Drug Database
NI

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

PubMedMicrobial pathogenesis2026-07-25

Competitive interactions between canine-derived lactic acid bacteria and Klebsiella michiganensis: Implications for probiotic potential in canine cystitis.

de Moraes Reiner Silveira RS, Teixiera Maria Eloisa ME, Núñez Teresa Alessandra de Lima TAL, Paschoal Natália Rodrigues NR et al.

The Klebsiella oxytoca complex comprises at least six bacterial species, including Klebsiella michiganensis, for which reports in veterinary medicine remain scarce, particularly in the context of urinary tract infections. This prospective in vitro study aimed to (i) molecularly characterize, using next-generation sequencing (NGS), a K. michiganensis strain isolated from canine cystitis, including its plasmid content and antimicrobial resistance gene repertoire; and (ii) identify, among six species-specific lactic acid bacteria (LAB) recovered from the urogenital tract of healthy dogs, candidate strains exhibiting in vitro antagonism against this pathogen and a probiotic phenotype compatible with future ex vivo and in vivo validation. The in vitro antagonism was performed through five bacterial competition assays: spot-on-the-lawn (SOTL), radial streak (RS), modified cross-streak (MCS), agar well diffusion (AWD), and liquid coculture (LCA) assays. The probiotic properties of LAB strains were assessed through resistance to artificial gastric juice, bile salt tolerance, hydrophobicity, growth capacity, hydrogen peroxide production, antimicrobial susceptibility, complemented by class 1 integron genes screening and KEGG functional profile characterization. NGS analysis of K. michiganensis revealed the presence of IncF and IncR plasmids and 27 antimicrobial resistance genes. KEGG orthology analysis of the LAB strains revealed strain-specific metabolic KOs in four out of the six isolates. Among the tested strains, Enterococcus faecalis showed greater inhibition in the SOTL assays, whereas Lacticaseibacillus casei exhibited significantly greater inhibitory activity in the RS (p < 0.0001). Although some E. faecalis strains showed limited inhibition in the AWD and MCS assays, both species effectively inhibited the pathogen in the LCA. All LAB strains demonstrated tolerance to gastrointestinal conditions, moderate to high hydrophobicity, and hydrogen peroxide production, with no class 1 integron genes detected. Overall, K. michiganensis was identified as a novel causative agent of canine cystitis, and LAB strains, particularly L. casei, displayed key probiotic traits, supporting its potential for therapeutic application.

PMID 42498045
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PubMedTurkish journal of biology = Turk biyoloji dergisi2026-07-25

An in vitro mechanistic study of cholinergic-associated mechanisms relevant to MASLD in HepG2 cells.

Sönmez Gamze G, Gök Müslüm M, Sari Suat S, Bodur Ebru E

Polyunsaturated fatty acids (PUFAs) and the hepatic cholinergic axis are critical regulators of lipid metabolism and inflammatory signaling; however, their time-dependent interplay in hepatocytes remains incompletely understood. Clarifying how n-6 and n-3 PUFAs interact with cholinergic pathways may provide mechanistic insight into metabolic dysfunction-associated steatotic liver disease (MASLD). HepG2 cells were used to examine the combined effects of butyrylcholinesterase (BChE) overexpression and PUFA exposure. Cells were treated with linoleic acid (LA; n-6) or α-linolenic acid (α-LA; n-3) for 24 or 48 h. Gene expression analyses were performed to assess pathways involved in de novo lipogenesis, β-oxidation, cholinergic signaling, and inflammatory responses. Cholinesterase activities were measured enzymatically, secreted cytokines were profiled, and molecular docking simulations were performed to evaluate potential α-LA interactions with the α7 nicotinic acetylcholine receptor (α7 nAChR) and M3 muscarinic acetylcholine receptor (M3 mAChR). An early antilipogenic profile and changes suggestive of increased fatty-acid oxidation (↓SREBP-1c, ↓ACC1, and ↑CPT1A) were induced by α-LA at 24 h and were partially attenuated by 48 h. LA exhibited a biphasic pattern characterized by modest early suppression followed by a pronounced proinflammatory profile at 48 h (↑TNF, ↑IL6, and ↑COX-2). BChE overexpression was associated with increased expression of lipogenic and triglyceride-related genes, whereas cotreatment with PUFAs resulted in time- and class-specific modulation. Cholinergic markers exhibited divergent expression patterns: BCHE + α-LA increased CHAT and CHRNA7 expression at 48 h, whereas ACHE mRNA expression increased under both BCHE + LA and BCHE + α-LA conditions. Enzymatic analyses demonstrated increased total cholinesterase activity in the BChE and α-LA groups, while molecular docking supported the potential accommodation of α-LA within the binding pockets of α7 nAChR and M3 mAChR. PUFA class and exposure duration jointly shape hepatocellular metabolic and inflammatory states, with cholinergic signaling acting as a modulatory node relevant to MASLD.

PMID 42500687
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PubMedJournal of controlled release : official journal of the Controlled Release Society2026-07-25

Tumor-targeted CD40 ligand-functionalized extracellular vesicle mimetics enable chemoimmunotherapy for neuroblastoma.

Wang Jinkui J, Luo Junyi J, Li Jiahui J, Zhang Zhaoxia Z et al.

Neuroblastoma remains one of the most lethal pediatric solid tumors, and durable control of high-risk disease is hindered not only by inefficient tumor-selective drug delivery but also by a profoundly immunosuppressive tumor microenvironment. To address these dual barriers, we developed a chemoimmunotherapeutic vesicle-mimetic platform, DAS/CD40L-EM@DOX, by engineering CD40L-overexpressing HEK-293 T donor cells, generating extracellular vesicle mimetics through extrusion, decorating the membrane with a neuroblastoma-targeting DAS peptide, and post-loading doxorubicin. The resulting formulation preserved a nanoscale vesicular morphology, displayed CD40L on the membrane, and showed favorable particle size and zeta potential characteristics. In neuroblastoma cells, DAS decoration enhanced uptake in an α7 nicotinic acetylcholine receptor-associated manner and increased the cytotoxic and immunogenic effects of doxorubicin, as evidenced by augmented apoptosis, calreticulin exposure, and HMGB1 release. In macrophage assays, CD40L-containing vesicles shifted M2-like cells toward an M1-like phenotype, increasing CD86, TNF-α and IL-6 while decreasing CD206, IL-10 and TGF-β. Functionally, this repolarization enhanced tumor-cell phagocytosis and promoted CD8+ T-cell effector responses, including increased granzyme B, IFN-γ and IL-2 production. In tumor-bearing mice, DAS modification improved tumor accumulation and reduced off-target sequestration relative to unmodified vesicles. Therapeutically, DAS/CD40L-EM@DOX exerted the strongest inhibition of tumor growth, reduced tumor burden, prolonged survival, increased intratumoural M1-like macrophages and CD8+ T cells, decreased M2-like macrophages and regulatory T cells, and enhanced immunogenic cell-death markers in situ. Together, these findings support DAS/CD40L-EM@DOX as a dual-function vesicle-mimetic nanomedicine that couples neuroblastoma-targeted chemotherapy with macrophage reprogramming to remodel the tumor immune microenvironment and improve antitumour efficacy.

PMID 42498231
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PubMedCanadian journal of ophthalmology. Journal canadien d'ophtalmologie2026-07-25

Bisphosphonates and glaucoma: a pharmacovigilance signal detection analysis using the FAERS database.

Zhang Yan Y, Huang Yi Hong YH, Xiao Yan Ling YL, Zhu Xin Xing XX et al.

To detect and characterize disproportionality signals between individual bisphosphonates and glaucoma subtypes using the U.S. Food and Drug Administration Adverse Event Reporting System (FAERS). A retrospective pharmacovigilance disproportionality analysis. Participant data were drawn from adverse event reports from the FAERS database (Q1 2004-Q1 2025). Disproportionality analysis was conducted using the reporting odds ratio (ROR), proportional reporting ratio (PRR), and Bayesian confidence propagation neural network (BCPNN). Adverse events were coded using Medical Dictionary for Regulatory Activities (version 27.1). A significant signal required ≥3 cases and meeting thresholds (ROR 95% CI lower limit >1, PRR ≥2 with χ² ≥4, or BCPNN IC025 >0). Among 539 reports, significant disproportionality signals were identified for alendronic acid (ROR = 2.42; 95% CI: 2.18-2.70) and pamidronic acid (ROR = 2.23; 95% CI: 1.69-2.93) at the group level. Subtype-level signals included alendronic acid with open-angle glaucoma (ROR = 5.67) and normal-tension glaucoma (ROR = 4.60); pamidronic acid with open-angle glaucoma (ROR = 8.62); and risedronic acid with angle-closure glaucoma (ROR = 2.93). Median time-to-onset varied from 10 days (risedronic acid) to 1579 days (pamidronic acid). This pharmacovigilance analysis identifies distinct disproportionality signals linking specific bisphosphonates to different glaucoma subtypes, with heterogeneous time-to-onset patterns. The findings highlight potential safety signals warranting further clinical and mechanistic investigation.

PMID 42498257
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PubMedBritish journal of pharmacology2026-07-25

Rosemary metabolite carnosic acid opens Kv1.1 via its voltage sensor and corrects Kv1.1-linked episodic ataxia in mice.

Manville Rían W RW, Yoshimura Ryan F RF, Nguyen Hanh A HA, Zhao Ruiming R et al.

Episodic ataxia type 1 (EA1) is an autosomal dominant neurological disorder caused primarily by loss-of-function mutations in the voltage-gated potassium channel Kv1.1 (KCNA1). Small molecules that restore Kv1.1 activity hold promise as targeted therapies for EA1, yet current pharmacological strategies remain limited. Two electrode voltage-clamp electrophysiology and the Xenopus laevis oocyte expression system were used to study effects of carnosic acid, a phenolic diterpene from Salvia rosmarinus (rosemary) leaf extract on Kv1.1-linked EA1 mutant channels. We assessed ataxia therapeutic efficacy by comparing performance of Kcna1+/+ and Kcna1E283K/+ mice, a model of human EA1, on a balance beam under isoproterenol challenge in the absence or presence of 0.3-mg·kg-1 carnosic acid. Rosemary leaf extract and rosemary metabolite carnosic acid are efficacious Kv1.1 openers. Carnosic acid fully or partially corrects heterozygous, heteromeric Kv1.1 EA1 mutant channel activity in vitro and restores normal function in Kv1.1E283K/+ mice at 0.3 mg·kg-1. Experimental validation of unbiased in silico docking reveals carnosic acid occupies a binding pocket between the S1 and S4 helices of the voltage-sensing domain (VSD) of Kv1.1. Finally, we determined the chemical properties that endow carnosic acid with the ability to open Kv1.1 channels. Our findings uncover a Kv1.1 opener with the potential to reverse EA1 and other Kv1.1-linked disorders.

PMID 42498701
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PubMedPoultry science2026-07-25

Dietary glutamine modulates egg albumen and yolk composition in laying quails: effects of age.

Tomaszewska Ewa E, Kasperek Kornel K, Drabik Kamil K, Puzio Iwona I et al.

This study evaluated the effects of dietary l-glutamine (Gln) supplementation on egg composition and amino acid profiles in laying Japanese quail (Coturnix japonica). A total of 320 birds were assigned to four dietary treatments containing 0.0%, 0.5%, 1.0%, or 1.5% Gln for 12 wk. Eggs were collected at 12 and 19 wk of age, representing the early and late stages of the peak laying period, for analyses of yolk and albumen composition. Dietary Gln supplementation significantly affected the concentration of several amino acids in both yolk and albumen, although the response depended on bird age and Gln inclusion level. The effects were more pronounced in late peak-lay birds and were generally greatest at moderate supplementation levels (0.5% or 1.0% Gln). In albumen, increasing dietary Gln was associated with selective changes in amino acid composition, whereas yolk amino acid responses showed more evident age-dependent patterns. Proximate composition of egg fractions was affected to a lesser extent than amino acid profiles. Overall, the results indicate that dietary Gln modulates amino acid deposition in egg components in an age-dependent manner rather than uniformly enhancing egg nutritional value. This study demonstrates for the first time that dietary Gln supplementation can alter yolk and albumen amino acid profiles in laying quail, supporting its role as a dietary factor influencing amino acid deposition during different stages of lay.

PMID 42497588
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