FK866, a highly specific noncompetitive inhibitor of nicotinamide phosphoribosyltransferase, represents a novel mechanism for induction of tumor cell apoptosis.

By M. Hasmann, I. Schemainda. Cancer Research, 2003

655 citations recorded by the source corpus.

View Paper: https://www.semanticscholar.org/paper/c6b4f08bd44feaa01798300efc78c46dd54a721d

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Citations in the corpus

Nampt/PBEF/Visfatin regulates insulin secretion in beta cells as a systemic NAD biosynthetic enzyme. (2007, methodology): “To further confirm the effect of NMN on NAD biosynthesis and insulin secretion, we measured NAD levels in primary islets cultured overnight with NMN and/or FK866, a potent chemical inhibitor of Nampt (Hasmann and Schemainda, 2003).”
The secret life of NAD+: an old metabolite controlling new metabolic signaling pathways. (2010, background): “In several cell models, FK866 showed great promise by depleting NAD levels and thereby influencing not only tumorigenesis, but also metastasis and angiogenesis (31, 184).”
NAD+/NADH and NADP+/NADPH in Cellular Functions and Cell Death: Regulation and Biological Consequences (2008, unknown): “synthesis can induce apoptosis (117), and that NADH/NADPH”
Targeting cancer metabolism: a therapeutic window opens (2011, background): “Interestingly, NAMPT, the enzyme that is involved in regenerating NAD + from nicotinamide and phosphoribosyl pyrophosphate via a salvage pathway, was identified as the target of a molecule that was discovered in a screen to find novel cytotoxic compound”
Clinical Applications of Metabolomics in Oncology: A Review (2009, background): “Current examples of using metabolomics in developmental therapeutics are with tyrosine kinase inhibitors, proapoptotic agents, and heat shock protein inhibitors (57-63).”
NAD+ metabolism and the control of energy homeostasis - a balancing act between mitochondria and the nucleus (2015, background): “NAMPT has been found to be overexpressed in several types of tumors, and its expression is associated to tumor progression (Bi et al., 2011; Hasmann and Schemainda, 2003; Van Beijnum et al., 2002; Wang et al., 2011).”
Glucose restriction inhibits skeletal myoblast differentiation by activating SIRT1 through AMPK-mediated regulation of Nampt. (2008, methodology): “We then probed the role of the enzymatic activity of Nampt with FK866, a highly specific inhibitor (Hasmann and Schemainda, 2003) (Khan et al., 2006).”
Nicotinamide mononucleotide, a key NAD+ intermediate, treats the pathophysiology of diet- and age-induced diabetes in mice (2011, background): “NMN was also able to overcome NAD deficits caused by a potent NAMPT inhibitor FK866 (Hasmann and Schemainda, 2003), but it was unable to alleviate the NAD reduction, due to the inhibition of nicotinamide/nicotinic acid mononucleotide adenylyltransferases (NMNATs) by their potent inhibitor, gallotann”
Inhibition of lactate dehydrogenase A induces oxidative stress and inhibits tumor progression (2010, background): “We found that the NAMPT inhibitor of NAD+ synthesis, FK866, also increased ROS production (Fig.”