PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
16625543-15	2006	Combination therapy with ipratropium plus a short-acting beta-2 agonist conferred benefits over a short-acting beta-2 agonist alone in terms of post-bronchodilator lung function.	Ipratropium	25-36	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	111-117
16625543-17	2006	AUTHORS" CONCLUSIONS: The available data from the trials included in this review suggest that the advantage of regular long term use of ipratropium alone or in combination with a short-acting beta-2 agonist or over a beta-2 agonist alone are small, if the aim is to improve lung function, symptoms and exercise tolerance.	Ipratropium	136-147	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	217-223
15219176-0	2004	A short-term comparison of fluticasone propionate/salmeterol with ipratropium bromide/albuterol for the treatment of COPD.	Ipratropium	66-85	COPD	Homo sapiens	117-121
14966821-0	2004	Efficacy and safety of ipratropium bromide plus fenoterol inhaled via Respimat Soft Mist Inhaler vs. a conventional metered dose inhaler plus spacer in children with asthma.	Ipratropium	23-42	POC1 centriolar protein A	Homo sapiens	79-83
15500180-4	2004	Anticholinergic bronchodilators, such as ipratropium bromide and especially tiotropium, are first-line anticholinergic agents that can be used alone or in combination with long-acting or short-acting beta2-agonists to achieve these primary goals of COPD treatment.	Ipratropium	41-60	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	200-205
15500180-4	2004	Anticholinergic bronchodilators, such as ipratropium bromide and especially tiotropium, are first-line anticholinergic agents that can be used alone or in combination with long-acting or short-acting beta2-agonists to achieve these primary goals of COPD treatment.	Ipratropium	41-60	COPD	Homo sapiens	249-253
15219176-10	2004	CONCLUSIONS: Short-term treatment with the combined inhaled corticosteroid and long-acting beta(2)-adrenoceptor agonist fluticasone propionate/salmeterol resulted in greater control of lung function and symptoms than combined ipratropium bromide/albuterol bronchodilator therapy, in patients with COPD.	Ipratropium	226-245	adrenoceptor beta 2	Homo sapiens	91-111
16129327-4	2005	Ipratropium bromide can be added in the nebulisation, depending on the severity of the attack and the response to beta-2-agonists.	Ipratropium	0-19	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	114-120
15219176-1	2004	BACKGROUND: This is the first comparison of two combination therapies, fluticasone propionate/salmeterol and ipratropium bromide/albuterol (salbutamol), for the treatment of patients with COPD.	Ipratropium	109-128	COPD	Homo sapiens	188-192
12637127-11	2003	The ICER for ipratropium over placebo was $273.03; for formoterol 12 microg over ipratropium, $1611.32.	Ipratropium	13-24	cAMP responsive element modulator	Homo sapiens	4-8
12796167-1	2003	STUDY OBJECTIVE: This study tests the hypothesis that the administration of multiple doses of inhaled albuterol (A), ipratropium bromide (IB), and flunisolide (F) provides an additional benefit to adults with acute severe asthma compared with the administration of A plus IB (A/IB) or A plus F (A/F).	Ipratropium	117-136	ANIB1	Homo sapiens	138-140
12395958-1	2002	OBJECTIVE: To determine whether a combined formulation consisting of ipratropium and an inhaled beta2 agonist (2-in-1 therapy) leads to lower respiratory-related healthcare use and charges and improved compliance compared with treatment with separate ipratropium and beta2-agonist inhalers (separate inhaler therapy).	Ipratropium	69-80	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	267-272
12578401-7	2003	Current evidence suggests that long-acting beta(2)-adrenoreceptor agonists such as salmeterol and the new long-acting anticholinergic agent tiotropium bromide are more efficacious than their shorter acting equivalents such as salbutamol and ipratropium bromide in terms of bronchodilation, improved well-being and a reduction in acute exacerbation rates.	Ipratropium	241-260	adrenoceptor beta 2	Homo sapiens	43-65
10679537-9	2000	In patients with asthma, however, there was a slight increase in the relative risk of mortality associated with the use of ipratropium (RR 1.24; 95% CI 1.11 to 1.39).	Ipratropium	123-134	ribonucleotide reductase catalytic subunit M1	Homo sapiens	136-140
11980113-10	2002	CONCLUSION: Severe complication of BA is treated more effectively with combination of beta 2-adrenomimetic with atrovent.	Ipratropium	112-120	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	86-92
11605121-4	2001	Using an oscillating PEP-system in the expiratory outlet of a nebulizer does not only increase the bronchodilatory effect of ipratropiumbromide but also shortens by combining inhalation and physiotherapy the time necessary for therapy in those patients.	Ipratropium	125-143	prolyl endopeptidase	Homo sapiens	21-24
11718499-5	2001	Ipratropium should be considered in patients who fail or cannot tolerate beta2-agonists.	Ipratropium	0-11	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	73-78
11303413-9	2001	Since the publication of these guidelines, several new pharmacological products have been approved for use in patients with COPD including a combination of an anticholinergic and selective beta 2-adrenergic agonist [ipratropium/salbutamol (albuterol)] and a long-acting beta 2-adrenergic agonist (salmeterol).	Ipratropium	216-227	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	189-195
11714074-7	2001	Use of nebulized ipratropium/beta2-agonist combination therapy was associated with a pooled 7.3% improvement in forced expiratory volume in 1 sec [95% confidence interval (CI), 3.8-10.9%] and a 22.1% improvement in peak expiratory flow (95% CI, 11.0-33.2%) compared with patients who received beta2-agonist without ipratropium.	Ipratropium	17-28	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	293-298
11714074-7	2001	Use of nebulized ipratropium/beta2-agonist combination therapy was associated with a pooled 7.3% improvement in forced expiratory volume in 1 sec [95% confidence interval (CI), 3.8-10.9%] and a 22.1% improvement in peak expiratory flow (95% CI, 11.0-33.2%) compared with patients who received beta2-agonist without ipratropium.	Ipratropium	315-326	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	29-34
9230720-3	1997	We hypothesized that ipratropium bromide, an anticholinergic agent without vascular effects, should block PAF-induced bronchoconstriction but not interfere with its systemic, neutropenic, and gas exchange effects.	Ipratropium	21-40	PCNA clamp associated factor	Homo sapiens	106-109
9555617-10	1998	Decrease in Tal score after 15 min meant p < 0.01 for salbutamol-ipratropium and salbutamol vs. ipratropium.	Ipratropium	68-79	transaldolase 1	Homo sapiens	12-15
9532321-7	1998	Both doses of ipratropium bromide nasal spray significantly reduced the hypersecretion associated with PAR, compared with placebo.	Ipratropium	14-33	jumping translocation breakpoint	Homo sapiens	103-106
9353399-11	1997	Pretreatment of dogs with inhaled ipratropium bromide (0.01%) slightly, but significantly reduced the increase in lung resistance due to NKA challenge but had no effect on the decrease of dynamic lung compliance or on the respiratory responses to NKA.	Ipratropium	34-53	tachykinin precursor 1	Homo sapiens	137-140
8966503-4	1996	In an overview the action, indications and side effects of beta-2 sympathomimetics, ipratropium bromide, anti-allergens and inhaled steroids are discussed.	Ipratropium	84-103	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	59-65
9164362-11	1997	CONCLUSIONS: Ipratropium nasal spray 0.03% administered at a dose of 42 micrograms/nostril bid is a safe and effective new therapy for control of anterior rhinorrhea in pediatric patients with PNAR.	Ipratropium	13-24	BH3 interacting domain death agonist	Homo sapiens	91-94
9400690-8	1997	Thus, nebulized ipratropium bromide imparts a small improvement in lung function when compared with salbutamol alone; however, further studies are needed to determine if multiple doses of combined anticholinergic/beta 2-agonist treatment reduce need for admission.	Ipratropium	16-35	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	213-219
8549206-0	1996	Bronchodilating effects of combined therapy with clinical dosages of ipratropium bromide and salbutamol for stable COPD.	Ipratropium	69-88	COPD	Homo sapiens	115-119
8549208-0	1996	Bronchodilating effects of combined therapy with clinical dosages of ipratropium bromide and salbutamol for stable COPD.	Ipratropium	69-88	COPD	Homo sapiens	115-119
8658369-3	1996	The aim of the present study was to determine the dose of ipratropium bromide aerosol that improves exercise performance using progressive cycle ergometry in patients with stable COPD.	Ipratropium	58-77	COPD	Homo sapiens	179-183
8658369-12	1996	CONCLUSIONS: A dose of at least four times the standard dose of ipratropium bromide from an MDI with a spacer device was necessary to improve maximal cycle exercise capacity in patients with stable COPD.	Ipratropium	64-83	COPD	Homo sapiens	198-202
7982121-0	1994	Effects of ipratropium bromide on bradykinin nasal provocation in chronic allergic rhinitis.	Ipratropium	11-30	kininogen 1	Homo sapiens	34-44
1696438-0	1990	Influence of antihistamine (astemizole) and anticholinergic drugs (ipratropium bromide) on bronchoconstriction induced by substance P.	Ipratropium	67-86	tachykinin precursor 1	Homo sapiens	122-133
8441333-6	1993	The half-lives in hours were: Ba 679-Hm3: 34.7, -Hm1: 14.6, -Hm2: 3.6; ipratropium-Hm3: 0.26, -Hm1: 0.11, -Hm2: 0.035.	Ipratropium	71-82	cholinergic receptor muscarinic 3	Homo sapiens	83-86
2145136-0	1990	A comparison of the effects of ipratropium bromide and metaproterenol sulfate in acute exacerbations of COPD.	Ipratropium	31-50	COPD	Homo sapiens	104-108
2145136-13	1990	We concluded that for acute exacerbations of COPD, both ipratropium and metaproterenol are effective medications when administered via an MDI attached to a device (Inspirease).	Ipratropium	56-67	COPD	Homo sapiens	45-49
1387041-5	1992	Bradykinin challenge induced mean maximal increases of 57%, 59%, 77% and 72% in NAR on the placebo, terfenadine, ipratropium bromide and terfenadine plus ipratropium bromide pretreatment days respectively.	Ipratropium	113-132	kininogen 1	Homo sapiens	0-10
1387041-5	1992	Bradykinin challenge induced mean maximal increases of 57%, 59%, 77% and 72% in NAR on the placebo, terfenadine, ipratropium bromide and terfenadine plus ipratropium bromide pretreatment days respectively.	Ipratropium	154-173	kininogen 1	Homo sapiens	0-10
1387041-8	1992	Bradykinin nasal challenge caused a mean maximal increase in albumin levels in recovered nasal lavages of 11.5, 13.0, 12.2 and 12.3 times of baseline levels on the placebo, terfenadine, ipratropium bromide and terfenadine plus ipratroprium bromide pretreatment days respectively.	Ipratropium	186-205	kininogen 1	Homo sapiens	0-10
1835292-8	1991	Ipratropium may also be effective when beta 2 agonists are not effective.	Ipratropium	0-11	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	39-45
1837707-8	1991	2) Inhibitory effects of ipratropium bromide inhalation of ACE inhibitor-induced cough were noted in 83.3% of the patients, but their coughs did not completely disappear.	Ipratropium	25-44	angiotensin I converting enzyme	Homo sapiens	59-62
1840360-7	1991	One of the advantages of adding ipratropium to nebulised beta-agonist treatment might be that it permits the use of lower doses of beta 2-agonist and thereby reduces the systemic side-effects of the treatment.	Ipratropium	32-43	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	131-137
35569122-10	2022	CMap analysis showed that the small molecules scriptaid, torasemide, dexpropranolol, ipratropium bromide, and harmine were potential negative regulators of TGIF1.	Ipratropium	85-104	TGFB induced factor homeobox 1	Homo sapiens	156-161
1972192-10	1990	Bradykinin-induced stimulation of tracheal ciliary beat frequency is blocked by hexamethonium bromide, ipratropium bromide or indomethacin.	Ipratropium	103-122	kininogen 1	Canis lupus familiaris	0-10
34884730-4	2021	All OCT2 substrates cis-inhibited DiASP uptake in OCT2-overexpressing HEK293 cells, with IC50 values ranging from 0.24 microM (for ipratropium) to 2.39 mM (for dopamine).	Ipratropium	131-142	solute carrier family 22 member 2	Homo sapiens	4-8
34884730-4	2021	All OCT2 substrates cis-inhibited DiASP uptake in OCT2-overexpressing HEK293 cells, with IC50 values ranging from 0.24 microM (for ipratropium) to 2.39 mM (for dopamine).	Ipratropium	131-142	solute carrier family 22 member 2	Homo sapiens	50-54
35563491-9	2022	Human OCT1 transported ipratropium with 5.2-fold higher capacity but 8.4-fold lower affinity than dog OCT1.	Ipratropium	23-34	solute carrier family 22 member 1	Homo sapiens	6-10
2971708-8	1988	Ipratropium bromide administration, like VIP administration, significantly raised the PD20 value.	Ipratropium	0-19	vasoactive intestinal peptide	Homo sapiens	41-44
2951804-0	1986	Prevention of fog-induced bronchospasm by Duovent and its components (fenoterol, ipratropium bromide) in asthmatics.	Ipratropium	81-100	zinc finger protein, FOG family member 1	Homo sapiens	14-17
2962075-5	1987	Studies indicate that ipratropium bromide is effective in some pre-term babies who have airways obstruction following positive pressure ventilation but it can be a useful agent in the first 18 months of life, when beta 2-stimulants are rarely effective.	Ipratropium	22-41	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	214-220
2943921-6	1986	The age, baseline values of FVC and FEV1, and the increases in FEV1 and 1/Zrs with ipratropium did not differ between the two.	Ipratropium	83-94	limb development membrane protein 1	Homo sapiens	74-77
2943921-7	1986	Isoproterenol-phenylephrine aerosol following ipratropium produced further increases in FEV1 and 1/Zrs in asthmatic patients but no additive increases in bronchitic patients.	Ipratropium	46-57	limb development membrane protein 1	Homo sapiens	99-102
3529052-3	1986	Following pretreatment with nebulized ipratropium bromide, VIP infusion caused a significant (p less than 0.02) bronchodilation of 25 l/min.	Ipratropium	38-57	vasoactive intestinal peptide	Homo sapiens	59-62
2968227-0	1988	Ipratropium in patients with COPD receiving cholinesterase inhibitors.	Ipratropium	0-11	butyrylcholinesterase	Homo sapiens	44-58
2968227-1	1988	Three patients with chronic obstructive lung disease (COPD) and myasthenia gravis whose pulmonary symptoms were worsened by therapy with cholinesterase inhibitors were improved by inhaled ipratropium bromide.	Ipratropium	188-207	butyrylcholinesterase	Homo sapiens	137-151
2968227-5	1988	This experience suggests that ipratropium may be the bronchodilator drug of choice in patients with obstructive lung disease aggravated by cholinesterase inhibitors.	Ipratropium	30-41	butyrylcholinesterase	Homo sapiens	139-153
3541715-8	1987	However, ipratropium bromide (0.25 mg by nebulizer) significantly inhibited the effect of bradykinin, the PD35 being 0.8 mumol (range, 0.16 to 3.4) and 0.15 mumol (range, 0.047 to 1.15) after active dose and placebo, respectively (p less than 0.05).	Ipratropium	9-28	kininogen 1	Homo sapiens	90-100
2882568-2	1986	The studies suggest that the use of a combination of anticholinergic and beta 2-adrenergic drugs is justified, because the dominant mechanism in bronchospasm is the effect of acetylcholine on muscarinic receptors and because ipratropium bromide increases the action of fenoterol, so as to obtain prolonged bronchospasmolytic and antibronchoconstrictive effects with halved doses of beta 2-agonist.	Ipratropium	225-244	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	73-79
2951808-0	1986	Prevention of fog-induced bronchospasm by high doses of ipratropium bromide in asthmatics.	Ipratropium	56-75	zinc finger protein, FOG family member 1	Homo sapiens	14-17
3157668-6	1985	Ipratropium bromide (0.25 mg by inhalation) significantly (P less than 0.05) reduced the bronchoconstriction (maximum falls 34 +/- 14 and 15 +/- 9% after saline and ipratropium bromide, respectively; means +/- SD n = 6), indicating that it was dependent on a cholinergic vagal reflex rather than on local release of substance P from nerves in the airway.	Ipratropium	0-19	tachykinin precursor 1	Homo sapiens	316-327
2861067-1	1985	The aim of this study was to investigate the effects of nebulized ipratropium in patients with acute asthma in order to determine whether it augments the bronchodilator effect of a beta agonist drug.	Ipratropium	66-77	amyloid beta precursor protein	Homo sapiens	179-185
6226224-6	1983	Thus, acetylcholinesterase inhibitor therapy in subjects with myasthenia gravis with airflow limitation led to significant increase in airways resistance that could be completely reversed by the inhalation of the muscarinic receptor blocker ipratropium bromide.	Ipratropium	241-260	acetylcholinesterase (Cartwright blood group)	Homo sapiens	6-26
32707498-5	2020	After treatment with ipratropium bromide (IB) or dexamethasone (DEX), the expression of OCTN1/2 was upregulated compared with that in the CSE-LPS model group, while the expression of inflammatory factors was significantly downregulated.	Ipratropium	21-40	solute carrier family 22 member 4	Homo sapiens	88-95
6216870-0	1981	[Effects of ipratropium bromide in aerosol administration on airway resistance and MEFV curves].	Ipratropium	12-31	MEFV innate immuity regulator, pyrin	Homo sapiens	83-87
6219156-9	1983	It is concluded that when the anticholinergic drug ipratropium is administered concurrently with an inhaled beta 2 agonist and an oral theophylline derivative, increased bronchodilatation occurs with no detectable additional side effects.	Ipratropium	51-62	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	108-114
6461333-2	1982	Ipratropium bromide has not only an anticholinergic effect but also has an attenuating one on the contractile responses induced by serotonin, prostaglandin F2 alpha, histamine and bradykinin, and has a potentiating one on the relaxation responses induced by prostaglandin E2, isoprenaline and adrenaline.	Ipratropium	0-19	kininogen 1	Homo sapiens	180-190
6448137-3	1980	As with the beta 2-adrenoceptor agonists, the onset of maximum effect with ipratropium (about 1.5 to 2 hours) is slower than with isoprenaline (although significant bronchodilation usually occurs within seconds or minutes of ipratropium inhalation), and the duration of effect (about 4 to 6 hours) is longer.	Ipratropium	75-86	adrenoceptor beta 2	Homo sapiens	12-31
6448137-4	1980	Studies of concomitant use of ipratropium and other agents such as beta 2-adrenoceptor agonists, theophylline, or sodium cromoglycate, have usually shown a greater response in many patients than with single drug therapy, as might be expected from  the different mechanisms of action of these groups of drugs.	Ipratropium	30-41	adrenoceptor beta 2	Homo sapiens	67-86
6448137-8	1980	Ipratropium may also be useful in the occasional patient in whom side effects such as palpitations or tremor are troublesome with usual inhaled doses of beta 2-adrenoceptor agonists.	Ipratropium	0-11	adrenoceptor beta 2	Homo sapiens	153-172
159510-1	1979	The effects of (a) regular use for one week and (b) a single dose of a synthetic anticholinergic (ipratropium bromide) on lung mucociliary clearance and as a bronchodilator was ascertained in a controlled, double-blind, cross-over study in 12 patients with reversible airways obstruction (mean increase in FEV after isoprenaline: 17% range 10-50%).	Ipratropium	98-117	FEV transcription factor, ETS family member	Homo sapiens	306-309
32707498-5	2020	After treatment with ipratropium bromide (IB) or dexamethasone (DEX), the expression of OCTN1/2 was upregulated compared with that in the CSE-LPS model group, while the expression of inflammatory factors was significantly downregulated.	Ipratropium	42-44	solute carrier family 22 member 4	Homo sapiens	88-95
28990234-6	2018	Of these events only LRTI was significant for Atrovent  naive patients [ID1 /IDR = 1.42 (99% CI: 1.04, 1.95)].	Ipratropium	46-54	inhibitor of DNA binding 1, HLH protein	Homo sapiens	72-75
31930755-1	2020	BACKGROUND: Ipratropium bromide (IB), when administered with beta2-agonists, is effective in reducing hospital admissions of children presenting to the emergency department (ED) with severe asthma.	Ipratropium	12-31	ATPase H+ transporting V0 subunit a2	Homo sapiens	61-66
31930755-1	2020	BACKGROUND: Ipratropium bromide (IB), when administered with beta2-agonists, is effective in reducing hospital admissions of children presenting to the emergency department (ED) with severe asthma.	Ipratropium	33-35	ATPase H+ transporting V0 subunit a2	Homo sapiens	61-66
32027707-6	2020	In both cell models, L-carnitine uptake on the apical side was significantly inhibited by the bronchodilators glycopyrrolate and tiotropium, that hence can be considered substrates of ATB0,+; ipratropium was instead effective on the basolateral side, indicating its interaction with OCTN2.	Ipratropium	192-203	solute carrier family 22 member 5	Homo sapiens	283-288
31658507-10	2020	Furthermore, phosphorylated Akt (p-Akt) protein levels increased in CD4+ T cells from both controls and AR patients after coculture with D-U87 cells and decreased after IB treatment.	Ipratropium	169-171	AKT serine/threonine kinase 1	Homo sapiens	28-31
31658507-10	2020	Furthermore, phosphorylated Akt (p-Akt) protein levels increased in CD4+ T cells from both controls and AR patients after coculture with D-U87 cells and decreased after IB treatment.	Ipratropium	169-171	AKT serine/threonine kinase 1	Homo sapiens	35-38
31658507-13	2020	CONCLUSION: In-vitro cholinergic nerve inhibition with IB decreased AR CD4+ T-cell polarization into Th2 cells partially through an Akt-dependent mechanism.	Ipratropium	55-57	AKT serine/threonine kinase 1	Homo sapiens	132-135
24607693-2	2014	Herein, by using a modified protocol, combining pilocarpine with ipratropium bromide, we unexpectedly observed a heretofore-unrecognized distinct cellular population expressing the neuroprogenitor marker doublecortin (DCX) on post insult days (PID) 10, 14 and 18, mainly located in the temporal segment of the hippocampal fissure (hf).	Ipratropium	65-84	doublecortin	Rattus norvegicus	218-221
27676604-4	2017	Overexpression of OCTs or MATEs in HEK293 cells resulted in an up to 63-fold increase in the uptake of ipratropium (Km of 0.32 mum to OCT2 and Vmax of 3.34 nmolxmg protein-1xmin-1 to MATE1).	Ipratropium	103-114	solute carrier family 22 member 2	Homo sapiens	134-138
27676604-4	2017	Overexpression of OCTs or MATEs in HEK293 cells resulted in an up to 63-fold increase in the uptake of ipratropium (Km of 0.32 mum to OCT2 and Vmax of 3.34 nmolxmg protein-1xmin-1 to MATE1).	Ipratropium	103-114	solute carrier family 47 member 1	Homo sapiens	183-188
27676604-5	2017	The transcellular transport of ipratropium was 16-fold higher in OCT2-MATE1 and 10-fold higher in OCT1-MATE1 overexpressing compared to control MDCKII cells.	Ipratropium	31-42	solute carrier family 22 member 2	Canis lupus familiaris	65-69
27676604-5	2017	The transcellular transport of ipratropium was 16-fold higher in OCT2-MATE1 and 10-fold higher in OCT1-MATE1 overexpressing compared to control MDCKII cells.	Ipratropium	31-42	solute carrier family 47 member 1	Homo sapiens	70-75
27676604-5	2017	The transcellular transport of ipratropium was 16-fold higher in OCT2-MATE1 and 10-fold higher in OCT1-MATE1 overexpressing compared to control MDCKII cells.	Ipratropium	31-42	solute carrier family 22 member 1	Homo sapiens	98-102
27676604-5	2017	The transcellular transport of ipratropium was 16-fold higher in OCT2-MATE1 and 10-fold higher in OCT1-MATE1 overexpressing compared to control MDCKII cells.	Ipratropium	31-42	solute carrier family 47 member 1	Homo sapiens	103-108
27676604-6	2017	Genetic polymorphisms in OCT1 and OCT2 affected ipratropium uptake and clinically relevant concentration of ondansetron and pyrithiamine inhibited ipratropium uptake via MATEs by more than 90%.	Ipratropium	48-59	solute carrier family 22 member 1	Homo sapiens	25-29
27676604-6	2017	Genetic polymorphisms in OCT1 and OCT2 affected ipratropium uptake and clinically relevant concentration of ondansetron and pyrithiamine inhibited ipratropium uptake via MATEs by more than 90%.	Ipratropium	48-59	solute carrier family 22 member 2	Homo sapiens	34-38
27676604-6	2017	Genetic polymorphisms in OCT1 and OCT2 affected ipratropium uptake and clinically relevant concentration of ondansetron and pyrithiamine inhibited ipratropium uptake via MATEs by more than 90%.	Ipratropium	147-158	solute carrier family 22 member 1	Homo sapiens	25-29
27676604-7	2017	This study suggests that OCT1, OCT2 and MATEs may be strongly involved in the renal and extra-renal elimination of ipratropium and other quaternary amine alkaloids.	Ipratropium	115-126	solute carrier family 22 member 1	Homo sapiens	25-29
27676604-7	2017	This study suggests that OCT1, OCT2 and MATEs may be strongly involved in the renal and extra-renal elimination of ipratropium and other quaternary amine alkaloids.	Ipratropium	115-126	solute carrier family 22 member 2	Homo sapiens	31-35
28035420-10	2017	Our analyses suggested that bisoprolol, celecoxib, and ipratropium bromide, are potential therapeutics for ASL-regulated HCC formation.	Ipratropium	55-74	argininosuccinate lyase	Homo sapiens	107-110
28824036-1	2017	BACKGROUND: Inhaled anticholinergics such as ipratropium bromide (IB), when administered with beta2-agonists, are effective in reducing hospital admissions of children presenting to the emergency department with moderate to severe asthma.	Ipratropium	45-64	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	94-99
28824036-1	2017	BACKGROUND: Inhaled anticholinergics such as ipratropium bromide (IB), when administered with beta2-agonists, are effective in reducing hospital admissions of children presenting to the emergency department with moderate to severe asthma.	Ipratropium	66-68	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	94-99
30715829-15	2016	There Is little evidence that ipratropium, an inhaled short-acting anti-muscarinic bronchodilator, improves COPD symptoms.	Ipratropium	30-41	COPD	Homo sapiens	108-112
27418820-0	2016	Efficacy and safety of ipratropium bromide/salbutamol sulphate administered in a hydrofluoroalkane metered-dose inhaler for the treatment of COPD.	Ipratropium	23-42	COPD	Homo sapiens	141-145
25937167-6	2015	HeLa OCTN1 was inhibited by spermine, NaCl (Na(+)), TEA, gamma-butyrobetaine, choline, acetylcarnitine and ipratropium but not by neostigmine.	Ipratropium	107-118	solute carrier family 22 member 4	Homo sapiens	5-10
25859173-0	2015	Continuous Inhalation of Ipratropium Bromide for Acute Asthma Refractory to beta2-agonist Treatment.	Ipratropium	25-44	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	76-81
25859173-1	2015	To present the case of a patient with persistent bronchospasm, refractory to treatment with beta2-agonists, that resolved promptly with continuous inhalation of large dose (1000 mcg/hr) ipratropium bromide, and to discuss the possibility of tolerance to beta2-agonists as the cause for his failure to respond to adrenergic medications.	Ipratropium	186-205	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	92-97
25859173-1	2015	To present the case of a patient with persistent bronchospasm, refractory to treatment with beta2-agonists, that resolved promptly with continuous inhalation of large dose (1000 mcg/hr) ipratropium bromide, and to discuss the possibility of tolerance to beta2-agonists as the cause for his failure to respond to adrenergic medications.	Ipratropium	186-205	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	254-259
25859173-6	2015	Continuous inhalation of large dose ipratropium bromide may be an effective regimen for the treatment of patients hospitalized with acute asthma who are deemed to be nonresponsive and/or tolerant to beta2-agonist therapy.	Ipratropium	36-55	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	199-204
25278282-0	2015	A comparative study of the beneficial effects of ipratropium and beclomethasone against insulin-induced tracheal tissue contraction in a guinea pig model.	Ipratropium	49-60	insulin	Cavia porcellus	88-95
25278282-1	2015	OBJECTIVE: To evaluate the acute effects of insulin on airway reactivity and the protective effects of beclomethasone and ipratropium against insulin-induced airway hyperresponsiveness on isolated tracheal smooth muscle in a guinea pig model.	Ipratropium	122-133	insulin	Cavia porcellus	142-149
24428969-10	2014	Interleukin-4 expression level was significantly higher in the allergic model group than in the control group and significantly decreased by ipratropium bromide (P < .05).	Ipratropium	141-160	interleukin 4	Mus musculus	0-13
24428969-11	2014	In contrast, the expression of forkhead box P3 was lower in the allergic model group than in the control group and increased with treatment by ipratropium bromide (P < .05).	Ipratropium	143-162	forkhead box P3	Mus musculus	31-46
24428969-13	2014	Expression of substance P and vasoactive intestinal peptide was significantly increased in allergic mice and decreased by ipratropium bromide.	Ipratropium	122-141	tachykinin 1	Mus musculus	14-25
21728272-1	2011	BACKGROUND: The addition of ipratropium, a synthetic cholinergic antagonist, to beta2-agonist therapy provides an additive improvement in adult with acute severe asthma and COPD because of increased vagal tone in the airways.	Ipratropium	28-39	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	80-85
23748234-7	2013	CCh-stimulated [(35)S]GTPgammaS binding to Galphaq was inhibited by mAChR antagonists, including scopolamine, ipratropium, atropine, 4-DAMP, pirenzepine, and AF-DX 116, with a rank order of potency consistent with previous studies of M1-expressing cells.	Ipratropium	110-121	G protein subunit alpha q	Rattus norvegicus	43-50
23656745-8	2013	Nebulised ipratropium bromide (via nebulisation or multidosing via pMDI-spacer combination) should be added if there is a poor response to three doses of beta2-agonist or if the symptoms are severe.	Ipratropium	10-29	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	154-159
22409290-12	2012	The cost-effectiveness studies of tiotropium versus placebo, ipratropium or salmeterol pointed towards a reduction in total COPD-related healthcare costs for tiotropium in many but not all studies.	Ipratropium	61-72	COPD	Homo sapiens	124-128
20962061-8	2011	The K(m) value of rOct2-mediated ipratropium uptake (0.143 +- 0.03 muM) was consistent with that of the high-affinity component.	Ipratropium	33-44	solute carrier family 22 member 2	Rattus norvegicus	18-23
20962061-9	2011	The OCT/Oct inhibitor corticosterone, at a concentration of 1 muM (IC(50), 1.11 +- 0.20 muM for rOct2-mediated ipratropium transport), inhibited ipratropium by 18.4%, suggesting that rOct2 is involved in renal secretion of ipratropium.	Ipratropium	111-122	plexin A2	Homo sapiens	4-7
20962061-3	2011	Uptake of radiolabeled ipratropium in rat kidney slices was significantly inhibited by OCT/Oct substrates including cimetidine, imipramine, and quinidine, but not by organic anion transporter substrates (e.g., p-aminohippuric acid and estrone-3-sulfate).	Ipratropium	23-34	plexin A2	Homo sapiens	87-90
20962061-3	2011	Uptake of radiolabeled ipratropium in rat kidney slices was significantly inhibited by OCT/Oct substrates including cimetidine, imipramine, and quinidine, but not by organic anion transporter substrates (e.g., p-aminohippuric acid and estrone-3-sulfate).	Ipratropium	23-34	plexin A2	Homo sapiens	91-94
20962061-9	2011	The OCT/Oct inhibitor corticosterone, at a concentration of 1 muM (IC(50), 1.11 +- 0.20 muM for rOct2-mediated ipratropium transport), inhibited ipratropium by 18.4%, suggesting that rOct2 is involved in renal secretion of ipratropium.	Ipratropium	111-122	plexin A2	Homo sapiens	8-11
20962061-9	2011	The OCT/Oct inhibitor corticosterone, at a concentration of 1 muM (IC(50), 1.11 +- 0.20 muM for rOct2-mediated ipratropium transport), inhibited ipratropium by 18.4%, suggesting that rOct2 is involved in renal secretion of ipratropium.	Ipratropium	111-122	solute carrier family 22 member 2	Rattus norvegicus	96-101
20962061-9	2011	The OCT/Oct inhibitor corticosterone, at a concentration of 1 muM (IC(50), 1.11 +- 0.20 muM for rOct2-mediated ipratropium transport), inhibited ipratropium by 18.4%, suggesting that rOct2 is involved in renal secretion of ipratropium.	Ipratropium	145-156	plexin A2	Homo sapiens	4-7
20962061-9	2011	The OCT/Oct inhibitor corticosterone, at a concentration of 1 muM (IC(50), 1.11 +- 0.20 muM for rOct2-mediated ipratropium transport), inhibited ipratropium by 18.4%, suggesting that rOct2 is involved in renal secretion of ipratropium.	Ipratropium	145-156	plexin A2	Homo sapiens	8-11
20962061-9	2011	The OCT/Oct inhibitor corticosterone, at a concentration of 1 muM (IC(50), 1.11 +- 0.20 muM for rOct2-mediated ipratropium transport), inhibited ipratropium by 18.4%, suggesting that rOct2 is involved in renal secretion of ipratropium.	Ipratropium	145-156	solute carrier family 22 member 2	Rattus norvegicus	96-101
20962061-9	2011	The OCT/Oct inhibitor corticosterone, at a concentration of 1 muM (IC(50), 1.11 +- 0.20 muM for rOct2-mediated ipratropium transport), inhibited ipratropium by 18.4%, suggesting that rOct2 is involved in renal secretion of ipratropium.	Ipratropium	145-156	plexin A2	Homo sapiens	4-7
20962061-9	2011	The OCT/Oct inhibitor corticosterone, at a concentration of 1 muM (IC(50), 1.11 +- 0.20 muM for rOct2-mediated ipratropium transport), inhibited ipratropium by 18.4%, suggesting that rOct2 is involved in renal secretion of ipratropium.	Ipratropium	145-156	plexin A2	Homo sapiens	8-11
20962061-9	2011	The OCT/Oct inhibitor corticosterone, at a concentration of 1 muM (IC(50), 1.11 +- 0.20 muM for rOct2-mediated ipratropium transport), inhibited ipratropium by 18.4%, suggesting that rOct2 is involved in renal secretion of ipratropium.	Ipratropium	145-156	solute carrier family 22 member 2	Rattus norvegicus	96-101
20826145-9	2010	In conclusion, formoterol alone or combined with ipratropium bromide partially protects the lungs against the chronic inflammation and airspace enlargement by reducing neutrophilic infiltration possibly via the inhibition of MMP-9 activity.	Ipratropium	49-68	matrix metallopeptidase 9	Rattus norvegicus	225-230
21311689-5	2010	RESULTS: With FSC as the reference, risk for a COPD-related hospitalization and/or emergency department visit was significantly higher for ipratropium (hazard ratio [HR] 1.64, 95% confidence interval [CI] 1.50-1.79) and tiotropium (HR 1.29, CI 1.17-1.41).	Ipratropium	139-150	COPD	Homo sapiens	47-51
21311689-6	2010	Mean adjusted 12-month COPD-related total health care costs were lower for FSC ($2068, standard deviation [SD] $1190) than for ipratropium ($2841, SD $1858) and tiotropium ($2408, SD $1511, both P <0.05).	Ipratropium	127-138	COPD	Homo sapiens	23-27
20477218-0	2008	Clinical efficacy and safety of the combination of ipratropium bromide and fenoterol inhaled via the Respimat Soft Mist inhaler for relief of airflow obstruction.	Ipratropium	51-70	cytokine dependent hematopoietic cell linker	Homo sapiens	115-119
19308904-0	2009	[Association of A/T polymorphism of the CHRM2 gene with bronchodilator response to ipratropium bromide in asthmatic children].	Ipratropium	83-102	cholinergic receptor muscarinic 2	Homo sapiens	40-45
18990976-10	2008	CONCLUSIONS: Our data suggest that, besides their positive effects on respiratory symptoms, budesonide, formoterol, ipratropium bromide, and NAC modulate MRP1 activity in bronchial epithelial cells.	Ipratropium	116-135	ATP binding cassette subfamily C member 1	Homo sapiens	154-158