nampt activator-1

NAMPT Activator-1 (compound 1) is an effective and specific activator of niacinamide phosphotransferase (Compound 1) with a wide range of EC50 (3.3-3.7 μM). NAMPT activator-1 effectively protects cultured cells from FK866-mediated toxicity and is a potential neuroprotective compound.

NAMPTactivator-9 (Compound DIPM) is an allosteric, non-competitive activator of NAMPT with an EC50 of 3.366 μM for hNAMPT. This compound enhances the enzymatic activity of NAMPT through its allosteric, non-competitive mechanism, subsequently increasing intracellular NAD+ levels. It has the capability to restore myotube diameter and reduce the expression of atrophy markers Atrogin-1 and MuRF1, making it suitable for studies related to muscle atrophy.

NAT is a nicotinamide phosphoribosyltransferase (NAMPT) activator that increases intracellular NAD levels and induces subsequent metabolic and transcriptional reprogramming. It exhibits neuroprotective effects in a chemotherapy-induced peripheral neuropathy (CIPN) mouse model and may be employed in studies of neurodegenerative diseases or conditions associated with reduced NAD levels.

NAMPT Activator-3, a derivative of NAT, is a potent activator of NAMPT, demonstrating an EC50 of 2.6 μM and KD of 132 nM. It effectively shields cultured cells against toxicity induced by FK866 and has demonstrated significant neuroprotective effects in a chemotherapy-induced peripheral neuropathy (CIPN) mouse model, without any apparent toxicity [1].

Nampt activator-4, a positive allosteric modulator (N-PAM) of nicotinamide phosphoribosyltransferase (NAMPT), has an EC50 of 0.058 μM and can enhance nicotinamide adenine dinucleotide (NAD+) levels in cells [1].

NAMPT activator-6 is a NAMPT activator that can regulate the NAMPT and NAD⁺-related optogenetic systems. NAMPT activator-6 can be used to construct high-efficiency photoswitchable PROTACs (PS-PROTACs), bidirectionally and reversibly regulate NAMPT and NAD⁺ levels in a light-dependent manner, and reduce the related toxicity caused by inhibitor-based PS-PROTACs.