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glycopyrronium bromide (Sialanar)

✓ Approved

Proveca · Small Molecule · Small Molecule

What is glycopyrronium bromide?

glycopyrronium bromide is a small molecule developed by Proveca. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesSialanar
CompanyProveca
Drug ClassSmall Molecule
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Proveca

Therapeutic Indications

glycopyrronium bromide is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Gastrointestinal disordersSalivary hypersecretion✓ Approved

Related Research Articles

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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PubMedAnalytica chimica acta2026-09-19

Surfactant deep eutectic solvents for extraction and HPLC-PDA analysis of antipsoriatic drugs in spiked water and lipophilic topical matrices.

Alamir Samy G SG, Magdy Nancy N, Ibrahim Adel Ehab AE, Hussein Lobna A LA et al.

Deep eutectic solvents (DESs) have garnered attention in various disciplines due to their unique properties. In this work, different surfactants were screened as hydrogen-bond acceptors in combination with structurally related phenols as hydrogen-bond donors (HBDs), and successful and unsuccessful pairings were discussed. Literature on successfully paired surfactants was also reviewed. Nevertheless, the screening results and reported classifications, together with the observed aqueous behavior and variable extraction performance across different matrices, prompted further investigation of composition-behavior relationships of these systems. Five surfactant-phenolic DESs were synthesized by mixing o-cresol (CRS) or catechol with dodecyltrimethylammonium bromide (DTAB), cetyltrimethylammonium bromide (CTAB), or Brij35 at 75.0 °C for 30.0 min. Although more hydrophobic HBDs were used than in previous studies, the resulting DESs displayed transient aqueous dispersion after vortexing and subsequently re-separated on standing. Their viscosity (64.21-1389 mPa s) and conductivity (1.00-447.00 μS/cm) also varied. 1H/13C nuclear magnetic resonance and Fourier-transform infrared spectroscopy indicated hydrogen bonding between phenolic hydroxyl groups and bromide/ether acceptors, with features suggesting π-cation association in cationic-surfactant systems. To probe their practicality, a high-performance liquid chromatography method with photodiode array detection was developed for betamethasone valerate, halobetasol propionate, fusidic acid, and tazarotene, achieving separation within 6 min, and compared with five reported chromatographic methods. Validation per the International Council for Harmonisation Q2 (R1) guidelines demonstrated linearity (R2 0.9997-0.9999), accuracy (98.2-102.4%), and precision (≤2.0%), with robustness evaluated through experimental design. Brij35-based systems showed reduced extraction recoveries for lipophilic topical formulations. After additional screening, CRSCTAB and CRSDTAB DESs were used with spiked water samples as a hydrophilic proof-of-concept matrix, employing salting-out-assisted liquid-liquid microextraction using ammonium acetate. The results suggest provisional amphiphilic-like rather than conventional hydrophobic-DES behavior; however, thermal phase diagrams, equilibrium water-solubility measurements, and broader thermodynamic investigations remain necessary before any formal reclassification.

PMID 42763156
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PubMedPathology, research and practice2026-09-19

Quercetin protects brain microvascular endothelial cells against hypoxia/reoxygenation-induced injury and ferroptosis by targeting the TCF3/ALOX15 axis: Implications for cerebral small vessel disease.

Cao Mengjie M, Ji Yingxiao Y, Zhang Bin B, Chen Kun K et al.

Cerebral small vessel disease (CSVD) is a leading cause of vascular cognitive impairment and stroke. Quercetin is a natural flavonoid with neuroprotective effects in various cerebrovascular disorders. However, its specific molecular targets and mechanisms in CSVD remain elusive. Bioinformatic analysis identified arachidonate 15-lipoxygenase (ALOX15) as a potential ferroptosis-related target of quercetin in CSVD. The human cerebral microvascular endothelial cells (HCMEC/D3) subjected to hypoxia/reoxygenation (H/R) treatment were used for in vitro experiments. Cell viability, apoptosis, and angiogenesis were measured via 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), flow cytometry, and tube formation assay, respectively. Ferroptosis markers, including Fe²⁺, superoxide dismutase (SOD), malondialdehyde (MDA), and lipid peroxidation were detected by commercial kits or flow cytometry. The expression of ALOX15, transcription factor 3 (TCF3), acyl-CoA synthetase long-chain family member 4 (ACSL4), and glutathione peroxidase 4 (GPX4) was assessed using western blot. Online prediction, dual-luciferase reporter assay, and chromatin immunoprecipitation (ChIP) were performed to validate the TCF3-ALOX15 transcriptional regulation. A bilateral common carotid artery occlusion (BCAO) rat model of CSVD was established for in vivo validation. Quercetin improved H/R-induced HCMEC/D3 cell viability, promoted angiogenesis, and reduced apoptosis. Quercetin also attenuated ferroptosis, characterized by decreased Fe²⁺ accumulation, MDA and lipid peroxidation levels, and restoration of SOD activity and GPX4 expression while suppressing ACSL4 (all P < 0.05). TCF3 was identified as a transcriptional activator of ALOX15. TCF3 knockdown mimicked quercetin's protective effects, which were reversed by ALOX15 overexpression. Conversely, TCF3 overexpression counteracted quercetin-mediated protection. In BCAO rats, quercetin treatment ameliorated hippocampal neuronal damage, reduced brain edema, improved spatial learning and memory, and suppressed expression of TCF3/ALOX15 and ferroptosis markers (all P < 0.05). Quercetin protected against H/R-induced endothelial injury and ferroptosis in CSVD by targeting the TCF3/ALOX15 transcriptional axis, providing mechanistic insights into quercetin's cerebrovascular protective effects.

PMID 42762583
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PubMedFrontiers in immunology2026-09-18

A case report of sequential efgartigimod and rituximab treatment for tSNMG.

Xie Hua H, Pan Ting Ting TT, Zhang Lin L

Trible-seronegative myasthenia gravis (tSNMG) is defined as myasthenia gravis (MG) without detectable or low affinity antibodies to acetylcholine receptor (AChR), muscle-specific kinase (MuSK) andlipoprotein related protein 4(LRP-4). This article reports a case of a 39-year-old married female patient with thymoma-associated seronegative myasthenia gravis (tSNMG), which was accompanied by multiple positive autoantibodies and a benign mediastinal lesion. The primary manifestation was generalized muscle weakness, involving the limbs, bulbar muscles, and respiratory muscles. After admission, the patient showed poor responses to treatments including pyridostigmine bromide, human immunoglobulin, glucocorticoids, and tacrolimus. Ultimately, following therapy with efgartigimod followed by rituximab, significant symptomatic improvement was observed. By analyzing the diagnosis and treatment process of this case alongside relevant literature, this report explores the therapeutic value of efgartigimod followed by rituximab for tSNMG, key points for individualized regimen adjustments, and the challenges in diagnosis and treatment, thereby providing a reference for the clinical management of such refractory cases.

PMID 42755762
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PubMedRSC advances2026-09-18

Preparation, characterization, and catalytic performance of a 2,3-dihydroxybenzoic acid-based deep eutectic solvent for the synthesis of chromenoquinolinones.

Goudarzi Hadis H, Habibi Davood D, Alizadeh Abdolhamid A, Monem Arezo A

An ethyltriphenylphosphonium bromide/2,3-dihydroxybenzoic acid deep eutectic solvent (ETPPBr/2,3-DHBA-DES, 1 : 2 molar ratio) was prepared and characterized by eutectic phase behavior analysis, FT-IR spectroscopy, 1H NMR spectroscopy, TGA/DTA, and density measurements, confirming the formation of a eutectic system. The DES was then employed as a recyclable catalyst for the one-pot three-component synthesis of 6H-benzo[h]chromeno[4,3-b]quinolin-6-ones via the condensation of 4-hydroxycoumarin, 1-naphthylamine, and aryl or heteroaryl aldehydes under solvent-free conditions. Under the optimized reaction conditions (0.50 mmol catalyst, 80 °C), ten target derivatives were obtained in 60.8-85.0% isolated yields within 45-90 min. The catalyst was readily recovered by aqueous extraction and reused for four consecutive cycles, affording product yields from 85% in the first run to 72% in the fourth. FT-IR analysis of the recovered catalyst indicated that its characteristic structural features were largely preserved after recycling. These results demonstrate that the ETPPBr/2,3-DHBA-DES is an effective and recyclable catalyst for the solvent-free synthesis of 6H-benzo[h]chromeno [4,3-b]quinolin-6-ones.

PMID 42757127
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PubMedCellular and molecular biology (Noisy-le-Grand, France)2026-09-18

Selegiline induces neuroprotection via PGC-1α/Nrf2 gene upregulation in H2O2 -treated hippocampal-derived neural stem/progenitor cells.

Abdanipour Alireza A, Nikfar Ali A, Feizi Hadi H

Oxidative stress mediated by reactive oxygen species (ROS) is a major contributor to the pathogenesis of neurodegenerative diseases, including Alzheimer's, Parkinson's, Huntington's, multiple sclerosis, and amyotrophic lateral sclerosis. Selegiline, a monoamine oxidase B inhibitor, has been reported to exert neuroprotective effects, although its precise cytoprotective mechanisms remain unclear. In this study, we investigated the effects of selegiline on apoptosis, necrosis, and cell survival in hydrogen peroxide (H₂O₂)-treated hippocampal-derived neural stem/progenitor cells (HD-NSPCs) in vitro. Passage 3 HD-NSPCs were treated with varying concentrations of selegiline (10⁻³ to 10⁻⁹ M) prior to exposure to 125 μM H₂O₂. Cell viability was assessed using the MTT assay, while apoptosis and necrosis were evaluated using TUNEL and acridine orange/ethidium bromide staining, respectively. Real-time RT-PCR was performed to quantify mRNA levels of PGC-1α, Nrf2, and Bcl-2. Treatment with 10⁻⁷ M selegiline significantly enhanced HD-NSC viability, reduced apoptotic and necrotic cell fractions, and upregulated PGC-1α, Nrf2, and Bcl-2 expression compared to untreated cells (P < 0.05). These findings suggest that selegiline mitigates oxidative stress-induced cytotoxicity by activating Nrf2/PGC-1α signaling and promoting anti-apoptotic gene expression, thereby preserving mitochondrial function and enhancing cell survival. Overall, selegiline may represent a promising therapeutic agent for protecting neural progenitor cells and alleviating neuronal damage in neurodegenerative disorders.

PMID 42758107
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