Ask about this productRelated genes to: MAOB antibody
- Gene:
- MAOB NIH gene
- Name:
- monoamine oxidase B
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- Xp11.3
- Locus Type:
- gene with protein product
- Date approved:
- 1986-01-01
- Date modifiied:
- 2016-10-05
Related products to: MAOB antibody
Related articles to: MAOB antibody
- Metabolic reprogramming plays a crucial role in cancer progression, therapeutic resistance, and tumor-microenvironment remodelling. Monoamine oxidase-B (MAO-B), a mitochondrial enzyme involved in oxidative deamination, has recently been identified as a metabolic regulator that influences reactive oxygen species (ROS) production, mitochondrial homeostasis, and redox-dependent signaling in tumors. Selegiline, an MAO-B inhibitor traditionally used in neurological disorders, is now gaining attention for its potential role in modulating tumor metabolism. Elevated MAO-B activity contributes to oxidative stress, genomic instability, immune suppression, and metabolic adaptations that support tumor survival. By inhibiting MAO-B, selegiline reduces ROS generation, alters mitochondrial respiration, regulates glycolytic flux, and disrupts hypoxia-associated pathways, making it a promising modulator of metabolic checkpoints in oncology. Relevant literature was collected from PubMed, Google Scholar, and ScienceDirect using keywords such as Selegiline, MAO-B inhibitor, tumor metabolism, oxidative stress, and drug repurposing in cancer. Relevant studies from the past 5 years, with inclusion criteria focusing on mechanistic, preclinical, and translational evidence related to MAO-B and selegiline-mediated metabolic regulation. Recent findings indicate that selegiline not only modulates cancer cell metabolism but also influences the tumor microenvironment by reducing inflammatory cytokine production, altering macrophage polarization, and enhancing susceptibility to therapeutic stress. Additionally, combination approaches with chemotherapeutics, metabolic inhibitors, and immunotherapies show synergistic potential. This review summarizes current insights into selegiline's role in metabolic reprogramming, highlights existing challenges, and discusses future opportunities for repositioning selegiline as a targeted metabolic modulator in cancer therapy. - Source: PubMed
Publication date: 2026/04/07
Jayachandran JayanthNambidi SibinKondaveeti Suresh BabuPathak SurajitRadhakrishnan ArunkumarBanerjee AntaraDutta Roy Asim K - A novel series of chromene-phenylpiperazine-chalcone hybrids was rationally designed, synthesized and evaluated as multi-target-directed ligands (MTDLs) for Alzheimer's disease (AD). Among them, compound 9 s exhibited selective equine serum butyrylcholinesterase (eqBuChE, IC = 0.13 μM) and concurrent monoamine oxidase B (MAO-B, IC = 1.63 μM) inhibitory activities. Kinetic and molecular docking studies indicated that 9 s acts as a mixed-type dual-site inhibitor. In silico modeling suggests that the binding pose is stabilized by a predicted pseudo-seven-membered ring. Furthermore, 9 s facilitated the disassembly of self-aggregated and Cu-induced Aβ fibrils. In BV-2 microglial cells, it demonstrated a high safety margin (> 380-fold effective concentration), accelerated intracellular Aβ clearance, and subsequently attenuated LPS-induced NO production. In vivo evaluations revealed low acute toxicity (LD > 1000 mg/kg). Oral administration of 9 s successfully reversed scopolamine-induced spatial working memory deficits in mice. These findings validate the drug-like 9 s as an orally efficacious MTDL candidate that provides symptomatic cognitive relief, while possessing promising in vitro disease-modifying potential for AD therapy. - Source: PubMed
Publication date: 2026/04/19
Liu YuanxiuJiang ZhenzeChen DieHe ZhixinNing WenjieWang SihongGuan Liping - Recent studies have highlighted the critical role of 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase-3 (PFKFB3) in inflammation, with inhibitors like 3PO showing therapeutic potential in various inflammatory diseases. However, its effect on asthma inflammation remains unclear. - Source: PubMed
Publication date: 2026/04/02
Huang SiqingWei ShunaLuo FangCheng Yuanxiong - In tauopathies, tau accumulation and neuroinflammation are associated with progressive synaptic and network alterations that contribute to neurodegeneration. We used 8 PS19 and 12 C57Bl/6 (WT) mice undergoing consecutive [F]UCB-H PET scans between 5.7 and 11.0 months of age to longitudinally evaluate SV2A expression levels, with terminal validation via immunohistochemistry. A desynchronization index (DI) quantified deviation from a reference-derived inter-regional SV2A expression pattern from whole-brain SV2A-PET data, and principal component analysis (PCA) further summarized these regional deviation profiles. Baseline translocator protein (TSPO, [F]GE-180) and monoamine oxidase B (MAO-B, [F]F-DED) imaging for activated microglia and reactive astrogliosis were performed to detect early neuroinflammation, which was subsequently correlated with serial SV2A expression, evaluated by the area under the curve (AUC) of [F]UCB-H z-scores (PS19 vs. WT). We observed phased SV2A expression alterations in PS19 mice in the neocortex, hippocampus CA1, brainstem, thalamus, hypothalamus, and cerebellum, showing an increasing trend from 8.4 to 10.0 months of age (+8.1% ± 3.0%), followed by a rapid decline towards 11.0 months of age (-18.4% ± 4.7%), together with greater later-stage inter-regional SV2A expression pattern deviation. Tau burden tended to show a broadly negative association with SV2A expression levels across primary and exploratory regions. Associations of SV2A-PET signal variation with early microglial activation and reactive astrogliosis differed between PS19 and WT mice. In summary, these findings suggest that longitudinal [F]UCB-H PET may provide a feasible approach for tracking stage-dependent regional SV2A expression alterations and inter-regional deviation in this mouse model of primary tauopathy. - Source: PubMed
Publication date: 2026/04/15
Li YunleiZatcepin ArtemPalumbo GiovannaOos RoselWind-Mark KarinLindner SimonGildehaus Franz-JosefGnörich JohannesWerner Rudolf ABrendel MatthiasKunze Lea H - Serotonin syndrome (SS) is a potentially life-threatening condition resulting from excessive serotonergic activity in the central nervous system. We present a fatal case of SS complicated by multiple organ failure in a 72-year-old patient with Parkinson's disease following the sequential administration of two selective serotonin reuptake inhibitors (sertraline and escitalopram) while on a stable regimen of the monoamine oxidase-B inhibitor rasagiline. Pharmacogenomic testing revealed a homozygous *10/*10 genotype, conferring an intermediate metabolizer phenotype, which is postulated to have contributed to serotonergic drug accumulation and resultant toxicity in combination with other significant pharmacodynamic and pharmacokinetic interactions. This case was distinguished by three key features: first, the sequential serotonergic challenge from two different SSRIs in combination with rasagiline; second, the unprecedented severity of clinical manifestations, including rhabdomyolysis, acute hepatic and renal injury, and a disseminated intravascular coagulation-like state; and finally, the pharmacogenetic findings that provide a partial mechanistic explanation for the extreme drug sensitivity. This report underscores the critical importance of pre-emptive pharmacogenomic screening in patients receiving complex polypharmacy, particularly when combining drugs with serotonergic properties. It also serves as a critical warning that even selective MAO-B inhibitors can precipitate life-threatening interactions with SSRIs in genetically susceptible individuals, thereby informing more stringent personalized therapeutic strategies. - Source: PubMed
Publication date: 2026/03/31
Liu Dong-YangYi Ya-HuiLi NaLuo Fang-MingGong Wei-Jing