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nicotinic acid (nicotinic acid ER / Niaspanor / Niaspan)

✓ Approved

Merck KGaA · HCAR2 · Small Molecule

What is nicotinic acid?

nicotinic acid is a small molecule developed by Merck KGaA. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand Namesnicotinic acid ER, Niaspanor, Niaspan
CompanyMerck KGaA
Drug ClassSmall Molecule
Molecular TargetHCAR2
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Merck KGaA

Mechanism of Action

Molecular Targets

nicotinic acid acts on 1 molecular target:

HCAR2hydroxycarboxylic acid receptor 2 (NIACR1, GPR109A)
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Therapeutic Indications

nicotinic acid is developed for 8 unique indications across 4 therapeutic areas.

Therapeutic AreaConditionPhase
Vascular disordersArteriosclerosis✓ Approved
Metabolism and nutrition disordersHypercholesterolaemia✓ Approved
Metabolism and nutrition disordersHypertriglyceridaemia✓ Approved
Cardiac disordersMyocardial infarction✓ Approved
Metabolism and nutrition disordersDyslipidaemia✓ Approved

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Related Research Articles

PubMedMolecular psychiatry2026-09-20

An mPFC-DMV cortical-autonomic-immune axis governs stress-induced immune dysregulation in sepsis.

Yin Lu L, Liu Fuhong F, Li Mengyun M, Wang Ye Y et al.

Chronic psychological stress is a major predisposing factor that worsens sepsis outcomes, yet the neural mechanisms linking stress exposure to immune dysregulation remain poorly understood. Here, using a mouse model of chronic restraint stress (CRS) followed by endotoxemia, we show that prior stress markedly aggravates mortality, systemic inflammation, and immune imbalance during sepsis. Mechanistically, we identify a stress-sensitive medial prefrontal cortex (mPFC)-dorsal motor nucleus of the vagus (DMV) circuit that functions as a central regulator of peripheral neuroimmune homeostasis. Chronic stress is associated with impaired mPFC-DMV circuit function, accompanied by reduced splenic nerve activity, disrupted splenic norepinephrine (NE) and acetylcholine (ACh) signaling, heightened inflammatory responses, and diminished regulatory T cell (Treg) activity. Chemogenetic activation of the mPFC-to-DMV pathway restores splenic autonomic output, normalizes neurotransmitter homeostasis, attenuates systemic inflammation, improves survival, and rescues stress-associated Treg dysfunction. Importantly, chemical sympathectomy with 6-hydroxydopamine (6-OHDA) largely attenuates the protective effects of circuit activation, including its regulation of splenic NE/ACh balance, inflammatory cytokine production, and Treg responses, indicating that intact splenic sympathetic neuroimmune signaling is required for mPFC-DMV-mediated immunomodulation. Furthermore, in vitro experiments reveal that exogenous ACh promotes macrophage-mediated Treg activation through α7 nicotinic acetylcholine receptors (α7nAChRs), providing a cellular mechanism through which autonomic neurotransmitter signaling regulates peripheral immune homeostasis. Together, these findings define a functional cortical-autonomic-immune axis through which chronic stress disrupts neuroimmune homeostasis during sepsis. Our findings further identify autonomic neurotransmitter signaling and α7nAChR-dependent macrophage-Treg communication as key mechanisms linking cortical circuit dysfunction to peripheral immune dysregulation, highlighting cortical-autonomic neuromodulation as a potential therapeutic strategy for stress-associated immune dysfunction in sepsis.

PMID 42763340
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PubMedLipids in health and disease2026-09-20

Real-world use of bempedoic acid for hypercholesterolaemia: a German multicentre, retrospective, cohort study.

Haberbosch Linus L, Baessler Andrea A, de Ruiter Ulrike U, Sinning David D et al.

Dyslipidaemia remains a leading cause of death in Germany despite an improving therapeutic landscape, with many patients not achieving guideline-recommended low-density lipoprotein cholesterol (LDL-C) goals. Bempedoic acid, an adenosine triphosphate citrate lyase inhibitor, is a recent addition to the therapeutic landscape with proven efficacy in randomised controlled trials; however, its use varies between centres. We aimed to assess the short-term, real-world effectiveness of bempedoic acid in lowering LDL-C levels in patients in Germany. This retrospective, observational study was conducted using data from patients with primary hypercholesterolaemia or mixed dyslipidaemia, collected before and approximately 3 months after initiating bempedoic acid in 7 specialised lipid outpatient clinics in Germany. Data were analysed from a total of 641 patients, with a mean age (standard deviation [SD]) of 63.2 (11.3) years. The addition of bempedoic acid significantly reduced LDL-C levels from a mean of 133.6 mg/dL at baseline to 101.8 mg/dL after 3 months (p < 0.001). The mean within-patient LDL-C reduction was 31.8 mg/dL and the mean patient-level percentage change was -17.5%. Mean patient-level changes were -4.9% for HDL-C and -12.0% for total cholesterol; triglycerides did not change significantly. At 3 months, patients not receiving any lipid-lowering therapy (LLT) other than bempedoic acid had a mean patient-level LDL-C reduction of 27.1%; corresponding mean reductions were 23.7% with ezetimibe, 20.3% with PCSK9 inhibitor therapy, 9.0% with statin therapy and 6.1% with statin plus ezetimibe. Suspected adverse events were documented in 218/641 patients (34.0%), and 171/641 (26.7%) had discontinued bempedoic acid by follow-up. Myalgia was the most commonly reported adverse event in patients discontinuing treatment (75 cases). Findings from this real-world, multicentre study conducted in Germany show that bempedoic acid may present an effective treatment option for patients with hypercholesterolaemia who are already receiving LLT, in addition to being an effective option for patients not receiving/tolerating other LLTs. The magnitude of LDL-C reduction differed across background treatment strategies, while suspected adverse events and treatment discontinuation were common in this specialist-care cohort.

PMID 42763399
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PubMedOpen life sciences2026-09-20

Comparative analysis of vitamin C derivatives on ATP homeostasis across diverse cell types.

Goc Anna A, Sumera Waldemar W, Niedzwiecki Aleksandra A

Cellular energy homeostasis is tightly regulated by mitochondrial function and substrate availability. Vitamin C is a redox-active molecule with emerging roles in cellular metabolism; however, the metabolic impacts of structurally distinct vitamin C derivatives remain incompletely defined. In this study, we systematically compared l-ascorbic acid, dehydroascorbic acid, 6-O-palmitoyl-l-ascorbate, and mineral ascorbates (calcium, magnesium, sodium, and potassium salts) across multiple mammalian cell types. Cells were exposed to concentrations ranging from 60 to 500 µM, encompassing physiologically and pharmacologically relevant levels. The vitamin C derivatives induced cell type- and concentration-dependent modulation of intracellular ATP levels. Notably, HepG2 and renal epithelial cells exhibited robust ATP increases, whereas fibroblasts, myocytes, microglia, and skeletal muscle models displayed variable responses depending on the derivative and dose. Moreover, in skeletal muscle cells, co-treatment of standard l-ascorbic acid with select fatty acids did not yield additive bioenergetic effects, suggesting a localized, substrate-specific plateau or shared regulatory step in this specific cell model. Exposure to l-ascorbic acid induced selective increases in COX-1 without changes in SDH-A, consistent with rapid functional modulation of mitochondrial activity in myocytes and microglial cells only. Collectively, these findings demonstrate that vitamin C derivatives modulate cellular ATP levels within existing metabolic networks in a context-dependent manner, consistent with the modulation of mitochondrial-associated energy metabolism.

PMID 42763556
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PubMedVeterinary research2026-09-20

Bovine viral diarrhea virus (BVDV) relies on cellular lipid droplet biogenesis and lipolysis to provide energy for viral replication.

Xiong Xiaoran X, Liu Yi Y, Zhu Yaohong Y, Wang Jiufeng J et al.

Bovine viral diarrhea virus (BVDV), one of the most important viral pathogens in cattle, causes serious economic losses due to immunosuppression and persistent infections. Previous studies have shown a tight connection between virus infection and lipid metabolism, particularly in the formation and degradation of lipid droplets (LDs). However, the pathogenic mechanism of BVDV infection and the molecular mechanisms by which viral proteins reprogram lipid metabolism remain unclear. We found that BVDV increased cellular LD accumulation by enhancing the production of new lipids, accelerating exogenous fatty acid uptake, and elevating diacylglycerol acyltransferase (DGAT)-dependent esterification of fatty acids (FAs). The generated LDs subsequently release free fatty acids (FFAs) via adipose triglyceride lipase/hormone-sensitive lipase (ATGL/HSL)-dependent lipolysis. This lipolysis-dependent release of FFAs is accelerated and transferred to mitochondria for oxidation by increasing contact between LDs and mitochondria, thereby promoting viral replication. Furthermore, BVDV core protein targets the surface of LDs, increasing and recruiting fatty acid synthase (FASN) and ATGL to promote LD mobilization. Meanwhile, the core protein interacts with mitochondria, linking mitochondria to LDs and facilitating the release of FAs for efficient fatty acid oxidation. Collectively, this study demonstrates that the BVDV core protein regulates cellular lipid metabolism to support BVDV replication, contributing to understanding the pathogenetic mechanisms by which BVDV interacts with host cells.

PMID 42763408
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PubMedCytotechnology2026-09-20

Antioxidant, genotoxic and cytotoxic effects of root extracts of Astragalus microcephalus: an assessment for alternative medicine.

Akbaba Giray Buğra GB, Öztürkkan Füreya Elif FE, Akdeniz Fikret F

The aim of this study is to evaluate the antioxidant, genotoxic and cytotoxic effects of root extracts of Astragalus microcephalus Willd. (A. microcephalus). Extracts were obtained using solvents such as ethanol, ethanol: n-hexane, n-hexane and methanol by Soxhlet extraction. The content of oil obtained from the n-hexane extracts of the plant was determined by Gas Chromatography with downstream Flame Ionization Detector (GC-FID) analysis. The antioxidant activity and total phenolic content of the extracts were determined by 2,2-diphenyl-1-picrylhydrazyl (DPPH) and Folin-Ciocalteu Methods, respectively. Genotoxic and cytotoxic properties of extracts at 50 and 100 µg/mL concentrations were investigated by Micronucleus (MN) and 3-(4,5-dimethylthiazol2-yl)-2,5-diphenyltetrazolium-bromide (MTT) assay, respectively. The roots of the plant contain an average of 2.53% oil. It was found that the most abundant fatty acid in the roots of the plant was linoleic acid. In addition, the roots of the plant contain palmitic, linolenic, 13,16-docosaadienoic, oleic and stearic acid. Methanolic extracts have the highest antioxidant activity and the richest in total phenolic content. All extracts obtained were determined to be genotoxic at 50 and 100 µg/mL. Methanol, ethanol: n-hexane and ethanol extracts of roots of A. microcephalus exhibit very low antioxidant activity even at high concentrations. Furthermore, except for the plant's ethanolic extract, all other extracts exhibit cytotoxicity at concentrations as low as 50 and 100 µg/mL. According to the results of this study, it isn't recommended to use the roots of A. microcephalus Willd. in the treatment of various diseases, considering their genotoxic and cytotoxic effects.

PMID 42763479
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PubMedIn vitro models2026-09-20

A flow cytometry-based assay system for the in vitro screening of anti-steatotic compounds.

Deshmukh Kajal K, Malladi Navya N, Banerjee Sanjay K SK

The rising prevalence of MASLD and the absence of approved therapies highlight the need for reliable, quantifiable in vitro assays to screen compounds targeting hepatic lipid accumulation. Current methods are often semi-quantitative and lack sensitivity. This study aimed to develop and validate a flow cytometry-based assay using HepG2 cells to assess lipid accumulation, a key early marker of hepatic steatosis and toxicity. Steatosis was induced using varying concentrations of oleic acid (0-800 μM) for 12-48 h. Lipid accumulation was quantified using Nile Red staining and flow cytometry. The data were compared with two other conventional methods, the absorbance/fluorescence-based and the image-based systems. The developed assay system was tested against various clinically used drugs known to have anti-hepatosteatosis properties. Compared to the conventional methods, Oleic acid-induced fat accumulation, measured by flow cytometry in the hepatocyte-specific HepG2 cell line, was observed to be dose-dependent and time-dependent, with significant lipid accumulation at 400 μM oleic acid after 24 h. The assay was validated using known anti-steatotic drugs, where Saroglitazar, Pioglitazone, Empagliflozin, and Atorvastatin significantly reduced lipid accumulation in HepG2 cells. Further, the sensitivity of the assay was checked by calculating the IC₅₀ values, where Saroglitazar and Triacsin C showed IC₅₀ values of 0.16 μM and 0.15 μM, respectively. This study successfully developed a flow cytometry-based in vitro assay using HepG2 cells to screen drugs against MASLD. The present flow cytometry assay is a human cell-based and animal-free system that offers a sensitive, accurate, and high-throughput platform for evaluating anti-steatotic compounds, with clear advantages over conventional methods for early-stage drug discovery. The online version contains supplementary material available at https://doi.org/10.1007/s44164-026-00110-4.

PMID 42763509
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