NNMT Antibody
- Known as:
- NNMT Antibody
- Catalog number:
- XW-7951
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- NNMT Antibody
Related genes to: NNMT Antibody
- Gene:
- NNMT NIH gene
- Name:
- nicotinamide N-methyltransferase
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 11q23.1
- Locus Type:
- gene with protein product
- Date approved:
- 1994-04-18
- Date modifiied:
- 2014-11-19
Related products to: NNMT Antibody
Related articles to: NNMT Antibody
- Nicotinamide N-methyltransferase (NNMT) is an enzyme that helps regulate how cells balance energy and methylation potential; however, its abnormal activation can disrupt this balance, fueling diseases such as diabetes, obesity, fibrosis, and cancer. As a result, small-molecule inhibitors targeting NNMT have been developed to reduce this elevated activity, but insufficient target engagement, reduced bioavailability, and unknown safety profiles have led to limited preclinical success across diseases. Advances in NNMT small-molecule inhibitor development have yielded a number of compounds that address these concerns, resulting in drug-like compounds with high affinities for cellular NNMT and promising safety profiles. In this review, we assess the growing therapeutic potential of NNMT inhibitors by highlighting recent developments in NNMT pathophysiology and inhibitor medicinal chemistry. - Source: PubMed
Publication date: 2026/04/30
Puleo NoahAllega Maria FrancescaNiemann Claus ULengyel Ernst - Accumulating evidence suggests reciprocal risk factors between periodontitis (PD) and systemic sclerosis (SSc). Ferroptosis, an iron-dependent and immune-related form of cell death, has been implicated in both diseases, yet its shared molecular mechanisms remain largely unclear. - Source: PubMed
Publication date: 2026/04/02
Zhang ShengchaoYang ShengweiGe CuiJi ChaoLin RuohanXue WenjuanLiu DongxiuChen Fulin - Drug resistance in patients remains a significant obstacle to successful treatment, even with improvements in cancer treatment strategies. Resistance to taxanes, such as docetaxel (Dtx) and cabazitaxel (Cbz), frequently emerges in castration resistant prostate cancer (CRPC). Through pulse selection of the parental cells (DU145), we established Dtx- and Cbz-resistant CRPC cell models and integrated different omic approaches, including transcriptomics and proteomics, to determine the molecular signatures underlying taxane resistance. Interestingly, several genes were regulated in the same direction (up- or down-regulation) at both the gene and protein expression levels in resistant cells compared to parental cells, suggesting that alterations primarily occur at the transcriptional level and manifest at the protein level. Among the differentially regulated genes, Cysteine Rich Protein 2 (CRIP2), a gene associated with tumor suppressor function, has been found to be the most downregulated in taxane-resistant cells. Conversely, Nicotinamide N-Methyltransferase (NNMT) exhibited a significant upregulation and has been validated in the context of taxane resistance. Its overexpression was shown to promote taxane resistance in two different CRPC cell lines, whereas depletion via siRNA or gRNA, as well as treatment with 1-methylnicotinamide (1-MNA, used as a feedback inhibitor)resensitized the resistant cells. RNA-sequencing of NNMT-knockout (CRISPR-Cas9) cells has indicated involvement of TGFβ signaling, and suppressing this pathway has further increased the taxane sensitivity. Epithelial Mesenchymal Transition (EMT) was another pathway depleted upon knockout, and subsequent analysis revealed a significant correlation between NNMT and EMT-related genes (VIM, CDH2, FN1, TGFB1, and ZEB2) in both the Cancer Cell Line Encyclopedia (CCLE) panel and patient data. Additionally, in cancers other than PC, NNMT has been observed to predict treatment outcomes, and notably, among the patients with a high EMT signature, elevated NNMT levels were associated with decreased overall survival. More importantly, NNMT-high patients were found to be non-responders to taxane-containing chemotherapy regimens. Collectively, our findings suggest that targeting NNMT and the pathways it affects, such as TGFβ, offers a viable approach for addressing taxane-resistant PC. - Source: PubMed
Publication date: 2026/04/17
Cevatemre BuseKaryemez EzgiBulut IpekSyed HamzahGönen MehmetBaykal Ahmet TarikBagci-Onder TugbaAcilan Ceyda - Nicotinamide -methyltransferase (NNMT) has emerged as a regulator of cellular methylation, epigenetic remodeling, and energy homeostasis. Its aberrant expression has been implicated in cancer, metabolic disorders, and renal diseases. Although several NNMT inhibitors have been reported, most lack selectivity, cellular activity, or favorable pharmacokinetic properties. Here, we describe the discovery and optimization of a novel non-SAM-mimetic bisubstrate inhibitor of NNMT originating from high-throughput screening. Guided by structure-based design, systematic modifications of hit compound yielded lead compound with over 1000-fold improved potency (IC for compounds and = 10 μM and 0.0084 μM, respectively). Compound exhibited sub-micromolar cell-based activity and high selectivity for a subfamily of methyltransferases. In rodents, compound exhibited pronounced renal distribution and moderate bioavailability, while achieving dose-dependent renal NNMT inhibition in a renal fibrosis model. These results highlight compound as a promising probe and a starting point for NNMT-targeted drug discovery. - Source: PubMed
Publication date: 2026/03/06
Yoshida ShuheiKondo NoriyasuUehara ShotaYoshimura NoritoSako YusukeYamamoto ShihoKitade MikikoTachibana Yuki - Cancer-associated fibroblasts (CAFs) drive immunosuppression in hepatocellular carcinoma (HCC). However, their metabolic regulation remains poorly defined. We investigated the role of nicotinamide N-methyltransferase (NNMT) in CAFs. - Source: PubMed
Publication date: 2026/04/14
Lu ShounanKe ShanjiaYu HongjunMeng ZhanzhiBai MiaoyuXu YananZhu HuiYang JinwenQian BaolinYin BingWang ChaoqunFeng ZhigangLi ZhongyuZhou YongzhiLi ZihaoLi XinglongHua YongliangFu YaoTang WeiWu YaohuaMa Yong