PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24403854-0	2013	Supplementation of nicotinic acid with NAMPT inhibitors results in loss of in vivo efficacy in NAPRT1-deficient tumor models.	Niacin	19-33	nicotinamide phosphoribosyltransferase	Homo sapiens	39-44	
24097869-2	2013	EXPERIMENTAL DESIGN: We use a NAMPT inhibitor, GNE-617, to evaluate nicotinic acid rescue status in a panel of more than 400 cancer cell lines.	Niacin	68-82	nicotinamide phosphoribosyltransferase	Homo sapiens	30-35	
29054982-0	2017	Discovery of a Highly Selective NAMPT Inhibitor That Demonstrates Robust Efficacy and Improved Retinal Toxicity with Nicotinic Acid Coadministration.	Niacin	117-131	nicotinamide phosphoribosyltransferase	Homo sapiens	32-37	
24204194-3	2013	While cells proficient for nicotinic acid phosphoribosyl transferase (NAPRT1) can be protected from NAMPT inhibition as they convert nicotinic acid (NA) to NAD independent of the salvage pathway, this protection only occurs if NA is added before NAD depletion.	Niacin	27-41	nicotinamide phosphoribosyltransferase	Homo sapiens	100-105	
35396381-5	2022	Here we show that tumor environment enriched in vitamin B3 (NAM) or nicotinic acid (NA) significantly lowers the anti-tumor efficacy of APO866, a prototypic NAMPT inhibitor.	Niacin	68-82	nicotinamide phosphoribosyltransferase	Homo sapiens	157-162	
32266141-1	2020	Nicotinamide phosphoribosyltransferase (NAMPT) and nicotinate phosphoribosyltransferase (NAPRT) are two intracellular enzymes that catalyze the first step in the biosynthesis of NAD from nicotinamide and nicotinic acid, respectively.	Niacin	204-218	nicotinamide phosphoribosyltransferase	Homo sapiens	40-45	
29949049-10	2018	We found that the effects of GMX1778 and STF-31 could be partially abolished by (i) nicotinic acid (NA) only in nicotinic acid phosphoribosyltransferase (NAPRT) expressing cells and (ii) nicotinamide mononucleotide (NMN) in all cells tested, supporting the classification of these compounds as NAMPT inhibitors.	Niacin	84-98	nicotinamide phosphoribosyltransferase	Homo sapiens	294-299	
25201160-7	2014	Particularly, mutations that decrease NAPRT1 expression can predict the usefulness of Nicotinic Acid in tumor treatments with NAMPT inhibitors.	Niacin	86-100	nicotinamide phosphoribosyltransferase	Homo sapiens	126-131	
27783203-8	2017	This toxicity was mitigated in vitro by co-administration of nicotinic acid (NA), which can enable NAD production through the NAMPT-independent pathway; however, this resulted in only partial mitigation in in vivo studies.	Niacin	61-75	nicotinamide phosphoribosyltransferase	Homo sapiens	126-131	
25894564-0	2015	Preclinical models of nicotinamide phosphoribosyltransferase inhibitor-mediated hematotoxicity and mitigation by co-treatment with nicotinic acid.	Niacin	131-145	nicotinamide phosphoribosyltransferase	Homo sapiens	22-60	
25894564-8	2015	We further demonstrate that the MK toxicity is on-target based on the evidence that nicotinic acid (NA), which is converted to NAD via a NAMPT-independent pathway, can mitigate NAMPTi toxicity to human CFU-MK in vitro and was also protective for the hematotoxicity in rats in vivo.	Niacin	84-98	nicotinamide phosphoribosyltransferase	Homo sapiens	137-142	
26675378-3	2016	Knowledge of the expression patterns of both genes in tissues and tumors is critical for the use of nicotinic acid (NA) as cytoprotective in therapies using NAMPT inhibitors.	Niacin	100-114	nicotinamide phosphoribosyltransferase	Homo sapiens	157-162