PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
28176915-10	2017	Caspase-8 inhibitor Ac-IETD-CHO significantly decreased the activation of caspase cascade, indicating that the extrinsic pathway may have a vital role in the apoptotic events induced by SiDcR3/TRAIL.	Ac-IETD-CHO	20-31	caspase 8	Homo sapiens	0-9
28176915-10	2017	Caspase-8 inhibitor Ac-IETD-CHO significantly decreased the activation of caspase cascade, indicating that the extrinsic pathway may have a vital role in the apoptotic events induced by SiDcR3/TRAIL.	Ac-IETD-CHO	20-31	TNF superfamily member 10	Homo sapiens	193-198
14719118-11	2004	Incubating cells with a caspase-8-specific inhibitor Ac-IETD-CHO prior to Ad-p53 infection inhibited caspase-8 activity and apoptosis.	Ac-IETD-CHO	53-64	caspase 8	Homo sapiens	101-110
22130238-5	2011	These decreases in CD31 and CD47 levels on the apoptotic cell surface were almost completely suppressed by the caspase 3 inhibitor, Ac-DEVD-CHO, and partially suppressed by caspase 8 (Ac-IETD-CHO) and caspase 9 (Ac-LEHE-CHO) inhibitors but not by the metalloproteinase inhibitors GM6001 and TAPI-0.	Ac-IETD-CHO	184-195	platelet and endothelial cell adhesion molecule 1	Homo sapiens	19-23
22130238-5	2011	These decreases in CD31 and CD47 levels on the apoptotic cell surface were almost completely suppressed by the caspase 3 inhibitor, Ac-DEVD-CHO, and partially suppressed by caspase 8 (Ac-IETD-CHO) and caspase 9 (Ac-LEHE-CHO) inhibitors but not by the metalloproteinase inhibitors GM6001 and TAPI-0.	Ac-IETD-CHO	184-195	CD47 molecule	Homo sapiens	28-32
18404518-6	2005	In addition, a specific caspase-8 inhibitor, Ac-IETD-CHO, significantly attenuated BzATP-induced caspase-9 and caspase-3 activation, suggesting that P2X(7)R-mediated apoptosis in rPCNs occurs primarily through an intrinsic caspase-8/9/3 activation pathway.	Ac-IETD-CHO	45-56	caspase 8	Rattus norvegicus	24-33
18404518-6	2005	In addition, a specific caspase-8 inhibitor, Ac-IETD-CHO, significantly attenuated BzATP-induced caspase-9 and caspase-3 activation, suggesting that P2X(7)R-mediated apoptosis in rPCNs occurs primarily through an intrinsic caspase-8/9/3 activation pathway.	Ac-IETD-CHO	45-56	caspase 3	Rattus norvegicus	111-120
18404518-6	2005	In addition, a specific caspase-8 inhibitor, Ac-IETD-CHO, significantly attenuated BzATP-induced caspase-9 and caspase-3 activation, suggesting that P2X(7)R-mediated apoptosis in rPCNs occurs primarily through an intrinsic caspase-8/9/3 activation pathway.	Ac-IETD-CHO	45-56	caspase 8	Rattus norvegicus	223-232
14719118-11	2004	Incubating cells with a caspase-8-specific inhibitor Ac-IETD-CHO prior to Ad-p53 infection inhibited caspase-8 activity and apoptosis.	Ac-IETD-CHO	53-64	caspase 8	Homo sapiens	24-33
14719118-11	2004	Incubating cells with a caspase-8-specific inhibitor Ac-IETD-CHO prior to Ad-p53 infection inhibited caspase-8 activity and apoptosis.	Ac-IETD-CHO	53-64	tumor protein p53	Homo sapiens	77-80
16542823-12	2006	Finally, we show that the caspase 8 inhibitor Ac-IETD-CHO was more effective at blocking seizure-induced cell death than the caspase 9 inhibitor Ac-LEHD-CHO.	Ac-IETD-CHO	46-57	caspase 8	Rattus norvegicus	26-35
15451068-7	2004	Ac-IETD-CHO, a caspase-8 inhibitor, suppresses Bid cleavage and DNA fragmentation.	Ac-IETD-CHO	0-11	caspase 8	Homo sapiens	15-24
15451068-7	2004	Ac-IETD-CHO, a caspase-8 inhibitor, suppresses Bid cleavage and DNA fragmentation.	Ac-IETD-CHO	0-11	BH3 interacting domain death agonist	Homo sapiens	47-50
12660414-5	2003	Administration of a caspase-9 inhibitor (Ac-IETD-CHO) effectively prevented both ureteric bud branching and nephrogenesis, the same as a caspase-3 inhibitor (Ac-DEVD-CHO).	Ac-IETD-CHO	41-52	caspase 9	Mus musculus	20-29
12911332-3	2003	Ac-IETD-CHO (acetyl-Ile-Glu-Thr-Asp-aldehyde), which has a certain preference for inhibiting caspase-8, or Fas-antagonistic antibody, significantly inhibited cisplatin-induced apoptosis in both parental and cisplatin-selected HeLa cell lines.	Ac-IETD-CHO	0-11	caspase 8	Homo sapiens	93-102
12888916-4	2003	The enhancement of Fas-induced apoptosis by pre-treatment with neuraminidase was inhibited by z-VAD-fmk, a broad caspase inhibitor, and Ac-LEHD-CHO, an inhibitor of caspase-9, but not by Ac-IETD-CHO an inhibitor of caspase-8 or 6, imipramine, an inhibitor of acidic sphingomyelinase, glutathione, an inhibitor of neutral sphingomyelinase and Fumonisin B1, an inhibitor of ceramide synthase.	Ac-IETD-CHO	187-198	neuraminidase 1	Homo sapiens	63-76
11566177-6	2001	Ac-LEHD-CHO, a caspase-9 inhibitor or Ac-IETD-CHO, a caspase-8 inhibitor, inhibited cisplatin-induced caspase-3 activation and apoptosis similarly in both cell lines.	Ac-IETD-CHO	38-49	caspase 8	Homo sapiens	53-62
11956588-11	2002	Furthermore, the synergistic cytotoxicity of TRAIL and DOX was completely inhibited by Z-VAD-FMK, and partly inhibited by Ac-IETD-CHO, Ac-DQTD-CHO, or Ac-DMQD-CHO.	Ac-IETD-CHO	122-133	TNF superfamily member 10	Homo sapiens	45-50
12048029-6	2002	By using specific caspase inhibitors (Ac-DEVD-CHO, Ac-IETD-CHO and zVAD-fmk), we showed that caspase-3 and -7 (DEVDases) are major effector caspases during EV-induced apoptosis in permissive L929 and RK-13 cell cultures.	Ac-IETD-CHO	51-62	caspase 3	Mus musculus	93-102
11566177-6	2001	Ac-LEHD-CHO, a caspase-9 inhibitor or Ac-IETD-CHO, a caspase-8 inhibitor, inhibited cisplatin-induced caspase-3 activation and apoptosis similarly in both cell lines.	Ac-IETD-CHO	38-49	caspase 3	Homo sapiens	102-111
11599886-12	2001	An inhibitor of caspase-8, Ac-IETD-CHO, partially inhibited UVC-induced apoptosis.	Ac-IETD-CHO	27-38	caspase 8	Homo sapiens	16-25
11465715-11	2001	Furthermore, apoptosis induced by CD95 stimulation and proteasome inhibitors was blocked by the caspase 8-specific inhibitor Ac-IETD-CHO.	Ac-IETD-CHO	125-136	Fas cell surface death receptor	Homo sapiens	34-38
11465715-11	2001	Furthermore, apoptosis induced by CD95 stimulation and proteasome inhibitors was blocked by the caspase 8-specific inhibitor Ac-IETD-CHO.	Ac-IETD-CHO	125-136	caspase 8	Homo sapiens	96-105
11281652-8	2001	Moreover, Bax translocation, cytochrome c release, and caspase 9 activation were blocked by the broad-spectrum caspase inhibitor, Z-VAD-fmk and the caspase 8-preferential inhibitor, Ac-IETD-CHO, suggesting that the mitochondria might participate in apoptosis by amplifying the upstream death signals.	Ac-IETD-CHO	182-193	BCL2 associated X, apoptosis regulator	Homo sapiens	10-13
11281652-8	2001	Moreover, Bax translocation, cytochrome c release, and caspase 9 activation were blocked by the broad-spectrum caspase inhibitor, Z-VAD-fmk and the caspase 8-preferential inhibitor, Ac-IETD-CHO, suggesting that the mitochondria might participate in apoptosis by amplifying the upstream death signals.	Ac-IETD-CHO	182-193	cytochrome c, somatic	Homo sapiens	29-41
11281652-8	2001	Moreover, Bax translocation, cytochrome c release, and caspase 9 activation were blocked by the broad-spectrum caspase inhibitor, Z-VAD-fmk and the caspase 8-preferential inhibitor, Ac-IETD-CHO, suggesting that the mitochondria might participate in apoptosis by amplifying the upstream death signals.	Ac-IETD-CHO	182-193	caspase 9	Homo sapiens	55-64
11281652-8	2001	Moreover, Bax translocation, cytochrome c release, and caspase 9 activation were blocked by the broad-spectrum caspase inhibitor, Z-VAD-fmk and the caspase 8-preferential inhibitor, Ac-IETD-CHO, suggesting that the mitochondria might participate in apoptosis by amplifying the upstream death signals.	Ac-IETD-CHO	182-193	caspase 8	Homo sapiens	148-157
11044257-5	2000	Using various tetrapeptide inhibitors for caspase and its associated factor, we additionally demonstrated that inhibitors for caspase 3 (Ac-DEVD-CHO) and caspase 8/granzyme B (Ac-IETD-CHO) suppressed CTL-induced cell death, but an inhibitor for Fas-activated serine proteinase, which acts for the caspase 3 activator, did not, suggesting that CTL-induced cell death was initiated by the Perforin/Granzyme B system, rather than the Fas ligand/Fas system.	Ac-IETD-CHO	176-187	caspase 3	Homo sapiens	126-135
11044257-5	2000	Using various tetrapeptide inhibitors for caspase and its associated factor, we additionally demonstrated that inhibitors for caspase 3 (Ac-DEVD-CHO) and caspase 8/granzyme B (Ac-IETD-CHO) suppressed CTL-induced cell death, but an inhibitor for Fas-activated serine proteinase, which acts for the caspase 3 activator, did not, suggesting that CTL-induced cell death was initiated by the Perforin/Granzyme B system, rather than the Fas ligand/Fas system.	Ac-IETD-CHO	176-187	caspase 8	Homo sapiens	154-163
11044257-5	2000	Using various tetrapeptide inhibitors for caspase and its associated factor, we additionally demonstrated that inhibitors for caspase 3 (Ac-DEVD-CHO) and caspase 8/granzyme B (Ac-IETD-CHO) suppressed CTL-induced cell death, but an inhibitor for Fas-activated serine proteinase, which acts for the caspase 3 activator, did not, suggesting that CTL-induced cell death was initiated by the Perforin/Granzyme B system, rather than the Fas ligand/Fas system.	Ac-IETD-CHO	176-187	granzyme B	Homo sapiens	164-174
11044257-5	2000	Using various tetrapeptide inhibitors for caspase and its associated factor, we additionally demonstrated that inhibitors for caspase 3 (Ac-DEVD-CHO) and caspase 8/granzyme B (Ac-IETD-CHO) suppressed CTL-induced cell death, but an inhibitor for Fas-activated serine proteinase, which acts for the caspase 3 activator, did not, suggesting that CTL-induced cell death was initiated by the Perforin/Granzyme B system, rather than the Fas ligand/Fas system.	Ac-IETD-CHO	176-187	caspase 3	Homo sapiens	297-306
11044257-5	2000	Using various tetrapeptide inhibitors for caspase and its associated factor, we additionally demonstrated that inhibitors for caspase 3 (Ac-DEVD-CHO) and caspase 8/granzyme B (Ac-IETD-CHO) suppressed CTL-induced cell death, but an inhibitor for Fas-activated serine proteinase, which acts for the caspase 3 activator, did not, suggesting that CTL-induced cell death was initiated by the Perforin/Granzyme B system, rather than the Fas ligand/Fas system.	Ac-IETD-CHO	176-187	granzyme B	Homo sapiens	396-406
11044257-5	2000	Using various tetrapeptide inhibitors for caspase and its associated factor, we additionally demonstrated that inhibitors for caspase 3 (Ac-DEVD-CHO) and caspase 8/granzyme B (Ac-IETD-CHO) suppressed CTL-induced cell death, but an inhibitor for Fas-activated serine proteinase, which acts for the caspase 3 activator, did not, suggesting that CTL-induced cell death was initiated by the Perforin/Granzyme B system, rather than the Fas ligand/Fas system.	Ac-IETD-CHO	176-187	Fas ligand	Homo sapiens	431-441
11032765-10	2000	In addition, pretreatment with the caspase-3 inhibitor Ac-DEVD-CHO and the caspase-8 inhibitor Ac-IETD-CHO (25 microM, 8 h) significantly decreased caspase-3 activation following exposure to 1 mM PSP and parathion (p < 0.05).	Ac-IETD-CHO	95-106	caspase 8	Homo sapiens	75-84
11032765-10	2000	In addition, pretreatment with the caspase-3 inhibitor Ac-DEVD-CHO and the caspase-8 inhibitor Ac-IETD-CHO (25 microM, 8 h) significantly decreased caspase-3 activation following exposure to 1 mM PSP and parathion (p < 0.05).	Ac-IETD-CHO	95-106	caspase 3	Homo sapiens	148-157
11032765-12	2000	Alteration of OP compound-induced nuclear fragmentation or caspase-3 activation by pretreatment with cyclosporin A, Ac-IETD-CHO, or PMSF suggested that OP compound-induced cytotoxicity may be modulated through multiple sites, including mitochondrial permeability pores, receptor-mediated caspase pathways, or serine proteases.	Ac-IETD-CHO	116-127	caspase 3	Homo sapiens	59-68
11210827-6	2000	A broad-spectrum caspase inhibitor, z-VAD-fmk, completely prevented all apoptotic changes, except for the depletion of delta psi m. Both Ac-DEVD-CHO and Ac-IETD-CHO, inhibitors of caspase -3 and -8, respectively, effectively inhibited typical chromatin condensation to almost the same extent.	Ac-IETD-CHO	153-164	caspase 8	Homo sapiens	17-24
10721769-3	2000	In addition to the involvement of caspase 3 in arsenic trioxide-induced apoptosis of NB4 cells, the activation of caspase 8 was also shown to be involved by Western blot analysis or by apoptosis inhibition assay using caspase 8 inhibitor Ac-IETD-CHO.	Ac-IETD-CHO	238-249	caspase 8	Homo sapiens	114-123