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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

PubMedCells2026-10-26

Timeline of Achieving a Differentiated RPE Phenotype and Specialised Metabolism of ARPE-19 Cells Under Physiologically Relevant-Inducing Culture Conditions.

Matei Ioan V IV, Grimes Daniel D, Suwanmanee Gunticha G, Bagnall James J et al.

ARPE-19 cells are widely used to investigate and model retinal pigmented epithelium (RPE). Naïve ARPE-19 cells do not fully replicate RPE features. Previous reports show that under defined conditions, ARPE-19 differentiate towards an RPE phenotype, with protocols relying on prolonged or shorter-term cultures, the latter of which do not achieve full pigmentation. In particular, bioenergetics and mitochondrial dynamics have been assessed in a limited manner to date. The present work aims to characterise ARPE-19 under long-term physiologically relevant phenotype-inducing culture conditions, monitoring the timeline of RPE phenotype acquisition, with a focus on mitochondrial function and bioenergetics alongside structural and functional markers. Low passage ARPE-19 were cultured for 4 months using low-serum, pyruvate and nicotinamide-supplemented DMEM. Monthly assessments measured pigmentation, TER, gene/protein expression, mitochondrial parameters, and metabolism. ARPE-19 acquired relevant features early (1 month), including polarisation, expression of visual cycle and mitochondrial dynamic drivers, as well as increases in mitochondrial potential, mass/area and branching. Melanin accumulation was increased beginning at 1 month. Bioenergetic assays revealed a shift towards increased reliance on oxidative phosphorylation compared to glycolysis. Under these conditions, ARPE-19 acquired specific RPE features supporting functional assays after 1 month. Time-dependent accumulation of RPE-like features suggests that, for certain applications, later differentiation times are suitable. Appropriately differentiated ARPE-19 are a viable model to study key RPE physiological functions when accompanied by evidence of specific phenotypic and metabolic characterization.

PMID 42929819
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PubMedPhotochemistry and photobiology2026-10-25

Protection against ultraviolet-A and -B with systemic nicotinamide and Polypodium leucotomos extract-A narrative review.

Faisal A A, Pihl C C, Bjerring P P, Haedersdal M M et al.

Keratinocyte cancers (KCs) are increasing in incidence, and ultraviolet radiation (UVR) remains the main environmental risk factor. While topical sunscreens are effective photoprotectants, imperfect use has led to interest in oral supplements. This narrative review summarizes wavelength-specific mechanisms of two widely studied oral agents-nicotinamide (NAM) and Polypodium leucotomos (PL), across UVB, UVA, and solar-simulated radiation (SSR), focusing on DNA damage, erythema, immunosuppression, inflammation, oxidative stress, and tumor development. A PRISMA-informed search of PubMed, Embase, and Cochrane (inception to 28 November 2025) identified 36 eligible studies (18 NAM; 18 PL), including in vitro, animal, and human models. For NAM, clinical data demonstrated reduced KC incidence in immunocompetent patients, while no consistent changes in UVR-induced cyclobutane pyrimidine dimers (CPDs) or minimal erythema dose (MED) were seen. In murine SSR models, NAM reproducibly delayed KC development, supporting effects downstream of initial DNA damage. In vitro, NAM reduced inflammation and oxidative stress and, in limited data, oxidative stress signaling following UVA. For PL, human studies more consistently reported reduced erythema and oxidative stress, whereas effects on DNA damage were heterogeneous and limited, particularly for UVA in humans. Across both agents, mechanistic and wavelength-specific evidence remains incomplete, and study heterogeneity in UVR sources and endpoints limits comparability. Future research should establish standardized methods for UVR exposure assessment and focus on outcomes that are clinically relevant, to determine if the molecular effects observed lead to in vivo photoprotection.

PMID 42924584
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PubMedTransactions of the American Clinical and Climatological Association2026-10-25

THE KIDNEY AS A WINDOW INTO MAMMALIAN AGING: METABOLIC FRAILTY, MITOCHONDRIAL RESILIENCE, AND THE CONTINUUM FROM INJURY TO AGING.

Parikh Samir M SM

Aging-related decline of kidney function bears major medical and biological implications: chronic kidney disease (CKD) and acute kidney injury (AKI) risk rise sharply with age, and tubular epithelial cells in the kidney are paradoxically long-lived despite engaging in intense oxidative metabolic work. Mitochondrial relation to kidney physiology may unveil new hallmarks of mammalian aging. Our work has identified the central redox cofactor, nicotinamide adenine dinucleotide, as both a measurable and modifiable target to augment energy metabolism within the kidney and confer resistance to acute stressors that otherwise provoke AKI. More recently, we found that aging and transient injuries indefinitely degrade the fidelity of the kidney's mitochondrial DNA (mtDNA). Moreover, mtDNA mutation burden correlates with CKD severity and predicts future AKI events. These findings identify mtDNA mutations as a new, measurable determinant of kidney health and resilience, in turn proposing novel ways to track resilience in related organs.

PMID 42927019
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PubMedBiomedicine & pharmacotherapy = Biomedecine & pharmacotherapie2026-10-25

Nicotinate Phosphoribosyltransferase controls aggressiveness, Ca2+ homeostasis, and NAD+-derived Ca2+ mobilizing second messengers in triple-negative breast cancer.

Astigiano Cecilia C, Lori Laura L, Euro Liliya L, Caffa Irene I et al.

Triple-negative breast cancer (TNBC) represents the most aggressive form of breast cancer (BC), being characterized by a high metastatic rate and a poor prognosis due to its tendency to relapse and the lack of targeted therapies. Inhibition of NAD+ synthesis, mostly by targeting Nicotinamide Phosphoribosyltransferase in the salvage pathway, showed promise as anticancer therapy, as NAD+ is implicated in tumor growth, energy production, motion and invasiveness, immune response, and multi-drug resistance. We investigated the role of Nicotinate Phosphoribosyltransferase (NAPRT), the rate-limiting enzyme for NAD+ synthesis starting from nicotinate, in TNBC proliferation, invasiveness, also through the use of a 3D culture model, and in Ca2+ homeostasis. Our results demonstrated that NAPRT promotes tumor aggression and determines the concomitant increase of the cytosolic Ca2+ levels and the decrease in state of replenishment of Thapsigargin-sensitive ER Ca2+ stores. Also, NAPRT overexpression increased the levels of the Ca2+-mobilizing messengers cyclic ADPR and Nicotinic Acid Adenine Dinucleotide Phosphate (measurements with a newly developed assay) and the pharmacological CD38 or SARM1 inhibition reverted the NAPRT-induced changes in Ca2+ homeostasis. Therefore, targeting NAPRT may represent a promising strategy to slow down TNBC growth and progression.

PMID 42925766
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PubMedJournal of dental sciences2026-10-25

Sesamin suppresses high glucose-induced cyclooxygenase-2 and prostaglandin E2 production through Toll-like receptor 2-dependent oxidative stress in human gingival fibroblasts.

Li Ya-Lun YL, Hsu Yu-Chia YC, Fan Fang-Yu FY, Wang Yung-Li YL et al.

Hyperglycemia contributes to periodontal inflammation through oxidative stress and inflammatory mediator production in gingival fibroblasts. Sesamin, a major lignan from sesame, has antioxidant and anti-inflammatory properties. This study investigated whether sesamin attenuates high glucose (HG)-induced cyclooxygenase-2 (COX-2) expression and prostaglandin E2 (PGE2) production in human gingival fibroblasts (HGFs), and examined the involvement of Toll-like receptor 2 (TLR2)-dependent oxidative signaling. HGFs were exposed to HG in the presence or absence of sesamin. Cell viability, reactive oxygen species (ROS) generation, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, COX-2 expression, and PGE2 production were evaluated. The roles of TLR2, myeloid differentiation primary response 88 (MyD88), phosphoinositide 3-kinase (PI3K), Akt, and hypoxia-inducible factor-1α (HIF-1α) were examined using pathway-targeting approaches. HG increased TLR2 expression, enhanced NADPH oxidase-dependent ROS generation, and activated PI3K/Akt and HIF-1α signaling in HGFs. These responses were accompanied by increased COX-2 expression and PGE2 production. Sesamin suppressed HG-induced ROS generation, NADPH oxidase activity, PI3K/Akt and HIF-1α activation, COX-2 upregulation, and PGE2 release. Blockade of TLR2, MyD88, ROS generation, PI3K/Akt signaling, or HIF-1α also reduced HG-induced COX-2 expression and PGE2 production, supporting a TLR2/MyD88-dependent oxidative mechanism. Overall, the data indicate that sesamin targets upstream receptor-associated oxidative events rather than only terminal prostaglandin production. Sesamin attenuates HG-induced inflammatory responses in HGFs by suppressing TLR2/MyD88-mediated ROS generation and downstream PI3K/Akt/HIF-1α signaling. These findings suggest that sesamin may have potential as an adjunctive anti-inflammatory and antioxidant agent for modulating hyperglycemia-associated gingival inflammatory responses under diabetic-like conditions relevant to periodontal disease.

PMID 42923647
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PubMedbioRxiv : the preprint server for biology2026-10-25

An Inducible Model of RPE-Associated Hydroxyapatite Mineralization with Relevance to Drusen Formation in Age-Related Macular Degeneration.

Yang Julian J, Daniel Steffi S, Hulleman John D JD

A cardinal feature of nonexudative age-related macular degeneration (AMD) is the accumulation of drusen between the retinal pigment epithelium (RPE) and Bruch's membrane, yet the mechanisms that initiate and promote drusen formation remain to be fully understood. Hydroxyapatite (HAP), a calcium-phosphate mineral identified within human drusen, has been proposed to contribute to drusen nucleation and is associated with increased likelihood of RPE atrophy. However, mechanistic studies providing insight into RPE-associated mineralization have been limited by a lack of easy-to-use and manipulatable culture models. Here, we established a rapid, inducible ARPE-19-based model of HAP mineralization. We found that ARPE-19 cells cultured in minimum essential media (MEM) supplemented with nicotinamide (NIC), sodium phosphate, and ascorbic acid (NaPAA) reproducibly formed HAP positive deposits, whereas mineralization was not observed while using standard DMEM/F12 medium, DMEM/F12 with NaPAA, MEM-NIC medium, or MEM-NIC medium with alternative osteogenic supplements (such as β-glycerophosphate, ascorbic acid, and dexamethasone). Scanning electron microscopy with energy dispersive X ray spectroscopy demonstrated that the formed deposits were enriched in calcium (Ca) and phosphorus (P) with Ca/P ratios comparable to drusen-associated HAP deposits from AMD donor tissue. ARPE-19-based HAP deposits were also closely associated with neutral lipid-rich material, staining positive for BODIPY around their core structure. Bulk RNA sequencing of mineralized ARPE-19 cells revealed extracellular matrix, angiogenic, inflammatory, and metabolic transcriptional changes in the absence of strong enrichment of canonical osteogenic pathways. Co-treatment of mineralizing cells with either pyrophosphate, EDTA, or sodium citrate significantly reduced mineral deposition, but these approaches were not able to reverse it. Together, these findings establish a tractable RPE mineralization model that recapitulates key features of AMD-associated HAP and provides a platform for investigating mechanisms of drusen-associated mineral formation.

PMID 42926770
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