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Last update 08 May 2025

NADK

Last update 08 May 2025

Basic Info

Synonyms

FLJ13052, NAD kinase, NADK

+ [1]

Introduction-

Drugs associated with NADK

NKI-1

Target

NADK

Mechanism

NADK inhibitors

Active Org.

Universite de Montpellier II [+2]

Originator Org.

Institut Pasteur

Active Indication

Staphylococcal Infections

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with NADK

100 Translational Medicine associated with NADK

0 Patents (Medical) associated with NADK

390

Literatures (Medical) associated with NADK

01 May 2025·Phytomedicine

Schisandra total lignans ameliorate neuronal ferroptosis in 3xTg-AD mice via regulating NADK/NADPH/GSH pathway

Article

Author: Wang, Mengyao ; Guo, Minsong ; Wu, Yuying ; Yu, Hengyuan ; Zhou, Yuan ; Wei, Mengying ; Chen, Yong ; Xu, Tengfei

BACKGROUNDAlzheimer's disease (AD) is a progressive neurodegenerative disorder with limited treatments. Schisandra total lignans (STL), the primary active component of Schisandra chinensis, shows potential in alleviating AD-related symptoms, though the mechanisms remain unclear.PURPOSEConsidering the promoting effect of neuronal ferroptosis on AD and the neuroprotective activity of STL, this study aimed to investigate the impact of STL on AD neuronal ferroptosis and elucidate its underlying mechanisms.METHODSThis study used 3xTg-AD mice and SH-SY5Y cells overexpressing APPswe as models. UHPLC/Q-TOF-MS was applied for identifying components in STL extract and the plasma of 3xTg-AD mice, as well as to detect cellular endogenous metabolites for one-carbon metabolism analysis. Behavioral tests, including the Y maze, novel object recognition, Morris water maze, and open field, were conducted to assess the cognitive function and emotional state. Histopathological examinations were performed using immunofluorescence, immunohistochemistry, Nissl staining, and transmission electron microscopy. The GSH, GSSG, NAD(H), NADP(H), and MDA levels, as well as GPX and GR activity were measured using assay kits. ROS, Fe²⁺, and lipid peroxidation levels were detected with probes. Protein expression was evaluated by Western blot. Molecular docking, molecular dynamics simulations and cellular thermal shift assay were performed to analyze the STL-NADK interactions.RESULTSBehavioral tests indicated that STL alleviated cognitive impairments and anxiety in 3xTg-AD mice. Histological analysis showed that STL decreased hippocampal Aβ levels, inhibited hippocampal neuronal ferroptosis, and mitigated synaptic damage. Cellular assays demonstrated that STL alleviated APPswe overexpression-induced ferroptosis and synaptic damage by activating the NADK/NADPH/GSH pathway, with NADK knockdown abolishing this neuroprotective effect of STL. Computational analysis and cellular thermal shift assay identified Gomisin D as the key STL component with strong affinity for NADK, driving its neuroprotective effects.CONCLUSIONNADK emerges as a novel potential therapeutic target for AD, with STL activating NADK, promoting NADPH and GSH production, thereby mitigating neuronal ferroptosis in AD.

01 Apr 2025·International Journal of Biological Macromolecules

Neuritin improves cognitive impairments in APP/PS1 Alzheimer's disease mice model by mitigating neuronal ferroptosis via PI3K/Akt activation

Article

Author: Tan, Xiaohua ; Song, Dandan ; Gui, Fei ; Hong, Chenglin ; Huang, Jin ; Li, Guoxiang ; Sun, Jiawei ; Zhuang, Shuai

The neurotrophic factor Neuritin is known to enhance cognitive capacity and to mitigate synaptic impairments in the APP/PS1 Alzheimer's disease (AD) mouse model, suggesting therapeutic potential for clinical treatment. However, the core molecular mechanisms remain elusive. Ferroptosis, a form of programmed cell death linked to iron dysregulation and oxidative stress, contributes to neurodegeneration in AD in part by accelerating amyloid-β deposition and neurofibrillary tangle formation. Here we examined if Neuritin can mitigate cognitive decline and neural degeneration in AD model mice by suppressing ferroptosis. Age-dependent cognitive decline was associated with Neuritin downregulation and increased ferroptosis in the hippocampus. Intracerebroventricular injection of exogenous Neuritin mitigated spatial and fear learning deficits as well as neural oxidative stress, apoptosis, and ferroptosis in the hippocampus without causing deleterious side effects. Neuritin injection also upregulated the activity of NAD+ kinase (NADK), the enzyme responsible for converting NAD to anti-ferroptotic NADPH, in the hippocampus of AD mice as well as in cultured hippocampal neurons. Reduced Neuritin expression in the hippocampus AD mice was associated with reduced phosphorylation (activation) of Akt (p-Akt), and Neuritin administration enhanced p-Akt expression in both HT22 cells and AD model mice. Conversely, blocking the PI3K/Akt pathway in HT22 cells reversed the Neuritin-induced increase in NADK activity and reduction in ferroptosis, indicating that Neuritin protects neurons from AD-induced damage by enhancing NADK activity through the PI3K/Akt pathway. Collectively, our results support Neuritin upregulation as a potential therapeutic strategy for early-phase AD.

01 Apr 2025·Food Chemistry: X

The role of respiration metabolism in dicyclohexylcarbodiimide and disodium succinate regulating the pulp breakdown occurrence of fresh longan (Dimocarpus longan Lour.) during storage

Article

Author: Lin, Hetong ; Wang, Hui ; Chen, Yihui ; Sang, Yueying ; Zheng, Yi ; Lin, Yifen ; Fan, Zhongqi ; Lin, Yixiong ; Wen, Hongyi ; Lin, Mengshi

Compared to control longan, on day 6, DCC-treated longan presented 18 %, 2 %, 15 %, 34 %, 21 %, 26 % and 10 % higher levels of pulp breakdown index, fruit respiration rate, PGI, SDH, NAD, NADH and QH₂, respectively. Meanwhile, DCC-treated longan displayed 25 %, 5 %, 8 % and 12 % higher activities of respiratory terminal oxidases including CCO, AOX, PPO and AAO, respectively. However, DCC-treated longan presented 9 %, 27 %, 24 %, 25 % and 16 % lower levels of NADK, G-6-PDH + 6-PGDH, NADP, NADPH and Q, respectively. These data indicate that DCC-hastened longan pulp breakdown occurrence was owing to the diminished PPP, and the elevated EMP, TCA cycle and CCP, thereby leading to an increased respiration rate. However, DS treatment displayed contrary effects, indicating DS restrained longan pulp breakdown occurrence through diminishing the respiration metabolism and depressing the respiration rate of fresh longan.

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