PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
26359375-13	2015	Likewise, the Ano1 inhibitor T16Ainh-A01 reduced Ano1(+0) more than Ano1(-0).	T16AInh-A01	29-40	anoctamin 1	Homo sapiens	14-18
26530828-7	2016	When TRPM5 was inhibited by triphenylphosphine oxide (TPPO), ionomycin stimulated a small but resolvable inward current that was eliminated by anion channel blockers, including T16Ainh-A01 (T16), a specific Ano1 antagonist.	T16AInh-A01	177-188	transient receptor potential cation channel, subfamily M, member 5	Mus musculus	5-10
26530828-7	2016	When TRPM5 was inhibited by triphenylphosphine oxide (TPPO), ionomycin stimulated a small but resolvable inward current that was eliminated by anion channel blockers, including T16Ainh-A01 (T16), a specific Ano1 antagonist.	T16AInh-A01	177-188	anoctamin 1, calcium activated chloride channel	Mus musculus	207-211
26359375-13	2015	Likewise, the Ano1 inhibitor T16Ainh-A01 reduced Ano1(+0) more than Ano1(-0).	T16AInh-A01	29-40	anoctamin 1	Homo sapiens	49-53
26359375-13	2015	Likewise, the Ano1 inhibitor T16Ainh-A01 reduced Ano1(+0) more than Ano1(-0).	T16AInh-A01	29-40	anoctamin 1	Homo sapiens	49-53
25749771-10	2015	T16Ainh-A01, a TMEM16A inhibitor, attenuated these IL-13-induced effects.	T16AInh-A01	0-11	anoctamin 1	Homo sapiens	15-22
25749771-10	2015	T16Ainh-A01, a TMEM16A inhibitor, attenuated these IL-13-induced effects.	T16AInh-A01	0-11	interleukin 13	Homo sapiens	51-56
25914185-4	2015	Control experiments were performed in static concentrations of calcium and using the specific TMEM16A inhibitor T16Ainh-A01 [2-[(5-ethyl-1,6-dihydro-4-methyl-6-oxo-2-pyrimidinyl)thio]-N-[4-(4-methoxyphenyl)-2-thia zolyl]acetamide].	T16AInh-A01	112-123	anoctamin 1	Homo sapiens	94-101
26130088-11	2015	In addition, repeated administration of CaCCs inhibitors (T16Ainh-A01, CaCCinh-A01 or NFA) or anti-anoctamin-1 antibody prevented spinal nerve ligation-induced rises in anoctamin-1 mRNA and protein expression.	T16AInh-A01	58-69	anoctamin 1	Rattus norvegicus	169-180
24823391-5	2014	Patch-clamp analysis on freshly isolated GCs identified an outwardly rectifying Ca(2+)-activated Cl(-) current that was completely blocked by a selective ANO1 inhibitor T16Ainh-A01.	T16AInh-A01	169-180	anoctamin 1, calcium activated chloride channel	Mus musculus	154-158
25298423-6	2014	Most importantly, iodide release by PCCl3 and FRTL-5 cells is efficiently blocked by T16Ainh-A01, an ANO1-specific inhibitor, and upon ANO1 knockdown by RNA interference.	T16AInh-A01	85-96	anoctamin 1	Rattus norvegicus	101-105
34961937-7	2022	In vivo knockdown of TMEM16A with adenovirus harboring TMEM16A-shRNA or inhibition of TMEM16A channel activity with its specific inhibitor CaCCinh-A01 or T16Ainh-A01 effectively prevented UUO-induced renal fibrosis and decreased protein expression of fibronectin, alpha-SMA and collagen in the obstructed kidneys.	T16AInh-A01	154-165	anoctamin 1, calcium activated chloride channel	Mus musculus	86-93
25848051-6	2015	Similarly, in mouse dorsal root ganglion neurons, capsaicin-activated inward currents were inhibited significantly by a specific ANO1 antagonist, T16Ainh-A01 (A01), in the presence of a high concentration of EGTA but not in the presence of BAPTA [1,2-bis(o-aminophenoxy)ethane-N,N,N",N"-tetraacetic acid].	T16AInh-A01	146-157	anoctamin 1, calcium activated chloride channel	Mus musculus	129-133
34961937-7	2022	In vivo knockdown of TMEM16A with adenovirus harboring TMEM16A-shRNA or inhibition of TMEM16A channel activity with its specific inhibitor CaCCinh-A01 or T16Ainh-A01 effectively prevented UUO-induced renal fibrosis and decreased protein expression of fibronectin, alpha-SMA and collagen in the obstructed kidneys.	T16AInh-A01	154-165	anoctamin 1, calcium activated chloride channel	Mus musculus	21-28
34406600-13	2021	Electrophysiological recording showed that CaCC current increases and intrathecal application of T16Ainh-A01, a selective TMEM16A inhibitor, reverses the hyperexcitability of DRG neurons harvested from rats after SNI.	T16AInh-A01	97-108	anoctamin 1	Rattus norvegicus	122-129
34281197-5	2021	We analyzed the proliferation of HaCaT keratinocytes and ANO1-related ERK and AKT signaling pathways after ANO1 inhibitor (T16Ainh-A01 and Ani9) treatment and knock-down of ANO1.	T16AInh-A01	123-134	anoctamin 1, calcium activated chloride channel	Mus musculus	57-61
34281197-9	2021	In addition, the expression levels of IL-17A, IL-17F, IL-22, IL-23, IL-6, IL-1beta, and TNF-alpha increased after applying IMQ and were significantly reduced by coapplying IMQ and T16Ainh-A01.	T16AInh-A01	180-191	interleukin 17A	Mus musculus	38-44
34281197-8	2021	Coapplication of IMQ and T16Ainh-A01 on ears of mice reduced not only symptoms of IMQ-induced psoriasis such as thickening and erythema, but also expression of ANO1 and pERK1/2 compared to that of application of IMQ alone.	T16AInh-A01	25-36	anoctamin 1, calcium activated chloride channel	Mus musculus	160-164
34281197-9	2021	In addition, the expression levels of IL-17A, IL-17F, IL-22, IL-23, IL-6, IL-1beta, and TNF-alpha increased after applying IMQ and were significantly reduced by coapplying IMQ and T16Ainh-A01.	T16AInh-A01	180-191	interleukin 17F	Mus musculus	46-52
35370660-9	2022	Spontaneous contractions sensitive to a specific inhibitor of TMEM16A channels, T16Ainh-A01, were reduced in BDL-PVSMs.	T16AInh-A01	80-91	anoctamin 1, calcium activated chloride channel	Mus musculus	62-69
34281197-9	2021	In addition, the expression levels of IL-17A, IL-17F, IL-22, IL-23, IL-6, IL-1beta, and TNF-alpha increased after applying IMQ and were significantly reduced by coapplying IMQ and T16Ainh-A01.	T16AInh-A01	180-191	interleukin 22	Mus musculus	54-59
34281197-9	2021	In addition, the expression levels of IL-17A, IL-17F, IL-22, IL-23, IL-6, IL-1beta, and TNF-alpha increased after applying IMQ and were significantly reduced by coapplying IMQ and T16Ainh-A01.	T16AInh-A01	180-191	interleukin 23, alpha subunit p19	Mus musculus	61-66
34281197-9	2021	In addition, the expression levels of IL-17A, IL-17F, IL-22, IL-23, IL-6, IL-1beta, and TNF-alpha increased after applying IMQ and were significantly reduced by coapplying IMQ and T16Ainh-A01.	T16AInh-A01	180-191	interleukin 6	Mus musculus	68-72
34281197-9	2021	In addition, the expression levels of IL-17A, IL-17F, IL-22, IL-23, IL-6, IL-1beta, and TNF-alpha increased after applying IMQ and were significantly reduced by coapplying IMQ and T16Ainh-A01.	T16AInh-A01	180-191	interleukin 1 alpha	Mus musculus	74-82
34281197-9	2021	In addition, the expression levels of IL-17A, IL-17F, IL-22, IL-23, IL-6, IL-1beta, and TNF-alpha increased after applying IMQ and were significantly reduced by coapplying IMQ and T16Ainh-A01.	T16AInh-A01	180-191	tumor necrosis factor	Mus musculus	88-97
33109690-10	2021	Another important negative-sense RNA respiratory pathogen influenza virus was also inhibited by the TMEM16A-specific inhibitor T16Ainh-A01.	T16AInh-A01	127-138	anoctamin 1	Homo sapiens	100-107
35203658-3	2022	Here we used EACT and T16Ainh-A01, potent activator and inhibitor of calcium-activated channels transmembrane protein 16A (TMEM16A), respectively, to probe the role of these channels in the pathophysiology of acoustically evoked seizures in the GEPR-3s.	T16AInh-A01	22-33	anoctamin 1	Rattus norvegicus	96-121
35203658-3	2022	Here we used EACT and T16Ainh-A01, potent activator and inhibitor of calcium-activated channels transmembrane protein 16A (TMEM16A), respectively, to probe the role of these channels in the pathophysiology of acoustically evoked seizures in the GEPR-3s.	T16AInh-A01	22-33	anoctamin 1	Rattus norvegicus	123-130
32110998-7	2020	In perforated current-clamping method, the application of T16Ainh-A01 and reduction of Cl- extended excitation periods in rod bipolar cells, revealing that ANO1 induces repolarization during excitation.	T16AInh-A01	58-69	anoctamin 1, calcium activated chloride channel	Mus musculus	156-160
32358165-6	2020	In t-BBEC117 cells, whole-cell Cl- currents were sensitive to the ClCa channel blockers, 100 muM niflumic acid and 10 muM T16Ainh-A01, and were also reduced markedly by small-interfering RNA (siRNA) knockdown of TMEM16A.	T16AInh-A01	122-133	anoctamin 1, calcium activated chloride channel	Mus musculus	212-219
32110998-5	2020	The voltage-dependent component of ANO1 has outward rectifying and sustained characteristics and is clearly isolated by the inhibitory effect of Cl- reduction and T16Ainh-A01, a selective ANO1 inhibitor, in high EGTA, a Ca2+ chelator.	T16AInh-A01	163-174	anoctamin 1, calcium activated chloride channel	Mus musculus	35-39
32110998-5	2020	The voltage-dependent component of ANO1 has outward rectifying and sustained characteristics and is clearly isolated by the inhibitory effect of Cl- reduction and T16Ainh-A01, a selective ANO1 inhibitor, in high EGTA, a Ca2+ chelator.	T16AInh-A01	163-174	anoctamin 1, calcium activated chloride channel	Mus musculus	188-192
32959891-14	2020	Additionally, the PKA inhibitor H89 and the TMEM16A (Ca2+ -activated chloride channel) inhibitor T16Ainh-A01 significantly reduced the nicotine-effect.	T16AInh-A01	97-108	anoctamin 1, calcium activated chloride channel	Mus musculus	44-51
32514271-8	2020	Pretreatment of the HNECs with T16Ainh-A01 and LY294002 attenuated these EGF-induced effects.	T16AInh-A01	31-42	epidermal growth factor	Homo sapiens	73-76
31294840-9	2020	However, prior treatment of T16Ainh-A01 (10 muM) did not inhibit the CCis" actions, although it decreased [Cl- ]i by 10% and CBD by 15%.	T16AInh-A01	28-39	latexin	Homo sapiens	44-47
31747299-6	2020	Pretreatment with two different TMEM16A antagonists, benzbromarone or T16Ainh-A01, completely attenuated these Eact-induced contractions.	T16AInh-A01	70-81	anoctamin 1	Homo sapiens	32-39
31489251-5	2019	Suppression of ANO1 activity either by selective inhibitor (T16Ainh-A01) or by siRNA significantly attenuated the migration and invasion of ATC cells.	T16AInh-A01	60-71	anoctamin 1	Homo sapiens	15-19
30762024-3	2019	A TMEM16A selective antagonist (10 mug T16Ainh-A01) was intrathecally injected at L5-6.	T16AInh-A01	39-50	anoctamin 1	Rattus norvegicus	2-9
30762024-12	2019	These findings were inhibited by T16Ainh-A01 and confirm that TMEM16A plays a key role in persistent chronic constriction injury-induced hyperalgesia.	T16AInh-A01	33-44	anoctamin 1	Rattus norvegicus	62-69
30089032-10	2018	Inhibition of TMEM16A with T16Ainh-A01 impaired the pressure-induced myogenic contraction in perfused afferent arterioles.	T16AInh-A01	27-38	anoctamin 1	Rattus norvegicus	14-21
30821158-10	2019	Moreover, T16Ainh-A01, a specific TMEM16A inhibitor or shRNA targeting TMEM16A somewhat inhibited lung tumor cell growth and invasion as evident from in vitro studies and from in vivo xenograft-tumor growth.	T16AInh-A01	10-21	anoctamin 1	Homo sapiens	34-41
29870694-5	2018	Accordingly, repeated (3 times) intrathecal injection of the anoctamin-1 blocker T16Ainh-A01 (0.1-1 microg) or MONNA (1-10 microg) partially reverted SNL-induced mechanical allodynia in a dose-dependent manner.	T16AInh-A01	81-92	anoctamin 1	Rattus norvegicus	61-72
30328351-6	2018	Inhibition of TMEM16A by small molecule inhibitor (T16Ainh-A01) resulted in impaired embryo implantation and decidualization in mice.	T16AInh-A01	51-62	anoctamin 1, calcium activated chloride channel	Mus musculus	14-21
29870694-7	2018	Interestingly, intrathecal injection of T16Ainh-A01 (1 microg) or MONNA (10 microg) prevented SNL-induced up-regulation of anoctamin-1, ATF-3 and caspase-3 in injured L5 DRG.	T16AInh-A01	40-51	caspase 3	Rattus norvegicus	146-155
29870694-7	2018	Interestingly, intrathecal injection of T16Ainh-A01 (1 microg) or MONNA (10 microg) prevented SNL-induced up-regulation of anoctamin-1, ATF-3 and caspase-3 in injured L5 DRG.	T16AInh-A01	40-51	anoctamin 1	Rattus norvegicus	123-134
29870694-7	2018	Interestingly, intrathecal injection of T16Ainh-A01 (1 microg) or MONNA (10 microg) prevented SNL-induced up-regulation of anoctamin-1, ATF-3 and caspase-3 in injured L5 DRG.	T16AInh-A01	40-51	activating transcription factor 3	Rattus norvegicus	136-141
27588910-5	2016	Further investigation of the HBE16 cells revealed that TMEM16A knockdown or specific chloride channel inhibitor T16Ainh-A01 could suppress the CaCC currents and consequently reduce the extracellular regulated kinase (ERK1/2) phosphorylation, accompanying a dramatical decrease in MUC5AC expression.	T16AInh-A01	112-123	mitogen-activated protein kinase 3	Homo sapiens	217-223
27732935-7	2016	Furthermore, both ANO1 inhibitors CaCCinh-A01 and T16Ainh-A01 significantly suppressed cell migration.	T16AInh-A01	50-61	anoctamin 1, calcium activated chloride channel	Mus musculus	18-22
29600587-5	2018	In this study, we evaluated the effects of two TMEM16A antagonists on capacitation, acrosome reaction, and motility in guinea pig sperm; these antagonists were T16Ainh-A01, belonging to a second generation of potent antagonists of TMEM16A, and niflumic acid (NFA), a well-known antagonist of TMEM16A (CaCCs).	T16AInh-A01	160-171	anoctamin 1	Homo sapiens	47-54
29600587-5	2018	In this study, we evaluated the effects of two TMEM16A antagonists on capacitation, acrosome reaction, and motility in guinea pig sperm; these antagonists were T16Ainh-A01, belonging to a second generation of potent antagonists of TMEM16A, and niflumic acid (NFA), a well-known antagonist of TMEM16A (CaCCs).	T16AInh-A01	160-171	anoctamin 1	Homo sapiens	231-238
29600587-5	2018	In this study, we evaluated the effects of two TMEM16A antagonists on capacitation, acrosome reaction, and motility in guinea pig sperm; these antagonists were T16Ainh-A01, belonging to a second generation of potent antagonists of TMEM16A, and niflumic acid (NFA), a well-known antagonist of TMEM16A (CaCCs).	T16AInh-A01	160-171	anoctamin 1	Homo sapiens	231-238
29600587-8	2018	Inhibition of TMEM16A by T16Ainh-A01 affected sperm physiology by reducing capacitation, blocking the progesterone-induced acrosome reaction under optimal capacitation conditions, inhibiting progressive motility, and the acquisition of hyperactivated motility, diminishing [Ca2+ ]i, and increasing [Cl- ]i.	T16AInh-A01	25-36	anoctamin 1	Homo sapiens	14-21
29187602-4	2018	Treatment with the ClCa channel blockers, niflumic acid or T16Ainh-A01, significantly reduced melatonin secretion in pineal glands.	T16AInh-A01	59-70	chloride channel accessory 5	Rattus norvegicus	19-23
30165368-13	2018	T16Ainh-A01 showed a marked inhibitory effect on the mRNA levels of ANO1 and alpha-SMA, but had a negligible effect on ANO1 at the protein level.	T16AInh-A01	0-11	anoctamin 1	Rattus norvegicus	68-72
30165368-13	2018	T16Ainh-A01 showed a marked inhibitory effect on the mRNA levels of ANO1 and alpha-SMA, but had a negligible effect on ANO1 at the protein level.	T16AInh-A01	0-11	actin gamma 2, smooth muscle	Rattus norvegicus	77-86
29416639-8	2018	In MCF7 and MDA-MB-231 breast carcinoma cells, inhibition of ANO1 with T16Ainh-A01 or siRNA for ANO1 significantly suppressed the proliferation of cells.	T16AInh-A01	71-82	anoctamin 1	Homo sapiens	61-65
27588910-5	2016	Further investigation of the HBE16 cells revealed that TMEM16A knockdown or specific chloride channel inhibitor T16Ainh-A01 could suppress the CaCC currents and consequently reduce the extracellular regulated kinase (ERK1/2) phosphorylation, accompanying a dramatical decrease in MUC5AC expression.	T16AInh-A01	112-123	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	280-286
27413167-6	2016	Blockade of ANO1 currents with aminophenylthiazole (T16Ainh-A01) was highly dependent on [Ca(2+)]i Increasing [Ca(2+)]i reduced the potency of this blocker.	T16AInh-A01	52-63	anoctamin 1	Homo sapiens	12-16