PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
33030105-0	2022	Molecular dynamics analysis predicts ritonavir and naloxegol strongly block the SARS-CoV-2 spike protein-hACE2 binding.	naloxegol	51-60	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	91-96
33030105-0	2022	Molecular dynamics analysis predicts ritonavir and naloxegol strongly block the SARS-CoV-2 spike protein-hACE2 binding.	naloxegol	51-60	angiotensin converting enzyme 2	Homo sapiens	105-110
33030105-9	2022	Finally, a long MD analysis revealed two select candidate ligands, including ritonavir and naloxegol, highly stabilizing those key residues engaged in RBD-hACE2 interaction.	naloxegol	91-100	angiotensin converting enzyme 2	Homo sapiens	155-160
26678015-0	2016	Effects of CYP3A Modulators on the Pharmacokinetics of Naloxegol.	naloxegol	55-64	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	11-16
28035588-8	2017	Naloxegol is a sensitive substrate of cytochrome P450 (CYP) 3A4 and its exposure can be significantly altered by strong or moderate CYP3A modulators.	naloxegol	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	38-63
28336575-4	2017	At the human micro-opioid receptor in vitro, naloxegol was a potent inhibitor of binding (Ki = 7.42 nM) and a neutral competitive antagonist (pA2 - 7.95); agonist effects were <10% up to 30 muM and identical to those of naloxone.	naloxegol	45-54	latexin	Homo sapiens	193-196
27342744-5	2016	This analysis estimates the impact of naloxegol on the health state utility of LIR patients, examines if this utility impact is driven by the change in OIC status, and estimates the utility impact of relief of OIC.	naloxegol	38-47	CD300c molecule	Homo sapiens	79-82
27342744-11	2016	RESULTS: Compared with placebo, LIR patients treated with naloxegol 25 mg reported a 0.08 improvement in the EQ-5D overall score after 12 weeks of treatment.	naloxegol	58-67	CD300c molecule	Homo sapiens	32-35
27582887-7	2016	Naloxegol is substrate for the P-glycoprotein (P-gp) transporter.	naloxegol	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	31-45
27582887-10	2016	Naloxegol is metabolised through CYP3A4 to six metabolites, with the majority of the dose (68%) excreted with faeces and less (16%) with urine.	naloxegol	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	33-39
26678015-2	2016	This study evaluated the effects of CYP3A inhibition and induction on the pharmacokinetics, safety, and tolerability of naloxegol.	naloxegol	120-129	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	36-41
26678015-5	2016	Naloxegol was generally safe and well tolerated when given alone or coadministered with the respective CYP3A modulators; 1 subject discontinued because of elevations in liver enzymes attributed to rifampin.	naloxegol	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	103-108
26678015-6	2016	The exposure of naloxegol was affected substantially by ketoconazole, diltiazem, and rifampin, suggesting that it is a sensitive in vivo substrate of CYP3A4.	naloxegol	16-25	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	150-156
26248047-2	2016	Naloxegol is metabolized by CYP3A, and its properties as a substrate for the P-glycoprotein (PGP) transporter limit its central nervous system (CNS) permeability.	naloxegol	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	77-91
27299937-1	2016	Naloxegol, a peripherally acting mu-opioid receptor antagonist for the treatment of opioid-induced constipation, is a substrate for cytochrome P450 (CYP) 3A4/3A5 and the P-glycoprotein (P-gp) transporter.	naloxegol	0-9	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	132-161
27299937-1	2016	Naloxegol, a peripherally acting mu-opioid receptor antagonist for the treatment of opioid-induced constipation, is a substrate for cytochrome P450 (CYP) 3A4/3A5 and the P-glycoprotein (P-gp) transporter.	naloxegol	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	170-184
27299937-4	2016	The moderate CYP3A4 inducer efavirenz was predicted to reduce naloxegol exposure by ~50%, whereas weak CYP3A inhibitors were predicted to minimally affect exposure.	naloxegol	62-71	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	13-19
27299937-4	2016	The moderate CYP3A4 inducer efavirenz was predicted to reduce naloxegol exposure by ~50%, whereas weak CYP3A inhibitors were predicted to minimally affect exposure.	naloxegol	62-71	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	13-18
27299937-5	2016	In summary, the PBPK models reasonably estimated interactions with various CYP3A modulators and can be used to guide dosing in clinical practice when naloxegol is coadministered with such agents.	naloxegol	150-159	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	75-80
26248047-2	2016	Naloxegol is metabolized by CYP3A, and its properties as a substrate for the P-glycoprotein (PGP) transporter limit its central nervous system (CNS) permeability.	naloxegol	0-9	ATP binding cassette subfamily B member 1	Homo sapiens	93-96
26248047-5	2016	Coadministration of quinidine and naloxegol increased naloxegol"s AUC 1.4-fold and Cmax 2.5-fold but did not antagonize morphine-induced miosis, suggesting that PGP inhibition does not increase the CNS penetration of naloxegol.	naloxegol	34-43	ATP binding cassette subfamily B member 1	Homo sapiens	161-164
26248047-5	2016	Coadministration of quinidine and naloxegol increased naloxegol"s AUC 1.4-fold and Cmax 2.5-fold but did not antagonize morphine-induced miosis, suggesting that PGP inhibition does not increase the CNS penetration of naloxegol.	naloxegol	54-63	ATP binding cassette subfamily B member 1	Homo sapiens	161-164
26248047-5	2016	Coadministration of quinidine and naloxegol increased naloxegol"s AUC 1.4-fold and Cmax 2.5-fold but did not antagonize morphine-induced miosis, suggesting that PGP inhibition does not increase the CNS penetration of naloxegol.	naloxegol	54-63	ATP binding cassette subfamily B member 1	Homo sapiens	161-164
23726675-1	2013	Naloxegol (previously known as NKTR-118) is a peripherally acting mu-opioid receptor antagonist engineered using polymer conjugate technology in development as an oral, once-daily agent for the treatment of opioid-induced constipation (OIC).	naloxegol	0-9	natural killer cell triggering receptor	Homo sapiens	31-35
26317320-10	2016	Simulations indicated concomitant strong CYP3A4 inhibitors or inducers had relevant effects on naloxegol exposure.	naloxegol	95-104	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	41-47
26317320-11	2016	CONCLUSIONS: Administration of strong CYP3A4 inhibitors or inducers had a clinically relevant influence on naloxegol pharmacokinetics.	naloxegol	107-116	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	38-44
26535126-2	2015	OBJECTIVE: Assess the efficacy and safety of orally administered naloxegol in patients with prospectively confirmed OIC and LIR.	naloxegol	65-74	CD300c molecule	Homo sapiens	124-127
26535126-3	2015	METHODS: We analyzed pooled data from two identical randomized, double-blind, placebo-controlled, Phase 3 trials of naloxegol in patients with non-cancer pain, OIC and LIR in which naloxegol (12.5 mg, n = 240; 25 mg, n = 241) or placebo (n = 239) were administered daily.	naloxegol	116-125	CD300c molecule	Homo sapiens	168-171
26535126-9	2015	CONCLUSIONS: Naloxegol was efficacious, generally safe and well tolerated in the patients with OIC and LIR, while preserving opioid analgesia.	naloxegol	13-22	CD300c molecule	Homo sapiens	103-106
27137716-2	2015	Naloxegol (previously NKTR-118), a PEGylated derivative of naloxone that has minimal penetration of the central nervous system, has received regulatory approval as an oral therapy for OIC.	naloxegol	0-9	natural killer cell triggering receptor	Homo sapiens	22-26