Drug Database
NI

nicotinamide (Papulex)

✓ Approved

Wockhardt Limited · Small Molecule · Small Molecule

What is nicotinamide?

nicotinamide is a small molecule developed by Wockhardt Limited. It is approved for therapeutic indications via topical.

Drug Profile

Brand NamesPapulex
CompanyWockhardt Limited
Drug ClassSmall Molecule
RouteTopical
StatusApproved
Sources: ClinicalTrials.gov, Wockhardt Limited

Therapeutic Indications

nicotinamide is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Skin and subcutaneous tissue disordersAcne✓ Approved

Related Research Articles

PubMedSmall (Weinheim an der Bergstrasse, Germany)2026-08-25

Polyethylene Nanoplastic Exposure Causes Miscarriage by Impairing Trophoblast NAD+ Metabolism via Mitochondrial Dysfunction.

Rao Hanyu H, Zhang Yijun Y, Hong Wei W, Pan Zhiyi Z et al.

Micro- and nanoplastics (MNPs) are emerging environmental pollutants of global concern, yet their reproductive toxicity and underlying mechanisms remain poorly understood. Here, we identify villous accumulation of polyethylene (PE) as a potential risk factor associated with miscarriage and investigate the underlying mechanisms using well-characterized PE nanoparticles. PE fragments were detected in all examined human villous tissues and higher levels of these fragments showed a positive association with miscarriage risk (OR = 1.13, 95% CI, 1.00-1.28). In mice, oral exposure to PE-MNPs led to dose-dependent embryo resorption. In trophoblasts, PE nanoplastics (PE-NPs) were efficiently internalized and subsequently impaired cell migration and invasion. Mechanistically, PE-NPs accumulated within mitochondria, causing structural damage, downregulation of nicotinamide phosphoribosyltransferase (NAMPT), and depletion of nicotinamide adenine dinucleotide (NAD+), which in turn suppressed fibroblast growth factor 2 (FGF2) expression, resulting in impaired trophoblast migration and invasion. Supplementation with mitochondria-protective peptide, NAD+ or FGF2 attenuated trophoblast dysfunction and reduced embryo resorption. These findings provide mechanistic insight into PE-NPs-induced reproductive toxicity and suggest a potential therapeutic target to mitigate the impact of NPs exposure on maternal-fetal health.

PMID 42639858
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PubMedInvestigative ophthalmology & visual science2026-08-25

Nicotinamide Mononucleotide Attenuates Inflammatory Activation, Choroidal Neovascularization, and Lesion-Associated Remodeling.

Wang Jue J, Osada Hideto H, Chen Steve S, Yamaguchi Shintaro S et al.

To evaluate the therapeutic potential of nicotinamide mononucleotide (NMN) for modulating the neurovascular inflammatory microenvironment and blunting tissue remodeling in neovascular age-related macular degeneration (nAMD). A laser-induced choroidal neovascularization (CNV) model was established in C57BL/6J mice, and CNV lesion size was quantified on RPE/choroid flat mounts. Immunostaining evaluated myeloid cell accumulation and fibrosis-associated remodeling. Quantitative RT-PCR and Western blotting assessed inflammatory/angiogenic gene expression and signaling activation in the retina and RPE/choroid. In vitro, lipopolysaccharide (LPS)-stimulated bEnd.3 and primary mouse RPE cells and TGF-β-stimulated THP-1-derived macrophage cells were used to model inflammatory and profibrotic responses. NMN treatment significantly reduced CNV size in the laser-induced CNV model. This was accompanied by decreased myeloid cell accumulation within CNV lesions. NMN attenuated inflammatory and angiogenesis-related gene expression in the RPE/choroid and neural retina and reduced downstream signaling activation. In vitro, NMN suppressed LPS-induced inflammatory and proangiogenic responses in primary RPE cells and bEnd.3 endothelial cells and inhibited NF-κB activation. NMN further attenuated tissue remodeling, as shown by reduced collagen I-positive area under prolonged and delayed dosing regimens, together with decreased F4/80-positive area and α-smooth muscle actin-positive area within CNV lesions. In TGF-β-induced THP-1-derived macrophage cells, NMN suppressed profibrotic responses. Our findings indicate that NMN reduces inflammatory signaling and alleviates the inflammatory microenvironment in CNV, accompanied by decreased angiogenesis-related gene expression and fibrosis-related remodeling. By attenuating inflammatory activation and tissue remodeling processes, NMN warrants further evaluation as an adjunctive approach to limit CNV progression and late-stage tissue remodeling in nAMD.

PMID 42640154
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PubMedJournal of traditional Chinese medicine = Chung i tsa chih ying wen pan2026-08-25

Taohong Huazhuo decoction alleviates carbon tetrachloride-induced hepatic fibrosis in rats by inhibiting the nicotinamide adenine dinucleotide phosphate oxidase 4/nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 signaling pathway.

Yuan Ren R, Xiangni Chen C, Lei Shi S, Minghua Mao M et al.

To explore the mechanism underlying the anti-fibrotic effects of Taohong Huazhuo decoction (THHZD, ). Forty percent carbon tetrachloride (CCl4) dissolved in olive oil (2 mL/kg) was intraperitoneally injected twice a week for 8 weeks to induce hepatic fibrosis in rats. The normal group received the same volume of olive oil alone. At week 5, rats injected with CCl4 were intragastrically administered normal saline, 0.1 mg/kg colchicine, 3.285 g/kg THHZD, 6.57 g/kg THHZD, and 13.14 g/kg THHZD once a day for 4 weeks. A biochemical analyzer was used to detect the levels of serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), and total bilirubin (TBIL). Hematoxylin and eosin (HE) staining and Masson staining were performed to evaluate pathological changes in the liver. Enzyme-linked immunosorbent assay (ELISA) was used to determine glutathione (GSH) and malondialdehyde (MDA) levels in the liver, and interleukin-1β (IL-1β), and IL-18 in serum. The levels of α-smooth muscle actin (α-SMA) and reactive oxygen species (ROS) in liver tissues were analyzed by immunohistochemistry and immunofluorescence, respectively. Western blot (WB) was used to analyze the expression levels of nicotinamide adenine dinucleotide phosphate oxidase 4 (NOX4), nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3), IL-1β, IL-18, caspase-1, and collagen I in liver. Finally, in vitro experiments were conducted using hepatic stellate cells (HSC-T6). THHZD improved the pathological changes caused by CCl4 in the liver. Compared with the normal group, the levels of serum ALT, AST, TBIL, IL-1β, and IL-18 in the model group were significantly increased. NOX4, ROS, NLRP3, IL-1β, IL-18, caspase-1, collagen I, α-SMA, and MDA levels were increased in the liver, while GSH levels were decreased. The administration of THHZD to CCl4-exposed rats significantly reversed or eliminated the changes in the above-mentioned indicators. Moreover, THHZD inhibited transforming growth factor-β1 (TGF-β1)-induced high expression of α-SMA and collagen I in HSC-T6 cells, while downregulating the expression of proteins related to the NOX4/NLRP3 signaling pathway in vitro. THHZD reduced the activation of HSCs by inhibiting the NOX4/NLRP3 signaling pathway, thereby exerting anti-hepatic fibrosis effects.

PMID 42639772
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PubMedAngewandte Chemie (International ed. in English)2026-08-25

Theranostic Potential of an NAD(P)H-Activatable Fluorophore: Assessing Cancer Aggressiveness and Triggering Apoptosis.

Cha Yujin Y, Oh Taehoon T, Kim Hui Joo HJ, Kang Minju M et al.

Molecular theranostics, integrating precise diagnosis with targeted therapy, represents a cornerstone of personalized medicine. As a pivotal metabolic cofactor, reduced nicotinamide adenine dinucleotide (phosphate) (NAD(P)H) is intrinsically linked to cancer progression and survival when dysregulated. In this study, we report DE-CQ, an NAD(P)H-activatable fluorophore that enables both cancer imaging and apoptosis. DE-CQ allows the real-time quantification and visualization of intracellular NAD(P)H, serving as a robust molecular indicator of cancer malignancy. Beyond its diagnostic utility, DE-CQ preferentially induces mitochondria- and ER stress-dependent, caspase-mediated apoptosis in aggressive MDA-MB-231 cancer cells while maintaining minimal toxicity toward normal cells. Our findings demonstrate that DE-CQ functions as a potent theranostic agent, simultaneously providing diagnostic insights into cancer aggressiveness and triggering cell death. Given its dual functionality and high selectivity, DE-CQ holds significant potential as a next-generation platform for advanced, personalized cancer treatment.

PMID 42639950
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PubMedBioresource technology2026-08-24

Reinforced biofilm-mediated electron transfer and perfluorooctanoic acid removal: Neglected macrophyte roles in iron-biochar-based constructed wetlands.

Qian Xiuwen X, Huang Juan J, Shi Ying Y, Zhang Yuanyan Y et al.

This study evaluated how macrophytes regulated biofilm-mediated electron transfer and perfluorooctanoic acid (PFOA) fate in iron-carbon (IC)-based constructed wetlands (CWs). Compared with unplanted systems, Iris pseudacorus markedly enhanced intracellular electron transfer and energy metabolism, increasing final electron transport system activity by 51.3%, and raising ratio of oxidized nicotinamide adenine dinucleotide to reduced nicotinamide adenine dinucleotide by up to 5.9-fold and adenosine triphosphate content by 308.1% in IC layer after long-term PFOA exposure. Plants increased alpha diversity, optimized microbial community, and enriched functional microorganisms (like Geobacter and Shewanella) and up-regulated genes (belonging to Complex I/III/V, extracellular polymeric substance synthesis, and quinone), which were closely related to electron transfer and iron/sulfur-cycling. Consequently, macrophytes contributed to higher PFOA removal in IC-based CW (74.0-92.6%) than unplanted group (41.5-71.3%), with increased defluorination rate (by up to 30.7%), greater degradation contribution (28.5%), lower short-chain PFCA accumulation, and continuously enhanced nutrient removal. These findings innovatively proposed macrophytes as key regulators for sustainable PFOA treatment in IC-based CWs.

PMID 42636905
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PubMedCureus2026-08-24

Nicotinamide Mononucleotide (NMN) Prevents Age-Associated Transcriptional Drift in a Tissue-Dependent Manner: Mechanistic Leads From Ras-Related Protein Rab-11A-Mediated Trafficking and Carnitine Palmitoyltransferase 2-Linked Fatty Acid Oxidation.

Cheung Ngo N

This study is a secondary computational reanalysis of the publicly available GSE85718 microarray dataset generated during the long-term nicotinamide mononucleotide (NMN) study. NMN has been reported to improve several age-sensitive physiological traits in mice, including energy metabolism, insulin sensitivity, plasma lipid profiles, and skeletal-muscle mitochondrial function. However, the transcriptional mechanisms behind these effects remain less clear than the broader nicotinamide adenine dinucleotide (NAD+) and sirtuin-centered model often used to explain NMN biology. The present analysis used a per-tissue age-by-treatment interaction model to test whether NMN modifies the rate of age-associated transcriptional change rather than simply shifting expression at one age. The model was expression ~ age × treatment, with the age-by-treatment term used as the central test. A gene was considered an NMN-rescue candidate only when it changed with age in control mice and showed an opposite-signed interaction term, consistent with NMN shifting old-age expression toward the young-control state. No individual gene reached genome-wide false discovery rate (FDR) <0.05 for age, NMN at six months, or the interaction term in skeletal muscle, liver, or white adipose tissue (WAT). Therefore, all gene-level results should be treated as hypothesis-generating. Using relaxed nominal criteria, 421 rescue candidates were identified in skeletal muscle, 355 in liver, and 397 in WAT. Only 35 genes were rescued in at least two tissues, 26 of which were direction-consistent, and none were rescued in all three tissues. Ras-related protein Rab-11A (RAB11A) emerged as the strongest cross-tissue candidate, with rescue in skeletal muscle and WAT, high confidence in at least one tissue, consistent directionality, and involvement in 39 gene set enrichment analysis (GSEA) leading-edge terms, largely related to trafficking and cellular transport. Carnitine palmitoyltransferase 2 (CPT2) was the only mitochondrial gene among the robust cross-tissue candidates and was consistently rescued in skeletal muscle and WAT, supporting a focused fatty-acid oxidation and substrate-handling hypothesis rather than broad mitochondrial activation. At the pathway level, liver showed the clearest signal: NMN was associated with suppression of fatty-acyl-coenzyme A (CoA) and long-chain fatty-acyl-CoA metabolic programs. These findings do not establish that NMN prevents transcriptional aging or that RAB11A or CPT2 mediates the physiological effects of NMN. Instead, they identify tissue-specific, testable candidates from a secondary reanalysis of an existing animal dataset. In particular, they support moving beyond a generic "NAD+ improves mitochondria" model toward testable mechanisms involving cellular logistics, membrane recycling, and substrate utilization.

PMID 42634749
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