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

PubMedAging cell2026-10-22

A Cilia-Centered Nicotinamide Adenine Dinucleotide (NAD+) Signaling Network Regulates Hypothalamic Lysosomal Homeostasis and Metabolic Aging.

Park Se Eun SE, Roh Eun E, Park Jae Woo JW, Kim Seong Jun SJ et al.

Nicotinamide adenine dinucleotide (NAD+) is an essential metabolite that regulates diverse cellular metabolic processes. Primary cilia, hair-like organelles on the cell surface, function as critical signaling hubs. Here, we demonstrate that cellular NAD+ levels are key regulators of both primary cilia growth and lysosomal function in hypothalamic neurons. NAD+ depletion induces ciliary shortening and diminishes lysosomal activity in a cilia-dependent manner. Mechanistically, the lysosomal repair complex protein CHMP4B translocates from periciliary satellites to lysosomes during lysosomal stress, a process impaired by ciliary dysgenesis. Disrupted lysosomal recruitment of CHMP4B leads to abnormal lysosomal Ca2+ signaling and lysosomal dysfunction. Aged mice with hypothalamic NAD+ deficiency exhibit shortened cilia and lysosomal stress phenotypes, both of which are restored by calorie restriction (CR). Moreover, CR improves aging-associated metabolic dysfunction, at least in part, through hypothalamic cilia-dependent mechanisms. These findings identify a primary cilium-mediated-NAD+ signaling axis that maintains lysosomal homeostasis in hypothalamic neurons, the disruption of which drives metabolic aging.

PMID 42902820
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PubMedPharmacology & therapeutics2026-10-20

Prospects for adiponectin-based therapeutics in myocardial ischemia reperfusion injury.

Bahit M Cecilia MC, Gibson C Michael CM, Lei Yubin Y, Hsu Henry H HH et al.

Adiponectin is an adipocyte-derived hormone with broad cardiometabolic benefits, circulating at high levels in healthy individuals but reduced in obesity, diabetes, and cardiovascular disease. Low adiponectin concentrations are strongly associated with coronary artery disease, myocardial infarction, myocardial ischemia-reperfusion injury (MIRI), and heart failure. MIRI remains a major unmet need in contemporary ST-segment-elevation myocardial infarction (STEMI) care. Although reperfusion is essential in limiting ischemic myocardial necrosis, it causes deleterious effects such as impaired carbohydrate oxidation, excessive fatty-acid oxidation, intracellular acidosis, calcium (Ca2+) overload, oxidative/nitrative stress, and mitochondrial fragmentation, that expand infarct size, worsen microvascular obstruction, and fuel adverse ventricular remodeling. Activation of the adiponectin-adiponectin receptor (AdipoR) axis directly counteracts these processes by stimulating adenosine monophosphate-activated protein kinase (AMPK)-dependent metabolic rebalancing, restoring mitochondrial fusion-fission homeostasis, enhancing oxidative capacity, reducing inducible nitric oxide synthase (iNOS-) and nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-mediated injury, improving endothelial nitric oxide (NO) bioavailability, and enhancing microvascular perfusion. In animal models, adiponectin or its mimetics consistently reduced infarct size, improved myocardial function, and attenuated apoptosis, inflammation, and no-reflow. A growing array of therapeutic strategies has emerged, each bringing its own pharmacologic nuances and implications for translation to the clinic. This review summarizes current strategies to enhance adiponectin action, highlights the progress in peptide and small-molecule mimetics, and discusses future directions for clinical translation in cardiometabolic diseases.

PMID 42901395
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PubMedACS nano2026-10-20

Self-Amplifying Cascade Enzymatic Nanoplatform Orchestrating Metabolic Reprogramming and Oxidative Stress for Antitumor Therapy.

Chen Yusheng Y, Liu Qiang Q, Gao Mengluan M, Zhang Lingjian L et al.

Nanocatalytic tumor therapy utilizes nanomaterials to catalyze chemical reactions, producing cytotoxic species that kill tumor cells; however, the metabolic heterogeneity of tumor cells significantly compromises therapeutic efficacy. Herein, we developed a self-amplifying cascade enzymatic nanoplatform (ReS2@GOx) for nanocatalytic tumor therapy by orchestrating metabolic reprogramming and oxidative stress. This nanoplatform integrates rhenium disulfide (ReS2) nanozyme possessing trimodal enzyme-mimetic activities (catalase (CAT)-like, nicotinamide adenine dinucleotide (NADH) oxidase (NOX)-like, and glutathione oxidase (GSHOx)-like activities) with glucose oxidase (GOx), enabling three interlocked therapeutic actions: (1) external energy-independent singlet oxygen (1O2) generation through ReS2-mediated hydrogen peroxide (H2O2) conversion involving a superoxide anion (•O2-) intermediate; (2) attenuation of metabolic circuits through NADH oxidation and glutathione depletion; and (3) a cyclic cascade reaction driven by GOx-mediated glucose oxidation and H2O2 production, coupled with CAT-mediated H2O2-to-O2 conversion, sustaining glucose oxidation and NADH consumption. Mechanistic studies reveal a noncanonical 1O2 generation pathway involving electron shuttle-mediated •O2- conversion, establishing a redox loop fueled by endogenous substrates (e.g., glucose, NADH). The coordinated enzymatic triad achieves dual tumor suppression, including blocking adenosine triphosphate (ATP) production by inhibiting glycolysis/oxidative phosphorylation (OXPHOS) and inducing lipid peroxidation. This work demonstrates a nanocatalytic tumor therapy strategy that orchestrates tumor metabolism to potentiate oxidative lethality, highlighting the therapeutic potential of metabolic regulation for tumor treatment.

PMID 42899762
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PubMedIUBMB life2026-10-20

Icariin Protects Against Mitochondrial Damage and Ferroptosis-Related Injury in Synovial Fibroblast-Like Synoviocytes Through SUMO1-Dependent Regulation of SIRT1.

Wu Zhiming Z, Mao Zeqing Z, Guo Jian J, Xiong Mingfeng M et al.

Rheumatoid arthritis (RA) is a chronic autoimmune disease characterized by persistent synovial inflammation and progressive joint destruction, in which fibroblast-like synoviocytes (FLSs) play a central pathogenic role. Ferroptosis and oxidative stress-driven mitochondrial dysfunction have recently been implicated in synovial cell injury during RA progression. Sirtuin 1 (SIRT1), a nicotinamide adenine dinucleotide-dependent deacetylase, is known to regulate inflammation, redox homeostasis, and cell survival; however, the upstream regulatory mechanisms controlling SIRT1 function and their relevance to ferroptosis in RA remain poorly defined. Primary rat FLSs and a complete Freund's adjuvant (CFA)-induced adjuvant arthritis (AA) rat model were used. SIRT1 transcription, protein expression, subcellular localization, and enzymatic activity were assessed using quantitative real-time PCR, Western blotting, immunofluorescence, and enzymatic assays. Oxidative stress, mitochondrial dysfunction, lipid peroxidation, and ferroptosis-related parameters were evaluated using biochemical assays and fluorescence-based probes. SUMO1 expression was manipulated by knockdown and overexpression approaches, and the interaction between SUMO1 and SIRT1 was examined by co-IP.Inflammatory stimulation with IL-1β impaired SIRT1 transcriptional expression, reduced its nuclear localization, and suppressed its enzymatic activity in FLSs, accompanied by enhanced reactive oxygen species accumulation, mitochondrial dysfunction, lipid peroxidation, and ferroptosis-related changes. ICA treatment restored SIRT1 expression and activity while alleviating oxidative stress and ferroptotic injury. ICA upregulated SUMO1 expression, while Co-IP analysis demonstrated an association between SUMO1 and SIRT1. SUMO1-dependent regulation was associated with increased SIRT1 nuclear localization and enzymatic activity. Disruption of SUMO1 expression or pharmacological inhibition of SIRT1 suppressed the protective effects of ICA in FLSs. Consistent regulatory effects were observed in arthritic rats following ICA administration. These findings support the involvement of SUMO1/SIRT1 regulation in ferroptosis-related injury and mitochondrial dysfunction in RA-associated synovial cells. ICA exerts protective effects by restoring coordinated SIRT1 regulation at multiple functional levels, highlighting SIRT1-centered pathways as potential therapeutic targets for RA.

PMID 42897413
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PubMedJournal of oral & facial pain and headache2026-10-19

Gut microbial and metabolomic alterations associated with herpetic trigeminal neuralgia: an exploratory multi-omics study.

Tian Mingyue M, Wang Yangyang Y, Li Cong C, Fan Jiaming J et al.

Herpetic trigeminal neuralgia (HTN) is a neuropathic pain disorder caused by varicella-zoster virus invasion of the trigeminal nerve, but its mechanisms remain poorly elucidated. Accumulating evidence implicates gut microbiota dysbiosis and metabolic perturbations in modulating chronic pain via the gut-brain axis, yet their roles in HTN have not been systematically explored. Integrated multi-omics analysis was performed on 19 patients with HTN and 18 healthy controls. Fecal metagenomic sequencing characterized gut microbial composition and function. Untargeted metabolomics profiled metabolic signatures in fecal and circulating samples. Weighted gene co-expression network analysis (WGCNA) and random forest modeling screened pivotal microbial and metabolic features associated with HTN. Correlation analysis between differential metabolites and clinical pain scores validated the translational potential of identified alterations. HTN patients showed significantly reduced gut microbial diversity, with enriched Proteobacteria, depleted butyrate-producing bacteria (including Faecalibacterium, Roseburia, and Lachnospira), and expanded opportunistic pathogens (Escherichia coli and [Ruminococcus] gnavus). Microbial pathways for pH homeostasis and oxidative stress defense were downregulated. Metabolomic analysis identified differential metabolites, primarily involving nicotinate/nicotinamide metabolism and retrograde endocannabinoid signaling. WGCNA and random forest analyses suggested fecal metabolites as potential candidate features, with associations between gut microbial dysregulation and systemic metabolic changes. Furthermore, screened metabolites correlated significantly with pain scores. This study provides multi-omics evidence of gut microbial and metabolic dysregulation in HTN, generating hypotheses for further mechanistic research. Large-scale, multicenter prospective cohorts with standardized metadata collection are needed to validate these findings.

PMID 42895014
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PubMedJournal of microbiology and biotechnology2026-10-19

Heat-treated Lactiplantibacillus plantarum MYO Improves Muscle Strength and Modulates Gut Microbiota in Older Adults with Reduced Muscle Strength.

Lee Jin Joo JJ, Song Ji-Won JW, Kim Hyeon Jeong HJ, In Jung Hoon JH et al.

Age-related sarcopenia is a condition characterized by a decline in muscle strength and physical function with aging, and its improvement is important given its close association with falls, fractures, and mortality. Recently, as the link between age-related gut microbiota dysbiosis and sarcopenia has been elucidated, modulation of the gut microbiota has gained attention as a therapeutic strategy for sarcopenia. In particular, with growing interest in paraprobiotics, various health-promoting effects-including gut microbiota modulation and improvement of muscle strength-have been reported. However, clinical evidence supporting the association between the gut microbiota and muscle strength remains limited. Accordingly, this clinical study was conducted to investigate the effects of heat-treated Lactiplantibacillus plantarum MYO (LPMYO) intake on quadriceps muscle strength, hand grip strength, muscle quality index (MQI) and gut microbiota composition in older adults with reduced muscle strength, and to examine the correlation between muscle strength and gut microbiota. After 12 weeks of heat-treated LPMYO supplementation, quadriceps muscle strength, hand grip strength and MQI were significantly improved compared with the placebo group. In addition, the abundance of beneficial bacteria, including Faecalibacterium, Lachnospira, Turicibacter, Megasphaera, and the [Eubacterium]_ventriosum group, was significantly increased. Notably, Turicibacter and Megasphaera showed positive correlations with muscle parameters. In addition, enrichment of predicted microbial functions, such as amino acid metabolism, nicotinate and nicotinamide metabolism, and oxidative phosphorylation (OXPHOS), was observed following supplementation with heat-treated LPMYO. Taken together, heat-treated LPMYO significantly improved muscle strength and muscle quality, and these muscle strength-enhancing effects may be associated with alterations in the gut microbiota.

PMID 42894972
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