methylnaltrexone profile

methylnaltrexone: RN given refers to parent cpd(5alpha)-isomer [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

ID Source	ID
PubMed CID	5361918
CHEMBL ID	1186579
CHEBI ID	136007
SCHEMBL ID	49356
MeSH ID	M0100795

Synonym
n-methylnaltrexone
quaternary ammonium naltrexone
methylnaltrexonium
17-(cyclopropylmethyl)-4,5-epoxy-3,14-dihydroxymorphinanium-6-one
naltrexone mb
mrz 2663
methylnaltrexone
17-(cyclopropylmethyl)-4,5alpha-epoxy-3,14-dihydroxy-17-methyl-6-oxomorphinanium
morphinanium, 17-(cyclopropylmethyl)-4,5-epoxy-3,14-dihydroxy-17-methyl-6-oxo-, (5alpha)-
CHEBI:136007
bdbm50278337
83387-25-1
CHEMBL1186579
(4r,4as,7ar,12bs)-3-(cyclopropylmethyl)-4a,9-dihydroxy-3-methyl-2,4,5,6,7a,13-hexahydro-1h-4,12-methanobenzofuro[3,2-e]isoquinoline-3-ium-7-one
gtpl7563
SCHEMBL49356
DTXSID20873339 ,
JVLBPIPGETUEET-GAAHOAFPSA-O
Q411515
NCGC00378877-01
dtxcid00820846

Excerpt	Reference	Relevance
"Methylnaltrexone is a peripherally acting µ-opioid receptor antagonist indicated for the treatment of OIC."	( First-Dose Efficacy of Methylnaltrexone in Patients with Severe Medical Illness and Opioid-Induced Constipation: A Pooled Analysis. Israel, RJ; Peacock, WF; Slatkin, NE; Stambler, N, 2022)	1.75
"Methylnaltrexone is a peripheral opioid antagonist that ameliorates opioid-induced gastrointestinal stasis in others species yet preserves the analgesic effects of buprenorphine."	( Effects of Buprenorphine, Methylnaltrexone, and Their Combination on Gastrointestinal Transit in Healthy New Zealand White Rabbits. Brooks, EP; Martin-Flores, M; Mitchell, LM; Singh, B; Taylor, L; Walsh, CA, 2017)	1.48
"Methylnaltrexone is an opioid receptor antagonist that can reverse opioid-induced constipation without affecting analgesia."	( Methylnaltrexone for opioid-induced constipation in pediatric oncology patients. Alexander, S; Dupuis, LL; Lau, E; Mattiussi, A; Rodrigues, A; Wong, C, 2013)	2.55
"Methylnaltrexone is a peripheral opioid receptor antagonist that does not cross the blood-brain barrier; so without interference with pain relief, it could reverse the peripheral opioid side effects such as constipation, pruritus, postoperative ileus, and urinary retention. "	( The effect of methylnaltrexone on the side effects of intrathecal morphine after orthopedic surgery under spinal anesthesia. Amini, A; Asadi, S; Farbood, A; Zand, F, 2015)	2.22
"Methylnaltrexone is a peripheral opioid antagonist that does not cross the blood-brain barrier and can reverse the peripheral side effects of opioids without affecting the desired central properties."	( Protocol for a randomised control trial of methylnaltrexone for the treatment of opioid-induced constipation and gastrointestinal stasis in intensive care patients (MOTION). Anjum, A; Brett, SJ; Cross, M; Gordon, AC; O'Callaghan, D; Patel, PB; Warwick, J, 2016)	1.42
"Methylnaltrexone is a peripherally acting mu-opioid receptor antagonist that has been shown to relieve severe opioid-induced constipation (OIC) in patients with advanced disease receiving palliative care. "	( Phase II trial of subcutaneous methylnaltrexone in the treatment of severe opioid-induced constipation (OIC) in cancer patients: an exploratory study. Ades, S; Ashikaga, T; Ji, Y; Kumar, S; Mori, M, 2017)	2.18
"Methylnaltrexone is a peripherally active mu-opioid receptor antagonist that has been shown to antagonize the inhibitory effects of opioids on GI transit without impairing analgesia."	( Methylnaltrexone, a new peripherally acting mu-opioid receptor antagonist being evaluated for the treatment of postoperative ileus. Kraft, MD, 2008)	2.51
"Methylnaltrexone is a promising drug for the treatment of opioid-induced constipation."	( Methylnaltrexone: the answer to opioid-induced constipation? Cannom, RR; Mason, RJ, 2009)	2.52
"Methylnaltrexone (MNTX) is a peripherally acting mu-opioid receptor antagonist and is currently indicated for the treatment of opioid-induced constipation in patients with advanced illness who are receiving palliative care, when response to laxative therapy has not been sufficient. "	( In vitro metabolism and identification of human enzymes involved in the metabolism of methylnaltrexone. Chandrasekaran, A; Demaio, W; Erve, JC; Hultin, T; Li, H; Rotshteyn, Y; Scatina, J; Talaat, R; Tong, Z, 2010)	2.03
"Methylnaltrexone is a selective mu-opioid receptor antagonist that has restricted ability to cross the blood-brain barrier, thus enabling reversal of opioid-induced peripheral effects, such as constipation, without affecting the central effects, such as pain relief. "	( Methylnaltrexone. Garnock-Jones, KP; McKeage, K, 2010)	3.25
"Methylnaltrexone (MNTX) is a peripheral mu-opioid receptor antagonist for subcutaneous administration, which does not evoke symptoms of opioid abstinence."	( The role of opioid receptor antagonists in the treatment of opioid-induced constipation: a review. Leppert, W, 2010)	1.08
"Methylnaltrexone bromide is a peripherally acting mu antagonist and is indicated for the treatment of opioid-induced constipation in patients with advanced illness, when response to standard laxative therapy has been inefficacious."	( Methylnaltrexone: treatment for opioid-induced constipation. Baumrucker, SJ; Licup, N, 2011)	2.53
"Methylnaltrexone is a peripherally restricted opioid antagonist with μ-opioid receptor selectivity that can reduce opioid activity in peripheral organs such as the gastrointestinal tract while sparing the pain relief afforded by the pain medications."	( Methylnaltrexone bromide: research update of pharmacokinetics following parenteral administration. Boyd, TA; Rotshteyn, Y; Yuan, CS, 2011)	2.53
"Methylnaltrexone is a methylated form of the mu-opioid antagonist naltrexone that blocks peripheral effects of opioids without affecting centrally mediated analgesia. "	( Methylnaltrexone for opioid-induced constipation in patients with advanced illness: a 3-month open-label treatment extension study. Cooney, GA; Israel, RJ; Karver, S; Lipman, AG; Stambler, N, 2011)	3.25
"Methylnaltrexone (MNTX) is a novel peripherally acting μ-opioid antagonist that prevents peripheral side effects of opioid drugs such as constipation without affecting the analgesia. "	( Quantitative determination of methylnaltrexone in human serum using liquid chromatography-tandem mass spectrometry. Oswald, S; Schumacher, G; Siegmund, W, 2011)	2.1
"Methylnaltrexone is a selective peripherally acting mu-opioid receptor antagonist that decreases the constipating effects of opioids without affecting centrally mediated analgesia. "	( Characterization of abdominal pain during methylnaltrexone treatment of opioid-induced constipation in advanced illness: a post hoc analysis of two clinical trials. Israel, RJ; Lynn, R; Slatkin, NE; Su, C; Wang, W, 2011)	2.08
"Methylnaltrexone is an investigational peripheral opioid receptor antagonist, a quaternary derivative of naltrexone. "	( Methylnaltrexone, a novel peripheral opioid receptor antagonist for the treatment of opioid side effects. Israel, RJ; Yuan, CS, 2006)	3.22
"Methylnaltrexone is a peripheral opioid receptor antagonist undergoing phase III clinical trials for the treatment of opioid-induced constipation in patients with advanced medical illness who are being treated with narcotics for pain. "	( Methylnaltrexone: MNTX. , 2006)	3.22
"Methylnaltrexone (MNTX) is a peripheral opioid antagonist currently under clinical investigation."	( A review of methylnaltrexone, a peripheral opioid receptor antagonist, and its role in opioid-induced constipation. Friedman, D; Jahdi, M; Rim, F; Shaiova, L, 2007)	1.44
"Methylnaltrexone (MNTX) is a quaternary derivative of naltrexone. "	( Efficacy of methylnaltrexone versus naloxone for reversal of morphine-induced depression of hypoxic ventilatory response. Amin, HM; Camporesi, EM; Esposito, BF; Foss, JF; Roizen, MF; Sopchak, AM, 1994)	2.11
"Methylnaltrexone is a quaternary opioid antagonist with limited ability to cross the blood-brain barrier and the potential to antagonize the peripherally mediated effects of opioids. "	( Methylnaltrexone prevents morphine-induced delay in oral-cecal transit time without affecting analgesia: a double-blind randomized placebo-controlled trial. Foss, JF; Moss, J; O'Connor, M; Roizen, MF; Toledano, A; Yuan, CS, 1996)	3.18
"Methylnaltrexone is a quaternary opioid antagonist with limited ability to cross the blood-brain barrier that has the potential to antagonize the peripherally mediated gastrointestinal effects of opioids. "	( The safety and efficacy of oral methylnaltrexone in preventing morphine-induced delay in oral-cecal transit time. Foss, JF; Moss, J; Osinski, J; Roizen, MF; Toledano, A; Yuan, CS, 1997)	2.02
"Methylnaltrexone (MNTX) is a novel quaternary derivative of naltrexone that does not cross the blood-brain barrier and acts as a selective peripheral opioid receptor antagonist."	( A review of the potential role of methylnaltrexone in opioid bowel dysfunction. Foss, JF, 2001)	1.31

Excerpt	Reference	Relevance
"Methylnaltrexone has a positive impact on symptoms in women with NBS, although treatment does induce transient pain following its administration. "	( Effects of methylnaltrexone in patients with narcotic bowel syndrome: a pilot observational study. Gibson, PR; Morrison, G, 2012)	2.21
"N-methylnaltrexone has a direct effect on circular smooth muscle of the equine jejunum and pelvic flexure resulting in an increase in contractile activity."	( In vitro evaluation of the effect of the opioid antagonist N-methylnaltrexone on motility of the equine jejunum and pelvic flexure. Boscan, PL; van Hoogmoed, LM, 2005)	1.29
"Methylnaltrexone (MNTX) has been used to prevent the effects of opioids on the bowel and could reduce the incidence of POI when administered preoperatively."	( Design and feasibility of a double-blind, randomized trial of peri-operative methylnaltrexone for postoperative ileus prevention after adult spinal arthrodesis. Farhadi, HF; Gifford, CS; McGahan, BG; Minnema, AJ; Miracle, SD; Murphy, CV; Vazquez, DE; Weaver, TE, 2022)	1.67
"Methylnaltrexone has proven effective in treating cancer patients with OIC who have not responded adequately to conventional laxative therapy, though use is relatively contraindicated in those with peritoneal carcinomatosis due to theoretical risk and reported cases of perforation."	( Methylnaltrexone is safe in cancer patients with peritoneal carcinomatosis. Mendelsohn, RB; Nelson, KK; Schattner, MA, 2019)	2.68
"Methylnaltrexone has been recently approved by the FDA in the subcutaneous form for the treatment of opioid-induced bowel dysfunction, whereas the intravenous and oral forms remain under investigation."	( Methylnaltrexone: the answer to opioid-induced constipation? Cannom, RR; Mason, RJ, 2009)	2.52
"Methylnaltrexone has been shown to be effective for treating opioid-induced constipation (OIC) in chronic settings, but its effects on acute OIC have not been studied."	( Subcutaneous methylnaltrexone for treatment of acute opioid-induced constipation: phase 2 study in rehabilitation after orthopedic surgery. Anissian, L; Carpenito, J; Ramakrishna, T; Schwartz, HW; Stambler, N; Vincent, HK; Vincent, K, 2012)	2.19
"Methylnaltrexone has a positive impact on symptoms in women with NBS, although treatment does induce transient pain following its administration. "	( Effects of methylnaltrexone in patients with narcotic bowel syndrome: a pilot observational study. Gibson, PR; Morrison, G, 2012)	2.21
"N-methylnaltrexone has a direct effect on circular smooth muscle of the equine jejunum and pelvic flexure resulting in an increase in contractile activity."	( In vitro evaluation of the effect of the opioid antagonist N-methylnaltrexone on motility of the equine jejunum and pelvic flexure. Boscan, PL; van Hoogmoed, LM, 2005)	1.29
"Methylnaltrexone has greater polarity and lower lipid solubility, thus it does not cross the blood-brain barrier in humans."	( Methylnaltrexone, a novel peripheral opioid receptor antagonist for the treatment of opioid side effects. Israel, RJ; Yuan, CS, 2006)	2.5
"Methylnaltrexone has the potential to prevent or treat opioid-induced peripherally mediated ADEs on bowel dysfunction without interfering with central analgesia. "	( Methylnaltrexone mechanisms of action and effects on opioid bowel dysfunction and other opioid adverse effects. Yuan, CS, 2007)	3.23

Excerpt	Reference	Relevance
"Methylnaltrexone reduced all-cause mortality vs placebo treatment across multiple trials, suggesting methylnaltrexone may confer survival benefits in patients with opioid-induced bowel disorders taking opioids for cancer-related or chronic noncancer pain."	( Reductions in All-Cause Mortality Associated with the Use of Methylnaltrexone for Opioid-Induced Bowel Disorders: A Pooled Analysis. Brenner, D; Israel, RJ; Slatkin, NE; Stambler, N; Webster, LR, 2023)	2.59

Excerpt	Reference	Relevance
"Methylnaltrexone-treated patients had a significantly reduced mortality risk compared with placebo regardless of age or gender."	( Reductions in All-Cause Mortality Associated with the Use of Methylnaltrexone for Opioid-Induced Bowel Disorders: A Pooled Analysis. Brenner, D; Israel, RJ; Slatkin, NE; Stambler, N; Webster, LR, 2023)	1.87

Excerpt	Reference	Relevance
" This study was designed to examine the safety and tolerance of methylnaltrexone in healthy human participants over a range of doses and to identify any adverse effects or toxicity associated with methylnaltrexone and the doses at which these adverse effects occur."	( Safety and tolerance of methylnaltrexone in healthy humans: a randomized, placebo-controlled, intravenous, ascending-dose, pharmacokinetic study. Foss, JF; Moss, J; Murphy, M; O'Connor, MF; Roizen, MF; Yuan, CS, 1997)	0.84
"Opioids are associated with a number of adverse effects, constipation being the most common long-term adverse effect in patients with advanced cancer."	( Clinical status of methylnaltrexone, a new agent to prevent and manage opioid-induced side effects. Yuan, CS, )	0.46
"To review the mechanisms of action of methylnaltrexone and its effects on opioid bowel dysfunction, as well as its effects on other opioid-induced adverse effects (ADEs), and its potential roles in clinical practice."	( Methylnaltrexone mechanisms of action and effects on opioid bowel dysfunction and other opioid adverse effects. Yuan, CS, 2007)	2.05
" Safety was evaluated via standard assessments (ie, adverse events and related withdrawals, physical examinations, laboratory tests, vital signs, electrocardiograms) and assessment of surgical complications."	( Safety and efficacy of methylnaltrexone in shortening the duration of postoperative ileus following segmental colectomy: results of two randomized, placebo-controlled phase 3 trials. Carpenito, J; Chun, HK; Randazzo, B; Schulman, S; Stambler, N; Tzanis, E; Yu, CS, 2011)	0.68
" Rates of adverse events and serious adverse events were comparable across all treatment groups in both studies."	( Safety and efficacy of methylnaltrexone in shortening the duration of postoperative ileus following segmental colectomy: results of two randomized, placebo-controlled phase 3 trials. Carpenito, J; Chun, HK; Randazzo, B; Schulman, S; Stambler, N; Tzanis, E; Yu, CS, 2011)	0.68
" The most common adverse events during methylnaltrexone treatment were abdominal pain (9."	( Efficacy and Safety of Methylnaltrexone for Opioid-Induced Constipation in Patients With Chronic Noncancer Pain: A Placebo Crossover Analysis. Barrett, AC; Forbes, WP; Paterson, C; Viscusi, ER, )	0.71
" Often the only therapeutic option is to use class 2 or 3 analgesic opioids in the WHO classification, as class 1 analgesics may be toxic or of limited efficacy."	( [Management of adverse effects of opioid therapy]. Wirz, S, 2017)	0.46
"The most common adverse events were gastrointestinal related (e."	( Long-Term Safety and Efficacy of Subcutaneous Methylnaltrexone in Patients with Opioid-Induced Constipation and Chronic Noncancer Pain: A Phase 3, Open-Label Trial. Harper, JR; Israel, RJ; Khan, A; Michna, E; Webster, LR, 2017)	0.71
"Constipation is the most common chronic adverse effect of opioid pain medications in patients who require long-term opioid administration, such as patients with advanced cancer, but conventional measures for ameliorating constipation often are insufficient."	( Identifying and Treating Opioid Side Effects: The Development of Methylnaltrexone. Moss, J, 2019)	0.75
" No opioid withdrawal was observed in any subject, and no significant adverse effects were reported by the subjects during the study."	( Identifying and Treating Opioid Side Effects: The Development of Methylnaltrexone. Moss, J, 2019)	0.75
" Three patients had adverse outcomes or complications, with only one (0."	( Methylnaltrexone is safe in cancer patients with peritoneal carcinomatosis. Mendelsohn, RB; Nelson, KK; Schattner, MA, 2019)	1.96
" The purpose of this study was to determine if MNTX is effective and safe for POI treatment."	( The Efficacy and Safety of Methylnaltrexone for the Treatment of Postoperative Ileus. Atchison, L; Beavers, J; Dennis, B; Guillamondegui, O; Medvecz, A; Orton, L; Smith, MC, 2022)	1.02

Excerpt	Reference	Relevance
" Pharmacokinetic analysis revealed an elimination half-life of 117."	( Safety and tolerance of methylnaltrexone in healthy humans: a randomized, placebo-controlled, intravenous, ascending-dose, pharmacokinetic study. Foss, JF; Moss, J; Murphy, M; O'Connor, MF; Roizen, MF; Yuan, CS, 1997)	0.6
" The serum drug concentration-time profile fitted a two-compartment pharmacokinetic model."	( Pharmacokinetic profile of epidurally administered methylnaltrexone, a novel peripheral opioid antagonist in a rabbit model. Chan, VW; El Behiery, H; Foss, JF; Murph, DB, 2001)	0.56
" pharmacokinetic data on 670 drugs representing, to our knowledge, the largest publicly available set of human clinical pharmacokinetic data."	( Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds. Lombardo, F; Obach, RS; Waters, NJ, 2008)	0.35
"Studies conducted to date indicate that methylnaltrexone has high bioavailability after subcutaneous administration at therapeutic dose levels, a terminal half-life of ∼ 8 - 9 h, minimal metabolism, elimination involving renal and non-renal routes, and a limited potential for drug-drug interactions."	( Methylnaltrexone bromide: research update of pharmacokinetics following parenteral administration. Boyd, TA; Rotshteyn, Y; Yuan, CS, 2011)	2.08

Excerpt	Reference	Relevance
" Bioavailability of MNTX is low after oral administration, and plasma levels do not correlate with its actions in the gut, suggesting a predominantly local luminal action of MNTX on the gut."	( A review of the potential role of methylnaltrexone in opioid bowel dysfunction. Foss, JF, 2001)	0.59
"Studies conducted to date indicate that methylnaltrexone has high bioavailability after subcutaneous administration at therapeutic dose levels, a terminal half-life of ∼ 8 - 9 h, minimal metabolism, elimination involving renal and non-renal routes, and a limited potential for drug-drug interactions."	( Methylnaltrexone bromide: research update of pharmacokinetics following parenteral administration. Boyd, TA; Rotshteyn, Y; Yuan, CS, 2011)	2.08
" Since the bioavailability of oral MNTX is low, it is necessary to explore the oral formulations of MNTX that increase its bioavailability."	( Bioavailability of oral methylnaltrexone increases with a phosphatidylcholine-based formulation. Gu, M; Lin, DH; McEntee, E; Qin, LF; Wang, CZ; Wang, JT; Xie, XX; Yuan, CS, 2014)	0.71
" The physicochemical properties of MNTX-PC were analyzed, and its bioavailability was evaluated in rats."	( Bioavailability of oral methylnaltrexone increases with a phosphatidylcholine-based formulation. Gu, M; Lin, DH; McEntee, E; Qin, LF; Wang, CZ; Wang, JT; Xie, XX; Yuan, CS, 2014)	0.71
" Thus, the relative bioavailability after the oral administration of MNTX-PC was 410% compared to that of control."	( Bioavailability of oral methylnaltrexone increases with a phosphatidylcholine-based formulation. Gu, M; Lin, DH; McEntee, E; Qin, LF; Wang, CZ; Wang, JT; Xie, XX; Yuan, CS, 2014)	0.71
"MNTX-PC formulation significantly enhanced the oral bioavailability of MNTX."	( Bioavailability of oral methylnaltrexone increases with a phosphatidylcholine-based formulation. Gu, M; Lin, DH; McEntee, E; Qin, LF; Wang, CZ; Wang, JT; Xie, XX; Yuan, CS, 2014)	0.71

Excerpt	Relevance	Reference
" An inverted-U dose-response curve was obtained."	( Pharmacological evidence of a central effect of naltrexone, morphine, and beta-endorphin and a peripheral effect of met- and leu-enkephalin on retention of an inhibitory response in mice. Baratti, CM; Introini, IB; McGaugh, JL, 1985)	0.27
" Dose-response curves were subsequently determined under conditions of no stress, restraint, corticosterone (3 mg/kg, IP), and saline."	( Effects of restraint stress and intra-ventral tegmental area injections of morphine and methyl naltrexone on the discriminative stimulus effects of heroin in the rat. Shaham, Y; Stewart, J, )	0.13
" Inclusion of a fixed dose of 3-O-methylnaltrexone significantly shifted the analgesic dose-response curves for 6-acetylmorphine and heroin without altering the morphine dose-response curves."	( Antagonism of heroin and morphine self-administration in rats by the morphine-6beta-glucuronide antagonist 3-O-methylnaltrexone. Izzo, E; King, M; Koob, GF; Pasternak, GW; Walker, JR, 1999)	0.79
" and co-administration of 3-methylnaltrexone shifted the dose-response curves for endomorphin-2 induced antinociception to the right by 4-fold."	( Differential antagonism of endomorphin-1 and endomorphin-2 supraspinal antinociception by naloxonazine and 3-methylnaltrexone. Fujimura, T; Hayashi, T; Kastin, AJ; Murayama, K; Sakurada, C; Sakurada, S; Sakurada, T; Sato, T; Takeshita, M; Yonezawa, A; Yuhki, M; Zadina, JE, 2002)	0.82
" Steady state was achieved rapidly, and after repeated dosing for 3 days, methylnaltrexone decreased oral-cecal transit time from a pretreatment baseline value of 101."	( Tolerability, gut effects, and pharmacokinetics of methylnaltrexone following repeated intravenous administration in humans. Charney, MR; Doshan, H; Israel, RJ; Karrison, T; Maleckar, SA; Moss, J; O'connor, M; Yuan, CS, 2005)	0.81
" Progenics is conducting clinical trials with three methylnaltrexone dosage forms: subcutaneous, IV and oral."	( Methylnaltrexone: MNTX. , 2006)	2.03
" There was no apparent dose-response above 5mg."	( Subcutaneous methylnaltrexone for the treatment of opioid-induced constipation in patients with advanced illness: a double-blind, randomized, parallel group, dose-ranging study. Galasso, FL; Israel, RJ; Moehl Boatwright, ML; Portenoy, RK; Stambler, N; Thomas, J; Tran, D; Von Gunten, CF, 2008)	0.72
" Further analyses of these data, clinical trial designs and the various dosage forms are necessary to determine the potential role of methylnaltrexone in the treatment of POI."	( Methylnaltrexone, a new peripherally acting mu-opioid receptor antagonist being evaluated for the treatment of postoperative ileus. Kraft, MD, 2008)	1.99
"To review the chemistry, pharmacodynamics, pharmacokinetics, clinical efficacy, tolerability, indications, and dosing and administration of methylnaltrexone methobromide, the first approved peripherally selective opioid receptor-antagonist."	( Methylnaltrexone methobromide: the first peripherally active, centrally inactive opioid receptor-antagonist. Guay, DR, 2009)	2
"Methylnaltrexone methobromide is administered into the upper arm, abdomen, or thigh once every other day, with the frequency of dosing being increased, if needed, to a maximum of once daily."	( Methylnaltrexone methobromide: the first peripherally active, centrally inactive opioid receptor-antagonist. Guay, DR, 2009)	3.24
"A total of 469 subjects on opioids for chronic non-malignant pain with opioid-induced constipation were randomized to methylnaltrexone SC with once daily (QD) or every other day (QOD) dosing or placebo for 4 weeks."	( Effect of subcutaneous methylnaltrexone on patient-reported constipation symptoms. Iyer, SS; Manley, AL; Randazzo, BP; Schulman, SL; Tzanis, EL; Wang, W; Zhang, H, 2011)	0.89
" Differences in change from baseline in abdominal symptoms and pain scores between the methylnaltrexone SC QD or QOD dosing arms and placebo were not significant."	( Effect of subcutaneous methylnaltrexone on patient-reported constipation symptoms. Iyer, SS; Manley, AL; Randazzo, BP; Schulman, SL; Tzanis, EL; Wang, W; Zhang, H, 2011)	0.9
"The results of our study indicate significant improvement in constipation symptoms with methylnaltrexone QD or QOD dosing compared to placebo without a significant effect on pain scores."	( Effect of subcutaneous methylnaltrexone on patient-reported constipation symptoms. Iyer, SS; Manley, AL; Randazzo, BP; Schulman, SL; Tzanis, EL; Wang, W; Zhang, H, 2011)	0.9
" Based on conservative extrapolation of data from adult dosing, a methylnaltrexone dosing regimen was selected and the naloxone was weaned over two days in an effort to avoid a relative opioid overdose."	( Methylnaltrexone in treatment of opioid-induced constipation in a pediatric patient. Lee, JM; Mooney, J, 2012)	2.06
" While the addition of naloxone to oxycodone seems to act by preventing OIC, the intermittent dosing of methylnaltrexone every other day seems to stimulate defaecation by provoking an intestinal withdrawal response."	( Non-analgesic effects of opioids: management of opioid-induced constipation by peripheral opioid receptor antagonists: prevention or withdrawal? Holzer, P, 2012)	0.59
" Demographic, clinical, efficacy, and safety data were collected, including; opioid, laxative, and methylnatrexone dosing and frequency."	( Methylnaltrexone for opioid-induced constipation in pediatric oncology patients. Alexander, S; Dupuis, LL; Lau, E; Mattiussi, A; Rodrigues, A; Wong, C, 2013)	1.83
"Subcutaneous methylnaltrexone (MNTX), dosed based on body weight, is efficacious and well tolerated in inducing bowel movements in patients with advanced illness and opioid-induced constipation (OIC); however, fixed-dose administration of MNTX may improve ease of administration."	( Fixed-Dose Subcutaneous Methylnaltrexone in Patients with Advanced Illness and Opioid-Induced Constipation: Results of a Randomized, Placebo-Controlled Study and Open-Label Extension. Barrett, AC; Bull, J; Forbes, WP; Israel, RJ; Paterson, C; Wellman, CV, 2015)	1.09
" MNTX in oral immediate-release (MNTX-IR) and extended-release (MNTX-ER) dosage forms may antagonize the opioid induced delay in oro-cecal transit time (OCT) as measured by using radiolabeled lactulose."	( Extended-release but not immediate-release and subcutaneous methylnaltrexone antagonizes the loperamide-induced delay of whole-gut transit time in healthy subjects. Kolbow, J; Maritz, MA; Modess, C; Oswald, S; Rey, H; Siegmund, W; Wegner, D; Weitschies, W, 2016)	0.68
"In this phase 3, double-blind trial, adults with chronic noncancer pain receiving opioid doses of ≥ 50 mg/day oral morphine equivalents with OIC were randomly assigned to oral methylnaltrexone (150, 300, or 450 mg) or placebo once daily (QD) for 4 weeks followed by as-needed dosing for 8 weeks."	( Randomized, Double-Blind Trial of Oral Methylnaltrexone for the Treatment of Opioid-Induced Constipation in Patients with Chronic Noncancer Pain. Harper, JR; Israel, RJ; Rauck, R; Slatkin, NE; Stambler, N, 2017)	0.92
" A significantly greater percentage of patients had an increase in mean percentage of dosing days resulting in an RFBM within 4 hours of dosing during weeks 1 through 4 (QD period; primary endpoint) with methylnaltrexone (300 mg/day [24."	( Randomized, Double-Blind Trial of Oral Methylnaltrexone for the Treatment of Opioid-Induced Constipation in Patients with Chronic Noncancer Pain. Harper, JR; Israel, RJ; Rauck, R; Slatkin, NE; Stambler, N, 2017)	0.91
" In the rat, but not the mouse, 2-year carcinogenicity study a change in tumour pattern with an increase in testicular Leydig cell tumours (LCT) was observed after dosing at high (supra-pharmacological) concentrations."	( Naloxegol, an opioid antagonist with reduced CNS penetration: Mode-of-action and human relevance for rat testicular tumours. Andersson, H; Floettmann, E; Johnson, N; Mitchard, T, 2017)	0.46
" Expert opinion: Methylnaltrexone has both subcutaneous injection and oral dosage forms available in the market."	( Methylnaltrexone bromide for the treatment of opioid-induced constipation. Abdollahi, M; Mozaffari, S; Nikfar, S, 2018)	2.26
" Additional studies will be needed to identify effective opioid receptor antagonist dosing regimens for patients undergoing either short- or long-segment spinal arthrodesis procedures."	( Perioperative subcutaneous methylnaltrexone does not enhance gastrointestinal recovery after posterior short-segment spinal arthrodesis surgery: a randomized controlled trial. Farhadi, HF; Gifford, CS; McGahan, BG; Minnema, AJ; Miracle, SD; Murphy, CV; Vazquez, DE; Weaver, TE, 2022)	1.02

Class	Description
phenanthrenes	Any benzenoid aromatic compound that consists of a phenanthrene skeleton and its substituted derivatives thereof.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein	Taxonomy	Measurement	Average (µ)	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Spike glycoprotein	Severe acute respiratory syndrome-related coronavirus	Potency	39.8107	0.0096	10.5250	35.4813	AID1479145
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Solute carrier family 22 member 1	Homo sapiens (human)	IC50 (µMol)	234.0000	0.2100	5.5537	10.0000	AID1526751
Mu-type opioid receptor	Homo sapiens (human)	Ki	0.0067	0.0000	0.4197	10.0000	AID1467158; AID1826712
Delta-type opioid receptor	Homo sapiens (human)	Ki	1.9776	0.0000	0.5978	9.9300	AID1467159; AID1826719
Kappa-type opioid receptor	Cavia porcellus (domestic guinea pig)	Ki	0.0200	0.0000	0.2018	6.4240	AID1467160
Kappa-type opioid receptor	Homo sapiens (human)	Ki	0.0321	0.0000	0.3624	10.0000	AID1826720
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Mu-type opioid receptor	Homo sapiens (human)	EC50 (µMol)	10.0000	0.0000	0.3263	9.4000	AID1826723
Delta-type opioid receptor	Homo sapiens (human)	EC50 (µMol)	10.0000	0.0000	0.4332	8.3000	AID1826737
Kappa-type opioid receptor	Homo sapiens (human)	EC50 (µMol)	10.0000	0.0000	0.2244	8.9900	AID1826734
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Solute carrier family 22 member 1	Homo sapiens (human)	Km	20.0000	0.4770	4.0308	9.0000	AID1526737
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Process	via Protein(s)	Taxonomy
xenobiotic metabolic process	Solute carrier family 22 member 1	Homo sapiens (human)
neurotransmitter transport	Solute carrier family 22 member 1	Homo sapiens (human)
serotonin transport	Solute carrier family 22 member 1	Homo sapiens (human)
establishment or maintenance of transmembrane electrochemical gradient	Solute carrier family 22 member 1	Homo sapiens (human)
organic cation transport	Solute carrier family 22 member 1	Homo sapiens (human)
quaternary ammonium group transport	Solute carrier family 22 member 1	Homo sapiens (human)
prostaglandin transport	Solute carrier family 22 member 1	Homo sapiens (human)
monoamine transport	Solute carrier family 22 member 1	Homo sapiens (human)
putrescine transport	Solute carrier family 22 member 1	Homo sapiens (human)
spermidine transport	Solute carrier family 22 member 1	Homo sapiens (human)
acetylcholine transport	Solute carrier family 22 member 1	Homo sapiens (human)
dopamine transport	Solute carrier family 22 member 1	Homo sapiens (human)
norepinephrine transport	Solute carrier family 22 member 1	Homo sapiens (human)
thiamine transport	Solute carrier family 22 member 1	Homo sapiens (human)
xenobiotic transport	Solute carrier family 22 member 1	Homo sapiens (human)
epinephrine transport	Solute carrier family 22 member 1	Homo sapiens (human)
serotonin uptake	Solute carrier family 22 member 1	Homo sapiens (human)
norepinephrine uptake	Solute carrier family 22 member 1	Homo sapiens (human)
thiamine transmembrane transport	Solute carrier family 22 member 1	Homo sapiens (human)
metanephric proximal tubule development	Solute carrier family 22 member 1	Homo sapiens (human)
purine-containing compound transmembrane transport	Solute carrier family 22 member 1	Homo sapiens (human)
dopamine uptake	Solute carrier family 22 member 1	Homo sapiens (human)
monoatomic cation transmembrane transport	Solute carrier family 22 member 1	Homo sapiens (human)
transport across blood-brain barrier	Solute carrier family 22 member 1	Homo sapiens (human)
(R)-carnitine transmembrane transport	Solute carrier family 22 member 1	Homo sapiens (human)
acyl carnitine transmembrane transport	Solute carrier family 22 member 1	Homo sapiens (human)
spermidine transmembrane transport	Solute carrier family 22 member 1	Homo sapiens (human)
cellular detoxification	Solute carrier family 22 member 1	Homo sapiens (human)
xenobiotic transport across blood-brain barrier	Solute carrier family 22 member 1	Homo sapiens (human)
histamine metabolic process	Solute carrier family 22 member 3	Homo sapiens (human)
organic cation transport	Solute carrier family 22 member 3	Homo sapiens (human)
quaternary ammonium group transport	Solute carrier family 22 member 3	Homo sapiens (human)
monoatomic ion transport	Solute carrier family 22 member 3	Homo sapiens (human)
neurotransmitter transport	Solute carrier family 22 member 3	Homo sapiens (human)
serotonin transport	Solute carrier family 22 member 3	Homo sapiens (human)
organic cation transport	Solute carrier family 22 member 3	Homo sapiens (human)
quaternary ammonium group transport	Solute carrier family 22 member 3	Homo sapiens (human)
organic anion transport	Solute carrier family 22 member 3	Homo sapiens (human)
monocarboxylic acid transport	Solute carrier family 22 member 3	Homo sapiens (human)
monoamine transport	Solute carrier family 22 member 3	Homo sapiens (human)
spermidine transport	Solute carrier family 22 member 3	Homo sapiens (human)
dopamine transport	Solute carrier family 22 member 3	Homo sapiens (human)
norepinephrine transport	Solute carrier family 22 member 3	Homo sapiens (human)
regulation of appetite	Solute carrier family 22 member 3	Homo sapiens (human)
xenobiotic transport	Solute carrier family 22 member 3	Homo sapiens (human)
epinephrine transport	Solute carrier family 22 member 3	Homo sapiens (human)
histamine transport	Solute carrier family 22 member 3	Homo sapiens (human)
serotonin uptake	Solute carrier family 22 member 3	Homo sapiens (human)
histamine uptake	Solute carrier family 22 member 3	Homo sapiens (human)
norepinephrine uptake	Solute carrier family 22 member 3	Homo sapiens (human)
epinephrine uptake	Solute carrier family 22 member 3	Homo sapiens (human)
purine-containing compound transmembrane transport	Solute carrier family 22 member 3	Homo sapiens (human)
dopamine uptake	Solute carrier family 22 member 3	Homo sapiens (human)
transport across blood-brain barrier	Solute carrier family 22 member 3	Homo sapiens (human)
spermidine transmembrane transport	Solute carrier family 22 member 3	Homo sapiens (human)
cellular detoxification	Solute carrier family 22 member 3	Homo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger	Mu-type opioid receptor	Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled acetylcholine receptor signaling pathway	Mu-type opioid receptor	Homo sapiens (human)
phospholipase C-activating G protein-coupled receptor signaling pathway	Mu-type opioid receptor	Homo sapiens (human)
sensory perception	Mu-type opioid receptor	Homo sapiens (human)
negative regulation of cell population proliferation	Mu-type opioid receptor	Homo sapiens (human)
sensory perception of pain	Mu-type opioid receptor	Homo sapiens (human)
G protein-coupled opioid receptor signaling pathway	Mu-type opioid receptor	Homo sapiens (human)
behavioral response to ethanol	Mu-type opioid receptor	Homo sapiens (human)
positive regulation of neurogenesis	Mu-type opioid receptor	Homo sapiens (human)
negative regulation of Wnt protein secretion	Mu-type opioid receptor	Homo sapiens (human)
positive regulation of ERK1 and ERK2 cascade	Mu-type opioid receptor	Homo sapiens (human)
calcium ion transmembrane transport	Mu-type opioid receptor	Homo sapiens (human)
cellular response to morphine	Mu-type opioid receptor	Homo sapiens (human)
regulation of cellular response to stress	Mu-type opioid receptor	Homo sapiens (human)
regulation of NMDA receptor activity	Mu-type opioid receptor	Homo sapiens (human)
neuropeptide signaling pathway	Mu-type opioid receptor	Homo sapiens (human)
immune response	Delta-type opioid receptor	Homo sapiens (human)
G protein-coupled receptor signaling pathway	Delta-type opioid receptor	Homo sapiens (human)
G protein-coupled receptor signaling pathway, coupled to cyclic nucleotide second messenger	Delta-type opioid receptor	Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled receptor signaling pathway	Delta-type opioid receptor	Homo sapiens (human)
phospholipase C-activating G protein-coupled receptor signaling pathway	Delta-type opioid receptor	Homo sapiens (human)
adult locomotory behavior	Delta-type opioid receptor	Homo sapiens (human)
negative regulation of gene expression	Delta-type opioid receptor	Homo sapiens (human)
negative regulation of protein-containing complex assembly	Delta-type opioid receptor	Homo sapiens (human)
positive regulation of CREB transcription factor activity	Delta-type opioid receptor	Homo sapiens (human)
positive regulation of peptidyl-serine phosphorylation	Delta-type opioid receptor	Homo sapiens (human)
response to nicotine	Delta-type opioid receptor	Homo sapiens (human)
G protein-coupled opioid receptor signaling pathway	Delta-type opioid receptor	Homo sapiens (human)
eating behavior	Delta-type opioid receptor	Homo sapiens (human)
regulation of mitochondrial membrane potential	Delta-type opioid receptor	Homo sapiens (human)
regulation of calcium ion transport	Delta-type opioid receptor	Homo sapiens (human)
cellular response to growth factor stimulus	Delta-type opioid receptor	Homo sapiens (human)
cellular response to hypoxia	Delta-type opioid receptor	Homo sapiens (human)
cellular response to toxic substance	Delta-type opioid receptor	Homo sapiens (human)
neuropeptide signaling pathway	Delta-type opioid receptor	Homo sapiens (human)
immune response	Kappa-type opioid receptor	Homo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled receptor signaling pathway	Kappa-type opioid receptor	Homo sapiens (human)
phospholipase C-activating G protein-coupled receptor signaling pathway	Kappa-type opioid receptor	Homo sapiens (human)
chemical synaptic transmission	Kappa-type opioid receptor	Homo sapiens (human)
sensory perception	Kappa-type opioid receptor	Homo sapiens (human)
locomotory behavior	Kappa-type opioid receptor	Homo sapiens (human)
sensory perception of pain	Kappa-type opioid receptor	Homo sapiens (human)
adenylate cyclase-inhibiting opioid receptor signaling pathway	Kappa-type opioid receptor	Homo sapiens (human)
response to insulin	Kappa-type opioid receptor	Homo sapiens (human)
positive regulation of dopamine secretion	Kappa-type opioid receptor	Homo sapiens (human)
negative regulation of luteinizing hormone secretion	Kappa-type opioid receptor	Homo sapiens (human)
response to nicotine	Kappa-type opioid receptor	Homo sapiens (human)
G protein-coupled opioid receptor signaling pathway	Kappa-type opioid receptor	Homo sapiens (human)
maternal behavior	Kappa-type opioid receptor	Homo sapiens (human)
eating behavior	Kappa-type opioid receptor	Homo sapiens (human)
response to estrogen	Kappa-type opioid receptor	Homo sapiens (human)
estrous cycle	Kappa-type opioid receptor	Homo sapiens (human)
response to ethanol	Kappa-type opioid receptor	Homo sapiens (human)
regulation of saliva secretion	Kappa-type opioid receptor	Homo sapiens (human)
behavioral response to cocaine	Kappa-type opioid receptor	Homo sapiens (human)
sensory perception of temperature stimulus	Kappa-type opioid receptor	Homo sapiens (human)
defense response to virus	Kappa-type opioid receptor	Homo sapiens (human)
cellular response to lipopolysaccharide	Kappa-type opioid receptor	Homo sapiens (human)
cellular response to glucose stimulus	Kappa-type opioid receptor	Homo sapiens (human)
positive regulation of p38MAPK cascade	Kappa-type opioid receptor	Homo sapiens (human)
positive regulation of potassium ion transmembrane transport	Kappa-type opioid receptor	Homo sapiens (human)
response to acrylamide	Kappa-type opioid receptor	Homo sapiens (human)
positive regulation of eating behavior	Kappa-type opioid receptor	Homo sapiens (human)
conditioned place preference	Kappa-type opioid receptor	Homo sapiens (human)
neuropeptide signaling pathway	Kappa-type opioid receptor	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
acetylcholine transmembrane transporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
neurotransmitter transmembrane transporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
dopamine:sodium symporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
norepinephrine:sodium symporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
protein binding	Solute carrier family 22 member 1	Homo sapiens (human)
monoamine transmembrane transporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
secondary active organic cation transmembrane transporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
organic anion transmembrane transporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
organic cation transmembrane transporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
prostaglandin transmembrane transporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
pyrimidine nucleoside transmembrane transporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
thiamine transmembrane transporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
putrescine transmembrane transporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
spermidine transmembrane transporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
quaternary ammonium group transmembrane transporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
toxin transmembrane transporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
identical protein binding	Solute carrier family 22 member 1	Homo sapiens (human)
xenobiotic transmembrane transporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
(R)-carnitine transmembrane transporter activity	Solute carrier family 22 member 1	Homo sapiens (human)
neurotransmitter transmembrane transporter activity	Solute carrier family 22 member 3	Homo sapiens (human)
protein binding	Solute carrier family 22 member 3	Homo sapiens (human)
monoamine transmembrane transporter activity	Solute carrier family 22 member 3	Homo sapiens (human)
organic anion transmembrane transporter activity	Solute carrier family 22 member 3	Homo sapiens (human)
organic cation transmembrane transporter activity	Solute carrier family 22 member 3	Homo sapiens (human)
spermidine transmembrane transporter activity	Solute carrier family 22 member 3	Homo sapiens (human)
quaternary ammonium group transmembrane transporter activity	Solute carrier family 22 member 3	Homo sapiens (human)
toxin transmembrane transporter activity	Solute carrier family 22 member 3	Homo sapiens (human)
G-protein alpha-subunit binding	Mu-type opioid receptor	Homo sapiens (human)
G protein-coupled receptor activity	Mu-type opioid receptor	Homo sapiens (human)
beta-endorphin receptor activity	Mu-type opioid receptor	Homo sapiens (human)
voltage-gated calcium channel activity	Mu-type opioid receptor	Homo sapiens (human)
protein binding	Mu-type opioid receptor	Homo sapiens (human)
morphine receptor activity	Mu-type opioid receptor	Homo sapiens (human)
G-protein beta-subunit binding	Mu-type opioid receptor	Homo sapiens (human)
neuropeptide binding	Mu-type opioid receptor	Homo sapiens (human)
G protein-coupled opioid receptor activity	Delta-type opioid receptor	Homo sapiens (human)
protein binding	Delta-type opioid receptor	Homo sapiens (human)
receptor serine/threonine kinase binding	Delta-type opioid receptor	Homo sapiens (human)
G protein-coupled enkephalin receptor activity	Delta-type opioid receptor	Homo sapiens (human)
neuropeptide binding	Delta-type opioid receptor	Homo sapiens (human)
G protein-coupled opioid receptor activity	Kappa-type opioid receptor	Homo sapiens (human)
protein binding	Kappa-type opioid receptor	Homo sapiens (human)
receptor serine/threonine kinase binding	Kappa-type opioid receptor	Homo sapiens (human)
dynorphin receptor activity	Kappa-type opioid receptor	Homo sapiens (human)
neuropeptide binding	Kappa-type opioid receptor	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
plasma membrane	Solute carrier family 22 member 1	Homo sapiens (human)
basal plasma membrane	Solute carrier family 22 member 1	Homo sapiens (human)
membrane	Solute carrier family 22 member 1	Homo sapiens (human)
basolateral plasma membrane	Solute carrier family 22 member 1	Homo sapiens (human)
apical plasma membrane	Solute carrier family 22 member 1	Homo sapiens (human)
lateral plasma membrane	Solute carrier family 22 member 1	Homo sapiens (human)
presynapse	Solute carrier family 22 member 1	Homo sapiens (human)
nuclear outer membrane	Solute carrier family 22 member 3	Homo sapiens (human)
plasma membrane	Solute carrier family 22 member 3	Homo sapiens (human)
endomembrane system	Solute carrier family 22 member 3	Homo sapiens (human)
membrane	Solute carrier family 22 member 3	Homo sapiens (human)
basolateral plasma membrane	Solute carrier family 22 member 3	Homo sapiens (human)
apical plasma membrane	Solute carrier family 22 member 3	Homo sapiens (human)
mitochondrial membrane	Solute carrier family 22 member 3	Homo sapiens (human)
neuronal cell body	Solute carrier family 22 member 3	Homo sapiens (human)
presynapse	Solute carrier family 22 member 3	Homo sapiens (human)
endosome	Mu-type opioid receptor	Homo sapiens (human)
endoplasmic reticulum	Mu-type opioid receptor	Homo sapiens (human)
Golgi apparatus	Mu-type opioid receptor	Homo sapiens (human)
plasma membrane	Mu-type opioid receptor	Homo sapiens (human)
axon	Mu-type opioid receptor	Homo sapiens (human)
dendrite	Mu-type opioid receptor	Homo sapiens (human)
perikaryon	Mu-type opioid receptor	Homo sapiens (human)
synapse	Mu-type opioid receptor	Homo sapiens (human)
plasma membrane	Mu-type opioid receptor	Homo sapiens (human)
neuron projection	Mu-type opioid receptor	Homo sapiens (human)
plasma membrane	Delta-type opioid receptor	Homo sapiens (human)
synaptic vesicle membrane	Delta-type opioid receptor	Homo sapiens (human)
dendrite membrane	Delta-type opioid receptor	Homo sapiens (human)
presynaptic membrane	Delta-type opioid receptor	Homo sapiens (human)
axon terminus	Delta-type opioid receptor	Homo sapiens (human)
spine apparatus	Delta-type opioid receptor	Homo sapiens (human)
postsynaptic density membrane	Delta-type opioid receptor	Homo sapiens (human)
neuronal dense core vesicle	Delta-type opioid receptor	Homo sapiens (human)
plasma membrane	Delta-type opioid receptor	Homo sapiens (human)
neuron projection	Delta-type opioid receptor	Homo sapiens (human)
nucleoplasm	Kappa-type opioid receptor	Homo sapiens (human)
mitochondrion	Kappa-type opioid receptor	Homo sapiens (human)
cytosol	Kappa-type opioid receptor	Homo sapiens (human)
plasma membrane	Kappa-type opioid receptor	Homo sapiens (human)
membrane	Kappa-type opioid receptor	Homo sapiens (human)
sarcoplasmic reticulum	Kappa-type opioid receptor	Homo sapiens (human)
T-tubule	Kappa-type opioid receptor	Homo sapiens (human)
dendrite	Kappa-type opioid receptor	Homo sapiens (human)
synaptic vesicle membrane	Kappa-type opioid receptor	Homo sapiens (human)
presynaptic membrane	Kappa-type opioid receptor	Homo sapiens (human)
perikaryon	Kappa-type opioid receptor	Homo sapiens (human)
axon terminus	Kappa-type opioid receptor	Homo sapiens (human)
postsynaptic membrane	Kappa-type opioid receptor	Homo sapiens (human)
plasma membrane	Kappa-type opioid receptor	Homo sapiens (human)
neuron projection	Kappa-type opioid receptor	Homo sapiens (human)
virion membrane	Spike glycoprotein	Severe acute respiratory syndrome-related coronavirus
[Information is prepared from geneontology information from the June-17-2024 release]

Assay ID	Title	Year	Journal	Article
AID1826721	Selectivity index, ratio of Ki for displacement of [3H]-DADLE from human recombinant delta opioid receptor to Ki for displacement of [3H]-DAMGO from human recombinant mu opioid receptor	2022	Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6	Rational Design, Chemical Syntheses, and Biological Evaluations of Peripherally Selective Mu Opioid Receptor Ligands as Potential Opioid Induced Constipation Treatment.
AID1526744	Substrate activity at human OCT1*3 allele mutant expressed in HEK293 cells assessed as increase in compound uptake at 0.1 uM incubated for 2 mins by LC-MS/MS analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1526743	Substrate activity at human OCT1*2 allele mutant expressed in HEK293 cells assessed as increase in compound uptake at 0.1 uM incubated for 2 mins by LC-MS/MS analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1467162	Half life in rat liver microsomes	2017	Bioorganic & medicinal chemistry letters, 07-01, Volume: 27, Issue:13	Discovery of N-substituted-endo-3-(8-aza-bicyclo[3.2.1]oct-3-yl)-phenol and -phenyl carboxamide series of μ-opioid receptor antagonists.
AID1826722	Selectivity index, ratio of Ki for displacement of [3H]-U69593 from human recombinant kappa opioid receptor to Ki for displacement of [3H]-DAMGO from human recombinant mu opioid receptor	2022	Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6	Rational Design, Chemical Syntheses, and Biological Evaluations of Peripherally Selective Mu Opioid Receptor Ligands as Potential Opioid Induced Constipation Treatment.
AID1526748	Substrate activity at human OCT1*8 allele mutant expressed in HEK293 cells assessed as increase in compound uptake at 0.1 uM incubated for 2 mins by LC-MS/MS analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1467164	Half life in human liver microsomes	2017	Bioorganic & medicinal chemistry letters, 07-01, Volume: 27, Issue:13	Discovery of N-substituted-endo-3-(8-aza-bicyclo[3.2.1]oct-3-yl)-phenol and -phenyl carboxamide series of μ-opioid receptor antagonists.
AID1526742	Substrate activity at human OCT3 expressed in HEK293 cells assessed as increase in compound uptake by measuring Km incubated for 2 mins by LC-MS/MS analysis based Michaelis-Menten plot analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID711137	Selectivity ratio of Ki for delta opioid receptor to Ki for mu opioid receptor	2012	Journal of medicinal chemistry, Nov-26, Volume: 55, Issue:22	Design, synthesis, and biological evaluation of 17-cyclopropylmethyl-3,14β-dihydroxy-4,5α-epoxy-6β-[(4'-pyridyl)carboxamido]morphinan derivatives as peripheral selective μ opioid receptor Agents.
AID711136	Selectivity ratio of Ki for kappa opioid receptor to Ki for mu opioid receptor	2012	Journal of medicinal chemistry, Nov-26, Volume: 55, Issue:22	Design, synthesis, and biological evaluation of 17-cyclopropylmethyl-3,14β-dihydroxy-4,5α-epoxy-6β-[(4'-pyridyl)carboxamido]morphinan derivatives as peripheral selective μ opioid receptor Agents.
AID540210	Clearance in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1526778	Ratio of unbound maximal portal vein concentration in human at 450 mg, po to inhibition of human OCT1 expressed in HEK293 cells assessed as reduction in ASP+ substrate uptake by microplate reader based analysis	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1526747	Substrate activity at human OCT1*6 allele mutant expressed in HEK293 cells assessed as increase in compound uptake at 0.1 uM incubated for 2 mins by LC-MS/MS analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1826712	Displacement of [3H]-DAMGO from human recombinant mu opioid receptor by radioligand binding assay	2022	Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6	Rational Design, Chemical Syntheses, and Biological Evaluations of Peripherally Selective Mu Opioid Receptor Ligands as Potential Opioid Induced Constipation Treatment.
AID1526736	Substrate activity at human OCT1 expressed in HEK293 cells assessed as increase in compound uptake by measuring Vmax incubated for 2 mins by LC-MS/MS analysis based Michaelis-Menten plot analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID540212	Mean residence time in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1467163	Half life in dog liver microsomes	2017	Bioorganic & medicinal chemistry letters, 07-01, Volume: 27, Issue:13	Discovery of N-substituted-endo-3-(8-aza-bicyclo[3.2.1]oct-3-yl)-phenol and -phenyl carboxamide series of μ-opioid receptor antagonists.
AID1526751	Inhibition of human OCT1 expressed in HEK293 cells assessed as reduction in ASP+ substrate uptake by microplate reader based analysis	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1826734	Antagonist activity at human recombinant kappa opioid receptor assessed as reduction in U50,488H-induced [3S]-GTPgammaS binding	2022	Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6	Rational Design, Chemical Syntheses, and Biological Evaluations of Peripherally Selective Mu Opioid Receptor Ligands as Potential Opioid Induced Constipation Treatment.
AID702643	Increase in gastrointestinal motility in sc dosed morphine-pelleted mouse administered 20 mins before forced charcoal meal measured after 30 mins	2012	Bioorganic & medicinal chemistry letters, Jul-15, Volume: 22, Issue:14	6β-N-heterocyclic substituted naltrexamine derivative NAP as a potential lead to develop peripheral mu opioid receptor selective antagonists.
AID1826719	Displacement of [3H]-DADLE from human recombinant delta opioid receptor by radioligand binding assay	2022	Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6	Rational Design, Chemical Syntheses, and Biological Evaluations of Peripherally Selective Mu Opioid Receptor Ligands as Potential Opioid Induced Constipation Treatment.
AID1526731	Substrate activity at human OCT1 expressed in HEK293 cells assessed as increase in compound uptake at 0.05 uM incubated for 2 mins by LC-MS/MS analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1526753	Intrinsic clearance in human liver microsomes	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1826738	Gastroprokinetic activity in Swiss Webster mouse assessed as stimulation of gastrointestinal motility by measuring time required to defecation of red fecal pellet at 10 mg/kg, po incubated for 5 mins followed by morphine addition at 5 mg/kg and measured a	2022	Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6	Rational Design, Chemical Syntheses, and Biological Evaluations of Peripherally Selective Mu Opioid Receptor Ligands as Potential Opioid Induced Constipation Treatment.
AID1526733	Substrate activity at human OCT1 expressed in HEK293 cells assessed as increase in compound uptake at 0.5 uM incubated for 2 mins by LC-MS/MS analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1526746	Substrate activity at human OCT1*5 allele mutant expressed in HEK293 cells assessed as increase in compound uptake at 0.1 uM incubated for 2 mins by LC-MS/MS analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1864493	Substrate activity at human OCT3 overexpressed in HEK293 cells assessed as uptake ratio incubated for 2 mins by LC-MS/MS analysis	2022	Journal of medicinal chemistry, 09-22, Volume: 65, Issue:18	Substrates and Inhibitors of the Organic Cation Transporter 3 and Comparison with OCT1 and OCT2.
AID1526739	Substrate activity at OCT1 in primary human hepatocytes assessed as increase in compound uptake at 0.1 uM incubated for 2 mins in presence of 2 mM MPP+ by LC-MS/MS analysis relative to control	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1526749	Substrate activity at human OCT1*7 allele mutant expressed in HEK293 cells assessed as increase in compound uptake at 0.1 uM incubated for 2 mins by LC-MS/MS analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1467158	Displacement of [3H]DPN from recombinant human mu opioid receptor expressed in CHOK1 cell membranes	2017	Bioorganic & medicinal chemistry letters, 07-01, Volume: 27, Issue:13	Discovery of N-substituted-endo-3-(8-aza-bicyclo[3.2.1]oct-3-yl)-phenol and -phenyl carboxamide series of μ-opioid receptor antagonists.
AID1526741	Substrate activity at human OCT3 expressed in HEK293 cells assessed as increase in compound uptake by measuring Vmax incubated for 2 mins by LC-MS/MS analysis based Michaelis-Menten plot analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1467161	Intrinsic activity at recombinant human mu opioid receptor expressed in CHOK1 cells by [35S]GTPgammaS binding assay relative to DAMGO	2017	Bioorganic & medicinal chemistry letters, 07-01, Volume: 27, Issue:13	Discovery of N-substituted-endo-3-(8-aza-bicyclo[3.2.1]oct-3-yl)-phenol and -phenyl carboxamide series of μ-opioid receptor antagonists.
AID1526774	Cmax in human at 450 mg, po	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1526745	Substrate activity at human OCT1*4 allele mutant expressed in HEK293 cells assessed as increase in compound uptake at 0.1 uM incubated for 2 mins by LC-MS/MS analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1526737	Substrate activity at human OCT1 expressed in HEK293 cells assessed as increase in compound uptake by measuring Km incubated for 2 mins by LC-MS/MS analysis based Michaelis-Menten plot analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1826720	Displacement of [3H]-U69593 from human recombinant kappa opioid receptor by radioligand binding assay	2022	Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6	Rational Design, Chemical Syntheses, and Biological Evaluations of Peripherally Selective Mu Opioid Receptor Ligands as Potential Opioid Induced Constipation Treatment.
AID540209	Volume of distribution at steady state in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1826737	Antagonist activity at human recombinant delta opioid receptor assessed as reduction in SNC80 induced [3S]-GTPgammaS binding	2022	Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6	Rational Design, Chemical Syntheses, and Biological Evaluations of Peripherally Selective Mu Opioid Receptor Ligands as Potential Opioid Induced Constipation Treatment.
AID1526752	Passive membrane permeability by LC-MS/MS analysis based PAMPA	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1526775	Unbound Cmax in human at 450 mg, po	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1467159	Displacement of [3H]DPN from recombinant human delta opioid receptor expressed in CHOK1 cell membranes	2017	Bioorganic & medicinal chemistry letters, 07-01, Volume: 27, Issue:13	Discovery of N-substituted-endo-3-(8-aza-bicyclo[3.2.1]oct-3-yl)-phenol and -phenyl carboxamide series of μ-opioid receptor antagonists.
AID1526735	Substrate activity at human OCT1 expressed in HEK293 cells assessed as increase in compound uptake at 0.1 uM incubated for 2 mins in presence of 2 mM MPP+ by LC-MS/MS analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1526776	Unbound maximal portal vein concentration of in human at 450 mg, po	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1526732	Substrate activity at human OCT1 expressed in HEK293 cells assessed as increase in compound uptake at 0.1 uM incubated for 2 mins by LC-MS/MS analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1526734	Substrate activity at human OCT1 expressed in HEK293 cells assessed as increase in compound uptake at 0.05 to 0.5 uM incubated for 2 mins in presence of 2 mM MPP+ by LC-MS/MS analysis relative to control empty vector transfected cells	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1526738	Substrate activity at OCT1 in primary human hepatocytes assessed as increase in compound uptake at 0.1 uM incubated for 2 mins by LC-MS/MS analysis relative to control	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1526740	Substrate activity at OCT1 in primary human hepatocytes assessed as increase in compound uptake at 1 uM incubated for 2 mins by LC-MS/MS analysis relative to control	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1526777	Ratio of unbound Cmax in human at 450 mg, po to inhibition of human OCT1 expressed in HEK293 cells assessed as reduction in ASP+ substrate uptake by microplate reader based analysis	2019	Journal of medicinal chemistry, 11-14, Volume: 62, Issue:21	Opioids as Substrates and Inhibitors of the Genetically Highly Variable Organic Cation Transporter OCT1.
AID1826740	Reversal of morphine induced constipation in Swiss Webster mouse at 10 mg/kg, po for 5 mins followed by morphine addition at 5 mg/kg and measured after 20 mins by carmine red dye assay	2022	Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6	Rational Design, Chemical Syntheses, and Biological Evaluations of Peripherally Selective Mu Opioid Receptor Ligands as Potential Opioid Induced Constipation Treatment.
AID540213	Half life in human after iv administration	2008	Drug metabolism and disposition: the biological fate of chemicals, Jul, Volume: 36, Issue:7	Trend analysis of a database of intravenous pharmacokinetic parameters in humans for 670 drug compounds.
AID1826723	Antagonist activity at human recombinant mu opioid receptor assessed as reduction in DAMGO-induced [3S]-GTPgammaS binding	2022	Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6	Rational Design, Chemical Syntheses, and Biological Evaluations of Peripherally Selective Mu Opioid Receptor Ligands as Potential Opioid Induced Constipation Treatment.
AID1467160	Displacement of [3H]DPN from guinea pig kappa opioid receptor expressed in CHOK1 cell membranes	2017	Bioorganic & medicinal chemistry letters, 07-01, Volume: 27, Issue:13	Discovery of N-substituted-endo-3-(8-aza-bicyclo[3.2.1]oct-3-yl)-phenol and -phenyl carboxamide series of μ-opioid receptor antagonists.
AID1346364	Human mu receptor (Opioid receptors)	2009	Bioorganic & medicinal chemistry letters, Apr-15, Volume: 19, Issue:8	Syntheses of novel high affinity ligands for opioid receptors.
AID1346361	Human delta receptor (Opioid receptors)	2009	Bioorganic & medicinal chemistry letters, Apr-15, Volume: 19, Issue:8	Syntheses of novel high affinity ligands for opioid receptors.
AID1346329	Human kappa receptor (Opioid receptors)	2009	Bioorganic & medicinal chemistry letters, Apr-15, Volume: 19, Issue:8	Syntheses of novel high affinity ligands for opioid receptors.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Timeframe	Studies, This Drug (%)	All Drugs %
pre-1990	41 (13.95)	18.7374
1990's	34 (11.56)	18.2507
2000's	77 (26.19)	29.6817
2010's	119 (40.48)	24.3611
2020's	23 (7.82)	2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Publication Type	This drug (%)	All Drugs (%)
Trials	56 (17.50%)	5.53%
Reviews	69 (21.56%)	6.00%
Case Studies	23 (7.19%)	4.05%
Observational	1 (0.31%)	0.25%
Other	171 (53.44%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (58)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
Methylnaltrexone vs Erythromycin for Facilitating Gastric Emptying Time in Critically Ill Patients Intolerant to Enteral Feeding [NCT01117376]	Phase 2	42 participants (Anticipated)	Interventional	2010-05-31	Terminated(stopped due to The study was prematurely terminated because of unavailibility of Methylnaltrexone in the region)
A Phase 1, Open-Label, Study of the Effect of Cimetidine, a Known Inhibitor of Active Renal Secretion, on the Single-Dose Pharmacokinetics of Intravenously-Administered Methylnaltrexone in Healthy Adults [NCT01366378]	Phase 1	18 participants (Actual)	Interventional	2007-01-31	Completed
A Phase II Double-Blind Randomized Parallel Group Study of Intravenous (IV) Methylnaltrexone (MNTX) in the Prevention of Post-Operative Ileus [NCT01367548]	Phase 2	65 participants (Actual)	Interventional	2003-07-31	Completed
The Effect Of Methylnaltrexone (Relistor™) on Gut Motility and Tolerance to Tube Feeding in Patients Treated With Opiate Therapy [NCT01360372]	Phase 3	0 participants (Actual)	Interventional	2010-10-31	Withdrawn(stopped due to No eligible subjects identified)
A Multiple-Dose, Open-Label Study to Evaluate the Pharmacokinetics of MNTX in Healthy Adult Subjects [NCT01366326]	Phase 1	20 participants (Actual)	Interventional	2010-07-31	Completed
An Open-Label, Phase I Study of the Pharmacokinetics and Bioavailability of Single, Ascending Subcutaneous Doses of Methylnaltrexone Versus Intravenous Dose in Normal, Healthy Male Volunteers [NCT01367496]	Phase 1	6 participants (Actual)	Interventional	2002-06-30	Completed
A Phase II Double-Blind, Randomized, Parallel Group, Dose Ranging Study of Subcutaneous Methylnaltrexone in Patients With Opioid-Induced Bowel Dysfunction [NCT01367574]	Phase 2	39 participants (Actual)	Interventional	2002-04-30	Completed
A Randomized, Double-Blind, Placebo/Positive Controlled, Evaluation of the Effects of MNTX on ECG Parameters and Cardiac Repolarization in Normal Volunteers [NCT01363323]	Phase 1	546 participants (Actual)	Interventional	2004-11-30	Completed
A Phase 1 Randomized, Double-Blind, Placebo Controlled Parallel Group Study of the Pharmacokinetics, Safety and Tolerability of Methylnaltrexone Bromide Administered as Single and Multiple Intravenous Doses to Healthy Adults and Elderly Male and Female Su [NCT01366365]	Phase 1	28 participants (Actual)	Interventional	2006-10-31	Completed
A Phase I, Randomized, Open-Label, Active- and Placebo-Controlled Parallel Group Study of the Effect of Subcutaneous and Intravenous Methylnaltrexone on CYP450 2D6 Activity in Healthy Extensive Metabolizers of Dextromethorphan [NCT01367535]	Phase 1	54 participants (Actual)	Interventional	2006-03-31	Completed
A Three-Month Open-Label Treatment Extension of Protocol MNTX 302 [NCT01367613]	Phase 3	89 participants (Actual)	Interventional	2004-03-31	Completed
A Compassionate Use Study of Methylnaltrexone in Patients With Opioid-Induced Side Effects [NCT01368562]		26 participants (Actual)	Interventional	2003-01-24	Completed
A Replicate Design, Double-Blind, Randomized, Placebo-Controlled Tolerance and Pharmacokinetics Study of N-Methylnaltrexone Tablets in Normal, Healthy Volunteers [NCT01366339]	Phase 1	37 participants (Actual)	Interventional	2003-10-31	Completed
A Phase 1, Open-Label Study to Evaluate Single Dose Pharmacokinetics, Safety, and Tolerability of Methylnaltrexone (MNTX) in Subjects With Impaired Renal Function [NCT01367509]	Phase 1	32 participants (Actual)	Interventional	2004-03-31	Completed
Safety and Gastrointestinal Effects of Multiple-Dosed Intravenous Methylnaltrexone in Healthy Human Volunteers [NCT01367587]	Phase 2	12 participants (Actual)	Interventional	2002-04-30	Completed
An Open-Label, Phase I, Single Dose Study of the Pharmacokinetics, Mass Balance and Disposition of Intravenously Administered 14C-Methylnaltrexone in Normal, Healthy Volunteers [NCT01367483]	Phase 1	6 participants (Anticipated)	Interventional	2005-06-30	Completed
A Phase 3, Double-Blind, Randomized, Parallel-Group, Placebo-Controlled Study of Intravenous (IV) Methylnaltrexone Bromide (MNTX) in the Treatment of Post-Operative Ileus (POI) [NCT00401375]	Phase 3	524 participants (Actual)	Interventional	2006-10-31	Completed
Pharmacokinetics and Bioavailability Comparison of Two Different Formulations of MNTX Tablets: A Double-Blind, Single Dose, Crossover, Phase 1 Study in Normal Volunteers [NCT01366352]	Phase 1	24 participants (Actual)	Interventional	2004-02-29	Completed
A Phase 1, Open-Label, Study to Evaluate Single Dose Pharmacokinetics, Safety, and Tolerability of Methylnaltrexone (MNTX) in Volunteers With Impaired Hepatic Function [NCT01367522]	Phase 1	24 participants (Actual)	Interventional	2004-03-31	Completed
A Three-Month Open-Label Treatment Extension of Protocol MNTX 301 [NCT01367600]	Phase 3	27 participants (Actual)	Interventional	2003-02-28	Completed
A Multicenter, Randomized, Double-Blind, Placebo-Controlled, And Parallel-Group Study Of Subcutaneous Methylnaltrexone (MOA-728) For The Treatment Of Opioid-Induced Constipation In Adult Subjects [NCT00936884]	Phase 3	50 participants (Actual)	Interventional	2009-07-31	Completed
Open-Label Extension Study To Assess The Safety Of A Fixed Dose Of Subcutaneous Methylnaltrexone In Subjects With Advanced Illness And Opioid-Induced Constipation [NCT00672139]	Phase 4	156 participants (Actual)	Interventional	2008-07-31	Completed
An Open-Label Study to Evaluate the Long-Term Safety of Subcutaneous MOA-728 for Treatment of Opioid-Induced Constipation in Subjects With Nonmalignant Pain [NCT00804141]	Phase 3	1,040 participants (Actual)	Interventional	2008-12-03	Completed
Methylnaltrexone (MNTX) for Treatment of Opioid-induced Constipation in Advanced Illness Patients : a Multicenter, Randomized, Double-blind , Placebo-controlled Trail [NCT02574819]	Phase 2/Phase 3	198 participants (Anticipated)	Interventional	2015-04-30	Recruiting
A Randomized, Double-Blind, Placebo-Controlled Study Of A Fixed Dose Of Subcutaneous Methylnaltrexone In Adults With Advanced Illness And Opioid-Induced Constipation: Efficacy, Safety, And Additional Health Outcomes [NCT00672477]	Phase 4	237 participants (Actual)	Interventional	2008-06-30	Completed
A Phase I Urodynamic Study of the Opioid Antagonist, Naloxone and Intravenous Methylnaltrexone Reverse Opioid Effects on Bladder Function in Healthy Volunteers [NCT01367561]	Phase 1	15 participants (Actual)	Interventional	2002-10-31	Completed
An Open-Label Extension Study to Evaluate the Safety and Efficacy of Oral Methylnaltrexone Bromide Tablets in Subjects With Advanced Pancreatic Cancer [NCT04151719]	Phase 3	0 participants (Actual)	Interventional	2020-02-03	Withdrawn(stopped due to Due to pandemic challenges and consideration of a different study design in the future.)
Effects of Peripherally Acting µ-opioid Receptor Antagonists on Acute Pancreatitis - An Investigator-initiated, Randomized, Placebo-controlled, Double-blind Clinical Trial [NCT04743570]	Phase 2/Phase 3	105 participants (Actual)	Interventional	2021-05-14	Completed
A Multicenter, Double-Blind, Randomized, Parallel-Group, Placebo Controlled Phase 2 Study of Once-Daily Subcutaneous Methylnaltrexone (MNTX) in the Treatment of Opioid-Induced Constipation During Rehabilitation After Orthopedic Procedures [NCT00640146]	Phase 2	37 participants (Actual)	Interventional	2007-10-19	Completed
A Multicenter, Randomized, Double-Blind, Placebo-Controlled, Parallel-Group Study of Intravenous Methylnaltrexone (MOA-728) for the Treatment of Post Operative Ileus After Ventral Hernia Repair [NCT00528970]	Phase 3	374 participants (Actual)	Interventional	2007-10-17	Completed
Pharmacokinetics of Once Daily Subcutaneous Methylnaltrexone in Neurointensive Care Patients With High Dose Sufentanil Analgosedation [NCT01889290]	Phase 1	9 participants (Actual)	Interventional	2014-02-28	Completed
Can Methylnaltrexone Safely Treat Opioid Related Constipation in the Emergency Department? [NCT00949377]	Phase 4	0 participants (Actual)	Interventional	2009-09-30	Withdrawn(stopped due to Unable to recruit enough patients at a single center.)
A Multicenter, Randomized, Double-blind, Placebo-controlled, Parallel-group Study of Intravenous Methylnaltrexone (MOA-728) for the Treatment of Post Operative Ileus. [NCT00387309]	Phase 3	495 participants	Interventional	2006-12-31	Completed
Clinical Evaluation of the Efficacy of Methylnaltrexone in Resolving Constipation Induced by Different Opioid Subtypes, Combined With Laboratory Analysis of Immunomodulatory and Antiangiogenic Effects of Methylnaltrexone [NCT01955213]		7 participants (Actual)	Observational	2012-07-31	Terminated
A Phase II/III Adaptive Study to Evaluate the Safety and Efficacy of Oral Methylnaltrexone Bromide Tablets in Subjects With Advanced Pancreatic Cancer [NCT04083651]	Phase 2/Phase 3	0 participants (Actual)	Interventional	2020-01-06	Withdrawn(stopped due to Due to pandemic challenges and consideration of a different study design in the future.)
A Randomized, Double-Blind, Placebo-Controlled Trial Evaluating the Safety and Efficacy of Subcutaneous Methylnaltrexone for the Treatment of Opioid-Induced Constipation in Subjects With Cancer-Related Pain [NCT00858754]	Phase 4	0 participants (Actual)	Interventional	2009-03-31	Withdrawn(stopped due to Withdrawn [This study was terminated early by Wyeth, prior to dosing any subjects, for business reasons not related to safety.)
Methylnaltrexone for the Reversal of Opiate-Induced Constipation in the Intensive Care Unit [NCT01050595]	Phase 3	80 participants (Anticipated)	Interventional	2009-12-31	Recruiting
Is the Opioid-induced Pharyngeal and Esophageal Dysfunction Peripherally or Central Mediated? [NCT01012960]	Phase 4	13 participants (Actual)	Interventional	2009-11-30	Completed
A Mulitcenter, Randomized, Double-Blind, Placebo-Controlled, Parallel-Group Study of Subcutaneous MOA-728 for the Treatment of Opioid-Induced Constipation in Subjects With Chronic Non-Malignant Pain [NCT00529087]	Phase 3	460 participants (Actual)	Interventional	2007-08-31	Completed
RELISTOR's Effects on Opioid-Induced Constipation in Postoperative 1-2 Level Anterior Lumbar Interbody Fusion Patients: A Case-Control Study [NCT04930237]		0 participants (Actual)	Observational	2021-07-01	Withdrawn(stopped due to PI request to close study)
A Phase 3, Multicenter, Randomized, Double-blind, Placebo-controlled, Parallel-group Study of Oral Methylnaltrexone for the Treatment of Opioid-Induced Constipation in Subjects With Chronic, Non-Malignant Pain [NCT01186770]	Phase 3	804 participants (Actual)	Interventional	2010-09-01	Completed
A Double-Blind, Phase 3, Two-Week, Placebo Controlled Study of Methylnaltrexone(MNTX) for the Relief of Constipation Due to Opioid Therapy in Advance Medical Illness. [NCT00402038]	Phase 3	134 participants (Actual)	Interventional	2004-02-29	Completed
Methylnaltrexone as a Method to imprOVE Platelet Inhibition of Ticagrelor in Morphine-treated Patients With ST-segMENT Elevation Myocardial Infarction: a Prospective, Single Blinded Randomized, Placebo-controlled Trial [NCT02942550]	Phase 4	82 participants (Actual)	Interventional	2016-11-30	Completed
A Double-Blind Placebo-Controlled Study of Methylnaltrexone (MNTX) for the Relief of Constipation Due to Chronic Opioid Therapy in Patients With Advanced Medical Illness [NCT00401362]	Phase 3	154 participants (Actual)	Interventional	2003-02-28	Completed
Methylnaltrexone Versus Naloxegol in the Treatment of Opioid-Induced Constipation in the Emergency Department [NCT03523520]	Phase 4	15 participants (Actual)	Interventional	2020-12-23	Completed
The Use of Methylnaltrexone to Reduce Post-operative Opioid-induced Constipation in the Pediatric Spinal Fusion Patient [NCT01773096]	Phase 4	60 participants (Anticipated)	Interventional	2013-05-31	Completed
Phase II Trial of Subcutaneous Methylnaltrexone in the Treatment of Severe Opioid-induced Constipation in Cancer Patients [NCT01004393]	Phase 2	12 participants (Actual)	Interventional	2009-10-31	Completed
The Effect of Naloxone and Mehtylnaltrexone on Esophageal Sensitivity in Healthy Volunteers: a Randomized, Double-blind, Placebo-controlled Study [NCT03014843]		12 participants (Actual)	Interventional	2013-10-31	Completed
Effects of Extended Release Methylnaltrexone Bromide (150 mg b.i.d.) in Comparison to Extended Release Naloxone Hydrochloride (20 mg b.i.d.) on Loperamide-induced Delay of the Oro-cecal, Whole-gut and Colon Transit Time in Healthy Subjects. [NCT01596764]	Phase 1	16 participants (Actual)	Interventional	2011-05-31	Completed
Effects of 500 mg Immediate Release and Extended Release Methylnaltrexone on Loperamide-induced Delay of the Oro-cecal and Whole-gut Transit Time in Healthy Subjects [NCT01596777]	Phase 1	15 participants (Actual)	Interventional	2010-01-31	Completed
Effect of the Peripheral Opioid Receptor Antagonist Methylnaltrexone on the Pharmacokinetic and Pharmacodynamic Profiles of Ticagrelor in Patients Receiving Morphine: a Prospective, Randomized Placebo-controlled Trial [NCT02403830]	Phase 4	30 participants (Actual)	Interventional	2015-08-31	Completed
Impact of Naloxegol on Prevention of Lower GI Tract Paralysis in Critically Ill Adults Initiated on Scheduled Intravenous Opioid Therapy: A Randomized, Double-Blind, Placebo-Controlled, Phase II, Single-Center, Proof of Concept Study [NCT02977286]	Phase 4	12 participants (Actual)	Interventional	2017-01-01	Terminated(stopped due to Poor enrollment)
Double-Blind, Randomized Trial of Peri-operative Subcutaneous Methylnaltrexone Versus Placebo for Postoperative Ileus Prevention After Adult Spinal Arthrodesis [NCT03852524]	Phase 2	82 participants (Actual)	Interventional	2019-02-21	Completed
Effect of Methylnaltrexone on Gastrointestinal and Colonic Transit in Health [NCT01055704]	Phase 4	48 participants (Actual)	Interventional	2009-11-30	Completed
"Methylnatrexone In Resectable Head and Neck Squamous Cell Carcinoma (MINK). A Window of Opportunity Pilot Study." [NCT06162377]	Phase 4	25 participants (Anticipated)	Interventional	2024-04-30	Not yet recruiting
A Multicenter, Randomized, Double-blind, Placebo-Controlled, Parallel-Group Study of Oral MOA-728 for the Treatment of Opioid- Induced Bowel Dysfunction in Subjects With Chronic Nonmalignant Pain [NCT00547586]	Phase 2	122 participants (Actual)	Interventional	2007-10-31	Completed
Opioid-Induced Swallowing Dysfunction - The Impact of Bolus Volume: a Randomized, Double-Blind Study in Healthy Volunteers [NCT03283020]	Phase 4	20 participants (Anticipated)	Interventional	2017-11-11	Recruiting
Role of Endogenous Opioid Peptides in HIV-associated Chronic Widespread Pain [NCT04787848]		200 participants (Anticipated)	Interventional	2021-11-15	Recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Trial	Outcome
NCT00401375 (4) [back to overview]	Time to Discharge Eligibility
NCT00401375 (4) [back to overview]	Time to Discharge Order Written From the End of Surgery
NCT00401375 (4) [back to overview]	Time to First Bowel Movement
NCT00401375 (4) [back to overview]	Number of Participants With Clinically Meaningful Events (CMEs) for Nausea or Retching/Vomiting at 0 or 24 Hours as Evaluated by the Opioid-Related Symptom Distress Scale (SDS)
NCT00528970 (4) [back to overview]	Number of Participants With Clinically Meaningful Events (CMEs) for Nausea or Retching/Vomiting at Day 2 (24 Hours) as Evaluated by the Opioid-Related Symptom Distress Scale (SDS)
NCT00528970 (4) [back to overview]	Time to Discharge Eligibility
NCT00528970 (4) [back to overview]	Time to Discharge Order Written From the End of Surgery
NCT00528970 (4) [back to overview]	Time to First Bowel Movement
NCT00529087 (22) [back to overview]	Change From Baseline in Weekly Number of Quality Rescue-free Bowel Movements (RFBM)
NCT00529087 (22) [back to overview]	Time to the First Rescue-free Bowel Movement (RFBM) After First Dose
NCT00529087 (22) [back to overview]	Percentage of Patients With Improvement in Straining Scale Score for Rescue-free Bowel Movements (RFBM) by 1 Point During Open Label Period
NCT00529087 (22) [back to overview]	Change in Weekly Number of Complete Rescue-free Bowel Movements (RFBM)
NCT00529087 (22) [back to overview]	Percentage of Patients With Improvement in Bristol Stool Form Scale Score for Rescue-free Bowel Movements (RFBM) by 1 Point During Open Label Period
NCT00529087 (22) [back to overview]	Percentage of Patients With Any Diarrhea or Watery Rescue-free Bowel Movements (RFBM) During Open-label Period.
NCT00529087 (22) [back to overview]	Percentage of Patients With an Increase of at Least 1 in the Weekly Rescue-free Bowel Movement (RFBM) Rate From Baseline for the Double-blind Period at 4 Weeks
NCT00529087 (22) [back to overview]	Percentage of Patients With a Weekly Rescue-free Bowel Movement (RFBM) Rate ≥ 3 and an Increase of at Least 1 in the Weekly RFBM Rate From Baseline for the Double-blind Period
NCT00529087 (22) [back to overview]	Percentage of Patients Having a Rescue-free Bowel Movement (RFBM) Within 4 Hours of the First Dose
NCT00529087 (22) [back to overview]	Change in Straining Scale Score of Rescue-free Bowel Movements (RFBM) From Baseline During Double-blind Period
NCT00529087 (22) [back to overview]	Percentage of Patients Achieving at Least 3 Rescue-free Bowel Movements (RFBM) Per Week in Double-blind Period
NCT00529087 (22) [back to overview]	Change in Weekly Number of Bowel Movements During Double-blind Period
NCT00529087 (22) [back to overview]	Percentage of Active Injections Resulting in Any Rescue-free Bowel Movement (RFBM) Within 4 Hours of Injection During the Double-blind Period
NCT00529087 (22) [back to overview]	Change From Baseline in Weekly Number of Rescue-free Bowel Movements (RFBM) for the Double-blind Period at 4 Weeks
NCT00529087 (22) [back to overview]	Change in Bristol Stool Form Scale Score for Rescue-free Bowel Movements (RFBM)
NCT00529087 (22) [back to overview]	Change in Percentage of Rescue-free Bowel Movements (RFBM) Classified as Diarrhea or Watery Stools From Baseline During Double-blind Period
NCT00529087 (22) [back to overview]	Change in Percentage of Rescue-free Bowel Movements (RFBM) With a Sensation of Complete Evacuation From Baseline During Double-blind Period
NCT00529087 (22) [back to overview]	Change in Percentage of Rescue-free Bowel Movements (RFBM) With Bristol Stool Form Scale in Type 3 or Type 4 From Baseline During Double-blind Period
NCT00529087 (22) [back to overview]	Change in Percentage of Rescue-free Bowel Movements (RFBM) With Straining Scale Scores of 0 or 1 (no, or Mild) From Baseline During Double-blind Period
NCT00529087 (22) [back to overview]	Weekly Number of Rescue-free Bowel Movements (RFBM) (Open-label Period)
NCT00529087 (22) [back to overview]	Percentage of Active Injections Resulting in Any Rescue-free Bowel Movement (RFBM) Within 1, 2, 3 and 6 Hour(s) in Double-blind Period
NCT00529087 (22) [back to overview]	Percentage of Injections Resulting in Any Rescue-free Bowel Movement (RFBM) Within 1, 2, 3, 4 and 6 Hours in Double-blind Period
NCT00547586 (1) [back to overview]	Percentage of Participants With a Spontaneous Bowel Movement (SBM) Within 1, 2, 3, 4, and 6 Hours of Treatment
NCT00640146 (3) [back to overview]	Time to First Rescue-Free Bowel Movement (Laxation)
NCT00640146 (3) [back to overview]	Percentage of Participants With Laxation Response Within 4 Hours of the First Dose
NCT00640146 (3) [back to overview]	Percentage of Participants With Laxation Response Within 2 Hours of the First Dose
NCT00672139 (1) [back to overview]	Number of Laxations Per Subject Within 24 Hours of Dosing Per Week.
NCT00672477 (2) [back to overview]	Time to First Rescue-free Laxation (Following the First Dose of Study Drug).
NCT00672477 (2) [back to overview]	The Proportion of Subjects Who Have a Rescue-free Laxation Response Within 4 Hours After at Least 2 of the First 4 Doses
NCT00804141 (2) [back to overview]	Number of Participants With Treatment-Emergent Adverse Events (TEAEs)
NCT00804141 (2) [back to overview]	Change From Baseline in Weekly Bowel Movement (BM) Rate Through Follow-up
NCT00936884 (3) [back to overview]	The Proportion of Subjects Having a Rescue-free Bowel Movement (RFBM) Within 4 Hours After the First Injection.
NCT00936884 (3) [back to overview]	Percentage of Injections Resulting in RFBM Within 4 Hours After Test Article Administration.
NCT00936884 (3) [back to overview]	The Proportion of Subjects Having a Rescue-free Bowel Movement (RFBM) Within 4 Hours After Each Dose During Double-blind Period.
NCT01004393 (8) [back to overview]	Rescue-free Laxation After Administration of Subcutaneous Methylnaltrexone
NCT01004393 (8) [back to overview]	Bowel Movement Assessment (Frequency, Consistency and Difficulty) After Administration of Subcutaneous Methylnaltrexone
NCT01004393 (8) [back to overview]	Constipation Assessment (Severity and Distress) After Administration of Subcutaneous Methylnaltrexone
NCT01004393 (8) [back to overview]	Laxation After Administration of Subcutaneous Methylnaltrexone
NCT01004393 (8) [back to overview]	Overall Pain Scores (0-10; 0=no Pain, 10=Worst Pain) After Administration of Subcutaneous Methylnaltrexone
NCT01004393 (8) [back to overview]	Patient Satisfaction With the Study Medication After Administration of Subcutaneous Methylnaltrexone
NCT01004393 (8) [back to overview]	Symptoms of Opioid Withdrawal (Modified Himmelsbach Withdrawal Scales (Ranging 7-28 in Total; 1=None - 4=Severe for 7 Items)) After Administration of Subcutaneous Methylnaltrexone
NCT01004393 (8) [back to overview]	Time to Laxation After Administration of Subcutaneous Methylnaltrexone
NCT01055704 (8) [back to overview]	Colonic Filling at 6 Hours
NCT01055704 (8) [back to overview]	Colonic Geometric Center at 24 Hours
NCT01055704 (8) [back to overview]	Colonic Geometric Center at 4 Hours
NCT01055704 (8) [back to overview]	Colonic Geometric Center at 48 Hours
NCT01055704 (8) [back to overview]	Stool Consistency as Reported From the Bristol Stool Scale
NCT01055704 (8) [back to overview]	Stool Frequency
NCT01055704 (8) [back to overview]	T1/2 of Ascending Colon Emptying
NCT01055704 (8) [back to overview]	T1/2 of Gastric Emptying of Solid
NCT01186770 (3) [back to overview]	Percentage of Participants Who Responded (Responder) to Study Drug During Weeks 1 to 4
NCT01186770 (3) [back to overview]	Change in Weekly Number of RFBMs From Baseline Over the Entire First 4 Weeks (28 Days) of Dosing
NCT01186770 (3) [back to overview]	Average Percentage of Dosing Days That Resulted in Rescue-Free Bowel Movements (RFBMs) Within 4 Hours of Dosing During Weeks 1 to 4
NCT01368562 (1) [back to overview]	Number of Participants With Opioid Induced Side Effects
NCT02403830 (3) [back to overview]	AUC of Ticagrelor Plasma Levels
NCT02403830 (3) [back to overview]	Platelet Reactivity Measured by VASP
NCT02403830 (3) [back to overview]	Platelet Reactivity Measured by VerifyNow P2Y12
NCT02977286 (17) [back to overview]	Daily Maximal Sedation Assessment Scale (SAS) Score
NCT02977286 (17) [back to overview]	Daily Presence of Delirium Using the Intensive Care Delirium Screening Checklist (ICDSC)
NCT02977286 (17) [back to overview]	Days Without Mechanical Ventilation Support for Duration of ICU Stay
NCT02977286 (17) [back to overview]	ICU Days Without a SBM
NCT02977286 (17) [back to overview]	Number of Patients With Loose and Unformed or Liquid SBM
NCT02977286 (17) [back to overview]	Occurrence of Lower GI Tract Paralysis (≥3 Days Without a SBM)
NCT02977286 (17) [back to overview]	Occurrence of Lower GI Tract Paralysis Requiring GI/Surgical Consultation
NCT02977286 (17) [back to overview]	Percentage of Daily Goal Reached for Enteral Nutrition Administration
NCT02977286 (17) [back to overview]	Time to First Episode of Diarrhea
NCT02977286 (17) [back to overview]	Time to First Spontaneous Bowel Movement (SBM)
NCT02977286 (17) [back to overview]	Time to First Spontaneous Bowel Movement (SBM) Administration
NCT02977286 (17) [back to overview]	Number of Patients That Required Use of the Study Laxative Protocol
NCT02977286 (17) [back to overview]	Abdominal Pressure Measurement
NCT02977286 (17) [back to overview]	Average Daily Opioid Requirement [in IV Fentanyl Equivalents (mcg Per Day)]
NCT02977286 (17) [back to overview]	Daily Difference in the Pre-dose and Post-dose Clinical Opioid Withdrawal Scale (COWS) Score
NCT02977286 (17) [back to overview]	Daily Fluid Balance
NCT02977286 (17) [back to overview]	Daily Maximal Pain Scale Score
NCT03852524 (4) [back to overview]	Daily Narcotics
NCT03852524 (4) [back to overview]	Time to Discharge
NCT03852524 (4) [back to overview]	Time to First Bowel Movement
NCT03852524 (4) [back to overview]	Time to Discharge

Time to Discharge Eligibility

Time to discharge eligibility was measured from the end of surgery (defined as the time when the last skin suture or staple was placed in the participant). Discharge eligibility was defined as both tolerance of solid food and at least one bowel movement. Participants were considered to have tolerated solid food when they have eaten greater than or equal to (≥) 50 percent (%), of the first of two successive solid food meals (based on the judgement of the investigator or designee), without vomiting or nausea. Participants readmitted to the hospital with a diagnosis of POI within 7 days of discharge were considered treatment failures. Analysis was performed by Kaplan-Meier estimate. (NCT00401375)
Timeframe: Day 1 (From the time of end of surgery [that is; from the first dose of study drug administration]) up to Day 10

Intervention	days (Mean)
MNTX 12 mg	5.8
MNTX 24 mg	7.0
Placebo	6.5

Intervention	percentage of active injections (Mean)
MOA-728 QD	28.9
MOA-728 QOD	30.2
Placebo QD (Only QOD Injections)	9.3
Placebo QD	9.4

Intervention	percentage of active injections (Mean)
	1 hour	2 hours	3 hours	6 hours
MOA-728 QD	17.8	24.2	27.0	31.1
MOA-728 QOD	17.3	24.1	28.0	32.5
Placebo	3.3	5.8	7.8	11.5
Placebo QD (Only QOD Injections)	3.2	5.4	7.5	11.1

Intervention	Participants (Count of Participants)
	Within 1 hour of 1st dose	Within 2 hours of 1st dose	Within 3 hours of 1st dose	Within 4 hours of 1st dose	Within 6 hours of 1st dose
150 mg	0	1	1	1	1
300 mg	0	1	2	4	4
450 mg	7	9	13	15	15
600 mg	2	5	9	14	17
Placebo	0	1	3	3	6

Intervention	Number of laxations (Mean)
	Lowest weekly average # laxations/week	Highest weekly average # laxations/week
Methylnaltrexone Bromide 12 mg	2.4	3.4
Methylnaltrexone Bromide 8 mg	1.7	2.6

Intervention	percentage of participants (Number)
	RFBM post second DB injection	RFBM post third DB injection	RFBM post fourth DB injection	RFBM post fifth DB injection	RFBM post sixth DB injection	RFBM post seventh DB injection	RFBM post eighth DB injection
Methylnaltrexone Double-blind	61.9	52.6	38.9	56.3	43.8	43.8	57.1
Placebo	8.7	8.7	8.7	4.5	0	0	7.7

Intervention	percentage of participants (Number)
	Frequency of ≥ 1 laxation (0-4 hours) (n=12)	Frequency of ≥ 1 laxation (4-24 hours) (n=12)	Frequency of ≥ 1 laxation (24-48 hours) (n=11)	Consistency (slight-very hard) (0-4 hours) (n=12)	Consistency (slight-very hard) (4-24 hours) (n=12)	Consistency (slight-very hard)(24-48 hours) (n=11)	Difficulty (severe-very severe) (0-4 hours) (n=12)	Difficulty (severe-very severe)(4-24 hours) (n=12)	Difficulty (severe-very severe)(24-48hours) (n=11)
Methylnaltrexone	33	42	73	8	8	9	42	42	18

Intervention	percentage of participants (Number)
	Severity (severe-very severe) (0-4 hours) (n=12)	Severity (severe-very severe) (4-24 hours) (n=12)	Severity (severe-very severe) (24-48 hours) (n=11)	Distress (severe-very severe) (0-4 hours) (n=12)	Distress (severe-very severe) (4-24 hours) (n=12)	Distress (severe-very severe) (24-48 hours) (n=11)
Methylnaltrexone	42	50	27	25	25	0

Intervention	percentage of participants (Number)
	Rescue-free Laxation within 24 hours (n=12)	Laxation within 48 hours (n=12)
Methylnaltrexone	42	83

Intervention	units on a scale (Mean)
	Average pain (0-4 hours) (n=12)	Average pain (4-24 hours) (n=12)	Average pain (24-48 hours) (n=12)
Methylnaltrexone	2.9	2.4	2.3

Intervention	percentage of participants (Number)
	Satisfied-very satisfied (0-4 hours) (n=12)	Satisfied-very satisfied (4-24 hours) (n=12)	Satisfied-very satisfied (24-48 hours) (n=11)
Methylnaltrexone	33	58	64

Intervention	units on a scale (Mean)
	0-4 hours (n=12)	4-24 hours (n=12)	24-48 hours (n=11)
Methylnaltrexone	8.8	9.2	8.8

Intervention	hours (Mean)
	Mean time to rescue-free laxation ≤4 hours (n=11)	Mean time to rescue-free laxation ≤24 hours (n=11)	Mean time to laxation ≤48 hours (n=11)
Methylnaltrexone	3.3	16	20

Intervention	Percentage (Mean)
Methylnaltrexone 0.30 mg/kg	21.9
Codeine 30 mg	23.7
Methylnaltrexone 0.30 mg/kg + Codeine 30 mg	28.0
Placebo	34.5

Intervention	Units on a scale (Mean)
Methylnaltrexone 0.30 mg/kg	0.236
Codeine 30 mg	0
Methylnaltrexone 0.30 mg/kg + Codeine 30 mg	0.379
Placebo	0.347

Intervention	Stools (Mean)
Methylnaltrexone 0.30 mg/kg	1.1
Codeine 30 mg	0.63
Methylnaltrexone 0.30 mg/kg + Codeine 30 mg	0.7
Placebo	1.5

Intervention	hours (Mean)
Methylnaltrexone 0.30 mg/kg	17.1
Codeine 30 mg	24.0
Methylnaltrexone 0.30 mg/kg + Codeine 30 mg	23.6
Placebo	14.1

Intervention	Minutes (Mean)
Methylnaltrexone 0.30 mg/kg	102.7
Codeine 30 mg	104.0
Methylnaltrexone 0.30 mg/kg + Codeine 30 mg	126.8
Placebo	101.1

Intervention	RFBMs (Mean)
	Baseline	Change during Weeks 1-4
MNTX 150 mg	1.46	1.98
MNTX 300 mg	1.35	2.43
MNTX 450 mg	1.37	2.44
Placebo	1.49	1.87

Intervention	percentage of days (Mean)
MNTX 150 mg	21.05
MNTX 300 mg	24.64
MNTX 450 mg	27.40
Placebo	18.18

Intervention	Participants (Count of Participants)
	Nausea	Myoclonus	Vomiting	Sedation	Constipation	Urinary retention	Mental clouding	Sweating	Pruritus
Methylnaltrexone	3	1	3	1	1	3	4	2	0

methylnaltrexone

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Studies (294)

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Research Demand Index: 63.64

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Clinical Trials (58)

Trial Overview

Trial Outcomes

Time to Discharge Eligibility

Time to Discharge Order Written From the End of Surgery

Time to First Bowel Movement

Number of Participants With Clinically Meaningful Events (CMEs) for Nausea or Retching/Vomiting at 0 or 24 Hours as Evaluated by the Opioid-Related Symptom Distress Scale (SDS)

Number of Participants With Clinically Meaningful Events (CMEs) for Nausea or Retching/Vomiting at Day 2 (24 Hours) as Evaluated by the Opioid-Related Symptom Distress Scale (SDS)

Time to Discharge Eligibility

Time to Discharge Order Written From the End of Surgery

Time to First Bowel Movement

Change From Baseline in Weekly Number of Quality Rescue-free Bowel Movements (RFBM)

Time to the First Rescue-free Bowel Movement (RFBM) After First Dose

Percentage of Patients With Improvement in Straining Scale Score for Rescue-free Bowel Movements (RFBM) by 1 Point During Open Label Period

Change in Weekly Number of Complete Rescue-free Bowel Movements (RFBM)

Percentage of Patients With Improvement in Bristol Stool Form Scale Score for Rescue-free Bowel Movements (RFBM) by 1 Point During Open Label Period

Percentage of Patients With Any Diarrhea or Watery Rescue-free Bowel Movements (RFBM) During Open-label Period.

Percentage of Patients With an Increase of at Least 1 in the Weekly Rescue-free Bowel Movement (RFBM) Rate From Baseline for the Double-blind Period at 4 Weeks

Percentage of Patients With a Weekly Rescue-free Bowel Movement (RFBM) Rate ≥ 3 and an Increase of at Least 1 in the Weekly RFBM Rate From Baseline for the Double-blind Period

Percentage of Patients Having a Rescue-free Bowel Movement (RFBM) Within 4 Hours of the First Dose

Change in Straining Scale Score of Rescue-free Bowel Movements (RFBM) From Baseline During Double-blind Period

Percentage of Patients Achieving at Least 3 Rescue-free Bowel Movements (RFBM) Per Week in Double-blind Period

Change in Weekly Number of Bowel Movements During Double-blind Period

Percentage of Active Injections Resulting in Any Rescue-free Bowel Movement (RFBM) Within 4 Hours of Injection During the Double-blind Period

Change From Baseline in Weekly Number of Rescue-free Bowel Movements (RFBM) for the Double-blind Period at 4 Weeks

Change in Bristol Stool Form Scale Score for Rescue-free Bowel Movements (RFBM)

Change in Percentage of Rescue-free Bowel Movements (RFBM) Classified as Diarrhea or Watery Stools From Baseline During Double-blind Period

Change in Percentage of Rescue-free Bowel Movements (RFBM) With a Sensation of Complete Evacuation From Baseline During Double-blind Period

Change in Percentage of Rescue-free Bowel Movements (RFBM) With Bristol Stool Form Scale in Type 3 or Type 4 From Baseline During Double-blind Period

Change in Percentage of Rescue-free Bowel Movements (RFBM) With Straining Scale Scores of 0 or 1 (no, or Mild) From Baseline During Double-blind Period

Weekly Number of Rescue-free Bowel Movements (RFBM) (Open-label Period)

Percentage of Active Injections Resulting in Any Rescue-free Bowel Movement (RFBM) Within 1, 2, 3 and 6 Hour(s) in Double-blind Period

Percentage of Injections Resulting in Any Rescue-free Bowel Movement (RFBM) Within 1, 2, 3, 4 and 6 Hours in Double-blind Period

Percentage of Participants With a Spontaneous Bowel Movement (SBM) Within 1, 2, 3, 4, and 6 Hours of Treatment

Time to First Rescue-Free Bowel Movement (Laxation)

Percentage of Participants With Laxation Response Within 4 Hours of the First Dose

Percentage of Participants With Laxation Response Within 2 Hours of the First Dose

Number of Laxations Per Subject Within 24 Hours of Dosing Per Week.

Time to First Rescue-free Laxation (Following the First Dose of Study Drug).

The Proportion of Subjects Who Have a Rescue-free Laxation Response Within 4 Hours After at Least 2 of the First 4 Doses

Number of Participants With Treatment-Emergent Adverse Events (TEAEs)

Change From Baseline in Weekly Bowel Movement (BM) Rate Through Follow-up

The Proportion of Subjects Having a Rescue-free Bowel Movement (RFBM) Within 4 Hours After the First Injection.

Percentage of Injections Resulting in RFBM Within 4 Hours After Test Article Administration.

The Proportion of Subjects Having a Rescue-free Bowel Movement (RFBM) Within 4 Hours After Each Dose During Double-blind Period.

Rescue-free Laxation After Administration of Subcutaneous Methylnaltrexone

Bowel Movement Assessment (Frequency, Consistency and Difficulty) After Administration of Subcutaneous Methylnaltrexone

Constipation Assessment (Severity and Distress) After Administration of Subcutaneous Methylnaltrexone

Laxation After Administration of Subcutaneous Methylnaltrexone

Overall Pain Scores (0-10; 0=no Pain, 10=Worst Pain) After Administration of Subcutaneous Methylnaltrexone

Patient Satisfaction With the Study Medication After Administration of Subcutaneous Methylnaltrexone

Symptoms of Opioid Withdrawal (Modified Himmelsbach Withdrawal Scales (Ranging 7-28 in Total; 1=None - 4=Severe for 7 Items)) After Administration of Subcutaneous Methylnaltrexone