell lung cancer (NSCLC) with KIF5B-RET rearrangements using existing RET inhibitors, such as cabozantinib, lenvatinib, vandetanib, sunitinib, ponatinib, and AUY922, have been swiftly initiated by the discovery of the KIF5B-RET fusion gene.	ponatinib	189-198	ret proto-oncogene	Homo sapiens	82-85
26206305-6	2015	We experimentally validated KAR predictions of FGFR and MTOR dependence in lung cancer cell line H1581, showing synergistic reduction in proliferation after combining ponatinib and AZD8055.	ponatinib	167-176	mechanistic target of rapamycin kinase	Homo sapiens	56-60
26432046-2	2015	Ponatinib is a more potent BCR-ABL1 inhibitor than all other tyrosine-kinase inhibitors and selectively suppresses the resistant T315I clones.	ponatinib	0-9	BCR activator of RhoGEF and GTPase	Homo sapiens	27-35
26359452-4	2015	We identified and validated a synthetic lethal interaction between MTOR and ponatinib in non-small cell lung carcinoma cells.	ponatinib	76-85	mechanistic target of rapamycin kinase	Homo sapiens	67-71
26254990-0	2015	Ponatinib ameliorates pulmonary fibrosis by suppressing TGF-beta1/Smad3 pathway.	ponatinib	0-9	transforming growth factor beta 1	Homo sapiens	56-65
26254990-0	2015	Ponatinib ameliorates pulmonary fibrosis by suppressing TGF-beta1/Smad3 pathway.	ponatinib	0-9	SMAD family member 3	Homo sapiens	66-71
26254990-4	2015	In this study, the effects of Ponatinib on TGF-beta1-mediated epithelial-mesenchymal transition (EMT) in A549 cells, on the proliferation of human lung fibroblasts (HLF-1), on the apoptosis of human type I alveolar epithelial cells (AT I) in vitro, and on bleomycin (BLM)-induced pulmonary fibrosis was investigated in vivo.	ponatinib	30-39	transforming growth factor beta 1	Homo sapiens	43-52
26254990-5	2015	Treatment with Ponatinib resulted in a reduction of EMT in A549 cells with a decrease in vimentin and p-Smad3, whereas an increase in E-cadherin.	ponatinib	15-24	vimentin	Homo sapiens	89-97
26254990-5	2015	Treatment with Ponatinib resulted in a reduction of EMT in A549 cells with a decrease in vimentin and p-Smad3, whereas an increase in E-cadherin.	ponatinib	15-24	SMAD family member 3	Homo sapiens	104-109
26254990-5	2015	Treatment with Ponatinib resulted in a reduction of EMT in A549 cells with a decrease in vimentin and p-Smad3, whereas an increase in E-cadherin.	ponatinib	15-24	cadherin 1	Homo sapiens	134-144
26254990-8	2015	Treatment with Ponatinib resulted in an amelioration of the BLM-induced pulmonary fibrosis in rats with reductions of the pathological score, collagen deposition, p-Smad3, alpha-SMA, PDGF-BB and FGF-2 expression.	ponatinib	15-24	SMAD family member 3	Rattus norvegicus	165-170
26254990-8	2015	Treatment with Ponatinib resulted in an amelioration of the BLM-induced pulmonary fibrosis in rats with reductions of the pathological score, collagen deposition, p-Smad3, alpha-SMA, PDGF-BB and FGF-2 expression.	ponatinib	15-24	fibroblast growth factor 2	Rattus norvegicus	195-200
26254990-9	2015	In summary, Ponatinib reversed the EMT, inhibited the apoptosis of AT I, as well as HLF-1 proliferation and prevented pulmonary fibrosis by suppressing the TGF-beta1/Smad3 pathway.	ponatinib	12-21	transforming growth factor beta 1	Homo sapiens	156-165
26254990-9	2015	In summary, Ponatinib reversed the EMT, inhibited the apoptosis of AT I, as well as HLF-1 proliferation and prevented pulmonary fibrosis by suppressing the TGF-beta1/Smad3 pathway.	ponatinib	12-21	SMAD family member 3	Homo sapiens	166-171
26458439-10	2015	Thus, a third-generation ABL TKI, ponatinib, was developed to inhibit all mutated BCR-ABL and showed clinical efficacy in CML cells harboring T315I.	ponatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-28
26458439-10	2015	Thus, a third-generation ABL TKI, ponatinib, was developed to inhibit all mutated BCR-ABL and showed clinical efficacy in CML cells harboring T315I.	ponatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
26320862-7	2015	We also determined the first crystal structure of RIPK2 bound to ponatinib, and identified an allosteric site for inhibitor development.	ponatinib	65-74	receptor interacting serine/threonine kinase 2	Homo sapiens	50-55
26195136-1	2015	A series of pyrimidine alkynyl derivatives were designed and synthesized as new Bcr-Abl inhibitors by hybriding the structural moieties from GNF-7, ponatinib and nilotinib.	ponatinib	148-157	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	80-87
27137144-1	2015	Ponatinib, an oral tyrosine kinase inhibitor with significant activity in heavily pretreated patients with chronic myeloid leukemia, is a CYP3A4 substrate.	ponatinib	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	138-144
25662515-11	2015	Bosutinib, dasatinib, and ponatinib are Src/multikinase inhibitors that are approved by the FDA for the treatment of chronic myelogenous leukemia and vandetanib is approved for the treatment of medullary thyroid cancer.	ponatinib	26-35	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	40-43
25712455-2	2015	Tyrosine kinase inhibitors (TKIs) are the central treatment strategy for CML patients and have significantly improved survival rates, but the T315I mutation in the kinase domain of BCR-ABL1 confers resistance to all clinically approved TKIs, except ponatinib.	ponatinib	249-258	BCR activator of RhoGEF and GTPase	Homo sapiens	181-189
25712455-6	2015	RESULTS: Our findings demonstrate the emergence of compound mutations in the BCR-ABL1 kinase domain following ponatinib treatment, and chromosomal structural variation data predicted amplification of BCL2.	ponatinib	110-119	BCR activator of RhoGEF and GTPase	Homo sapiens	77-85
25712455-7	2015	The primary CD34(+) CML cells from this patient showed increased sensitivity to the combination of ponatinib and ABT-263, a BCL2 inhibitor with a negligible effect against the normal CD34(+) cells.	ponatinib	99-108	CD34 molecule	Homo sapiens	12-16
25712455-7	2015	The primary CD34(+) CML cells from this patient showed increased sensitivity to the combination of ponatinib and ABT-263, a BCL2 inhibitor with a negligible effect against the normal CD34(+) cells.	ponatinib	99-108	BCL2 apoptosis regulator	Homo sapiens	124-128
25996294-7	2015	Ponatinib and pazopanib abrogated phosphorylation of mixed lineage kinase domain-like protein (MLKL) upon TNF-alpha-induced necroptosis, indicating that both agents target a component upstream of MLKL.	ponatinib	0-9	mixed lineage kinase domain like pseudokinase	Homo sapiens	53-93
25996294-7	2015	Ponatinib and pazopanib abrogated phosphorylation of mixed lineage kinase domain-like protein (MLKL) upon TNF-alpha-induced necroptosis, indicating that both agents target a component upstream of MLKL.	ponatinib	0-9	mixed lineage kinase domain like pseudokinase	Homo sapiens	95-99
25996294-7	2015	Ponatinib and pazopanib abrogated phosphorylation of mixed lineage kinase domain-like protein (MLKL) upon TNF-alpha-induced necroptosis, indicating that both agents target a component upstream of MLKL.	ponatinib	0-9	tumor necrosis factor	Homo sapiens	106-115
25996294-7	2015	Ponatinib and pazopanib abrogated phosphorylation of mixed lineage kinase domain-like protein (MLKL) upon TNF-alpha-induced necroptosis, indicating that both agents target a component upstream of MLKL.	ponatinib	0-9	mixed lineage kinase domain like pseudokinase	Homo sapiens	196-200
25996294-9	2015	We validated RIPK1, RIPK3 and transforming growth factor-beta-activated kinase 1 (TAK1) as novel, direct targets of ponatinib by using competitive binding, cellular thermal shift and recombinant kinase assays.	ponatinib	116-125	receptor interacting serine/threonine kinase 1	Homo sapiens	13-18
25996294-9	2015	We validated RIPK1, RIPK3 and transforming growth factor-beta-activated kinase 1 (TAK1) as novel, direct targets of ponatinib by using competitive binding, cellular thermal shift and recombinant kinase assays.	ponatinib	116-125	receptor interacting serine/threonine kinase 3	Homo sapiens	20-25
25996294-9	2015	We validated RIPK1, RIPK3 and transforming growth factor-beta-activated kinase 1 (TAK1) as novel, direct targets of ponatinib by using competitive binding, cellular thermal shift and recombinant kinase assays.	ponatinib	116-125	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	30-80
25996294-9	2015	We validated RIPK1, RIPK3 and transforming growth factor-beta-activated kinase 1 (TAK1) as novel, direct targets of ponatinib by using competitive binding, cellular thermal shift and recombinant kinase assays.	ponatinib	116-125	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	82-86
25996294-10	2015	Ponatinib inhibited both RIPK1 and RIPK3, while pazopanib preferentially targeted RIPK1.	ponatinib	0-9	receptor interacting serine/threonine kinase 1	Homo sapiens	25-30
25996294-10	2015	Ponatinib inhibited both RIPK1 and RIPK3, while pazopanib preferentially targeted RIPK1.	ponatinib	0-9	receptor interacting serine/threonine kinase 3	Homo sapiens	35-40
26056008-0	2015	Identification of ponatinib and other known kinase inhibitors with potent MEKK2 inhibitory activity.	ponatinib	18-27	mitogen-activated protein kinase kinase kinase 2	Homo sapiens	74-79
26056008-6	2015	We report that ponatinib, AT9283, AZD7762, JNJ-7706621, PP121 and hesperadin had potent MEKK2 enzyme inhibitory activities ranging from 4.7 to 60 nM IC50.	ponatinib	15-24	mitogen-activated protein kinase kinase kinase 2	Homo sapiens	88-93
26056008-7	2015	Ponatinib is an FDA-approved drug that potently inhibited MEKK2 enzyme activity with IC50 values of 10-16 nM.	ponatinib	0-9	mitogen-activated protein kinase kinase kinase 2	Homo sapiens	58-63
25894969-8	2015	One patient with lymphoid BC/Ph+ ALL who harbored a T315I ABL mutation and was treated with ponatinib was found to have developed a newly acquired V216M TP53 mutation (12% of transcripts) when becoming resistant to ponatinib.	ponatinib	92-101	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-61
25894969-8	2015	One patient with lymphoid BC/Ph+ ALL who harbored a T315I ABL mutation and was treated with ponatinib was found to have developed a newly acquired V216M TP53 mutation (12% of transcripts) when becoming resistant to ponatinib.	ponatinib	92-101	tumor protein p53	Homo sapiens	153-157
25894969-8	2015	One patient with lymphoid BC/Ph+ ALL who harbored a T315I ABL mutation and was treated with ponatinib was found to have developed a newly acquired V216M TP53 mutation (12% of transcripts) when becoming resistant to ponatinib.	ponatinib	215-224	tumor protein p53	Homo sapiens	153-157
25894969-9	2015	Ponatinib led to a decrease of ABL T315I positive transcripts from 47% before ponatinib treatment to 16% at the time of ponatinib resistance in this patient, suggesting that both TP53 and ABL mutations were present in the same clone and that the newly acquired TP53 mutation might have caused ponatinib resistance in this patient.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
25894969-9	2015	Ponatinib led to a decrease of ABL T315I positive transcripts from 47% before ponatinib treatment to 16% at the time of ponatinib resistance in this patient, suggesting that both TP53 and ABL mutations were present in the same clone and that the newly acquired TP53 mutation might have caused ponatinib resistance in this patient.	ponatinib	0-9	tumor protein p53	Homo sapiens	179-183
25894969-9	2015	Ponatinib led to a decrease of ABL T315I positive transcripts from 47% before ponatinib treatment to 16% at the time of ponatinib resistance in this patient, suggesting that both TP53 and ABL mutations were present in the same clone and that the newly acquired TP53 mutation might have caused ponatinib resistance in this patient.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	188-191
25894969-9	2015	Ponatinib led to a decrease of ABL T315I positive transcripts from 47% before ponatinib treatment to 16% at the time of ponatinib resistance in this patient, suggesting that both TP53 and ABL mutations were present in the same clone and that the newly acquired TP53 mutation might have caused ponatinib resistance in this patient.	ponatinib	0-9	tumor protein p53	Homo sapiens	261-265
25894969-9	2015	Ponatinib led to a decrease of ABL T315I positive transcripts from 47% before ponatinib treatment to 16% at the time of ponatinib resistance in this patient, suggesting that both TP53 and ABL mutations were present in the same clone and that the newly acquired TP53 mutation might have caused ponatinib resistance in this patient.	ponatinib	78-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
25894969-9	2015	Ponatinib led to a decrease of ABL T315I positive transcripts from 47% before ponatinib treatment to 16% at the time of ponatinib resistance in this patient, suggesting that both TP53 and ABL mutations were present in the same clone and that the newly acquired TP53 mutation might have caused ponatinib resistance in this patient.	ponatinib	120-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
25894969-9	2015	Ponatinib led to a decrease of ABL T315I positive transcripts from 47% before ponatinib treatment to 16% at the time of ponatinib resistance in this patient, suggesting that both TP53 and ABL mutations were present in the same clone and that the newly acquired TP53 mutation might have caused ponatinib resistance in this patient.	ponatinib	120-129	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-34
25801024-0	2015	Structure guided design of potent and selective ponatinib-based hybrid inhibitors for RIPK1.	ponatinib	48-57	receptor interacting serine/threonine kinase 1	Homo sapiens	86-91
25801024-2	2015	In the current work, we report that the Bcr-Abl inhibitor and anti-leukemia agent ponatinib is also a first-in-class dual inhibitor of RIPK1 and RIPK3.	ponatinib	82-91	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
25801024-2	2015	In the current work, we report that the Bcr-Abl inhibitor and anti-leukemia agent ponatinib is also a first-in-class dual inhibitor of RIPK1 and RIPK3.	ponatinib	82-91	receptor interacting serine/threonine kinase 1	Homo sapiens	135-140
25801024-2	2015	In the current work, we report that the Bcr-Abl inhibitor and anti-leukemia agent ponatinib is also a first-in-class dual inhibitor of RIPK1 and RIPK3.	ponatinib	82-91	receptor interacting serine/threonine kinase 3	Homo sapiens	145-150
25801024-3	2015	Ponatinib potently inhibited multiple paradigms of RIPK1- and RIPK3-dependent cell death and inflammatory tumor necrosis factor alpha (TNF-alpha) gene transcription.	ponatinib	0-9	receptor interacting serine/threonine kinase 1	Homo sapiens	51-56
25801024-3	2015	Ponatinib potently inhibited multiple paradigms of RIPK1- and RIPK3-dependent cell death and inflammatory tumor necrosis factor alpha (TNF-alpha) gene transcription.	ponatinib	0-9	tumor necrosis factor	Homo sapiens	106-133
25801024-3	2015	Ponatinib potently inhibited multiple paradigms of RIPK1- and RIPK3-dependent cell death and inflammatory tumor necrosis factor alpha (TNF-alpha) gene transcription.	ponatinib	0-9	tumor necrosis factor	Homo sapiens	135-144
25801024-4	2015	We further describe design strategies that utilize the ponatinib scaffold to develop two classes of inhibitors (CS and PN series), each with greatly improved selectivity for RIPK1.	ponatinib	55-64	receptor interacting serine/threonine kinase 1	Homo sapiens	174-179
25801024-5	2015	In particular, we detail the development of PN10, a highly potent and selective "hybrid" RIPK1 inhibitor, capturing the best properties of two different allosteric RIPK1 inhibitors, ponatinib and necrostatin-1.	ponatinib	182-191	receptor interacting serine/threonine kinase 1	Homo sapiens	89-94
25686603-4	2015	The BCR-ABL1 kinase domain gatekeeper mutation Thr315Ile (T315I) confers resistance to all approved ABL1 inhibitors except ponatinib, which has toxicity limitations.	ponatinib	123-132	BCR activator of RhoGEF and GTPase	Homo sapiens	4-12
25803811-8	2015	CHIR258, PKC 412, and ponatinib reduced the number of CFUs formed by EMS-iPS-induced CD34+ cells in a dose-dependent manner, whereas imatinib did not.	ponatinib	22-31	CD34 molecule	Homo sapiens	85-89
25686603-4	2015	The BCR-ABL1 kinase domain gatekeeper mutation Thr315Ile (T315I) confers resistance to all approved ABL1 inhibitors except ponatinib, which has toxicity limitations.	ponatinib	123-132	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
25239608-0	2014	Ponatinib inhibits polyclonal drug-resistant KIT oncoproteins and shows therapeutic potential in heavily pretreated gastrointestinal stromal tumor (GIST) patients.	ponatinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	45-48
25317566-4	2015	Structural analysis reveals that the covalent bond between FIIN-2 and a cysteine, uniquely present in the glycine-rich loop of FGFR kinases, facilitates the DFG-out conformation, which together with the internal flexibility of FIIN-2 enables FIIN-2 to avoid the steric clash with the gate-keeper mutation that causes the ponatinib resistance.	ponatinib	321-330	fibroblast growth factor receptor 4	Homo sapiens	127-131
25527332-0	2015	The BCR-ABL inhibitor ponatinib inhibits platelet immunoreceptor tyrosine-based activation motif (ITAM) signaling, platelet activation and aggregate formation under shear.	ponatinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	4-11
25527332-9	2015	As our results indicate that pobatinib inhibits platelet function, the adverse cardiovascular events observed in patients taking ponatinib may be the result of the effect of ponatinib on other organs or cell types, or disease-specific processes, such as BCR-ABL+cells undergoing apoptosis in response to chemotherapy, or drug-induced adverse effects on the integrity of the vascular endothelium in ponatinib-treated patients.	ponatinib	129-138	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	254-261
25304212-1	2015	Ponatinib, a multi-targeted TKI and potent pan-ABL inhibitor, approved for the treatment of Ph + ALL and CML, was temporarily withdrawn from the U.S. market due to severe vascular adverse events.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	47-50
25465127-0	2014	Structural insights into FGFR kinase isoform selectivity: diverse binding modes of AZD4547 and ponatinib in complex with FGFR1 and FGFR4.	ponatinib	95-104	fibroblast growth factor receptor 1	Homo sapiens	121-126
25662515-13	2015	Both ATP and targeted therapeutic Src protein kinase inhibitors such as dasatinib and ponatinib make hydrophobic contacts with catalytic spine residues and form hydrogen bonds with hinge residues connecting the small and large kinase lobes.	ponatinib	86-95	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	34-37
24766374-13	2015	After ponatinib therapy, the T315I mutation burden decreased down to undetectable levels and the BCR-ABL1 transcripts showed a very low value (0.011%).	ponatinib	6-15	BCR activator of RhoGEF and GTPase	Homo sapiens	97-105
25317566-2	2015	Here, we determined the first crystal structures of the human FGFR4 kinase domain (FGFR4K) alone and complexed with ponatinib, a promiscuous type-2 (DFG-out) kinase inhibitor, and an oncogenic FGFR4K harboring the V550L gate-keeper mutation bound to FIIN-2, a new type-1 irreversible inhibitor.	ponatinib	116-125	fibroblast growth factor receptor 4	Homo sapiens	62-67
25239608-3	2014	Here, we explore the KIT-inhibitory activity of ponatinib in preclinical models and describe initial characterization of its activity in patients with GIST.	ponatinib	48-57	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	21-24
25239608-4	2014	EXPERIMENTAL DESIGN: The cellular and in vivo activities of ponatinib, imatinib, sunitinib, and regorafenib against mutant KIT were evaluated using an accelerated mutagenesis assay and a panel of engineered and GIST-derived cell lines.	ponatinib	60-69	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	123-126
25239608-5	2014	The ponatinib-KIT costructure was also determined.	ponatinib	4-13	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	14-17
25239608-7	2014	RESULTS: In engineered and GIST-derived cell lines, ponatinib potently inhibited KIT exon 11 primary mutants and a range of secondary mutants, including those within the A-loop.	ponatinib	52-61	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	81-84
25239608-12	2014	CONCLUSION: Ponatinib possesses potent activity against most major clinically relevant KIT mutants and has demonstrated preliminary evidence of activity in patients with refractory GIST.	ponatinib	12-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	87-90
25382104-4	2014	Drugs that are currently available, such as imatinib and ponatinib, were also docked against BCR-ABL protein to set a cutoff value for our screening.	ponatinib	57-66	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	93-100
25219510-7	2014	The structures of FGFR4 in complex with the type I inhibitor Dovitinib and the type II inhibitor Ponatinib reveal the molecular interactions with different types of kinase inhibitors and may assist in the design and development of FGFR4 inhibitors.	ponatinib	97-106	fibroblast growth factor receptor 4	Homo sapiens	18-23
25219510-7	2014	The structures of FGFR4 in complex with the type I inhibitor Dovitinib and the type II inhibitor Ponatinib reveal the molecular interactions with different types of kinase inhibitors and may assist in the design and development of FGFR4 inhibitors.	ponatinib	97-106	fibroblast growth factor receptor 4	Homo sapiens	231-236
25367954-0	2014	BCR-ABL1 compound mutations drive ponatinib resistance.	ponatinib	34-43	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
25367954-1	2014	BCR-ABL1 compound mutations harboring T315I are resistant to multiple TKIs, including ponatinib.	ponatinib	86-95	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
25122427-9	2014	Stable cells became sensitized to the RET tyrosine kinase inhibitors, vandetanib and ponatinib.	ponatinib	85-94	ret proto-oncogene	Homo sapiens	38-41
25378936-0	2014	The effects of ponatinib, a multi-targeted tyrosine kinase inhibitor, against human U87 malignant glioblastoma cells.	ponatinib	15-24	small nucleolar RNA, C/D box 87	Homo sapiens	84-87
25536607-1	2014	PURPOSE: Ponatinib (P) has been used for the treatment of chronic myeloid leukemia (CML) and it is known that inhibition of BCR-ABL fusion protein by ponatinib induces apoptosis of CML cells.	ponatinib	9-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
25536607-1	2014	PURPOSE: Ponatinib (P) has been used for the treatment of chronic myeloid leukemia (CML) and it is known that inhibition of BCR-ABL fusion protein by ponatinib induces apoptosis of CML cells.	ponatinib	150-159	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	124-131
25536607-8	2014	RESULTS: IC50values of ponatinib and EGCG were 87.13 nM and 50muM, respectively.	ponatinib	23-32	latexin	Homo sapiens	62-65
24966347-3	2014	In a panel of pleural mesothelioma cell lines, FGFR1 and FGF2 were coexpressed in three of seven cell lines and were significantly associated with sensitivity to the FGFR-active tyrosine kinase inhibitor (TKI), ponatinib, both in vitro and in vivo using orthotopically propagated xenografts.	ponatinib	211-220	fibroblast growth factor receptor 1	Homo sapiens	47-52
24966347-3	2014	In a panel of pleural mesothelioma cell lines, FGFR1 and FGF2 were coexpressed in three of seven cell lines and were significantly associated with sensitivity to the FGFR-active tyrosine kinase inhibitor (TKI), ponatinib, both in vitro and in vivo using orthotopically propagated xenografts.	ponatinib	211-220	fibroblast growth factor 2	Homo sapiens	57-61
25132497-0	2014	BCR-ABL1 compound mutations combining key kinase domain positions confer clinical resistance to ponatinib in Ph chromosome-positive leukemia.	ponatinib	96-105	BCR activator of RhoGEF and GTPase	Homo sapiens	0-8
25132497-1	2014	Ponatinib is the only currently approved tyrosine kinase inhibitor (TKI) that suppresses all BCR-ABL1 single mutants in Philadelphia chromosome-positive (Ph(+)) leukemia, including the recalcitrant BCR-ABL1(T315I) mutant.	ponatinib	0-9	BCR activator of RhoGEF and GTPase	Homo sapiens	93-101
25132497-1	2014	Ponatinib is the only currently approved tyrosine kinase inhibitor (TKI) that suppresses all BCR-ABL1 single mutants in Philadelphia chromosome-positive (Ph(+)) leukemia, including the recalcitrant BCR-ABL1(T315I) mutant.	ponatinib	0-9	BCR activator of RhoGEF and GTPase	Homo sapiens	198-206
25132497-2	2014	However, emergence of compound mutations in a BCR-ABL1 allele may confer ponatinib resistance.	ponatinib	73-82	BCR activator of RhoGEF and GTPase	Homo sapiens	46-54
25132497-3	2014	We found that clinically reported BCR-ABL1 compound mutants center on 12 key positions and confer varying resistance to imatinib, nilotinib, dasatinib, ponatinib, rebastinib, and bosutinib.	ponatinib	152-161	BCR activator of RhoGEF and GTPase	Homo sapiens	34-42
25465127-0	2014	Structural insights into FGFR kinase isoform selectivity: diverse binding modes of AZD4547 and ponatinib in complex with FGFR1 and FGFR4.	ponatinib	95-104	fibroblast growth factor receptor 4	Homo sapiens	131-136
25465127-2	2014	Despite a high level of sequence homology in the ATP-binding site, the majority of reported inhibitors are selective for the FGFR1-3 isoforms and display much reduced potency toward FGFR4, an exception being the Bcr-Abl inhibitor ponatinib.	ponatinib	230-239	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	212-219
25465127-3	2014	Here we present the crystal structure of the FGFR4 kinase domain and show that both FGFR1 and FGFR4 kinase domains in complex with ponatinib adopt a DFG-out activation loop conformation.	ponatinib	131-140	fibroblast growth factor receptor 4	Homo sapiens	45-50
25465127-3	2014	Here we present the crystal structure of the FGFR4 kinase domain and show that both FGFR1 and FGFR4 kinase domains in complex with ponatinib adopt a DFG-out activation loop conformation.	ponatinib	131-140	fibroblast growth factor receptor 1	Homo sapiens	84-89
25465127-3	2014	Here we present the crystal structure of the FGFR4 kinase domain and show that both FGFR1 and FGFR4 kinase domains in complex with ponatinib adopt a DFG-out activation loop conformation.	ponatinib	131-140	fibroblast growth factor receptor 4	Homo sapiens	94-99
25465127-4	2014	Comparison with the structure of FGFR1 in complex with the candidate drug AZD4547, combined with kinetic characterization of the binding of ponatinib and AZD4547 to FGFR1 and FGFR4, sheds light on the observed differences in selectivity profiles and provides a rationale for developing FGFR4-selective inhibitors.	ponatinib	140-149	fibroblast growth factor receptor 1	Homo sapiens	33-38
25465127-4	2014	Comparison with the structure of FGFR1 in complex with the candidate drug AZD4547, combined with kinetic characterization of the binding of ponatinib and AZD4547 to FGFR1 and FGFR4, sheds light on the observed differences in selectivity profiles and provides a rationale for developing FGFR4-selective inhibitors.	ponatinib	140-149	fibroblast growth factor receptor 1	Homo sapiens	165-170
25465127-4	2014	Comparison with the structure of FGFR1 in complex with the candidate drug AZD4547, combined with kinetic characterization of the binding of ponatinib and AZD4547 to FGFR1 and FGFR4, sheds light on the observed differences in selectivity profiles and provides a rationale for developing FGFR4-selective inhibitors.	ponatinib	140-149	fibroblast growth factor receptor 4	Homo sapiens	175-180
25465127-4	2014	Comparison with the structure of FGFR1 in complex with the candidate drug AZD4547, combined with kinetic characterization of the binding of ponatinib and AZD4547 to FGFR1 and FGFR4, sheds light on the observed differences in selectivity profiles and provides a rationale for developing FGFR4-selective inhibitors.	ponatinib	140-149	fibroblast growth factor receptor 4	Homo sapiens	286-291
25053825-2	2014	Here, we demonstrate that cotreatment with JQ1 and the FLT3 tyrosine kinase inhibitor (TKI) ponatinib or AC220 synergistically induce apoptosis of cultured and primary CD34(+) human AML blast progenitor cells (BPC) expressing FLT3-ITD.	ponatinib	92-101	fms related receptor tyrosine kinase 3	Homo sapiens	55-59
25053825-2	2014	Here, we demonstrate that cotreatment with JQ1 and the FLT3 tyrosine kinase inhibitor (TKI) ponatinib or AC220 synergistically induce apoptosis of cultured and primary CD34(+) human AML blast progenitor cells (BPC) expressing FLT3-ITD.	ponatinib	92-101	CD34 molecule	Homo sapiens	168-172
25053825-2	2014	Here, we demonstrate that cotreatment with JQ1 and the FLT3 tyrosine kinase inhibitor (TKI) ponatinib or AC220 synergistically induce apoptosis of cultured and primary CD34(+) human AML blast progenitor cells (BPC) expressing FLT3-ITD.	ponatinib	92-101	fms related receptor tyrosine kinase 3	Homo sapiens	226-230
24552773-0	2014	Ponatinib induces apoptosis in imatinib-resistant human mast cells by dephosphorylating mutant D816V KIT and silencing beta-catenin signaling.	ponatinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	101-104
24768818-4	2014	Ponatinib is identified as the more potent molecule, which inhibits DDR1 and DDR2 with an IC50 of 9nM.	ponatinib	0-9	discoidin domain receptor tyrosine kinase 1	Homo sapiens	68-72
24768818-4	2014	Ponatinib is identified as the more potent molecule, which inhibits DDR1 and DDR2 with an IC50 of 9nM.	ponatinib	0-9	discoidin domain receptor tyrosine kinase 2	Homo sapiens	77-81
24768818-8	2014	Whereas imatinib and ponatinib bind potently to both the DDR and ABL kinases, the hydrophobic interactions of the ABL P-loop appear poorly satisfied by DDR1-IN-1 suggesting a structural basis for its DDR1 selectivity.	ponatinib	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	65-68
24771645-6	2014	RESULTS: Among 58 cell lines, 14 exhibited ponatinib sensitivity (IC50 values <= 50 nmol/L) that correlated with FGFR1 mRNA and protein expression, but not with FGFR1 GCN or histology.	ponatinib	43-52	fibroblast growth factor receptor 1	Homo sapiens	116-121
24771645-7	2014	Moreover, ponatinib sensitivity associated with mRNA expression of the ligands, FGF2 and FGF9.	ponatinib	10-19	fibroblast growth factor 2	Homo sapiens	80-84
24771645-7	2014	Moreover, ponatinib sensitivity associated with mRNA expression of the ligands, FGF2 and FGF9.	ponatinib	10-19	fibroblast growth factor 9	Homo sapiens	89-93
24407160-0	2014	Identification of Ponatinib as a potent inhibitor of growth, migration, and activation of neoplastic eosinophils carrying FIP1L1-PDGFRA.	ponatinib	18-27	factor interacting with PAPOLA and CPSF1	Homo sapiens	122-128
24407160-0	2014	Identification of Ponatinib as a potent inhibitor of growth, migration, and activation of neoplastic eosinophils carrying FIP1L1-PDGFRA.	ponatinib	18-27	platelet derived growth factor receptor alpha	Homo sapiens	129-135
24407160-10	2014	In addition, ponatinib was found to downregulate expression of the activation-linked surface antigen CD63 on EOL-1 cells and to suppress the growth of primary neoplastic eosinophils.	ponatinib	13-22	CD63 molecule	Homo sapiens	101-105
24407160-14	2014	Although several different PDGFR-targeting agents are effective, the most potent drug appears to be ponatinib.	ponatinib	100-109	platelet derived growth factor receptor beta	Homo sapiens	27-32
24481648-0	2014	Ponatinib enhances anticancer drug sensitivity in MRP7-overexpressing cells.	ponatinib	0-9	ATP binding cassette subfamily C member 10	Homo sapiens	50-54
24481648-4	2014	Ponatinib, a multi-targeted TKI, inhibits the activity of BCR-ABL with very high potency and broad specificity, including the T315I mutation which confers resistance to other TKIs.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
24481648-5	2014	It was reported that ponatinib was capable of reversing breast cancer resistance protein (BCRP)- and P-glycoprotein (P-gp)-mediated MDR.	ponatinib	21-30	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	56-88
24481648-5	2014	It was reported that ponatinib was capable of reversing breast cancer resistance protein (BCRP)- and P-glycoprotein (P-gp)-mediated MDR.	ponatinib	21-30	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	90-94
24481648-5	2014	It was reported that ponatinib was capable of reversing breast cancer resistance protein (BCRP)- and P-glycoprotein (P-gp)-mediated MDR.	ponatinib	21-30	ATP binding cassette subfamily B member 1	Homo sapiens	101-115
24481648-5	2014	It was reported that ponatinib was capable of reversing breast cancer resistance protein (BCRP)- and P-glycoprotein (P-gp)-mediated MDR.	ponatinib	21-30	ATP binding cassette subfamily B member 1	Homo sapiens	117-121
24481648-6	2014	In the present study, we report for the first time that ponatinib also potentiates the cytotoxicity of widely used therapeutic substrates of MRP7, such as paclitaxel, docetaxel, vincristine and vinblastine.	ponatinib	56-65	ATP binding cassette subfamily C member 10	Homo sapiens	141-145
24481648-7	2014	Ponatinib significantly enhances the accumulation of [3H]-paclitaxel in cells expressing MRP7.	ponatinib	0-9	ATP binding cassette subfamily C member 10	Homo sapiens	89-93
24481648-10	2014	In addition to inhibition of pump function, ponatinib also downregulated MRP7 protein expression in a time- and concentration-dependent manner.	ponatinib	44-53	ATP binding cassette subfamily C member 10	Homo sapiens	73-77
24408322-0	2014	Ponatinib overcomes FGF2-mediated resistance in CML patients without kinase domain mutations.	ponatinib	0-9	fibroblast growth factor 2	Homo sapiens	20-24
24408322-5	2014	Resistance could be overcome with ponatinib, a multikinase inhibitor that targets BCR-ABL and FGF receptor.	ponatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
24408322-8	2014	Moreover, FGF2 in the marrow decreased concurrently with response to ponatinib, further suggesting that FGF2-mediated resistance is interrupted by FGF receptor inhibition.	ponatinib	69-78	fibroblast growth factor 2	Homo sapiens	104-108
24550512-6	2014	Modeling of BCR-ABL1 in complex with the potent pan-BCR-ABL1 TKI ponatinib highlighted potentially effective therapeutic strategies for patients carrying these recalcitrant and complex BCR-ABL1 mutant proteins while unveiling unique mechanisms of escape to ponatinib therapy.	ponatinib	65-74	BCR activator of RhoGEF and GTPase	Homo sapiens	12-20
24550512-6	2014	Modeling of BCR-ABL1 in complex with the potent pan-BCR-ABL1 TKI ponatinib highlighted potentially effective therapeutic strategies for patients carrying these recalcitrant and complex BCR-ABL1 mutant proteins while unveiling unique mechanisms of escape to ponatinib therapy.	ponatinib	65-74	BCR activator of RhoGEF and GTPase	Homo sapiens	52-60
24550512-6	2014	Modeling of BCR-ABL1 in complex with the potent pan-BCR-ABL1 TKI ponatinib highlighted potentially effective therapeutic strategies for patients carrying these recalcitrant and complex BCR-ABL1 mutant proteins while unveiling unique mechanisms of escape to ponatinib therapy.	ponatinib	65-74	BCR activator of RhoGEF and GTPase	Homo sapiens	52-60
24550512-6	2014	Modeling of BCR-ABL1 in complex with the potent pan-BCR-ABL1 TKI ponatinib highlighted potentially effective therapeutic strategies for patients carrying these recalcitrant and complex BCR-ABL1 mutant proteins while unveiling unique mechanisms of escape to ponatinib therapy.	ponatinib	257-266	BCR activator of RhoGEF and GTPase	Homo sapiens	12-20
24550512-6	2014	Modeling of BCR-ABL1 in complex with the potent pan-BCR-ABL1 TKI ponatinib highlighted potentially effective therapeutic strategies for patients carrying these recalcitrant and complex BCR-ABL1 mutant proteins while unveiling unique mechanisms of escape to ponatinib therapy.	ponatinib	257-266	BCR activator of RhoGEF and GTPase	Homo sapiens	52-60
24550512-6	2014	Modeling of BCR-ABL1 in complex with the potent pan-BCR-ABL1 TKI ponatinib highlighted potentially effective therapeutic strategies for patients carrying these recalcitrant and complex BCR-ABL1 mutant proteins while unveiling unique mechanisms of escape to ponatinib therapy.	ponatinib	257-266	BCR activator of RhoGEF and GTPase	Homo sapiens	52-60
24596204-0	2014	Ponatinib circumvents FGF2-driven resistance to imatinib in CML.	ponatinib	0-9	fibroblast growth factor 2	Homo sapiens	22-26
25360237-1	2014	Five BCR-ABL1 tyrosine kinase inhibitors (TKIs), imatinib, nilotinib, dasatinib, bosutinib, and ponatinib, are currently approved for the treatment of chronic myeloid leukemia (CML).	ponatinib	96-105	BCR activator of RhoGEF and GTPase	Homo sapiens	5-13
24486648-8	2014	In contrast, ponatinib efficiently eradicated leukemic cells expressing Hes1 and the imatinib-resistant FLP1L1-PDGFRAlpha mutant in vitro and in vivo.	ponatinib	13-22	hes family bHLH transcription factor 1	Mus musculus	72-76
24486648-8	2014	In contrast, ponatinib efficiently eradicated leukemic cells expressing Hes1 and the imatinib-resistant FLP1L1-PDGFRAlpha mutant in vitro and in vivo.	ponatinib	13-22	platelet derived growth factor receptor, alpha polypeptide	Mus musculus	111-121
24552773-3	2014	The purpose of this investigation was aimed at exploring whether ponatinib (AP24534), a novel effective TKI against T315I Bcr-Abl, was active against D816V KIT.	ponatinib	65-74	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	156-159
24552773-3	2014	The purpose of this investigation was aimed at exploring whether ponatinib (AP24534), a novel effective TKI against T315I Bcr-Abl, was active against D816V KIT.	ponatinib	76-83	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
24552773-3	2014	The purpose of this investigation was aimed at exploring whether ponatinib (AP24534), a novel effective TKI against T315I Bcr-Abl, was active against D816V KIT.	ponatinib	76-83	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	156-159
24552773-4	2014	We discovered that ponatinib abrogated the phosphorylation of KIT harboring either V560G (sensitive to imatinib) or D816V mutation (resistant to imatinib) and the downstream signaling transduction.	ponatinib	19-28	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	62-65
24552773-5	2014	Ponatinib inhibited the growth of D816V KIT-expressing cells in culture and nude mouse xenografted tumor.	ponatinib	0-9	KIT proto-oncogene receptor tyrosine kinase	Mus musculus	40-43
24552773-6	2014	Ponatinib triggered apoptosis by inducing the release of cytochrome c and AIF, downregulation of Mcl-1.	ponatinib	0-9	cytochrome c, somatic	Homo sapiens	57-69
24552773-6	2014	Ponatinib triggered apoptosis by inducing the release of cytochrome c and AIF, downregulation of Mcl-1.	ponatinib	0-9	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	97-102
24552773-7	2014	Furthermore, ponatinib abrogated the phosphorylation of beta-catenin at the site Y654, suppressed the translocation of beta-catenin, and inhibited the transcription and DNA binding of TCF and the expression of its targets (e.g., AXIN2, c-MYC, and CCND1).	ponatinib	13-22	catenin beta 1	Homo sapiens	56-68
24552773-7	2014	Furthermore, ponatinib abrogated the phosphorylation of beta-catenin at the site Y654, suppressed the translocation of beta-catenin, and inhibited the transcription and DNA binding of TCF and the expression of its targets (e.g., AXIN2, c-MYC, and CCND1).	ponatinib	13-22	catenin beta 1	Homo sapiens	119-131
24552773-7	2014	Furthermore, ponatinib abrogated the phosphorylation of beta-catenin at the site Y654, suppressed the translocation of beta-catenin, and inhibited the transcription and DNA binding of TCF and the expression of its targets (e.g., AXIN2, c-MYC, and CCND1).	ponatinib	13-22	hepatocyte nuclear factor 4 alpha	Homo sapiens	184-187
24552773-7	2014	Furthermore, ponatinib abrogated the phosphorylation of beta-catenin at the site Y654, suppressed the translocation of beta-catenin, and inhibited the transcription and DNA binding of TCF and the expression of its targets (e.g., AXIN2, c-MYC, and CCND1).	ponatinib	13-22	axin 2	Homo sapiens	229-234
24552773-7	2014	Furthermore, ponatinib abrogated the phosphorylation of beta-catenin at the site Y654, suppressed the translocation of beta-catenin, and inhibited the transcription and DNA binding of TCF and the expression of its targets (e.g., AXIN2, c-MYC, and CCND1).	ponatinib	13-22	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	236-241
24552773-7	2014	Furthermore, ponatinib abrogated the phosphorylation of beta-catenin at the site Y654, suppressed the translocation of beta-catenin, and inhibited the transcription and DNA binding of TCF and the expression of its targets (e.g., AXIN2, c-MYC, and CCND1).	ponatinib	13-22	cyclin D1	Homo sapiens	247-252
24552773-8	2014	Moreover, ponatinib was highly active against xenografted D816V KIT tumors in nude mice and significantly prolonged the survival of mice with aggressive systemic mastocytosis or mast cell leukemia by impeding the expansion and infiltration of mast cells with imatinib-resistant D814Y KIT.	ponatinib	10-19	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	64-67
24552773-8	2014	Moreover, ponatinib was highly active against xenografted D816V KIT tumors in nude mice and significantly prolonged the survival of mice with aggressive systemic mastocytosis or mast cell leukemia by impeding the expansion and infiltration of mast cells with imatinib-resistant D814Y KIT.	ponatinib	10-19	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	284-287
24552773-9	2014	Our findings warrant a clinical trial of ponatinib in patients with systemic mastocytosis harboring D816V KIT.	ponatinib	41-50	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	106-109
24552773-0	2014	Ponatinib induces apoptosis in imatinib-resistant human mast cells by dephosphorylating mutant D816V KIT and silencing beta-catenin signaling.	ponatinib	0-9	catenin beta 1	Homo sapiens	119-131
24552773-3	2014	The purpose of this investigation was aimed at exploring whether ponatinib (AP24534), a novel effective TKI against T315I Bcr-Abl, was active against D816V KIT.	ponatinib	65-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
24297701-0	2014	BCR-ABL residues interacting with ponatinib are critical to preserve the tumorigenic potential of the oncoprotein.	ponatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
24586514-0	2014	Combining the ABL1 kinase inhibitor ponatinib and the histone deacetylase inhibitor vorinostat: a potential treatment for BCR-ABL-positive leukemia.	ponatinib	36-45	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	14-18
24586514-0	2014	Combining the ABL1 kinase inhibitor ponatinib and the histone deacetylase inhibitor vorinostat: a potential treatment for BCR-ABL-positive leukemia.	ponatinib	36-45	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	14-17
24586514-5	2014	In the current study, we analyzed the efficacy of ponatinib and vorinostat treatment by using BCR-ABL-positive cell lines.	ponatinib	50-59	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	98-101
24586514-7	2014	We found that ponatinib potently inhibited the growth of Ba/F3 cells ectopically expressing BCR-ABL T315I mutation.	ponatinib	14-23	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	96-99
24586514-11	2014	Caspase 3 and PARP activation increased after combination treatment with ponatinib and vorinostat.	ponatinib	73-82	caspase 3	Mus musculus	0-9
24586514-11	2014	Caspase 3 and PARP activation increased after combination treatment with ponatinib and vorinostat.	ponatinib	73-82	poly (ADP-ribose) polymerase family, member 1	Mus musculus	14-18
24586514-16	2014	Thus, combined administration of ponatinib and vorinostat may be a powerful strategy against BCR-ABL mutant cells and could enhance the cytotoxic effects of ponatinib in those BCR-ABL mutant cells.	ponatinib	33-42	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	97-100
24586514-16	2014	Thus, combined administration of ponatinib and vorinostat may be a powerful strategy against BCR-ABL mutant cells and could enhance the cytotoxic effects of ponatinib in those BCR-ABL mutant cells.	ponatinib	33-42	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	180-183
24586514-16	2014	Thus, combined administration of ponatinib and vorinostat may be a powerful strategy against BCR-ABL mutant cells and could enhance the cytotoxic effects of ponatinib in those BCR-ABL mutant cells.	ponatinib	157-166	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	180-183
24550739-8	2014	After progression on pazopanib, the same patient also had stable disease on ponatinib, a pan-FGFR inhibitor (in vitro, FGFR2 IC50 8 nM).	ponatinib	76-85	fibroblast growth factor receptor 2	Homo sapiens	119-124
24258348-7	2014	Thus, a third-generation ABL TKI, ponatinib, was developed to inhibit all mutated BCR-ABL and showed clinical efficacy in CML cells harbouring T315I.	ponatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-28
24258348-7	2014	Thus, a third-generation ABL TKI, ponatinib, was developed to inhibit all mutated BCR-ABL and showed clinical efficacy in CML cells harbouring T315I.	ponatinib	34-43	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	82-89
23888935-1	2013	WHAT IS KNOWN AND OBJECTIVE: Ponatinib is a potent oral tyrosine kinase inhibitor with activity against BCR-ABL, the primary driver of chronic myeloid leukaemia and Philadelphia chromosome-positive acute lymphoblastic leukaemia.	ponatinib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	104-111
24756787-9	2014	In conclusion, ponatinib has proved to be a powerful BCR-ABL inhibitor, which exhibits clinical activity both in BCR-ABL wild-type and mutant CML, including activity against the T315I mutation.	ponatinib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	53-60
24756787-9	2014	In conclusion, ponatinib has proved to be a powerful BCR-ABL inhibitor, which exhibits clinical activity both in BCR-ABL wild-type and mutant CML, including activity against the T315I mutation.	ponatinib	15-24	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
25593988-8	2014	In ponatinib assays performed on both non-mutated and T315I-mutated BCR-ABL1 cells, an increased number of resistant clones were observed in the presence of MS-5.	ponatinib	3-12	BCR activator of RhoGEF and GTPase	Mus musculus	68-76
24472312-0	2014	Ponatinib efficiently kills imatinib-resistant chronic eosinophilic leukemia cells harboring gatekeeper mutant T674I FIP1L1-PDGFRalpha: roles of Mcl-1 and beta-catenin.	ponatinib	0-9	FIP1 like 1 (S. cerevisiae)	Mus musculus	117-123
24472312-0	2014	Ponatinib efficiently kills imatinib-resistant chronic eosinophilic leukemia cells harboring gatekeeper mutant T674I FIP1L1-PDGFRalpha: roles of Mcl-1 and beta-catenin.	ponatinib	0-9	myeloid cell leukemia sequence 1	Mus musculus	145-150
24472312-0	2014	Ponatinib efficiently kills imatinib-resistant chronic eosinophilic leukemia cells harboring gatekeeper mutant T674I FIP1L1-PDGFRalpha: roles of Mcl-1 and beta-catenin.	ponatinib	0-9	catenin (cadherin associated protein), beta 1	Mus musculus	155-167
24472312-4	2014	The purpose of this study was to examine the effect of ponatinib on T674I FIP1L1-PDGFRalpha.	ponatinib	55-64	FIP1 like 1 (S. cerevisiae)	Mus musculus	74-80
24472312-7	2014	The in vivo antitumor activity of ponatinib was evaluated with xenografted BaF3-T674I FIP1L1-PDGFRalpha cells in nude mice models.	ponatinib	34-43	FIP1 like 1 (S. cerevisiae)	Mus musculus	86-92
24472312-9	2014	Ponatinib potently inhibited the phosphorylation of WT and T674I FIP1L1-PDGFRalpha and their downstream signaling molecules (e.g., Stat3, Stat5).	ponatinib	0-9	FIP1 like 1 (S. cerevisiae)	Mus musculus	65-71
24472312-9	2014	Ponatinib potently inhibited the phosphorylation of WT and T674I FIP1L1-PDGFRalpha and their downstream signaling molecules (e.g., Stat3, Stat5).	ponatinib	0-9	signal transducer and activator of transcription 3	Mus musculus	131-136
24472312-9	2014	Ponatinib potently inhibited the phosphorylation of WT and T674I FIP1L1-PDGFRalpha and their downstream signaling molecules (e.g., Stat3, Stat5).	ponatinib	0-9	signal transducer and activator of transcription 5A	Mus musculus	138-143
24472312-10	2014	Ponatinib strikingly inhibited the growth of both WT and T674I FIP1L1-PDGFRalpha-carrying CEL cells (IC50: 0.004-2.5 nM).	ponatinib	0-9	FIP1 like 1 (S. cerevisiae)	Mus musculus	63-69
24472312-12	2014	In vivo, ponatinib abrogated the growth of xenografted BaF3-T674I FIP1L1-PDGFRalpha cells in nude mice.	ponatinib	9-18	FIP1 like 1 (S. cerevisiae)	Mus musculus	66-72
24472312-13	2014	CONCLUSIONS: Ponatinib is a pan-FIP1L1-PDGFRalpha inhibitor, and clinical trials are warranted to investigate its efficacy in imatinib-resistant CEL.	ponatinib	13-22	FIP1 like 1 (S. cerevisiae)	Mus musculus	32-38
24236021-0	2013	Ponatinib is a pan-BCR-ABL kinase inhibitor: MD simulations and SIE study.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
24180494-1	2013	BACKGROUND: Ponatinib is a potent oral tyrosine kinase inhibitor of unmutated and mutated BCR-ABL, including BCR-ABL with the tyrosine kinase inhibitor-refractory threonine-to-isoleucine mutation at position 315 (T315I).	ponatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
24180494-1	2013	BACKGROUND: Ponatinib is a potent oral tyrosine kinase inhibitor of unmutated and mutated BCR-ABL, including BCR-ABL with the tyrosine kinase inhibitor-refractory threonine-to-isoleucine mutation at position 315 (T315I).	ponatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	109-116
24236021-3	2013	The pan-BCR-ABL kinase inhibitor ponatinib exhibits potent activity against native, T315I, and all other clinically relevant mutants, and showed better inhibition than the previously known inhibitors.	ponatinib	33-42	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-15
24236021-4	2013	We have studied the molecular dynamics simulations and calculated solvated interaction energies of native and fourteen mutant BCR-ABL kinases (M244V, G250E, Q252H, Y253F, Y253H, E255K, E255V, T315A, T315I, F317L, F317V, M351T, F359V and H396P) complexed with ponatinib.	ponatinib	259-268	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	126-133
24236021-5	2013	These studies revealed that the interactions between ponatinib and individual residues in BCR-ABL kinase are also affected due to the remote residue mutations.	ponatinib	53-62	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	90-97
24236021-7	2013	Our work provides the molecular mechanisms of native and mutant BCR-ABL kinases inhibition by ponatinib at atomic level that has not been studied before.	ponatinib	94-103	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	64-71
24159169-0	2013	Activity of omacetaxine mepesuccinate against ponatinib-resistant BCR-ABL-positive cells.	ponatinib	46-55	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	66-73
24124571-0	2013	Targeting wild-type and mutationally activated FGFR4 in rhabdomyosarcoma with the inhibitor ponatinib (AP24534).	ponatinib	92-101	fibroblast growth factor receptor 4	Homo sapiens	47-52
24124571-7	2013	We found ponatinib (AP24534) to be the most potent FGFR4 inhibitor with an IC50 in the nanomolar range.	ponatinib	9-18	fibroblast growth factor receptor 4	Homo sapiens	51-56
24124571-7	2013	We found ponatinib (AP24534) to be the most potent FGFR4 inhibitor with an IC50 in the nanomolar range.	ponatinib	20-27	fibroblast growth factor receptor 4	Homo sapiens	51-56
24124571-8	2013	Ponatinib inhibited the growth of RMS cells expressing wild-type or mutated FGFR4 through increased apoptosis.	ponatinib	0-9	fibroblast growth factor receptor 4	Homo sapiens	76-81
24124571-9	2013	Phosphorylation of wild-type and mutated FGFR4 as well as its downstream target STAT3 was also suppressed by ponatinib.	ponatinib	109-118	fibroblast growth factor receptor 4	Homo sapiens	41-46
24124571-9	2013	Phosphorylation of wild-type and mutated FGFR4 as well as its downstream target STAT3 was also suppressed by ponatinib.	ponatinib	109-118	signal transducer and activator of transcription 3	Homo sapiens	80-85
24124571-10	2013	Finally, ponatinib treatment inhibited tumor growth in a RMS mouse model expressing mutated FGFR4.	ponatinib	9-18	fibroblast growth factor receptor 4	Mus musculus	92-97
24124571-11	2013	Therefore, our data suggests that ponatinib is a potentially effective therapeutic agent for RMS tumors that are driven by a dysregulated FGFR4 signaling pathway.	ponatinib	34-43	fibroblast growth factor receptor 4	Homo sapiens	138-143
23801357-2	2013	In vitro studies suggested that metabolism of ponatinib is partially mediated by CYP3A4.	ponatinib	46-55	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	81-87
23915432-13	2013	Here, we show that using the most recently approved TKI, ponatinib (Iclusig), in combination with CC(mut3) allows a dose reduction of ponatinib and increased therapeutic efficacy in vitro measured by reduction in kinase activity, induction of apoptosis via caspase-3/7 and 7-AAD/Annexin V assays, and reduced transformative ability measured by a colony forming assay.	ponatinib	57-66	caspase 3	Homo sapiens	257-266
23915432-13	2013	Here, we show that using the most recently approved TKI, ponatinib (Iclusig), in combination with CC(mut3) allows a dose reduction of ponatinib and increased therapeutic efficacy in vitro measured by reduction in kinase activity, induction of apoptosis via caspase-3/7 and 7-AAD/Annexin V assays, and reduced transformative ability measured by a colony forming assay.	ponatinib	57-66	annexin A5	Homo sapiens	279-288
23915432-13	2013	Here, we show that using the most recently approved TKI, ponatinib (Iclusig), in combination with CC(mut3) allows a dose reduction of ponatinib and increased therapeutic efficacy in vitro measured by reduction in kinase activity, induction of apoptosis via caspase-3/7 and 7-AAD/Annexin V assays, and reduced transformative ability measured by a colony forming assay.	ponatinib	68-75	caspase 3	Homo sapiens	257-266
23915432-13	2013	Here, we show that using the most recently approved TKI, ponatinib (Iclusig), in combination with CC(mut3) allows a dose reduction of ponatinib and increased therapeutic efficacy in vitro measured by reduction in kinase activity, induction of apoptosis via caspase-3/7 and 7-AAD/Annexin V assays, and reduced transformative ability measured by a colony forming assay.	ponatinib	68-75	annexin A5	Homo sapiens	279-288
23539538-0	2013	Synergistic growth-inhibitory effects of ponatinib and midostaurin (PKC412) on neoplastic mast cells carrying KIT D816V.	ponatinib	41-50	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	110-113
23539538-4	2013	Ponatinib was found to inhibit the kinase activity of KIT G560V and KIT D816V in the human mast cell leukemia cell line HMC-1.	ponatinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	54-57
23539538-4	2013	Ponatinib was found to inhibit the kinase activity of KIT G560V and KIT D816V in the human mast cell leukemia cell line HMC-1.	ponatinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-71
23539538-5	2013	In addition, ponatinib was found to block Lyn- and STAT5 activity in neoplastic mast cells.	ponatinib	13-22	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	42-45
23539538-5	2013	In addition, ponatinib was found to block Lyn- and STAT5 activity in neoplastic mast cells.	ponatinib	13-22	signal transducer and activator of transcription 5A	Homo sapiens	51-56
23539538-6	2013	Ponatinib induced growth inhibition and apoptosis in HMC-1.1 cells (KIT G560V(+)) and HMC-1.2 cells (KIT G560V(+)/KIT D816V(+)) as well as in primary neoplastic mast cells.	ponatinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	68-71
23539538-6	2013	Ponatinib induced growth inhibition and apoptosis in HMC-1.1 cells (KIT G560V(+)) and HMC-1.2 cells (KIT G560V(+)/KIT D816V(+)) as well as in primary neoplastic mast cells.	ponatinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	101-104
23539538-6	2013	Ponatinib induced growth inhibition and apoptosis in HMC-1.1 cells (KIT G560V(+)) and HMC-1.2 cells (KIT G560V(+)/KIT D816V(+)) as well as in primary neoplastic mast cells.	ponatinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	101-104
23539538-7	2013	The effects of ponatinib were dose-dependent, but higher IC50-values were obtained in HMC-1 cells harboring KIT D816V than in those lacking KIT D816V.	ponatinib	15-24	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	108-111
23801357-3	2013	The effects of CYP3A4 inhibition on the pharmacokinetics of ponatinib and its CYP3A4-mediated metabolite, AP24567, were evaluated in a single-center, randomized, two-period, two-sequence crossover study in healthy volunteers.	ponatinib	60-69	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	15-21
23539538-9	2013	The ponatinib+midostaurin combination induced substantial inhibition of KIT-, Lyn-, and STAT5 activity, but did not suppress Btk.	ponatinib	4-13	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	72-75
23539538-9	2013	The ponatinib+midostaurin combination induced substantial inhibition of KIT-, Lyn-, and STAT5 activity, but did not suppress Btk.	ponatinib	4-13	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	78-81
23539538-9	2013	The ponatinib+midostaurin combination induced substantial inhibition of KIT-, Lyn-, and STAT5 activity, but did not suppress Btk.	ponatinib	4-13	signal transducer and activator of transcription 5A	Homo sapiens	88-93
23539538-10	2013	We then applied a Btk short interfering RNA and found that Btk knockdown sensitizes HMC-1 cells against ponatinib.	ponatinib	104-113	Bruton tyrosine kinase	Homo sapiens	18-21
23539538-10	2013	We then applied a Btk short interfering RNA and found that Btk knockdown sensitizes HMC-1 cells against ponatinib.	ponatinib	104-113	Bruton tyrosine kinase	Homo sapiens	59-62
23986642-5	2013	Ponatinib (Iclusig ), an orally available, pan-tyrosine kinase inhibitor has a unique binding mechanism allowing inhibition of BCR-ABL kinases, including those with the T315I point mutation.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
23986642-5	2013	Ponatinib (Iclusig ), an orally available, pan-tyrosine kinase inhibitor has a unique binding mechanism allowing inhibition of BCR-ABL kinases, including those with the T315I point mutation.	ponatinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	127-134
23908597-7	2013	Within the FGFR2(mutant) cell lines, three of seven showed marked resistance to PD173074 and relative resistance to dovitinib and ponatinib.	ponatinib	130-139	fibroblast growth factor receptor 2	Homo sapiens	11-16
23908597-10	2013	Biochemical in vitro kinase analyses also show that ponatinib is more effective than dovitinib at inhibiting FGFR2(N550K).	ponatinib	52-61	fibroblast growth factor receptor 2	Homo sapiens	109-114
23787070-4	2013	Ponatinib (AP24534) an orally active Bcr-Abl Tyrosine Kinase Inhibitor and Bafetinib (INNO-406) have efficacy against various point mutations in the Bcr-Abl kinase.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
23787070-4	2013	Ponatinib (AP24534) an orally active Bcr-Abl Tyrosine Kinase Inhibitor and Bafetinib (INNO-406) have efficacy against various point mutations in the Bcr-Abl kinase.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
23787070-4	2013	Ponatinib (AP24534) an orally active Bcr-Abl Tyrosine Kinase Inhibitor and Bafetinib (INNO-406) have efficacy against various point mutations in the Bcr-Abl kinase.	ponatinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
23787070-4	2013	Ponatinib (AP24534) an orally active Bcr-Abl Tyrosine Kinase Inhibitor and Bafetinib (INNO-406) have efficacy against various point mutations in the Bcr-Abl kinase.	ponatinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	149-156
23684619-0	2013	Efficacy of ponatinib against ABL tyrosine kinase inhibitor-resistant leukemia cells.	ponatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	30-33
23684619-10	2013	This study demonstrates that ponatinib has an anti-leukemia effect by reducing ABL and Lyn kinase activity and this information may be of therapeutic relevance.	ponatinib	29-38	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	79-82
23684619-10	2013	This study demonstrates that ponatinib has an anti-leukemia effect by reducing ABL and Lyn kinase activity and this information may be of therapeutic relevance.	ponatinib	29-38	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	87-90
23576564-5	2013	Among TKIs tested, ponatinib showed the most robust capacity for apoptotic commitment showing sustained suppression of BCR-ABL signaling even at low intracellular levels following extensive washout, consistent with high-affinity binding and slow dissociation from ABL kinase.	ponatinib	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	119-126
23576564-5	2013	Among TKIs tested, ponatinib showed the most robust capacity for apoptotic commitment showing sustained suppression of BCR-ABL signaling even at low intracellular levels following extensive washout, consistent with high-affinity binding and slow dissociation from ABL kinase.	ponatinib	19-28	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	123-126
23372106-2	2013	Five currently available BCR-ABL inhibitors form the mainstay of CML treatment, including first-generation imatinib and more potent second-generation BCR-ABL inhibitors dasatinib and nilotinib, with bosutinib and ponatinib having been recently approved for market inclusion.	ponatinib	213-222	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	25-32
23563700-0	2013	Novel FGFR inhibitor ponatinib suppresses the growth of non-small cell lung cancer cells overexpressing FGFR1.	ponatinib	21-30	fibroblast growth factor receptor 1	Homo sapiens	104-109
23563700-3	2013	The aim of this study was to investigate whether targeting fibroblast growth factor receptor 1 (FGFR1) with ponatinib inhibits the cell growth in both established and primary lung cancer cells overexpressing FGFR1.	ponatinib	108-117	fibroblast growth factor receptor 1	Homo sapiens	59-94
23563700-3	2013	The aim of this study was to investigate whether targeting fibroblast growth factor receptor 1 (FGFR1) with ponatinib inhibits the cell growth in both established and primary lung cancer cells overexpressing FGFR1.	ponatinib	108-117	fibroblast growth factor receptor 1	Homo sapiens	96-101
23563700-5	2013	We identified four cell lines and two newly established primary lung cancer cultures that showed high FGFR1 expression levels, and evaluated the effect of the novel FGFR1 inhibitor ponatinib on cell growth.	ponatinib	181-190	fibroblast growth factor receptor 1	Homo sapiens	165-170
23468082-0	2013	Combined targeting of FGFR2 and mTOR by ponatinib and ridaforolimus results in synergistic antitumor activity in FGFR2 mutant endometrial cancer models.	ponatinib	40-49	fibroblast growth factor receptor 2	Homo sapiens	22-27
23468082-0	2013	Combined targeting of FGFR2 and mTOR by ponatinib and ridaforolimus results in synergistic antitumor activity in FGFR2 mutant endometrial cancer models.	ponatinib	40-49	mechanistic target of rapamycin kinase	Homo sapiens	32-36
23468082-0	2013	Combined targeting of FGFR2 and mTOR by ponatinib and ridaforolimus results in synergistic antitumor activity in FGFR2 mutant endometrial cancer models.	ponatinib	40-49	fibroblast growth factor receptor 2	Homo sapiens	113-118
23468082-4	2013	METHODS: Ponatinib is an oral multitargeted kinase inhibitor that potently inhibits all 4 members of the FGFR family.	ponatinib	9-18	fibroblast growth factor receptor 2	Homo sapiens	105-109
23468082-7	2013	RESULTS: The combination of ponatinib and ridaforolimus had a synergistic effect on the in vitro growth of endometrial lines bearing an activating FGFR2 mutation, irrespective of PTEN status.	ponatinib	28-37	fibroblast growth factor receptor 2	Homo sapiens	147-152
23468082-10	2013	CONCLUSIONS: These encouraging preclinical findings suggest the inhibition of both FGFR2 and mTOR by the ponatinib-ridaforolimus combination may provide a new therapeutic strategy to treat advanced endometrial cancers with dual pathway dysregulation.	ponatinib	105-114	fibroblast growth factor receptor 2	Homo sapiens	83-88
23468082-10	2013	CONCLUSIONS: These encouraging preclinical findings suggest the inhibition of both FGFR2 and mTOR by the ponatinib-ridaforolimus combination may provide a new therapeutic strategy to treat advanced endometrial cancers with dual pathway dysregulation.	ponatinib	105-114	mechanistic target of rapamycin kinase	Homo sapiens	93-97
23430109-5	2013	Substitution of the FLT3 "gatekeeper" phenylalanine with leucine (F691L) conferred mild resistance to ponatinib, but substitutions at the FLT3 activation loop (AL) residue D835 conferred a high degree of resistance.	ponatinib	102-111	fms related receptor tyrosine kinase 3	Homo sapiens	20-24
23908597-0	2013	The N550K/H mutations in FGFR2 confer differential resistance to PD173074, dovitinib, and ponatinib ATP-competitive inhibitors.	ponatinib	90-99	fibroblast growth factor receptor 2	Homo sapiens	25-30
23908597-5	2013	Unlike PD173074, ponatinib effectively inhibited all the dovitinib-resistant FGFR2 mutants except the V565I gatekeeper mutation, suggesting ponatinib but not dovitinib targets the active conformation of FGFR2 kinase.	ponatinib	17-26	fibroblast growth factor receptor 2	Homo sapiens	77-82
23563700-7	2013	Ponatinib treatment of established NSCLC cell lines expressing higher levels of FGFR1 resulted in marked cell growth inhibition and suppression of clonogenicity.	ponatinib	0-9	fibroblast growth factor receptor 1	Homo sapiens	80-85
23563700-11	2013	Our data indicate that pharmacological inhibition of FGFR1 kinase activity with ponatinib may be effective for the treatment of lung cancer patients whose tumors overexpress FGFR1.	ponatinib	80-89	fibroblast growth factor receptor 1	Homo sapiens	53-58
23563700-11	2013	Our data indicate that pharmacological inhibition of FGFR1 kinase activity with ponatinib may be effective for the treatment of lung cancer patients whose tumors overexpress FGFR1.	ponatinib	80-89	fibroblast growth factor receptor 1	Homo sapiens	174-179
23526464-0	2013	Ponatinib (AP24534) is a novel potent inhibitor of oncogenic RET mutants associated with thyroid cancer.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	61-64
23526464-0	2013	Ponatinib (AP24534) is a novel potent inhibitor of oncogenic RET mutants associated with thyroid cancer.	ponatinib	11-18	ret proto-oncogene	Homo sapiens	61-64
23526464-3	2013	OBJECTIVE: We tested whether ponatinib inhibited RET kinase and oncogenic activity.	ponatinib	29-38	ret proto-oncogene	Homo sapiens	49-52
23526464-4	2013	METHODS: Ponatinib activity was studied by an in vitro RET immunocomplex kinase assay and immunoblotting.	ponatinib	9-18	ret proto-oncogene	Homo sapiens	55-58
23526464-7	2013	RESULTS: Ponatinib inhibited immunopurified RET kinase at the IC50 of 25.8 nM (95% confidence interval [CI] = 23.15-28.77 nM).	ponatinib	9-18	ret proto-oncogene	Homo sapiens	44-47
23526464-9	2013	Ponatinib blunted phosphorylation of point-mutant and rearranged RET-derived oncoproteins and inhibited proliferation of RET-transformed fibroblasts and RET mutant thyroid carcinoma cells.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	65-68
23526464-9	2013	Ponatinib blunted phosphorylation of point-mutant and rearranged RET-derived oncoproteins and inhibited proliferation of RET-transformed fibroblasts and RET mutant thyroid carcinoma cells.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	121-124
23526464-9	2013	Ponatinib blunted phosphorylation of point-mutant and rearranged RET-derived oncoproteins and inhibited proliferation of RET-transformed fibroblasts and RET mutant thyroid carcinoma cells.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	121-124
23526464-11	2013	Ponatinib-treated TT cell tumors displayed a reduction in the mitotic index, RET phosphorylation, and signaling.	ponatinib	0-9	ret proto-oncogene	Homo sapiens	77-80
23526464-12	2013	CONCLUSIONS: Ponatinib is a potent inhibitor of RET kinase and has promising preclinical activity in models of RET-driven medullary thyroid carcinoma.	ponatinib	13-22	ret proto-oncogene	Homo sapiens	48-51
23526464-12	2013	CONCLUSIONS: Ponatinib is a potent inhibitor of RET kinase and has promising preclinical activity in models of RET-driven medullary thyroid carcinoma.	ponatinib	13-22	ret proto-oncogene	Homo sapiens	111-114
23430109-0	2013	Activity of ponatinib against clinically-relevant AC220-resistant kinase domain mutants of FLT3-ITD.	ponatinib	12-21	fms related receptor tyrosine kinase 3	Homo sapiens	91-95
23430109-3	2013	Ponatinib has demonstrated early clinical efficacy in chemotherapy-resistant acute myeloid leukemia (AML) patients with internal tandem duplication (ITD) mutations in FLT3.	ponatinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	167-171
23430109-4	2013	We assessed the in vitro activity of ponatinib against clinically relevant FLT3-ITD mutant isoforms that confer resistance to AC220 or sorafenib.	ponatinib	37-46	fms related receptor tyrosine kinase 3	Homo sapiens	75-79
23616953-1	2013	Ponatinib is a novel, next-generation, small-molecule tyrosine kinase inhibitor with potent activity against the BCR-ABL fusion oncogene as well as all other ABL kinase domain mutations that confer resistance to earlier generation tyrosine kinase inhibitors.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	113-120
23319824-0	2013	Combination of ponatinib with Hedgehog antagonist vismodegib for therapy-resistant BCR-ABL1-positive leukemia.	ponatinib	15-24	BCR activator of RhoGEF and GTPase	Mus musculus	83-91
23319824-5	2013	RESULTS: We observed that combination with vismodegib and ponatinib helps to eliminate therapy-resistant NOD/SCID repopulating T315I BCR-ABL1-positive cells.	ponatinib	58-67	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	137-141
23319824-6	2013	The percentage of CD19-positive leukemia cells in peripheral blood was significantly lower in vismodegib + ponatinib-treated mice than that of the vehicle or ponatinib alone (P < 0.001).	ponatinib	107-116	CD19 antigen	Mus musculus	18-22
23223358-2	2013	The third-generation ABL1 TKI ponatinib is effective against BCR-ABL1 point mutants individually, but remains vulnerable to certain BCR-ABL1 compound mutants.	ponatinib	30-39	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
23223358-2	2013	The third-generation ABL1 TKI ponatinib is effective against BCR-ABL1 point mutants individually, but remains vulnerable to certain BCR-ABL1 compound mutants.	ponatinib	30-39	BCR activator of RhoGEF and GTPase	Homo sapiens	61-69
23223358-2	2013	The third-generation ABL1 TKI ponatinib is effective against BCR-ABL1 point mutants individually, but remains vulnerable to certain BCR-ABL1 compound mutants.	ponatinib	30-39	BCR activator of RhoGEF and GTPase	Homo sapiens	132-140
23190395-8	2012	Using 1 as a competitive probe, we determined the extent to which ponatinib, a clinical Bcr-Abl inhibitor, targets Src-family kinases.	ponatinib	66-75	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	88-95
23409026-14	2013	After the recent approval of nilotinib, dasatinib, bosutinib and ponatinib for treatment of chronic myeloid leukemia along with imatinib, all of which vary in their effectiveness against mutated BCR-ABL forms, detection of pre-existing BCR-ABL mutations can help in selection of appropriate first-line drug therapy.	ponatinib	65-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
23409026-14	2013	After the recent approval of nilotinib, dasatinib, bosutinib and ponatinib for treatment of chronic myeloid leukemia along with imatinib, all of which vary in their effectiveness against mutated BCR-ABL forms, detection of pre-existing BCR-ABL mutations can help in selection of appropriate first-line drug therapy.	ponatinib	65-74	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	236-243
23114643-4	2013	Nilotinib, ponatinib and sorafenib strongly suppressed doxorubicin-mediated phosphorylation of JNK and p38 MAPK.	ponatinib	11-20	mitogen-activated protein kinase 8	Mus musculus	95-98
23114643-4	2013	Nilotinib, ponatinib and sorafenib strongly suppressed doxorubicin-mediated phosphorylation of JNK and p38 MAPK.	ponatinib	11-20	mitogen-activated protein kinase 14	Mus musculus	103-111
22875613-0	2013	Ponatinib as targeted therapy for FGFR1 fusions associated with the 8p11 myeloproliferative syndrome.	ponatinib	0-9	fibroblast growth factor receptor 1	Homo sapiens	34-39
22875613-4	2013	Ponatinib-treated Ba/F3 cells transformed by ZMYM2-FGFR1 and BCR-FGFR1 and the FGFR1OP2-FGFR1 positive KG1A cell line showed reduced proliferation and decreased survival when compared to control cells.	ponatinib	0-9	zinc finger, MYM-type 2	Mus musculus	45-50
22875613-4	2013	Ponatinib-treated Ba/F3 cells transformed by ZMYM2-FGFR1 and BCR-FGFR1 and the FGFR1OP2-FGFR1 positive KG1A cell line showed reduced proliferation and decreased survival when compared to control cells.	ponatinib	0-9	fibroblast growth factor receptor 1	Mus musculus	51-56
22875613-4	2013	Ponatinib-treated Ba/F3 cells transformed by ZMYM2-FGFR1 and BCR-FGFR1 and the FGFR1OP2-FGFR1 positive KG1A cell line showed reduced proliferation and decreased survival when compared to control cells.	ponatinib	0-9	BCR activator of RhoGEF and GTPase	Mus musculus	61-70
22875613-4	2013	Ponatinib-treated Ba/F3 cells transformed by ZMYM2-FGFR1 and BCR-FGFR1 and the FGFR1OP2-FGFR1 positive KG1A cell line showed reduced proliferation and decreased survival when compared to control cells.	ponatinib	0-9	FGFR1 oncogene partner 2	Mus musculus	79-87
22875613-4	2013	Ponatinib-treated Ba/F3 cells transformed by ZMYM2-FGFR1 and BCR-FGFR1 and the FGFR1OP2-FGFR1 positive KG1A cell line showed reduced proliferation and decreased survival when compared to control cells.	ponatinib	0-9	fibroblast growth factor receptor 1	Mus musculus	65-70
22875613-7	2013	In one evaluable patient, ponatinib specifically reduced numbers of FGFR1-fusion gene positive colonies.	ponatinib	26-35	fibroblast growth factor receptor 1	Homo sapiens	68-73
22781593-3	2013	Ponatinib (AP24534), which potently inhibits native and mutant BCR-ABL, also targets the FGFR family.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
22781593-3	2013	Ponatinib (AP24534), which potently inhibits native and mutant BCR-ABL, also targets the FGFR family.	ponatinib	0-9	fibroblast growth factor receptor 1	Homo sapiens	89-93
22781593-3	2013	Ponatinib (AP24534), which potently inhibits native and mutant BCR-ABL, also targets the FGFR family.	ponatinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	63-70
22781593-3	2013	Ponatinib (AP24534), which potently inhibits native and mutant BCR-ABL, also targets the FGFR family.	ponatinib	11-18	fibroblast growth factor receptor 1	Homo sapiens	89-93
22781593-4	2013	Using murine BaF3 cells, stably transformed with six different FGFR1 fusion genes, as well as human KG1 cells expressing activated chimeric FGFR1 and five newly established murine SCLL cell lines, we show that ponatinib (<50 nM) can effectively inhibit phosphoactivation of the fusion kinases and their downstream effectors, such as PLCgamma, Stat5 and Src.	ponatinib	210-219	fibroblast growth factor receptor 1	Homo sapiens	140-145
22781593-4	2013	Using murine BaF3 cells, stably transformed with six different FGFR1 fusion genes, as well as human KG1 cells expressing activated chimeric FGFR1 and five newly established murine SCLL cell lines, we show that ponatinib (<50 nM) can effectively inhibit phosphoactivation of the fusion kinases and their downstream effectors, such as PLCgamma, Stat5 and Src.	ponatinib	210-219	signal transducer and activator of transcription 5A	Mus musculus	346-351
22781593-4	2013	Using murine BaF3 cells, stably transformed with six different FGFR1 fusion genes, as well as human KG1 cells expressing activated chimeric FGFR1 and five newly established murine SCLL cell lines, we show that ponatinib (<50 nM) can effectively inhibit phosphoactivation of the fusion kinases and their downstream effectors, such as PLCgamma, Stat5 and Src.	ponatinib	210-219	Rous sarcoma oncogene	Mus musculus	356-359
22781593-7	2013	Furthermore, we demonstrate that ponatinib specifically inhibits cell growth and clonogenicity of normal human CD34+ progenitor cells transformed by chimeric FGFR1 fusion kinases.	ponatinib	33-42	CD34 molecule	Homo sapiens	111-115
22781593-7	2013	Furthermore, we demonstrate that ponatinib specifically inhibits cell growth and clonogenicity of normal human CD34+ progenitor cells transformed by chimeric FGFR1 fusion kinases.	ponatinib	33-42	fibroblast growth factor receptor 1	Homo sapiens	158-163
22781593-8	2013	Overall, our data provide convincing evidence to suggest that pharmacologic inhibition of FGFR1 fusion kinases with ponatinib is likely to be beneficial for patients with SCLL and perhaps for other human disorders associated with dysregulated FGFR1 activity.	ponatinib	116-125	fibroblast growth factor receptor 1	Homo sapiens	90-95
22781593-8	2013	Overall, our data provide convincing evidence to suggest that pharmacologic inhibition of FGFR1 fusion kinases with ponatinib is likely to be beneficial for patients with SCLL and perhaps for other human disorders associated with dysregulated FGFR1 activity.	ponatinib	116-125	fibroblast growth factor receptor 1	Homo sapiens	243-248
23190395-8	2012	Using 1 as a competitive probe, we determined the extent to which ponatinib, a clinical Bcr-Abl inhibitor, targets Src-family kinases.	ponatinib	66-75	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	115-118
23190395-9	2012	Remarkably, while ponatinib had little effect on endogenous Fyn or Src, it potently blocked the critical T-cell kinase, Lck.	ponatinib	18-27	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	120-123
23238683-4	2012	In this line, ponatinib (AP24534) has emerged as a promising therapeutic option in patients with all kinds of BCR-ABL mutations, especially the T315I one.	ponatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	110-117
23238683-7	2012	Our results show that ponatinib is highly effective on both sensitive and resistant CML cell lines, whatever the mode of resistance and also on BaF3 murine B cells carrying native BCR-ABL or T315I mutation.	ponatinib	22-31	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	180-187
23190221-2	2012	Ponatinib (AP24534) is a potent oral tyrosine kinase inhibitor that blocks native and mutated BCR-ABL, including the gatekeeper mutant T315I, which is uniformly resistant to tyrosine kinase inhibitors.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
23044928-5	2012	Furthermore, the activity profile of ponatinib and DCC-2036 against a panel of 24 clinically relevant BCR/ABL mutants is presented and compared to the other TKIs.	ponatinib	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	102-109
23190221-2	2012	Ponatinib (AP24534) is a potent oral tyrosine kinase inhibitor that blocks native and mutated BCR-ABL, including the gatekeeper mutant T315I, which is uniformly resistant to tyrosine kinase inhibitors.	ponatinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-101
23190221-14	2012	CONCLUSIONS: Ponatinib was highly active in heavily pretreated patients with Ph-positive leukemias with resistance to tyrosine kinase inhibitors, including patients with the BCR-ABL T315I mutation, other mutations, or no mutations.	ponatinib	13-22	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	174-181
22301675-0	2012	Ponatinib is active against imatinib-resistant mutants of FIP1L1-PDGFRA and KIT, and against FGFR1-derived fusion kinases.	ponatinib	0-9	factor interacting with PAPOLA and CPSF1	Homo sapiens	58-64
23187745-7	2012	The third-generation TKI ponatinib is a BCR-ABL inhibitor that has demonstrated significant activity, including in patients with the TKI resistance mutation T315I.	ponatinib	25-34	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	40-47
22532521-0	2012	Platelet dysfunction associated with ponatinib, a new pan BCR-ABL inhibitor with efficacy for chronic myeloid leukemia resistant to multiple tyrosine kinase inhibitor therapy.	ponatinib	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
22778153-6	2012	The ponatinib IC(50) values of BCR-ABL-expressing K562 cells transfected with ABCB1 and ABCG2 were approximately the same as and 2-fold higher than that of K562, respectively, consistent with ponatinib being a substrate of both proteins, but inhibiting its own transport, and resistance was also attenuated to a small degree by ponatinib-induced downregulation of ABCB1 and ABCG2 cell-surface expression on resistant K562 cells.	ponatinib	4-13	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	88-93
22778153-6	2012	The ponatinib IC(50) values of BCR-ABL-expressing K562 cells transfected with ABCB1 and ABCG2 were approximately the same as and 2-fold higher than that of K562, respectively, consistent with ponatinib being a substrate of both proteins, but inhibiting its own transport, and resistance was also attenuated to a small degree by ponatinib-induced downregulation of ABCB1 and ABCG2 cell-surface expression on resistant K562 cells.	ponatinib	192-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
22778153-6	2012	The ponatinib IC(50) values of BCR-ABL-expressing K562 cells transfected with ABCB1 and ABCG2 were approximately the same as and 2-fold higher than that of K562, respectively, consistent with ponatinib being a substrate of both proteins, but inhibiting its own transport, and resistance was also attenuated to a small degree by ponatinib-induced downregulation of ABCB1 and ABCG2 cell-surface expression on resistant K562 cells.	ponatinib	192-201	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
22778153-7	2012	Ponatinib at pharmacologically relevant concentrations produced synergistic cytotoxicity with ABCB1 and ABCG2 substrate chemotherapy drugs and enhanced apoptosis induced by these drugs, including daunorubicin, mitoxantrone, topotecan, and flavopiridol, in cells overexpressing these transport proteins.	ponatinib	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	94-99
22778153-7	2012	Ponatinib at pharmacologically relevant concentrations produced synergistic cytotoxicity with ABCB1 and ABCG2 substrate chemotherapy drugs and enhanced apoptosis induced by these drugs, including daunorubicin, mitoxantrone, topotecan, and flavopiridol, in cells overexpressing these transport proteins.	ponatinib	0-9	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	104-109
22778153-0	2012	The novel BCR-ABL and FLT3 inhibitor ponatinib is a potent inhibitor of the MDR-associated ATP-binding cassette transporter ABCG2.	ponatinib	37-46	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	10-17
22778153-0	2012	The novel BCR-ABL and FLT3 inhibitor ponatinib is a potent inhibitor of the MDR-associated ATP-binding cassette transporter ABCG2.	ponatinib	37-46	fms related receptor tyrosine kinase 3	Homo sapiens	22-26
22778153-0	2012	The novel BCR-ABL and FLT3 inhibitor ponatinib is a potent inhibitor of the MDR-associated ATP-binding cassette transporter ABCG2.	ponatinib	37-46	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	124-129
22778153-1	2012	Ponatinib is a novel tyrosine kinase inhibitor with potent activity against BCR-ABL with mutations, including T315I, and also against fms-like tyrosine kinase 3.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	76-83
22778153-1	2012	Ponatinib is a novel tyrosine kinase inhibitor with potent activity against BCR-ABL with mutations, including T315I, and also against fms-like tyrosine kinase 3.	ponatinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	134-160
22778153-2	2012	We tested interactions between ponatinib at pharmacologically relevant concentrations of 50 to 200 nmol/L and the MDR-associated ATP-binding cassette (ABC) proteins ABCB1, ABCC1, and ABCG2.	ponatinib	31-40	ATP binding cassette subfamily B member 1	Homo sapiens	165-170
22778153-2	2012	We tested interactions between ponatinib at pharmacologically relevant concentrations of 50 to 200 nmol/L and the MDR-associated ATP-binding cassette (ABC) proteins ABCB1, ABCC1, and ABCG2.	ponatinib	31-40	ATP binding cassette subfamily C member 1	Homo sapiens	172-177
22778153-3	2012	Ponatinib enhanced uptake of substrates of ABCG2 and ABCB1, but not ABCC1, in cells overexpressing these proteins, with a greater effect on ABCG2 than on ABCB1.	ponatinib	0-9	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	43-48
22778153-3	2012	Ponatinib enhanced uptake of substrates of ABCG2 and ABCB1, but not ABCC1, in cells overexpressing these proteins, with a greater effect on ABCG2 than on ABCB1.	ponatinib	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	53-58
22778153-3	2012	Ponatinib enhanced uptake of substrates of ABCG2 and ABCB1, but not ABCC1, in cells overexpressing these proteins, with a greater effect on ABCG2 than on ABCB1.	ponatinib	0-9	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	140-145
22778153-3	2012	Ponatinib enhanced uptake of substrates of ABCG2 and ABCB1, but not ABCC1, in cells overexpressing these proteins, with a greater effect on ABCG2 than on ABCB1.	ponatinib	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	154-159
22778153-4	2012	Ponatinib potently inhibited [(125)I]-IAAP binding to ABCG2 and ABCB1, indicating binding to their drug substrate sites, with IC(50) values of 0.04 and 0.63 mumol/L, respectively.	ponatinib	0-9	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	54-59
22778153-4	2012	Ponatinib potently inhibited [(125)I]-IAAP binding to ABCG2 and ABCB1, indicating binding to their drug substrate sites, with IC(50) values of 0.04 and 0.63 mumol/L, respectively.	ponatinib	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	64-69
22778153-5	2012	Ponatinib stimulated ABCG2 ATPase activity in a concentration-dependent manner and stimulated ABCB1 ATPase activity at low concentrations, consistent with it being a substrate of both proteins at pharmacologically relevant concentrations.	ponatinib	0-9	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	21-26
22778153-5	2012	Ponatinib stimulated ABCG2 ATPase activity in a concentration-dependent manner and stimulated ABCB1 ATPase activity at low concentrations, consistent with it being a substrate of both proteins at pharmacologically relevant concentrations.	ponatinib	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	94-99
22778153-6	2012	The ponatinib IC(50) values of BCR-ABL-expressing K562 cells transfected with ABCB1 and ABCG2 were approximately the same as and 2-fold higher than that of K562, respectively, consistent with ponatinib being a substrate of both proteins, but inhibiting its own transport, and resistance was also attenuated to a small degree by ponatinib-induced downregulation of ABCB1 and ABCG2 cell-surface expression on resistant K562 cells.	ponatinib	4-13	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	31-38
22778153-6	2012	The ponatinib IC(50) values of BCR-ABL-expressing K562 cells transfected with ABCB1 and ABCG2 were approximately the same as and 2-fold higher than that of K562, respectively, consistent with ponatinib being a substrate of both proteins, but inhibiting its own transport, and resistance was also attenuated to a small degree by ponatinib-induced downregulation of ABCB1 and ABCG2 cell-surface expression on resistant K562 cells.	ponatinib	4-13	ATP binding cassette subfamily B member 1	Homo sapiens	78-83
22301675-0	2012	Ponatinib is active against imatinib-resistant mutants of FIP1L1-PDGFRA and KIT, and against FGFR1-derived fusion kinases.	ponatinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	65-71
22301675-0	2012	Ponatinib is active against imatinib-resistant mutants of FIP1L1-PDGFRA and KIT, and against FGFR1-derived fusion kinases.	ponatinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	76-79
22301675-0	2012	Ponatinib is active against imatinib-resistant mutants of FIP1L1-PDGFRA and KIT, and against FGFR1-derived fusion kinases.	ponatinib	0-9	fibroblast growth factor receptor 1	Homo sapiens	93-98
22238366-2	2012	Ponatinib (AP24534) is an oral multitargeted tyrosine kinase inhibitor being explored in a pivotal phase II trial in patients with chronic myelogenous leukemia due to its potent activity against BCR-ABL.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
22519766-6	2012	Ponatinib, a pan BCR-ABL TKI, while still under investigation, is very hopeful with its ability to overcome T315I mutations in resistant CML and Ph + ALL patients.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	17-24
22409268-0	2012	Ponatinib may overcome resistance of FLT3-ITD harbouring additional point mutations, notably the previously refractory F691I mutation.	ponatinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	37-41
22409268-4	2012	We investigated the cellular effects of the recently characterised FLT3-TKI ponatinib (AP24534) on murine myeloid cells transfected with FLT3-ITD with or without additional point mutations of the FLT3-TKD including the (so far) multi-resistant F691I mutation.	ponatinib	76-85	FMS-like tyrosine kinase 3	Mus musculus	67-71
22409268-4	2012	We investigated the cellular effects of the recently characterised FLT3-TKI ponatinib (AP24534) on murine myeloid cells transfected with FLT3-ITD with or without additional point mutations of the FLT3-TKD including the (so far) multi-resistant F691I mutation.	ponatinib	76-85	FMS-like tyrosine kinase 3	Mus musculus	137-141
22409268-4	2012	We investigated the cellular effects of the recently characterised FLT3-TKI ponatinib (AP24534) on murine myeloid cells transfected with FLT3-ITD with or without additional point mutations of the FLT3-TKD including the (so far) multi-resistant F691I mutation.	ponatinib	76-85	FMS-like tyrosine kinase 3	Mus musculus	137-141
22409268-5	2012	Ponatinib effectively induced apoptosis not only in the parental FLT3-ITD cell line but also in all stably transfected subclones harbouring additional FLT3-TKD point mutations (N676D, F691I or G697R).	ponatinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	65-69
22409268-5	2012	Ponatinib effectively induced apoptosis not only in the parental FLT3-ITD cell line but also in all stably transfected subclones harbouring additional FLT3-TKD point mutations (N676D, F691I or G697R).	ponatinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	151-155
22409268-6	2012	These observations correlated with a strong inhibition of FLT3-ITD and its downstream targets STAT5, AKT and ERK1/2 upon ponatinib incubation, as determined by Western blotting.	ponatinib	121-130	fms related receptor tyrosine kinase 3	Homo sapiens	58-62
22409268-6	2012	These observations correlated with a strong inhibition of FLT3-ITD and its downstream targets STAT5, AKT and ERK1/2 upon ponatinib incubation, as determined by Western blotting.	ponatinib	121-130	signal transducer and activator of transcription 5A	Homo sapiens	94-99
22409268-6	2012	These observations correlated with a strong inhibition of FLT3-ITD and its downstream targets STAT5, AKT and ERK1/2 upon ponatinib incubation, as determined by Western blotting.	ponatinib	121-130	AKT serine/threonine kinase 1	Homo sapiens	101-104
22409268-6	2012	These observations correlated with a strong inhibition of FLT3-ITD and its downstream targets STAT5, AKT and ERK1/2 upon ponatinib incubation, as determined by Western blotting.	ponatinib	121-130	mitogen-activated protein kinase 3	Homo sapiens	109-115
22409268-7	2012	We conclude that ponatinib represents a promising FLT3-TKI that should be further investigated in clinical trials.	ponatinib	17-26	fms related receptor tyrosine kinase 3	Homo sapiens	50-54
22409268-8	2012	The targeted therapy of FLT3-ITD-positive AML with ponatinib might be associated with a lower frequency of secondary resistance caused by acquired FLT3-TKD mutations.	ponatinib	51-60	fms related receptor tyrosine kinase 3	Homo sapiens	24-28
22409268-8	2012	The targeted therapy of FLT3-ITD-positive AML with ponatinib might be associated with a lower frequency of secondary resistance caused by acquired FLT3-TKD mutations.	ponatinib	51-60	fms related receptor tyrosine kinase 3	Homo sapiens	147-151
22503441-3	2012	Here we review structure-based approaches underlying the development of several molecules that are currently in clinical trials, including the cMet inhibitor ARQ197 and the Bcr-Abl inhibitor ponatinib.	ponatinib	191-200	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	173-180
22238366-2	2012	Ponatinib (AP24534) is an oral multitargeted tyrosine kinase inhibitor being explored in a pivotal phase II trial in patients with chronic myelogenous leukemia due to its potent activity against BCR-ABL.	ponatinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	195-202
22238366-4	2012	In Ba/F3 cells engineered to express activated FGFR1-4, ponatinib potently inhibited FGFR-mediated signaling and viability with IC(50) values <40 nmol/L, with substantial selectivity over parental Ba/F3 cells.	ponatinib	56-65	fibroblast growth factor receptor 1	Mus musculus	47-54
22238366-7	2012	Importantly, the potency of ponatinib in these models is similar to that previously observed in BCR-ABL-driven models and plasma levels of ponatinib that exceed the IC(50) values for FGFR1-4 inhibition can be sustained in patients.	ponatinib	139-148	fibroblast growth factor receptor 1	Homo sapiens	183-188
22956142-5	2012	Using Imatinib and BCR/ABL as a paradigm for a drug-target pair, we reported a retroviral vector-based screening strategy to identify the spectrum of resistance-conferring mutations, which has helped in designing the next-generation BCR/ABL inhibitors such as Nilotinib, Dasatinib, and Ponatinib.	ponatinib	286-295	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	19-26
22956142-5	2012	Using Imatinib and BCR/ABL as a paradigm for a drug-target pair, we reported a retroviral vector-based screening strategy to identify the spectrum of resistance-conferring mutations, which has helped in designing the next-generation BCR/ABL inhibitors such as Nilotinib, Dasatinib, and Ponatinib.	ponatinib	286-295	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	233-240
34614211-8	2022	The estimated 5-year survival rate for patients with Philadelphia chromosome-positive acute lymphoblastic leukemia (ALL) exceeds 70% with intensive chemotherapy and ponatinib, a third-generation BCR-ABL1 TKI, and more recent nonchemotherapy regimens using dasatinib or ponatinib with blinatumomab are producing outstanding results.	ponatinib	165-174	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	199-203
21482694-0	2011	Potent activity of ponatinib (AP24534) in models of FLT3-driven acute myeloid leukemia and other hematologic malignancies.	ponatinib	19-28	fms related receptor tyrosine kinase 3	Homo sapiens	52-56
21482694-1	2011	Ponatinib (AP24534) is a novel multitargeted kinase inhibitor that potently inhibits native and mutant BCR-ABL at clinically achievable drug levels.	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
21482694-1	2011	Ponatinib (AP24534) is a novel multitargeted kinase inhibitor that potently inhibits native and mutant BCR-ABL at clinically achievable drug levels.	ponatinib	11-18	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-110
21482694-2	2011	Ponatinib also has in vitro inhibitory activity against a discrete set of kinases implicated in the pathogenesis of other hematologic malignancies, including FLT3, KIT, fibroblast growth factor receptor 1 (FGFR1), and platelet derived growth factor receptor alpha (PDGFRalpha).	ponatinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	158-162
21482694-2	2011	Ponatinib also has in vitro inhibitory activity against a discrete set of kinases implicated in the pathogenesis of other hematologic malignancies, including FLT3, KIT, fibroblast growth factor receptor 1 (FGFR1), and platelet derived growth factor receptor alpha (PDGFRalpha).	ponatinib	0-9	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	164-167
21482694-2	2011	Ponatinib also has in vitro inhibitory activity against a discrete set of kinases implicated in the pathogenesis of other hematologic malignancies, including FLT3, KIT, fibroblast growth factor receptor 1 (FGFR1), and platelet derived growth factor receptor alpha (PDGFRalpha).	ponatinib	0-9	fibroblast growth factor receptor 1	Homo sapiens	169-204
21482694-2	2011	Ponatinib also has in vitro inhibitory activity against a discrete set of kinases implicated in the pathogenesis of other hematologic malignancies, including FLT3, KIT, fibroblast growth factor receptor 1 (FGFR1), and platelet derived growth factor receptor alpha (PDGFRalpha).	ponatinib	0-9	fibroblast growth factor receptor 1	Homo sapiens	206-211
21482694-2	2011	Ponatinib also has in vitro inhibitory activity against a discrete set of kinases implicated in the pathogenesis of other hematologic malignancies, including FLT3, KIT, fibroblast growth factor receptor 1 (FGFR1), and platelet derived growth factor receptor alpha (PDGFRalpha).	ponatinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	218-263
21482694-2	2011	Ponatinib also has in vitro inhibitory activity against a discrete set of kinases implicated in the pathogenesis of other hematologic malignancies, including FLT3, KIT, fibroblast growth factor receptor 1 (FGFR1), and platelet derived growth factor receptor alpha (PDGFRalpha).	ponatinib	0-9	platelet derived growth factor receptor alpha	Homo sapiens	265-275
21482694-4	2011	The activity of ponatinib against the FLT3-ITD mutant, found in up to 30% of acute myeloid leukemia (AML) patients, was particularly notable.	ponatinib	16-25	fms related receptor tyrosine kinase 3	Homo sapiens	38-42
21482694-5	2011	In MV4-11 (FLT3-ITD(+/+)) but not RS4;11 (FLT3-ITD(-/-)) AML cells, ponatinib inhibited FLT3 signaling and induced apoptosis at concentrations of less than 10 nmol/L.	ponatinib	68-77	fms related receptor tyrosine kinase 3	Homo sapiens	11-15
21482694-7	2011	Ponatinib inhibited viability of primary leukemic blasts from a FLT3-ITD positive AML patient (IC50 4 nmol/L) but not those isolated from 3 patients with AML expressing native FLT3.	ponatinib	0-9	fms related receptor tyrosine kinase 3	Homo sapiens	64-68
21482694-8	2011	Overall, these results support the investigation of ponatinib in patients with FLT3-ITD-driven AML and other hematologic malignancies driven by KIT, FGFR1, or PDGFRalpha.	ponatinib	52-61	fms related receptor tyrosine kinase 3	Homo sapiens	79-83
21482694-8	2011	Overall, these results support the investigation of ponatinib in patients with FLT3-ITD-driven AML and other hematologic malignancies driven by KIT, FGFR1, or PDGFRalpha.	ponatinib	52-61	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	144-147
21482694-8	2011	Overall, these results support the investigation of ponatinib in patients with FLT3-ITD-driven AML and other hematologic malignancies driven by KIT, FGFR1, or PDGFRalpha.	ponatinib	52-61	fibroblast growth factor receptor 1	Homo sapiens	149-154
21482694-8	2011	Overall, these results support the investigation of ponatinib in patients with FLT3-ITD-driven AML and other hematologic malignancies driven by KIT, FGFR1, or PDGFRalpha.	ponatinib	52-61	platelet derived growth factor receptor alpha	Homo sapiens	159-169
21098337-5	2011	The leading third-generation clinical candidate for treatment-refractory CML, including patients with the T315I mutation, is ponatinib (AP24534), a pan-BCR-ABL inhibitor that has entered pivotal phase 2 testing.	ponatinib	125-134	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	152-159
19878872-3	2009	We report design and preclinical evaluation of AP24534, a potent, orally available multitargeted kinase inhibitor active against T315I and other BCR-ABL mutants.	ponatinib	47-54	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
19878872-5	2009	Our work supports clinical evaluation of AP24534 as a pan-BCR-ABL inhibitor for treatment of CML.	ponatinib	41-48	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
33774681-0	2021	The role of ponatinib in adult BCR-ABL1 positive acute lymphoblastic leukemia after allogeneic transplantation: a real-life retrospective multicenter study.	ponatinib	12-21	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	35-39
22157290-8	2011	Ponatinib represents the last generation of TKI, and this drug has been developed with the aim of targeting a specific BCR-ABL1 mutation (T315I), which arises in the setting of prolonged TKI therapy and leads to resistance to all commercially available TKI.	ponatinib	0-9	BCR activator of RhoGEF and GTPase	Homo sapiens	119-127
21700550-6	2011	The first evaluations of AP24534 present this drug as a potent multi-targeted kinase inhibitor active against T315I and all other BCR-ABL mutants.	ponatinib	25-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	130-137
34837846-9	2022	MEK inhibitor showed synergy with multikinase inhibitor ponatinib, ABL inhibitor nilotinib, PI3K/mTOR inhibitor pictilisib, and pan-RAF inhibitor LY3009120.	ponatinib	56-65	mitogen-activated protein kinase kinase 7	Homo sapiens	0-3
34959482-5	2021	The first, second, and third generation inhibitors (imatinib, dasatinib, nilotinib, bosutinib, and ponatinib) of BCR-ABL1 and the allosteric inhibitor asciminib showed deep genetic and molecular remission rates in CML, leading to the evaluation of treatment discontinuation in prospective trials.	ponatinib	99-108	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-121
34699866-6	2021	Mechanistically, the ponatinib/gossypol combination significantly increased apoptotic markers p53, Bax, and caspase-9 while decreasing anti-apoptotic marker Bcl-2.	ponatinib	21-30	transformation related protein 53, pseudogene	Mus musculus	94-97
34850536-3	2022	Cell-based screening of FGFR inhibitors with potential for clinical repurposing (NVP-BGJ398, nintedanib, dovitinib and ponatinib) revealed greater sensitivity of fusion-gene-positive versus -negative rhabdomyosarcoma cell lines and was shown to be correlated with high expression of FGFR2 and its specific ligand, FGF7.	ponatinib	119-128	fibroblast growth factor receptor 2	Homo sapiens	283-288
34850536-3	2022	Cell-based screening of FGFR inhibitors with potential for clinical repurposing (NVP-BGJ398, nintedanib, dovitinib and ponatinib) revealed greater sensitivity of fusion-gene-positive versus -negative rhabdomyosarcoma cell lines and was shown to be correlated with high expression of FGFR2 and its specific ligand, FGF7.	ponatinib	119-128	fibroblast growth factor 7	Homo sapiens	314-318
34842047-0	2021	STAT5 inhibitor Pimozide as a probable therapeutic option in overcoming Ponatinib resistance in K562 leukemic cells.	ponatinib	72-81	signal transducer and activator of transcription 5A	Homo sapiens	0-5
34842047-5	2021	Combination therapy of Pimozide and Ponatinib demonstrated that STAT5 was a significant protein for regaining chemosensitivity to Ponatinib when its expression was suppressed both at mRNA and protein level.	ponatinib	36-45	signal transducer and activator of transcription 5A	Homo sapiens	64-69
34842047-5	2021	Combination therapy of Pimozide and Ponatinib demonstrated that STAT5 was a significant protein for regaining chemosensitivity to Ponatinib when its expression was suppressed both at mRNA and protein level.	ponatinib	130-139	signal transducer and activator of transcription 5A	Homo sapiens	64-69
34843980-0	2022	Sodium-glucose cotransporter type 2 inhibitors prevent ponatinib-induced endothelial senescence and disfunction: A potential rescue strategy.	ponatinib	55-64	solute carrier family 5 member 2	Homo sapiens	0-35
34885009-0	2021	Receptor-Tyrosine Kinase Inhibitor Ponatinib Inhibits Meningioma Growth In Vitro and In Vivo.	ponatinib	35-44	TYRO3 protein tyrosine kinase 3	Mus musculus	0-24
34984405-0	2022	Phase 1 Clinical Trial of Trametinib and Ponatinib in Patients With NSCLC Harboring KRAS Mutations.	ponatinib	41-50	KRAS proto-oncogene, GTPase	Homo sapiens	84-88
34984405-3	2022	Compensatory activation of FGFR1 was identified as a mechanism of trametinib resistance in KRAS-mutant NSCLC, and combination therapy with trametinib and ponatinib was synergistic in in vitro and in vivo models.	ponatinib	154-163	fibroblast growth factor receptor 1	Homo sapiens	27-32
34984405-5	2022	Methods: A phase 1 dose escalation study of trametinib and ponatinib was conducted in patients with advanced NSCLC with KRAS mutations.	ponatinib	59-68	KRAS proto-oncogene, GTPase	Homo sapiens	120-124
34699069-1	2022	The BCR-ABL1 inhibitor ponatinib is approved for the treatment of adults with chronic myeloid leukemia or Philadelphia chromosome-positive acute lymphoblastic leukemia, including those with the T315I mutation.	ponatinib	23-32	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	8-12
34461124-0	2021	PI3K/mTOR dual-inhibition with VS-5584 enhances anti-leukemic efficacy of ponatinib in blasts and Ph-negative LSCs of chronic myeloid leukemia.	ponatinib	74-83	mechanistic target of rapamycin kinase	Homo sapiens	5-9
34461124-2	2021	We evaluated the potential of ponatinib and PI3K/mTOR dual-inhibitor VS-5584 combination (PoVS) therapy to increase the anti-leukemic effects of ponatinib and investigated the underlying mechanisms at the molecular level.	ponatinib	145-154	mechanistic target of rapamycin kinase	Homo sapiens	49-53
34699866-6	2021	Mechanistically, the ponatinib/gossypol combination significantly increased apoptotic markers p53, Bax, and caspase-9 while decreasing anti-apoptotic marker Bcl-2.	ponatinib	21-30	BCL2-associated X protein	Mus musculus	99-102
34699866-6	2021	Mechanistically, the ponatinib/gossypol combination significantly increased apoptotic markers p53, Bax, and caspase-9 while decreasing anti-apoptotic marker Bcl-2.	ponatinib	21-30	caspase 9	Mus musculus	108-117
34699866-6	2021	Mechanistically, the ponatinib/gossypol combination significantly increased apoptotic markers p53, Bax, and caspase-9 while decreasing anti-apoptotic marker Bcl-2.	ponatinib	21-30	B cell leukemia/lymphoma 2	Mus musculus	157-162
34102636-0	2021	Durable Molecular Remission in an Elderly Patient Affected by Relapsed Ph'+ Acute Lymphoblastic Leukemia with T315I and Concomitant p190 and p210 Expression Achieved by Inotuzumab and Ponatinib.	ponatinib	189-198	contactin associated protein 1	Homo sapiens	137-141
34403880-1	2021	Tyrosine kinase inhibitors (TKIs) such as imatinib, nilotinib, dasatinib, and ponatinib have significantly improved the life expectancy of Philadelphia chromosome-positive (Ph+) acute lymphocytic leukemia (ALL) patients; however, resistance to TKIs remains a major clinical challenge.	ponatinib	78-87	phenylalanine hydroxylase	Homo sapiens	173-175
34117218-5	2021	Apoptosis of IM-resistant Ph+ALL cells with T315I mutation of BCR-ABL was also upregulated by LEN in the presence of the newly developed TKI ponatinib.	ponatinib	141-150	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	62-69
34593434-5	2021	In addition, upon glycoprotein VI (GPVI) receptor activation, a significantly lower percentage of PAC1 binding platelets (p<=0.05) was observed at 1,000 nM final concentration of ponatinib.	ponatinib	179-188	dual specificity phosphatase 2	Homo sapiens	98-102
34196168-0	2021	Therapeutic potential of ruxolitinib and ponatinib in patients with EPOR-rearranged Philadelphia chromosome-like acute lymphoblastic leukemia.	ponatinib	41-50	erythropoietin receptor	Homo sapiens	68-72
34659899-0	2021	Asciminib and ponatinib exert synergistic anti-neoplastic effects on CML cells expressing BCR-ABL1 T315I-compound mutations.	ponatinib	14-23	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	94-98
34659899-1	2021	Ponatinib is a tyrosine kinase inhibitor (TKI) directed against BCR-ABL1 which is successfully used in patients with BCR-ABL1 T315I+ chronic myeloid leukemia (CML).	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	68-72
34659899-1	2021	Ponatinib is a tyrosine kinase inhibitor (TKI) directed against BCR-ABL1 which is successfully used in patients with BCR-ABL1 T315I+ chronic myeloid leukemia (CML).	ponatinib	0-9	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-125
34659899-4	2021	We demonstrate that asciminib synergizes with ponatinib in inducing growth-arrest and apoptosis in patient-derived CML cell lines and murine Ba/F3 cells harboring BCR-ABL1 T315I or T315I-including compound mutations.	ponatinib	46-55	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	167-171
34659899-5	2021	Asciminib and ponatinib also produced cooperative effects on CRKL phosphorylation in BCR-ABL1-transformed cells.	ponatinib	14-23	CRK like proto-oncogene, adaptor protein	Homo sapiens	61-65
34659899-5	2021	Asciminib and ponatinib also produced cooperative effects on CRKL phosphorylation in BCR-ABL1-transformed cells.	ponatinib	14-23	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	89-93
34659899-6	2021	The growth-inhibitory effects of the drug combination "asciminib+ponatinib" was further enhanced by hydroxyurea (HU), a drug which has lately been described to suppresses the proliferation of BCR-ABL1 T315I+ CML cells.	ponatinib	65-74	c-abl oncogene 1, non-receptor tyrosine kinase	Mus musculus	196-200
34659899-8	2021	Most importantly, we were able to show that the combinations "asciminib+ponatinib" and "asciminib+ponatinib+HU" produce synergistic apoptosis-inducing effects in CD34+/CD38- CML stem cells obtained from patients with chronic phase CML or BCR-ABL1 T315I+ CML blast phase.	ponatinib	72-81	CD34 molecule	Homo sapiens	162-166
34659899-8	2021	Most importantly, we were able to show that the combinations "asciminib+ponatinib" and "asciminib+ponatinib+HU" produce synergistic apoptosis-inducing effects in CD34+/CD38- CML stem cells obtained from patients with chronic phase CML or BCR-ABL1 T315I+ CML blast phase.	ponatinib	72-81	CD38 molecule	Homo sapiens	168-172
34659899-8	2021	Most importantly, we were able to show that the combinations "asciminib+ponatinib" and "asciminib+ponatinib+HU" produce synergistic apoptosis-inducing effects in CD34+/CD38- CML stem cells obtained from patients with chronic phase CML or BCR-ABL1 T315I+ CML blast phase.	ponatinib	72-81	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	242-246
34659899-8	2021	Most importantly, we were able to show that the combinations "asciminib+ponatinib" and "asciminib+ponatinib+HU" produce synergistic apoptosis-inducing effects in CD34+/CD38- CML stem cells obtained from patients with chronic phase CML or BCR-ABL1 T315I+ CML blast phase.	ponatinib	98-107	CD34 molecule	Homo sapiens	162-166
34659899-8	2021	Most importantly, we were able to show that the combinations "asciminib+ponatinib" and "asciminib+ponatinib+HU" produce synergistic apoptosis-inducing effects in CD34+/CD38- CML stem cells obtained from patients with chronic phase CML or BCR-ABL1 T315I+ CML blast phase.	ponatinib	98-107	CD38 molecule	Homo sapiens	168-172
34659899-9	2021	Together, asciminib, ponatinib and HU synergize in producing anti-leukemic effects in multi-resistant CML cells, including cells harboring T315I+ BCR-ABL1 compound mutations and CML stem cells.	ponatinib	21-30	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	150-154
34276365-7	2021	Moreover, employing immortalized cell lines and primary CD34-positive progenitors, we demonstrate that these modifications lead to reduced BCR-ABL1 sensitivity to imatinib, dasatinib and ponatinib but not nilotinib.	ponatinib	187-196	CD34 molecule	Homo sapiens	56-60
34276365-7	2021	Moreover, employing immortalized cell lines and primary CD34-positive progenitors, we demonstrate that these modifications lead to reduced BCR-ABL1 sensitivity to imatinib, dasatinib and ponatinib but not nilotinib.	ponatinib	187-196	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	143-147
34071707-0	2021	Connexin 43 and Connexin 26 Involvement in the Ponatinib-Induced Cardiomyopathy: Sex-Related Differences in a Murine Model.	ponatinib	47-56	gap junction protein, alpha 1	Mus musculus	0-11
34071707-0	2021	Connexin 43 and Connexin 26 Involvement in the Ponatinib-Induced Cardiomyopathy: Sex-Related Differences in a Murine Model.	ponatinib	47-56	gap junction protein, beta 2	Mus musculus	16-27
34071707-4	2021	Altered connexin expression and localization have been described in diseased myocardium and the aim of this study is to assess the involvement of Cx43, Cx26, and some related molecules in ponatinib-induced cardiac toxicity.	ponatinib	188-197	gap junction protein, alpha 3	Mus musculus	146-150
34071707-4	2021	Altered connexin expression and localization have been described in diseased myocardium and the aim of this study is to assess the involvement of Cx43, Cx26, and some related molecules in ponatinib-induced cardiac toxicity.	ponatinib	188-197	gap junction protein, beta 2	Mus musculus	152-156
34071707-8	2021	The altered cardiac function and the change in Cxs expression observed in mice after ponatinib treatment, were results dependent on the Notch1 pathway and sex.	ponatinib	85-94	notch 1	Mus musculus	136-142
34071707-10	2021	The downmodulation of cardiac Cx43, Cx26 and miR-122, high pS368-Cx43 phosphorylation, cell viability and survival activation could represent some of the female adaptative/compensatory reactions to ponatinib cardiotoxicity.	ponatinib	198-207	gap junction protein, alpha 3	Mus musculus	30-34
34071707-10	2021	The downmodulation of cardiac Cx43, Cx26 and miR-122, high pS368-Cx43 phosphorylation, cell viability and survival activation could represent some of the female adaptative/compensatory reactions to ponatinib cardiotoxicity.	ponatinib	198-207	gap junction protein, beta 2	Mus musculus	36-40
34071707-10	2021	The downmodulation of cardiac Cx43, Cx26 and miR-122, high pS368-Cx43 phosphorylation, cell viability and survival activation could represent some of the female adaptative/compensatory reactions to ponatinib cardiotoxicity.	ponatinib	198-207	microRNA 122	Mus musculus	45-52
34071707-10	2021	The downmodulation of cardiac Cx43, Cx26 and miR-122, high pS368-Cx43 phosphorylation, cell viability and survival activation could represent some of the female adaptative/compensatory reactions to ponatinib cardiotoxicity.	ponatinib	198-207	gap junction protein, alpha 3	Mus musculus	65-69
35551463-2	2022	The approval of BCR::ABL1 tyrosine kinase inhibitors (TKI) such as imatinib, dasatinib, nilotinib and ponatinib marked a milestone in targeted therapy only for a subset of patients carrying the translocation t(9;22)(q34;q11).	ponatinib	102-111	BCR activator of RhoGEF and GTPase	Homo sapiens	16-19
35551463-2	2022	The approval of BCR::ABL1 tyrosine kinase inhibitors (TKI) such as imatinib, dasatinib, nilotinib and ponatinib marked a milestone in targeted therapy only for a subset of patients carrying the translocation t(9;22)(q34;q11).	ponatinib	102-111	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	21-25
35544670-6	2022	EXPERT OPINION: Ponatinib is a potent pan-BCR-ABL1 TKI with substantial activity in patients with more resistant or advanced CML.	ponatinib	16-25	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	46-50
35603651-0	2022	(Ponatinib inhibits the proliferation of SNU-449 human hepatocellular cancer cells and blocks MAPK and PDK1/AKT/mTOR signaling pathways).	ponatinib	1-10	pyruvate dehydrogenase kinase 1	Homo sapiens	103-107
35603651-0	2022	(Ponatinib inhibits the proliferation of SNU-449 human hepatocellular cancer cells and blocks MAPK and PDK1/AKT/mTOR signaling pathways).	ponatinib	1-10	AKT serine/threonine kinase 1	Homo sapiens	108-111
35603651-0	2022	(Ponatinib inhibits the proliferation of SNU-449 human hepatocellular cancer cells and blocks MAPK and PDK1/AKT/mTOR signaling pathways).	ponatinib	1-10	mechanistic target of rapamycin kinase	Homo sapiens	112-116
35603651-11	2022	A number of kinase signaling pathways were inhibited by ponatinib, including the Src signaling pathway, MAPK pathway and PDK1/AKT/mTOR pathway.	ponatinib	56-65	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	81-84
35603651-11	2022	A number of kinase signaling pathways were inhibited by ponatinib, including the Src signaling pathway, MAPK pathway and PDK1/AKT/mTOR pathway.	ponatinib	56-65	pyruvate dehydrogenase kinase 1	Homo sapiens	121-125
35603651-11	2022	A number of kinase signaling pathways were inhibited by ponatinib, including the Src signaling pathway, MAPK pathway and PDK1/AKT/mTOR pathway.	ponatinib	56-65	AKT serine/threonine kinase 1	Homo sapiens	126-129
35603651-11	2022	A number of kinase signaling pathways were inhibited by ponatinib, including the Src signaling pathway, MAPK pathway and PDK1/AKT/mTOR pathway.	ponatinib	56-65	mechanistic target of rapamycin kinase	Homo sapiens	130-134
35603651-12	2022	Conclusion Ponatinib can inhibit the proliferation, promote the apoptosis and cell cycle arrest of hepatocellular cancer cells and block MAPK and PDK1/AKT/mTOR signaling pathways, which might be a potential agent for liver cancer treatment.	ponatinib	11-20	pyruvate dehydrogenase kinase 1	Homo sapiens	146-150
35603651-12	2022	Conclusion Ponatinib can inhibit the proliferation, promote the apoptosis and cell cycle arrest of hepatocellular cancer cells and block MAPK and PDK1/AKT/mTOR signaling pathways, which might be a potential agent for liver cancer treatment.	ponatinib	11-20	AKT serine/threonine kinase 1	Homo sapiens	151-154
35603651-12	2022	Conclusion Ponatinib can inhibit the proliferation, promote the apoptosis and cell cycle arrest of hepatocellular cancer cells and block MAPK and PDK1/AKT/mTOR signaling pathways, which might be a potential agent for liver cancer treatment.	ponatinib	11-20	mechanistic target of rapamycin kinase	Homo sapiens	155-159
35172577-2	2022	Here, we report the design of unique hybrid molecules by combining the two pharmacophores of clinically approved BCR-ABL inhibitor (ponatinib) and HDAC inhibitor (vorinostat) and results of in vitro studies in drug-resistant CML cells.	ponatinib	132-141	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	117-120
34939982-4	2022	The downstream molecules of cyclin B1 and D1 were significantly increased in ponatinib-treated melanocytes.	ponatinib	77-86	cyclin B1	Homo sapiens	28-44
35057108-2	2022	Targeted therapies based on tyrosine kinase inhibitors (TKIs), such as imatinib, dasatinib, nilotinib, bosutinib, and ponatinib, have revolutionized the treatment of BCR-ABL1-driven leukemia, particularly chronic myeloid leukemia (CML).	ponatinib	118-127	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	170-174
35412404-2	2022	AREAS COVERED: In this review, the authors discuss the role of ponatinib, an oral pan-inhibitor of BCR-ABL1, with potent activity in heavily pretreated patients, including T315I mutation.	ponatinib	63-72	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	103-107
35091442-16	2022	CONCLUSION: Ponatinib demonstrated activity in advanced GIST, particularly in KIT ex11-positive disease.	ponatinib	12-21	KIT proto-oncogene, receptor tyrosine kinase	Homo sapiens	78-81
35207746-12	2022	We also used NCC-PMP1-C1 cells to screen drugs, which demonstrated a significant response to daunorubicin HCl, homoharringtonine, mitomycin C, and ponatinib.	ponatinib	147-156	peroxisomal biogenesis factor 19	Homo sapiens	17-21
35091541-0	2022	Venetoclax-ponatinib for T315I/compound-mutated Ph+ acute lymphoblastic leukemia.	ponatinib	11-20	phenylalanine hydroxylase	Homo sapiens	48-50