PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
34740946-0	2022	Ixazomib induces apoptosis and suppresses proliferation in esophageal squamous cell carcinoma through activation of the c-Myc/NOXA pathway.	ixazomib	0-8	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	120-125
34740946-0	2022	Ixazomib induces apoptosis and suppresses proliferation in esophageal squamous cell carcinoma through activation of the c-Myc/NOXA pathway.	ixazomib	0-8	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	126-130
34740946-6	2022	RT-PCR results showed that the expression of endoplasmic reticulum stress-related gene NOXA and c-Myc significant increase after treatment with ixazomib in ESCC cell.	ixazomib	144-152	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	87-91
34740946-6	2022	RT-PCR results showed that the expression of endoplasmic reticulum stress-related gene NOXA and c-Myc significant increase after treatment with ixazomib in ESCC cell.	ixazomib	144-152	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	96-101
34740946-7	2022	Then we knockdown the NOXA and c-Myc by siRNA, the therapeutic effect of ixazomib markedly decrease, which confirmed that c-Myc/NOXA pathway played a key role in the treatment of ESCC with ixazomib.	ixazomib	73-81	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	22-26
34740946-7	2022	Then we knockdown the NOXA and c-Myc by siRNA, the therapeutic effect of ixazomib markedly decrease, which confirmed that c-Myc/NOXA pathway played a key role in the treatment of ESCC with ixazomib.	ixazomib	73-81	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	31-36
34740946-7	2022	Then we knockdown the NOXA and c-Myc by siRNA, the therapeutic effect of ixazomib markedly decrease, which confirmed that c-Myc/NOXA pathway played a key role in the treatment of ESCC with ixazomib.	ixazomib	73-81	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	122-127
34740946-7	2022	Then we knockdown the NOXA and c-Myc by siRNA, the therapeutic effect of ixazomib markedly decrease, which confirmed that c-Myc/NOXA pathway played a key role in the treatment of ESCC with ixazomib.	ixazomib	73-81	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	128-132
34740946-7	2022	Then we knockdown the NOXA and c-Myc by siRNA, the therapeutic effect of ixazomib markedly decrease, which confirmed that c-Myc/NOXA pathway played a key role in the treatment of ESCC with ixazomib.	ixazomib	189-197	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	22-26
34740946-7	2022	Then we knockdown the NOXA and c-Myc by siRNA, the therapeutic effect of ixazomib markedly decrease, which confirmed that c-Myc/NOXA pathway played a key role in the treatment of ESCC with ixazomib.	ixazomib	189-197	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	31-36
34740946-7	2022	Then we knockdown the NOXA and c-Myc by siRNA, the therapeutic effect of ixazomib markedly decrease, which confirmed that c-Myc/NOXA pathway played a key role in the treatment of ESCC with ixazomib.	ixazomib	189-197	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	122-127
34740946-7	2022	Then we knockdown the NOXA and c-Myc by siRNA, the therapeutic effect of ixazomib markedly decrease, which confirmed that c-Myc/NOXA pathway played a key role in the treatment of ESCC with ixazomib.	ixazomib	189-197	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	128-132
34740946-10	2022	These results suggested that ixazomib is known to suppress proliferation and induce apoptosis in an ESCC cell lines, and this effect was likely mediated by increased activation of the c-Myc/NOXA signaling pathways.	ixazomib	29-37	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	184-189
34740946-10	2022	These results suggested that ixazomib is known to suppress proliferation and induce apoptosis in an ESCC cell lines, and this effect was likely mediated by increased activation of the c-Myc/NOXA signaling pathways.	ixazomib	29-37	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	190-194
34378191-11	2021	FCE showed significant synergistic activity in vitro and in vivo with ixazomib.	ixazomib	70-78	ferrochelatase	Homo sapiens	0-3
34485305-10	2021	Furthermore, integrated analysis of S100 gene expression and ex vivo drug sensitivity data showed significant negative correlation between expression of S100 family members (S100A8, S100A9, and S100A12) and sensitivity to some drugs used in current MM treatment, including proteasome inhibitors (bortezomib, carfilzomib, and ixazomib) and histone deacetylase inhibitor panobinostat.	ixazomib	325-333	S100 calcium binding protein A1	Homo sapiens	36-40
34485305-10	2021	Furthermore, integrated analysis of S100 gene expression and ex vivo drug sensitivity data showed significant negative correlation between expression of S100 family members (S100A8, S100A9, and S100A12) and sensitivity to some drugs used in current MM treatment, including proteasome inhibitors (bortezomib, carfilzomib, and ixazomib) and histone deacetylase inhibitor panobinostat.	ixazomib	325-333	S100 calcium binding protein A8	Homo sapiens	174-180
34485305-10	2021	Furthermore, integrated analysis of S100 gene expression and ex vivo drug sensitivity data showed significant negative correlation between expression of S100 family members (S100A8, S100A9, and S100A12) and sensitivity to some drugs used in current MM treatment, including proteasome inhibitors (bortezomib, carfilzomib, and ixazomib) and histone deacetylase inhibitor panobinostat.	ixazomib	325-333	S100 calcium binding protein A9	Homo sapiens	182-188
34485305-10	2021	Furthermore, integrated analysis of S100 gene expression and ex vivo drug sensitivity data showed significant negative correlation between expression of S100 family members (S100A8, S100A9, and S100A12) and sensitivity to some drugs used in current MM treatment, including proteasome inhibitors (bortezomib, carfilzomib, and ixazomib) and histone deacetylase inhibitor panobinostat.	ixazomib	325-333	S100 calcium binding protein A12	Homo sapiens	194-201
35485606-4	2022	The expression of autophagy proteins (LC3A/B and Beclin-1) and UPS protein (ubiquitin) in MDA-MB-231 and MCF-7 cells following doxorubicin, ixazomib, and/or hydroxychloroquine were determined by western blot.	ixazomib	140-148	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	38-44
35485606-6	2022	Doxorubicin and ixazomib cotreatment increased Beclin-1 (3.8- and 3.5-fold) and LC3-II expression (13.5- and 1.9-fold) in MDA-MB-231 and MCF-7 cells, respectively.	ixazomib	16-24	beclin 1	Homo sapiens	47-55
33647537-0	2021	Ixazomib inhibits myeloma cell proliferation by targeting UBE2K.	ixazomib	0-8	ubiquitin conjugating enzyme E2 K	Homo sapiens	58-63
33647537-3	2021	The purpose of this study was to investigate the relationship between ixazomib and UBE2K in myeloma cells.	ixazomib	70-78	ubiquitin conjugating enzyme E2 K	Homo sapiens	83-88
33647537-6	2021	Furthermore, the regulatory effects of ixazomib on UBE2K and its downstream targets were investigated following the overexpression of UBE2K.	ixazomib	39-47	ubiquitin conjugating enzyme E2 K	Homo sapiens	51-56
33647537-8	2021	Ixazomib significantly increased the expression of HIST1H2BD, MNAT1, NEK3, and TARS2, while decreasing the expression of HSPA1B and UBE2K.	ixazomib	0-8	H2B clustered histone 5	Homo sapiens	51-60
33647537-8	2021	Ixazomib significantly increased the expression of HIST1H2BD, MNAT1, NEK3, and TARS2, while decreasing the expression of HSPA1B and UBE2K.	ixazomib	0-8	MNAT1 component of CDK activating kinase	Homo sapiens	62-67
33647537-8	2021	Ixazomib significantly increased the expression of HIST1H2BD, MNAT1, NEK3, and TARS2, while decreasing the expression of HSPA1B and UBE2K.	ixazomib	0-8	NIMA related kinase 3	Homo sapiens	69-73
33647537-8	2021	Ixazomib significantly increased the expression of HIST1H2BD, MNAT1, NEK3, and TARS2, while decreasing the expression of HSPA1B and UBE2K.	ixazomib	0-8	threonyl-tRNA synthetase 2, mitochondrial	Homo sapiens	79-84
33647537-8	2021	Ixazomib significantly increased the expression of HIST1H2BD, MNAT1, NEK3, and TARS2, while decreasing the expression of HSPA1B and UBE2K.	ixazomib	0-8	heat shock protein family A (Hsp70) member 1B	Homo sapiens	121-127
33647537-8	2021	Ixazomib significantly increased the expression of HIST1H2BD, MNAT1, NEK3, and TARS2, while decreasing the expression of HSPA1B and UBE2K.	ixazomib	0-8	ubiquitin conjugating enzyme E2 K	Homo sapiens	132-137
33647537-9	2021	In addition, ixazomib inhibited the proliferation of myeloma cells, blocked cell cycle, induced cell apoptosis, and increased the production of reactive oxygen species by inhibiting UBE2K expression.	ixazomib	13-21	ubiquitin conjugating enzyme E2 K	Homo sapiens	182-187
33647537-10	2021	Lastly, ixazomib regulates mitosis- and apoptosis-related genes by lowering UBE2K expression.	ixazomib	8-16	ubiquitin conjugating enzyme E2 K	Homo sapiens	76-81
33647537-11	2021	CONCLUSION: In summary, ixazomib leads to impaired proliferation of myeloma cells by targeting UBE2K.	ixazomib	24-32	ubiquitin conjugating enzyme E2 K	Homo sapiens	95-100
33310890-7	2021	In subcutaneous tumor models, combination of ixazomib and alectinib prominently induced tumor regression and apoptosis even though the tumors were generated from ALK-rearranged NSCLC cells with non-functional p53.	ixazomib	45-53	ALK receptor tyrosine kinase	Homo sapiens	162-165
33310890-7	2021	In subcutaneous tumor models, combination of ixazomib and alectinib prominently induced tumor regression and apoptosis even though the tumors were generated from ALK-rearranged NSCLC cells with non-functional p53.	ixazomib	45-53	tumor protein p53	Homo sapiens	209-212
33641211-5	2021	METHODS: This is a single-center phase Ib study with a 3+3 design of fulvestrant and the proteasome inhibitor ixazomib (MLN9708) in patients with advanced ER+ breast cancer that was progressing on fulvestrant.	ixazomib	110-118	estrogen receptor 1	Homo sapiens	155-157
33670955-0	2021	Oral Proteasomal Inhibitors Ixazomib, Oprozomib, and Delanzomib Upregulate the Function of Organic Anion Transporter 3 (OAT3): Implications in OAT3-Mediated Drug-Drug Interactions.	ixazomib	28-36	solute carrier family 22 member 8	Homo sapiens	91-118
33670955-0	2021	Oral Proteasomal Inhibitors Ixazomib, Oprozomib, and Delanzomib Upregulate the Function of Organic Anion Transporter 3 (OAT3): Implications in OAT3-Mediated Drug-Drug Interactions.	ixazomib	28-36	solute carrier family 22 member 8	Homo sapiens	120-124
33670955-0	2021	Oral Proteasomal Inhibitors Ixazomib, Oprozomib, and Delanzomib Upregulate the Function of Organic Anion Transporter 3 (OAT3): Implications in OAT3-Mediated Drug-Drug Interactions.	ixazomib	28-36	solute carrier family 22 member 8	Homo sapiens	143-147
33670955-4	2021	Therefore, this study investigated the effects of ixazomib, oprozomib, and delanzomib on the expression and transport activity of OAT3 and elucidated the underlying mechanisms.	ixazomib	50-58	solute carrier family 22 member 8	Homo sapiens	130-134
33670955-7	2021	Together, our study discovered a novel role of anticancer agents ixazomib, oprozomib, and delanzomib in upregulating OAT3 function, unveiled the proteasome as a promising target for OAT3 regulation, and provided implication of OAT3-mediated drug-drug interactions, which should be warned against during combination therapies with proteasome inhibitor drugs.	ixazomib	65-73	solute carrier family 22 member 8	Homo sapiens	117-121
33670955-7	2021	Together, our study discovered a novel role of anticancer agents ixazomib, oprozomib, and delanzomib in upregulating OAT3 function, unveiled the proteasome as a promising target for OAT3 regulation, and provided implication of OAT3-mediated drug-drug interactions, which should be warned against during combination therapies with proteasome inhibitor drugs.	ixazomib	65-73	solute carrier family 22 member 8	Homo sapiens	182-186
33670955-7	2021	Together, our study discovered a novel role of anticancer agents ixazomib, oprozomib, and delanzomib in upregulating OAT3 function, unveiled the proteasome as a promising target for OAT3 regulation, and provided implication of OAT3-mediated drug-drug interactions, which should be warned against during combination therapies with proteasome inhibitor drugs.	ixazomib	65-73	solute carrier family 22 member 8	Homo sapiens	182-186
32607595-6	2021	Similar results were obtained with next-generation proteasome inhibitors ixazomib and carfilzomib, indicating that induction of HSF2 expression is a general response to proteasome dysfunction.	ixazomib	73-81	heat shock transcription factor 2	Homo sapiens	128-132
33296126-0	2021	Ixazomib, an oral proteasome inhibitor, exhibits potential effect in dystrophin-deficient mdx mice.	ixazomib	0-8	dystrophin, muscular dystrophy	Mus musculus	69-79
33296126-12	2021	There was an increase in the expression of dystrophin and utrophin in the TA and DIA muscles and a reduction in the expression of osteopontin and TGF-beta in the DIA muscle of mdx mice treated with ixazomib.	ixazomib	198-206	dystrophin, muscular dystrophy	Mus musculus	43-53
33296126-12	2021	There was an increase in the expression of dystrophin and utrophin in the TA and DIA muscles and a reduction in the expression of osteopontin and TGF-beta in the DIA muscle of mdx mice treated with ixazomib.	ixazomib	198-206	utrophin	Mus musculus	58-66
33296126-12	2021	There was an increase in the expression of dystrophin and utrophin in the TA and DIA muscles and a reduction in the expression of osteopontin and TGF-beta in the DIA muscle of mdx mice treated with ixazomib.	ixazomib	198-206	secreted phosphoprotein 1	Mus musculus	130-141
33296126-12	2021	There was an increase in the expression of dystrophin and utrophin in the TA and DIA muscles and a reduction in the expression of osteopontin and TGF-beta in the DIA muscle of mdx mice treated with ixazomib.	ixazomib	198-206	transforming growth factor alpha	Mus musculus	146-154
33296126-13	2021	Ixazomib was thus shown to increase the expression of dystrophin and utrophin associated with improved pathological and functional changes in the dystrophic muscles of mdx mice.	ixazomib	0-8	dystrophin, muscular dystrophy	Mus musculus	54-64
33296126-13	2021	Ixazomib was thus shown to increase the expression of dystrophin and utrophin associated with improved pathological and functional changes in the dystrophic muscles of mdx mice.	ixazomib	0-8	utrophin	Mus musculus	69-77
33406639-0	2021	Activation of Serum/Glucocorticoid Regulated Kinase 1/Nuclear Factor-kappaB Pathway Are Correlated with Low Sensitivity to Bortezomib and Ixazomib in Resistant Multiple Myeloma Cells.	ixazomib	138-146	serum/glucocorticoid regulated kinase 1	Homo sapiens	14-53
33406639-7	2021	The SGK1 inhibitor enhances the cytotoxic effects of bortezomib and ixazomib; however, FGFR1 and CCR2 inhibitors do not show such effect in KMS-20 cells.	ixazomib	68-76	serum/glucocorticoid regulated kinase 1	Homo sapiens	4-8
33406639-8	2021	Moreover, SGK1 activation induces the phosphorylation of NF-kappaB p65, and an NF-kappaB inhibitor enhances the sensitivity of KMS-20 cells to bortezomib and ixazomib.	ixazomib	158-166	serum/glucocorticoid regulated kinase 1	Homo sapiens	10-14
33406639-8	2021	Moreover, SGK1 activation induces the phosphorylation of NF-kappaB p65, and an NF-kappaB inhibitor enhances the sensitivity of KMS-20 cells to bortezomib and ixazomib.	ixazomib	158-166	nuclear factor kappa B subunit 1	Homo sapiens	57-66
33406639-10	2021	These results indicate that the activation of the SGK1/NF-kappaB pathway correlates with a low sensitivity to bortezomib and ixazomib, and a combination of bortezomib and ixazomib with an SGK1 or NF-kappaB inhibitor may be involved in the treatment of MM via activation of the SGK1/NF-kappaB pathway.	ixazomib	125-133	serum/glucocorticoid regulated kinase 1	Homo sapiens	50-54
33406639-10	2021	These results indicate that the activation of the SGK1/NF-kappaB pathway correlates with a low sensitivity to bortezomib and ixazomib, and a combination of bortezomib and ixazomib with an SGK1 or NF-kappaB inhibitor may be involved in the treatment of MM via activation of the SGK1/NF-kappaB pathway.	ixazomib	125-133	nuclear factor kappa B subunit 1	Homo sapiens	55-64
33406639-10	2021	These results indicate that the activation of the SGK1/NF-kappaB pathway correlates with a low sensitivity to bortezomib and ixazomib, and a combination of bortezomib and ixazomib with an SGK1 or NF-kappaB inhibitor may be involved in the treatment of MM via activation of the SGK1/NF-kappaB pathway.	ixazomib	171-179	serum/glucocorticoid regulated kinase 1	Homo sapiens	50-54
33406639-10	2021	These results indicate that the activation of the SGK1/NF-kappaB pathway correlates with a low sensitivity to bortezomib and ixazomib, and a combination of bortezomib and ixazomib with an SGK1 or NF-kappaB inhibitor may be involved in the treatment of MM via activation of the SGK1/NF-kappaB pathway.	ixazomib	171-179	nuclear factor kappa B subunit 1	Homo sapiens	55-64
33406639-10	2021	These results indicate that the activation of the SGK1/NF-kappaB pathway correlates with a low sensitivity to bortezomib and ixazomib, and a combination of bortezomib and ixazomib with an SGK1 or NF-kappaB inhibitor may be involved in the treatment of MM via activation of the SGK1/NF-kappaB pathway.	ixazomib	171-179	serum/glucocorticoid regulated kinase 1	Homo sapiens	188-192
33406639-10	2021	These results indicate that the activation of the SGK1/NF-kappaB pathway correlates with a low sensitivity to bortezomib and ixazomib, and a combination of bortezomib and ixazomib with an SGK1 or NF-kappaB inhibitor may be involved in the treatment of MM via activation of the SGK1/NF-kappaB pathway.	ixazomib	171-179	nuclear factor kappa B subunit 1	Homo sapiens	196-205
33406639-10	2021	These results indicate that the activation of the SGK1/NF-kappaB pathway correlates with a low sensitivity to bortezomib and ixazomib, and a combination of bortezomib and ixazomib with an SGK1 or NF-kappaB inhibitor may be involved in the treatment of MM via activation of the SGK1/NF-kappaB pathway.	ixazomib	171-179	serum/glucocorticoid regulated kinase 1	Homo sapiens	188-192
33406639-10	2021	These results indicate that the activation of the SGK1/NF-kappaB pathway correlates with a low sensitivity to bortezomib and ixazomib, and a combination of bortezomib and ixazomib with an SGK1 or NF-kappaB inhibitor may be involved in the treatment of MM via activation of the SGK1/NF-kappaB pathway.	ixazomib	171-179	nuclear factor kappa B subunit 1	Homo sapiens	196-205
32931083-3	2020	Here, we report that the proteasome inhibitors bortezomib and ixazomib markedly increased protein levels of the osteoblastic key transcription factor osterix/Sp7 (Osx).	ixazomib	62-70	Sp7 transcription factor	Homo sapiens	150-161
32931083-3	2020	Here, we report that the proteasome inhibitors bortezomib and ixazomib markedly increased protein levels of the osteoblastic key transcription factor osterix/Sp7 (Osx).	ixazomib	62-70	Sp7 transcription factor	Homo sapiens	163-166
32653622-12	2020	B-cell activating factor (BAFF) plasma levels were significantly higher after ixazomib dosing in those who remained cGVHD-free compared to those developed cGVHD.	ixazomib	78-86	TNF superfamily member 13b	Homo sapiens	0-24
32653622-12	2020	B-cell activating factor (BAFF) plasma levels were significantly higher after ixazomib dosing in those who remained cGVHD-free compared to those developed cGVHD.	ixazomib	78-86	TNF superfamily member 13b	Homo sapiens	26-30
32350909-0	2020	Clinical benefit of ixazomib plus lenalidomide-dexamethasone in myeloma patients with non-canonical NF-kappaB pathway activation.	ixazomib	20-28	nuclear factor kappa B subunit 1	Homo sapiens	100-109
32350909-6	2020	CONCLUSIONS: Adding ixazomib to Rd provides clinical benefit in MM tumors with increased non-canonical NF-kappaB pathway activity.	ixazomib	20-28	nuclear factor kappa B subunit 1	Homo sapiens	103-112
32453773-6	2020	We have previously shown that ixazomib (IXA), a proteasome inhibitor used for treating multiple myeloma, effectively reduced the size of the infarct produced by global ischemia in isolated rat hearts and prevented degradation of the sarcoplasmic reticulum calcium release channel RyR2.	ixazomib	30-38	ryanodine receptor 2	Rattus norvegicus	280-284
32019102-0	2020	Ixazomib Improves Bone Remodeling and Counteracts sonic Hedgehog signaling Inhibition Mediated by Myeloma Cells.	ixazomib	0-8	sonic hedgehog signaling molecule	Homo sapiens	50-64
32019102-7	2020	Given the key role of Sonic Hedgehog (SHH) signaling in bone homeostasis, we further investigated Ixazomib-induced SHH pathway activation.	ixazomib	98-106	sonic hedgehog signaling molecule	Homo sapiens	115-118
32019102-8	2020	This set of experiments showed that Ixazomib, but not Bortezomib, was able to bind the Smoothened (SMO) receptor leading to nuclear translocation of GLI1 in human MSCs.	ixazomib	36-44	GLI family zinc finger 1	Homo sapiens	149-153
32019102-10	2020	In conclusion, our data demonstrated that Ixazomib regulates bone remodeling by decreasing osteoclastogenesis and prompting osteoblast differentiation via the canonical SHH signaling pathway activation, thus, representing a promising therapeutic option to improve the complex pathological condition of MM patients.	ixazomib	42-50	sonic hedgehog signaling molecule	Homo sapiens	169-172
31452195-0	2020	Combinatorial ixazomib and belinostat therapy induces NFE2L2-dependent apoptosis in Hodgkin and T-cell lymphoma.	ixazomib	14-22	NFE2 like bZIP transcription factor 2	Homo sapiens	54-60
31452195-3	2020	In ixazomib-treated TCL and HL cells, transient inhibition followed by full recovery of proteasomal activity observed was accompanied by induction of proteasomal gene expression with NFE2L2 (also termed NRF2) as a prominent upstream regulator.	ixazomib	3-11	NFE2 like bZIP transcription factor 2	Homo sapiens	183-189
31452195-3	2020	In ixazomib-treated TCL and HL cells, transient inhibition followed by full recovery of proteasomal activity observed was accompanied by induction of proteasomal gene expression with NFE2L2 (also termed NRF2) as a prominent upstream regulator.	ixazomib	3-11	NFE2 like bZIP transcription factor 2	Homo sapiens	203-207
31452195-5	2020	In addition, CRISPR/Cas9 mediated knockdown of NFE2L2 in Jurkat cells resulted in a significant decrease in cell viability with ixazomib compared with untreated control cells.	ixazomib	128-136	NFE2 like bZIP transcription factor 2	Homo sapiens	47-53
31452195-6	2020	Using transcriptomic and proteasomal activity evaluation of ixazomib, belinostat, or ixazomib + belinostat treated cells, we observed that NFE2L2, proteasome gene expression and functional recovery were abrogated by ixazomib + belinostat combination, resulting in synergistic drug activity in ixazomib-sensitive and -resistant cell lines and primary cells.	ixazomib	60-68	NFE2 like bZIP transcription factor 2	Homo sapiens	139-145
31452195-6	2020	Using transcriptomic and proteasomal activity evaluation of ixazomib, belinostat, or ixazomib + belinostat treated cells, we observed that NFE2L2, proteasome gene expression and functional recovery were abrogated by ixazomib + belinostat combination, resulting in synergistic drug activity in ixazomib-sensitive and -resistant cell lines and primary cells.	ixazomib	85-93	NFE2 like bZIP transcription factor 2	Homo sapiens	139-145
31452195-6	2020	Using transcriptomic and proteasomal activity evaluation of ixazomib, belinostat, or ixazomib + belinostat treated cells, we observed that NFE2L2, proteasome gene expression and functional recovery were abrogated by ixazomib + belinostat combination, resulting in synergistic drug activity in ixazomib-sensitive and -resistant cell lines and primary cells.	ixazomib	85-93	NFE2 like bZIP transcription factor 2	Homo sapiens	139-145
31452195-6	2020	Using transcriptomic and proteasomal activity evaluation of ixazomib, belinostat, or ixazomib + belinostat treated cells, we observed that NFE2L2, proteasome gene expression and functional recovery were abrogated by ixazomib + belinostat combination, resulting in synergistic drug activity in ixazomib-sensitive and -resistant cell lines and primary cells.	ixazomib	85-93	NFE2 like bZIP transcription factor 2	Homo sapiens	139-145
31452195-7	2020	Altogether, these results suggest that the synergistic activity of ixazomib + belinostat is mediated via inhibition NFE2L2-dependent proteasomal recovery and extended proteasomal inhibition culminating in increased cell death.	ixazomib	67-75	NFE2 like bZIP transcription factor 2	Homo sapiens	116-122
31540997-5	2019	Herein we show that bortezomib and next-generation proteasome inhibitors ixazomib and carfilzomib markedly induce AIRAP expression in human melanoma at concentrations comparable to plasma-levels in treated patients.	ixazomib	73-81	zinc finger AN1-type containing 2A	Homo sapiens	114-119
31273172-9	2019	Patients with an estimated glomerular filtration rate of less than 50mL/min/1.73m2 received a lower cumulative dose of ixazomib and lenalidomide than those with other rates.	ixazomib	119-127	CD59 molecule (CD59 blood group)	Homo sapiens	72-77
30487243-9	2019	Mechanistically, ixazomib treatment resulted in the accumulation of polyubiquitinated proteins, including phosphorylated IkappaBalpha with a significant reduction of p65 subunit nuclear translocation.	ixazomib	17-25	NFKB inhibitor alpha	Homo sapiens	121-133
30487243-9	2019	Mechanistically, ixazomib treatment resulted in the accumulation of polyubiquitinated proteins, including phosphorylated IkappaBalpha with a significant reduction of p65 subunit nuclear translocation.	ixazomib	17-25	RELA proto-oncogene, NF-kB subunit	Homo sapiens	166-169
30487243-11	2019	IMPLICATIONS: This preclinical study supports the use of oral proteasome inhibitor ixazomib for targeting NF-kappaB signaling in the treatment of EBV-associated B-cell neoplasms.Visual Overview: http://mcr.aacrjournals.org/content/molcanres/17/4/839/F1.large.jpg.	ixazomib	83-91	nuclear factor kappa B subunit 1	Homo sapiens	106-115
30902965-8	2019	MLN9708, a proteasome inhibitor, potently induced autophagy via the induction of MAP1LC3B and sensitized the cell to autophagy-mediated cell death in VHL-deficient and VHL-mutant (L101A) cells.	ixazomib	0-7	microtubule-associated protein 1 light chain 3 beta	Mus musculus	81-89
30359552-0	2019	Ixazomib promotes CHOP-dependent DR5 induction and apoptosis in colorectal cancer cells.	ixazomib	0-8	DNA damage inducible transcript 3	Homo sapiens	18-22
30359552-0	2019	Ixazomib promotes CHOP-dependent DR5 induction and apoptosis in colorectal cancer cells.	ixazomib	0-8	TNF receptor superfamily member 10b	Homo sapiens	33-36
30359552-4	2019	Western blotting and real-time RT-PCR were performed to detect ixazomib-induced DR5 upregulation.	ixazomib	63-71	TNF receptor superfamily member 10b	Homo sapiens	80-83
30359552-8	2019	Our findings indicated that ixazomib treatment induces CHOP-dependent DR5 induction, irrespective of p53 status.	ixazomib	28-36	DNA damage inducible transcript 3	Homo sapiens	55-59
30359552-8	2019	Our findings indicated that ixazomib treatment induces CHOP-dependent DR5 induction, irrespective of p53 status.	ixazomib	28-36	TNF receptor superfamily member 10b	Homo sapiens	70-73
30359552-9	2019	Furthermore, DR5 is necessary for ixazomib-mediated apoptosis.	ixazomib	34-42	TNF receptor superfamily member 10b	Homo sapiens	13-16
30359552-10	2019	Ixazomib also synergized with TRAIL to induce marked apoptosis via DR5 in CRC cells.	ixazomib	0-8	TNF receptor superfamily member 10b	Homo sapiens	67-70
30359552-11	2019	CONCLUSIONS: Our findings further suggested that ixazomib sensitizes TRAIL/death receptor signaling pathway-targeted CRC and suggested that DR5 induction could be a valuable indicator of ixazomib sensitivity.	ixazomib	49-57	TNF superfamily member 10	Homo sapiens	69-74
30359552-11	2019	CONCLUSIONS: Our findings further suggested that ixazomib sensitizes TRAIL/death receptor signaling pathway-targeted CRC and suggested that DR5 induction could be a valuable indicator of ixazomib sensitivity.	ixazomib	187-195	TNF receptor superfamily member 10b	Homo sapiens	140-143
30089730-9	2018	Finally, we performed proof-of-principle experiments using a currently approved proteasome inhibitor, ixazomib, to target FOXM1 and demonstrated a therapeutic response in AML patient samples and animal models of AML that correlates with the suppression of FOXM1 and its transcriptional targets.	ixazomib	102-110	forkhead box M1	Homo sapiens	122-127
30089730-9	2018	Finally, we performed proof-of-principle experiments using a currently approved proteasome inhibitor, ixazomib, to target FOXM1 and demonstrated a therapeutic response in AML patient samples and animal models of AML that correlates with the suppression of FOXM1 and its transcriptional targets.	ixazomib	102-110	forkhead box M1	Homo sapiens	256-261
29699990-12	2018	Finally, a potential therapeutic application of proteasome inhibitors (bortezomib and ixazomib), which are known to inhibit NF-kappaB, was identified through their ability to decrease proliferation and increase apoptosis in LGL leukemia cell lines and primary patient cells.	ixazomib	86-94	nuclear factor kappa B subunit 1	Homo sapiens	124-133
29643240-6	2018	Ixazomib, a proteasome inhibitor in clinical use, blocks this pathway, increasing the abundance of Casp8p41 and causing more cells to die in a Casp8p41-dependent manner.IMPORTANCE The Casp8p41 pathway of cell death is unique to HIV-infected cells yet is blocked by Bcl2.	ixazomib	0-8	caspase 8	Homo sapiens	99-105
29643240-6	2018	Ixazomib, a proteasome inhibitor in clinical use, blocks this pathway, increasing the abundance of Casp8p41 and causing more cells to die in a Casp8p41-dependent manner.IMPORTANCE The Casp8p41 pathway of cell death is unique to HIV-infected cells yet is blocked by Bcl2.	ixazomib	0-8	BCL2 apoptosis regulator	Homo sapiens	265-269
28800141-0	2018	Effects of Strong CYP3A Inhibition and Induction on the Pharmacokinetics of Ixazomib, an Oral Proteasome Inhibitor: Results of Drug-Drug Interaction Studies in Patients With Advanced Solid Tumors or Lymphoma and a Physiologically Based Pharmacokinetic Analysis.	ixazomib	76-84	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	18-23
28800141-2	2018	However, at higher than clinical concentrations, ixazomib was metabolized by multiple CYP isoforms, with the estimated relative contribution being highest for CYP3A at 42%.	ixazomib	49-57	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	159-164
28800141-9	2018	The clinical drug-drug interaction study results were reconciled well by a physiologically based pharmacokinetic model that incorporated a minor contribution of CYP3A to overall ixazomib clearance and quantitatively considered the strength of induction of CYP3A and intestinal P-glycoprotein by rifampin.	ixazomib	178-186	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	161-166
28800141-10	2018	On the basis of these study results, the ixazomib prescribing information recommends that patients should avoid concomitant administration of strong CYP3A inducers with ixazomib.	ixazomib	41-49	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	149-154
28800141-10	2018	On the basis of these study results, the ixazomib prescribing information recommends that patients should avoid concomitant administration of strong CYP3A inducers with ixazomib.	ixazomib	169-177	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	149-154
28842936-4	2017	Significant reductions in cell viability, NF-kappaB activation, and GATA-3 expression were observed preclinically in ixazomib-treated cells.	ixazomib	117-125	GATA binding protein 3	Homo sapiens	68-74
28842936-6	2017	Concordant with our preclinical observations, a significant reduction in NF-kappaB activation and GATA-3 expression was observed in an exceptional responder following one month of treatment with ixazomib.	ixazomib	195-203	GATA binding protein 3	Homo sapiens	98-104
28842936-7	2017	While ixazomib had limited activity in this small and heterogeneous cohort of patients, inhibition of the NF-kappaB/GATA-3 axis in a single exceptional responder suggests that ixazomib may have utility in appropriately selected patients or in combination with other agents.	ixazomib	176-184	GATA binding protein 3	Homo sapiens	116-122
29416618-5	2018	In addition, we showed that ixazomib induces apoptosis and the DNA damage response pathway, through activation of the checkpoint kinase 2 (CHK2).	ixazomib	28-36	checkpoint kinase 2	Homo sapiens	118-137
29416618-5	2018	In addition, we showed that ixazomib induces apoptosis and the DNA damage response pathway, through activation of the checkpoint kinase 2 (CHK2).	ixazomib	28-36	checkpoint kinase 2	Homo sapiens	139-143
29416618-6	2018	Hence, pharmacological inhibition of CHK2 enhances the anti-tumor activity of ixazomib in DLBCL cells.	ixazomib	78-86	checkpoint kinase 2	Homo sapiens	37-41
28790851-13	2017	It exerted anticancer effects through targeting the expression of DEGs, such as HSPA6, APCDD1, TP53, and JUN, and affecting the signaling pathways including apoptosis and cell cycle pathway, which demonstrated the promising potential of ixazomib for CRC therapy.	ixazomib	237-245	heat shock protein family A (Hsp70) member 6	Homo sapiens	80-85
28790851-13	2017	It exerted anticancer effects through targeting the expression of DEGs, such as HSPA6, APCDD1, TP53, and JUN, and affecting the signaling pathways including apoptosis and cell cycle pathway, which demonstrated the promising potential of ixazomib for CRC therapy.	ixazomib	237-245	APC down-regulated 1	Homo sapiens	87-93
28790851-13	2017	It exerted anticancer effects through targeting the expression of DEGs, such as HSPA6, APCDD1, TP53, and JUN, and affecting the signaling pathways including apoptosis and cell cycle pathway, which demonstrated the promising potential of ixazomib for CRC therapy.	ixazomib	237-245	tumor protein p53	Homo sapiens	95-99
28495797-0	2017	Ixazomib enhances parathyroid hormone-induced beta-catenin/T-cell factor signaling by dissociating beta-catenin from the parathyroid hormone receptor.	ixazomib	0-8	hepatocyte nuclear factor 4 alpha	Homo sapiens	46-72
28495797-0	2017	Ixazomib enhances parathyroid hormone-induced beta-catenin/T-cell factor signaling by dissociating beta-catenin from the parathyroid hormone receptor.	ixazomib	0-8	catenin beta 1	Homo sapiens	46-58
27783987-9	2016	However, the combination of ixazomib with IFN-alpha significantly enhanced ixazomib"s ability to induce apoptotic cell death in BRAF V600E mutant and BRAF wild-type human melanoma tumor cells.	ixazomib	28-36	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	128-132
27783987-9	2016	However, the combination of ixazomib with IFN-alpha significantly enhanced ixazomib"s ability to induce apoptotic cell death in BRAF V600E mutant and BRAF wild-type human melanoma tumor cells.	ixazomib	28-36	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	150-154
27783987-9	2016	However, the combination of ixazomib with IFN-alpha significantly enhanced ixazomib"s ability to induce apoptotic cell death in BRAF V600E mutant and BRAF wild-type human melanoma tumor cells.	ixazomib	75-83	interferon alpha 1	Homo sapiens	42-51
27783987-9	2016	However, the combination of ixazomib with IFN-alpha significantly enhanced ixazomib"s ability to induce apoptotic cell death in BRAF V600E mutant and BRAF wild-type human melanoma tumor cells.	ixazomib	75-83	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	128-132
27783987-9	2016	However, the combination of ixazomib with IFN-alpha significantly enhanced ixazomib"s ability to induce apoptotic cell death in BRAF V600E mutant and BRAF wild-type human melanoma tumor cells.	ixazomib	75-83	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	150-154
27783987-10	2016	The combination of ixazomib and IFN-alpha also enhanced inhibition of cell proliferation in BRAF V600E mutant melanoma tumor cells; however, this was not seen in BRAF wild-type cells.	ixazomib	19-27	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	92-96
27783987-11	2016	Ixazomib-induced apoptosis was associated with processing of the pro-apoptotic proteins procaspase-3, -7, -8, and -9, and cleavage of poly-ADP-ribose polymerase (PARP).	ixazomib	0-8	caspase 3	Homo sapiens	88-116
27783987-11	2016	Ixazomib-induced apoptosis was associated with processing of the pro-apoptotic proteins procaspase-3, -7, -8, and -9, and cleavage of poly-ADP-ribose polymerase (PARP).	ixazomib	0-8	poly(ADP-ribose) polymerase 1	Homo sapiens	134-160
27783987-11	2016	Ixazomib-induced apoptosis was associated with processing of the pro-apoptotic proteins procaspase-3, -7, -8, and -9, and cleavage of poly-ADP-ribose polymerase (PARP).	ixazomib	0-8	poly(ADP-ribose) polymerase 1	Homo sapiens	162-166
27783987-12	2016	In an in vivo xenograft model of human melanoma, combination treatment with IFN-alpha-2b and ixazomib demonstrated a significant reduction in tumor volume when compared to vehicle (p = 0.005) and single therapy ixazomib (p = 0.017) and IFN-alpha-2b (p = 0.036).	ixazomib	93-101	interferon alpha 1	Homo sapiens	236-245
27783987-12	2016	In an in vivo xenograft model of human melanoma, combination treatment with IFN-alpha-2b and ixazomib demonstrated a significant reduction in tumor volume when compared to vehicle (p = 0.005) and single therapy ixazomib (p = 0.017) and IFN-alpha-2b (p = 0.036).	ixazomib	211-219	interferon alpha 1	Homo sapiens	76-85
27783987-13	2016	These pre-clinical results support further evaluation of combination treatment with ixazomib and IFN-alpha for the treatment of advanced BRAF V600E mutant melanoma.	ixazomib	84-92	B-Raf proto-oncogene, serine/threonine kinase	Homo sapiens	137-141
27325500-3	2016	When investigating the proteasome inhibitors bortezomib, carfilzomib, and ixazomib, we observed increased luminescence for bortezomib and ixazomib, but not for carfilzomib, in a pregnane-X-receptor (PXR) reporter gene assay, which was inconsistent with the mRNA expression levels of the main PXR target gene CYP3A4.	ixazomib	74-82	nuclear receptor subfamily 1 group I member 2	Homo sapiens	178-197
27325500-3	2016	When investigating the proteasome inhibitors bortezomib, carfilzomib, and ixazomib, we observed increased luminescence for bortezomib and ixazomib, but not for carfilzomib, in a pregnane-X-receptor (PXR) reporter gene assay, which was inconsistent with the mRNA expression levels of the main PXR target gene CYP3A4.	ixazomib	74-82	nuclear receptor subfamily 1 group I member 2	Homo sapiens	199-202
27325500-3	2016	When investigating the proteasome inhibitors bortezomib, carfilzomib, and ixazomib, we observed increased luminescence for bortezomib and ixazomib, but not for carfilzomib, in a pregnane-X-receptor (PXR) reporter gene assay, which was inconsistent with the mRNA expression levels of the main PXR target gene CYP3A4.	ixazomib	74-82	nuclear receptor subfamily 1 group I member 2	Homo sapiens	292-295
27325500-3	2016	When investigating the proteasome inhibitors bortezomib, carfilzomib, and ixazomib, we observed increased luminescence for bortezomib and ixazomib, but not for carfilzomib, in a pregnane-X-receptor (PXR) reporter gene assay, which was inconsistent with the mRNA expression levels of the main PXR target gene CYP3A4.	ixazomib	74-82	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	308-314
27325500-3	2016	When investigating the proteasome inhibitors bortezomib, carfilzomib, and ixazomib, we observed increased luminescence for bortezomib and ixazomib, but not for carfilzomib, in a pregnane-X-receptor (PXR) reporter gene assay, which was inconsistent with the mRNA expression levels of the main PXR target gene CYP3A4.	ixazomib	138-146	nuclear receptor subfamily 1 group I member 2	Homo sapiens	178-197
27325500-3	2016	When investigating the proteasome inhibitors bortezomib, carfilzomib, and ixazomib, we observed increased luminescence for bortezomib and ixazomib, but not for carfilzomib, in a pregnane-X-receptor (PXR) reporter gene assay, which was inconsistent with the mRNA expression levels of the main PXR target gene CYP3A4.	ixazomib	138-146	nuclear receptor subfamily 1 group I member 2	Homo sapiens	199-202
27325500-3	2016	When investigating the proteasome inhibitors bortezomib, carfilzomib, and ixazomib, we observed increased luminescence for bortezomib and ixazomib, but not for carfilzomib, in a pregnane-X-receptor (PXR) reporter gene assay, which was inconsistent with the mRNA expression levels of the main PXR target gene CYP3A4.	ixazomib	138-146	nuclear receptor subfamily 1 group I member 2	Homo sapiens	292-295
27325500-3	2016	When investigating the proteasome inhibitors bortezomib, carfilzomib, and ixazomib, we observed increased luminescence for bortezomib and ixazomib, but not for carfilzomib, in a pregnane-X-receptor (PXR) reporter gene assay, which was inconsistent with the mRNA expression levels of the main PXR target gene CYP3A4.	ixazomib	138-146	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	308-314
27529620-9	2016	Ixazomib also prevented the 50% reduction in RyR2 content observed after ischemia.	ixazomib	0-8	ryanodine receptor 2	Rattus norvegicus	45-49
27429848-0	2016	BH3 mimetic ABT-737 sensitizes colorectal cancer cells to ixazomib through MCL-1 downregulation and autophagy inhibition.	ixazomib	58-66	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	75-80
26988986-0	2016	Proteasomal Inhibition by Ixazomib Induces CHK1 and MYC-Dependent Cell Death in T-cell and Hodgkin Lymphoma.	ixazomib	26-34	checkpoint kinase 1	Homo sapiens	43-47
26988986-7	2016	The predicted activity for tumor suppressors and oncogenes, the impact on "hallmarks of cancer," and the analysis of key significant genes from global transcriptome analysis for ixazomib strongly favored tumor inhibition via downregulation of MYC and CHK1, its target genes.	ixazomib	178-186	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	243-246
26988986-7	2016	The predicted activity for tumor suppressors and oncogenes, the impact on "hallmarks of cancer," and the analysis of key significant genes from global transcriptome analysis for ixazomib strongly favored tumor inhibition via downregulation of MYC and CHK1, its target genes.	ixazomib	178-186	checkpoint kinase 1	Homo sapiens	251-255
26988986-8	2016	Furthermore, in ixazomib-treated lymphoma cells, we identified that CHK1 was involved in the regulation of MYC expression through chromatin modification involving histone H3 acetylation via chromatin immunoprecipitation.	ixazomib	16-24	checkpoint kinase 1	Homo sapiens	68-72
26988986-8	2016	Furthermore, in ixazomib-treated lymphoma cells, we identified that CHK1 was involved in the regulation of MYC expression through chromatin modification involving histone H3 acetylation via chromatin immunoprecipitation.	ixazomib	16-24	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	107-110
26988986-10	2016	Altogether, ixazomib significantly downregulates MYC and induces potent cell death in T-cell lymphoma and Hodgkin lymphoma, and we identified that combinatorial therapy with anti-CHK1 treatment represents a rational and novel therapeutic approach.	ixazomib	12-20	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	49-52
26988986-10	2016	Altogether, ixazomib significantly downregulates MYC and induces potent cell death in T-cell lymphoma and Hodgkin lymphoma, and we identified that combinatorial therapy with anti-CHK1 treatment represents a rational and novel therapeutic approach.	ixazomib	12-20	checkpoint kinase 1	Homo sapiens	179-183
27217076-6	2016	MLN9708 also enhanced Dox-induced JNK and p38 phosphorylation and inhibited Dox-induced IkappaBalpha degradation.	ixazomib	0-7	mitogen-activated protein kinase 14	Homo sapiens	42-45
27217076-6	2016	MLN9708 also enhanced Dox-induced JNK and p38 phosphorylation and inhibited Dox-induced IkappaBalpha degradation.	ixazomib	0-7	NFKB inhibitor alpha	Homo sapiens	88-100
26634271-0	2016	Selective Toxicity of Investigational Ixazomib for Human Leukemia Cells Expressing Mutant Cytoplasmic NPM1: Role of Reactive Oxygen Species.	ixazomib	38-46	nucleophosmin 1	Homo sapiens	102-106
26634271-4	2016	RESULTS: Apoptosis induced by ixazomib was abrogated by knockdown of NPM1/NPMc(+)expression using an inducible shRNA construct and enhanced by NPMc(+)overexpression.	ixazomib	30-38	nucleophosmin 1	Homo sapiens	69-73
26709701-0	2015	KRAS Genotype Correlates with Proteasome Inhibitor Ixazomib Activity in Preclinical In Vivo Models of Colon and Non-Small Cell Lung Cancer: Potential Role of Tumor Metabolism.	ixazomib	51-59	KRAS proto-oncogene, GTPase	Homo sapiens	0-4
26709701-4	2015	A survey of 14 non-small cell lung cancer (NSCLC) and 6 colon xenografts showed a striking relationship between ixazomib activity and KRAS genotype; tumors with wild-type (WT) KRAS were more sensitive to ixazomib than tumors harboring KRAS activating mutations.	ixazomib	112-120	KRAS proto-oncogene, GTPase	Homo sapiens	134-138
26709701-4	2015	A survey of 14 non-small cell lung cancer (NSCLC) and 6 colon xenografts showed a striking relationship between ixazomib activity and KRAS genotype; tumors with wild-type (WT) KRAS were more sensitive to ixazomib than tumors harboring KRAS activating mutations.	ixazomib	112-120	KRAS proto-oncogene, GTPase	Homo sapiens	176-180
26709701-4	2015	A survey of 14 non-small cell lung cancer (NSCLC) and 6 colon xenografts showed a striking relationship between ixazomib activity and KRAS genotype; tumors with wild-type (WT) KRAS were more sensitive to ixazomib than tumors harboring KRAS activating mutations.	ixazomib	112-120	KRAS proto-oncogene, GTPase	Homo sapiens	176-180
26709701-5	2015	To confirm the association between KRAS genotype and ixazomib sensitivity, we used SW48 isogenic colon cancer cell lines.	ixazomib	53-61	KRAS proto-oncogene, GTPase	Homo sapiens	35-39
26709701-7	2015	SW48 KRAS WT tumors, but neither SW48-KRAS-G13D tumors nor SW48-KRAS-G12V tumors, were sensitive to ixazomib in vivo.	ixazomib	100-108	KRAS proto-oncogene, GTPase	Homo sapiens	5-9
26709701-13	2015	The non-clinical data presented here show a correlation between KRAS genotype and ixazomib sensitivity in NSCLC and colon xenografts and provide new evidence of regulation of key metabolic pathways by proteasome inhibition.	ixazomib	82-90	KRAS proto-oncogene, GTPase	Homo sapiens	64-68
26141494-3	2015	METHODS: Nonclinical studies assessed (1) the in vitro binding of ixazomib to the hERG channel and (2) its effect on QT/QTc in dogs (N = 4) via telemetry.	ixazomib	66-74	ETS transcription factor ERG	Homo sapiens	82-86
26141494-6	2015	RESULTS: In vitro binding potency for ixazomib to the hERG channel was weak (K i 24.9 muM; IC50 59.6 muM), and nonclinical telemetry studies showed no QT/QTc prolongation at doses up to 4.2 mg/m(2).	ixazomib	38-46	ETS transcription factor ERG	Homo sapiens	54-58
26141494-6	2015	RESULTS: In vitro binding potency for ixazomib to the hERG channel was weak (K i 24.9 muM; IC50 59.6 muM), and nonclinical telemetry studies showed no QT/QTc prolongation at doses up to 4.2 mg/m(2).	ixazomib	38-46	latexin	Homo sapiens	86-89
26141494-6	2015	RESULTS: In vitro binding potency for ixazomib to the hERG channel was weak (K i 24.9 muM; IC50 59.6 muM), and nonclinical telemetry studies showed no QT/QTc prolongation at doses up to 4.2 mg/m(2).	ixazomib	38-46	latexin	Homo sapiens	101-104
25919767-0	2015	Calcineurin Inhibitor Minimization With Ixazomib, an Investigational Proteasome Inhibitor, for the Prevention of Antibody Mediated Rejection in a Preclinical Model.	ixazomib	40-48	calcineurin binding protein 1	Rattus norvegicus	0-21
25919767-5	2015	RESULTS: Compared to untreated animals, ixazomib alone or in combination with 1/2 dose CsA reduced donor-specific antibody, intragraft transcripts for chemokines CCL-21 and CXCL-13, and CD19 expression in both sensitized and naive transplants.	ixazomib	40-48	C-C motif chemokine ligand 21	Rattus norvegicus	162-168
25919767-5	2015	RESULTS: Compared to untreated animals, ixazomib alone or in combination with 1/2 dose CsA reduced donor-specific antibody, intragraft transcripts for chemokines CCL-21 and CXCL-13, and CD19 expression in both sensitized and naive transplants.	ixazomib	40-48	C-X-C motif chemokine ligand 13	Rattus norvegicus	173-180
25919767-5	2015	RESULTS: Compared to untreated animals, ixazomib alone or in combination with 1/2 dose CsA reduced donor-specific antibody, intragraft transcripts for chemokines CCL-21 and CXCL-13, and CD19 expression in both sensitized and naive transplants.	ixazomib	40-48	CD19 molecule	Rattus norvegicus	186-190
26099967-3	2015	All established PI (bortezomib and carfilzomib), as well as experimental drugs in the field (dalanzomib, oprozomib, and ixazomib), by design target the rate-limiting beta5 subunit.	ixazomib	120-128	adaptor related protein complex 5 subunit beta 1	Homo sapiens	166-171
25234165-5	2015	MiR-29b was significantly reduced in bortezomib-resistant cells as well as in cells resistant to second-generation PIs carfilzomib and ixazomib.	ixazomib	135-143	microRNA 29b-1	Homo sapiens	0-7
24120758-4	2014	Here, we show that similar to bortezomib, the novel proteasome inhibitors carfilzomib and ixazomib, as well as staurosporine and adaphostin, induce the generation of Mcl-1(128-350) in MM cells.	ixazomib	90-98	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	166-171
24292417-0	2013	(18)F-FDG-PET/CT imaging in an IL-6- and MYC-driven mouse model of human multiple myeloma affords objective evaluation of plasma cell tumor progression and therapeutic response to the proteasome inhibitor ixazomib.	ixazomib	205-213	interleukin 6	Mus musculus	31-44
24285522-0	2013	Syntheses of C-13 and C-14-labeled versions of the investigational proteasome inhibitor MLN9708.	ixazomib	88-95	homeobox C13	Homo sapiens	13-17