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nicotinamide (Papulex)

✓ Approved

Wockhardt Limited · 小分子 · 小分子

什么是 nicotinamide？

nicotinamide 是一种小分子，由Wockhardt Limited研发。该药已获批，用于治疗相关适应症，给药途径：Topical。

药物档案

商品名Papulex
公司Wockhardt Limited
药物类别小分子
给药途径Topical
状态Approved
来源： ClinicalTrials.gov, Wockhardt Limited

治疗适应症

nicotinamide 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Skin and subcutaneous tissue disordersAcne✓ Approved

相关研究文献

PubMedNature chemical biology2026-09-10

A sequence motif enables widespread use of noncanonical redox cofactors in natural enzymes.

Saleh Samer S, Hsu Ning-Hsiang NH, Luu Emma E, Martin Vincent C VC et al.

Noncanonical redox cofactors (NRCs) are low-cost alternatives to the natural redox cofactors nicotinamide adenine dinucleotide (NAD+) and nicotinamide adenine dinucleotide phosphate (NADP+) for biomanufacturing, offering exquisite electron-delivery control, yet their adoption is limited by the scarcity of compatible enzymes. Screening the aldehyde dehydrogenase (ALDH) family, we identified a conserved RH/QxxR motif that enables widespread NRC activity among natural enzymes. Bos taurus ALDH3a1 exhibits unprecedented turnover with nicotinamide mononucleotide (NMN+), with kcat values exceeding NAD+ and surpassing most engineered NRC-active enzymes by 10-105-fold. Structural analyses reveal that this motif reinforces cofactor positioning and preorganizes the active site independently of the NAD+ adenosine monophosphate moiety. This motif supports activity across simple-synthetic NRCs such as 1-(2-carbamoylmethyl)nicotinamide and, when introduced into diverse ALDH scaffolds, enhances NMN+ activity up to 60-fold. These findings elucidate nature's solution to engineering NRC-active enzymes and offer a blueprint to mine latent evolutionary plasticity in natural enzymes that serve as superior engineering starting points.

PMID 42717052
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PubMedAging cell2026-09-10

NAD+ Metabolic Reprogramming Drives CD8+ T Cells Senescence and Exacerbates Ulcerative Colitis.

Ye Maolin M, Zhou Qi Q, Kong Mingjia M, Zhao Suhan S et al.

While immunosenescence is increasingly implicated in chronic inflammatory disorders, its precise pathogenic contribution to ulcerative colitis (UC) remains elusive. Here, we identify senescent CD8+ T cells as a distinct pathogenic population that exacerbates colitis, demonstrating that systemic senolytic treatment significantly attenuates disease severity. Mechanistically, nicotinamide adenine dinucleotide (NAD+) metabolic dysregulation triggers mitochondrial dysfunction and cytosolic mitochondrial DNA leakage, promoting CD8+ T cell senescence through the activation of the cGAS-STING signaling pathway. Spatial transcriptomic mapping reveals that senescent CD8+ T cells are enriched within mucosal niches experiencing NAD+ metabolic dysregulation. Crucially, this senescent-metabolic signature correlates with severe disease phenotypes and predicts non-response to biologic therapies in UC patients. Collectively, our findings uncover a critical NAD+-cGAS-STING axis driving T cell senescence, establishing the clearance of senescent immune cells as a promising therapeutic strategy for UC.

PMID 42717261
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PubMedBiophotonics discovery2026-09-10

Autofluorescence lifetime imaging resolves cell heterogeneity within peripheral blood mononuclear cells.

Riendeau Jeremiah M JM, Hockerman Lucia L, Maly Elizabeth E, Samimi Kayvan K et al.

Standard methods to characterize peripheral blood mononuclear cells (PBMCs) are often destructive, lack metabolic information, or do not provide single-cell resolution. Label-free tools that nondestructively measure single-cell metabolism within PBMCs can provide new layers of information to characterize disease state and cell therapy potential. We aim to determine whether nondestructive fluorescence lifetime imaging microscopy (FLIM) of the endogenous metabolic cofactors nicotinamide adenine dinucleotide (phosphate) (reduced form) and flavin adenine dinucleotide (oxidized form), or optical metabolic imaging (OMI), can identify immune cell subsets and activation state within heterogeneous PBMC cultures. OMI measured single-cell metabolism of PBMCs from three different human donors in the quiescent or activated (phorbol 12-myristate 13-acetate and ionomycin) state. Fluorescent antibodies were used as ground truth labels for single-cell classifiers of immune cell subtypes. OMI identified quiescent versus activated PBMCs with 94% accuracy at only 2 h post-stimulation, identified monocytes within quiescent and activated PBMCs with 96% and 88% recall, respectively, and identified NK cells within quiescent and activated PBMCs with 74% recall. OMI identifies activation state and immune cell subpopulations within PBMCs, enabling single-cell and label-free measurements of metabolic heterogeneity within complex PBMC samples. Therefore, OMI could enhance PBMC immunophenotyping for diagnostic and therapeutic applications.

PMID 42719456
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PubMedRenal failure2026-09-10

Pharmacological activation of SIRT1 alleviates sepsis-associated acute kidney injury by improving renal mitochondrial energy metabolism.

Zhu Rui R, Yang Hairong H, Liu Li L, Gao Yuanyuan Y et al.

Sepsis-associated acute kidney injury (SA-AKI) is a frequent and severe complication of sepsis and is closely associated with increased mortality. Mitochondrial dysfunction and impaired energy metabolism are important contributors to SA-AKI pathogenesis. Silent information regulator 1 (SIRT1), a nicotinamide adenine dinucleotide (NAD+)-dependent deacetylase, regulates cellular metabolism, oxidative stress, and mitochondrial homeostasis. However, its role in septic renal mitochondrial dysfunction remains incompletely understood. In this study, an LPS-induced NRK-52E rat kidney epithelial cell injury model and a cecal ligation and puncture (CLP)-induced sepsis rat model were established. SIRT1-related signaling was pharmacologically modulated using the SIRT1 activator SRT1720 or the SIRT1 inhibitor EX-527. Cell viability, SIRT1 mRNA and protein abundance, mitochondrial ultrastructure, oxidative stress, mitochondrial membrane potential, ATP content, ATPase activity, and non-esterified fatty acid levels were assessed. LPS exposure reduced SIRT1 expression in NRK-52E cells and was accompanied by decreased cell viability, mitochondrial structural damage, oxidative stress, and impaired energy metabolism. SRT1720 attenuated these changes, whereas EX-527 aggravated them. Similarly, in CLP-induced septic rats, renal SIRT1 expression was decreased, together with renal injury and mitochondrial metabolic dysfunction. SRT1720 ameliorated renal pathological injury and mitochondrial-related abnormalities, whereas EX-527 worsened these changes. These findings suggest that SIRT1 activation attenuates SA-AKI, at least partly by maintaining renal mitochondrial energy homeostasis.

PMID 42717829
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PubMedNature synthesis2026-09-10

Engineering de novo formatotrophy in the non-model yeast Y. lipolytica.

Newell William W, Hapeta Piotr P, Bell David D, Ledesma-Amaro Rodrigo R

Formate is an exciting potential microbial feedstock as it can be derived from CO2 and electricity. Despite this, limited progress has been made in engineering formatotrophy in yeasts, and no yeasts grow using formate naturally. Here we use metabolic modelling to find two potential formatotrophy pathways in Yarrowia lipolytica. We then use C13 tracer analysis and computationally guided growth experiments to show that wild-type Y. lipolytica possesses strong formate dissimilation and a cyclical C1 pathway with similar architecture to the synthetic serine-threonine cycle, which it uses to co-assimilate formate and glycerol. Messenger RNA sequencing shows that formate exposure results in increased oxidative stress and changes in the tricarboxylic acid cycle, redox and C1 metabolism. Following this, we use model-guided adaptive laboratory evolution to produce a formatotrophic strain of Y. lipolytica using the eukaryotic serine-threonine cycle. We then use further messenger RNA sequencing to show that formatotrophy is supported by changes in adenosine triphosphate and reactive oxygen species metabolism. Subsequently, we engineer nicotinamide adenine dinucleotide phosphate (NADPH) and reactive oxygen species metabolism to create a strain with substantially improved growth. This strain reaches about 10% of the theoretical maximum biomass yield, highlighting its potential for additional engineering approaches. Finally, we show that beta-carotene production from formate is possible in our engineered strain, opening the door to formatotrophic eukaryote bioprocesses.

PMID 42718654
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PubMedJournal of clinical biochemistry and nutrition2026-09-10

Chemical generation of superoxide in the co-presence of riboflavin derivatives and NADH: evidence for a non-enzymatic redox pathway.

Sugita Rinka R, Iida Sayaka S, Nagase Midori M, Masaki Hitoshi H et al.

We recently reported that flavin-associated compounds such as riboflavin, flavin mononucleotide, and flavin adenine dinucleotide reduce oxidized coenzyme Q and vitamin K homologues to corresponding reduced forms in the presence of reduced β-nicotinamide adenine dinucleotide (NADH). In these processes, coenzyme Q or vitamin K acts as a terminal electron accepter. If oxygen can function as an electron acceptor instead of those quinones, resulting in the formation of superoxide. In this study, superoxide formation from the system of NADH and flavin-associated compounds was examined using a water-soluble tetrazolium salt (WST-1) and 2-methyl-6-(4-methoxyphenyl)-3,7-dihydroimidazo[1,2-a]pyrazin-3-one (MCLA) assays. Formation of WST-1 formazan and chemiluminescence from MCLA, both of which are specific to superoxide, increased during co-incubation with NADH and a flavin-associated compound, and significantly suppressed with the addition of superoxide dismutase (SOD). Superoxide is an important reactive oxygen species (ROS) that is converted to other ROS, such as hydrogen peroxide or peroxynitrite. HaCaT keratinocytes, immortalized human keratinocytes, were then cultivated with NADH and flavin-associated compounds. Cell viability declined with increasing NADH concentration but was significantly recovered following the addition of SOD and catalase. We propose a chemical pathway for flavin-associated compound and NADH-induced superoxide generation in vivo, in which extracellular SOD plays an important role in cell survival.

PMID 42719550
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