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atenolol + bendroflumethiazide (TenBen / Amoretic LD / Amoretic)

✓ Approved

Warner Chilcott PLC · ADRB1 · Small Molecule

What is atenolol + bendroflumethiazide?

atenolol + bendroflumethiazide is a small molecule developed by Warner Chilcott PLC. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesTenBen, Amoretic LD, Amoretic
CompanyWarner Chilcott PLC
Drug ClassSmall Molecule
Molecular TargetADRB1, SLC12A3
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Warner Chilcott PLC

Mechanism of Action

Molecular Targets

atenolol + bendroflumethiazide acts on 2 molecular targets:

ADRB1adrenoceptor beta 1 (B1AR, RHR)
SLC12A3solute carrier family 12 member 3 (NCCT, NCC)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

atenolol + bendroflumethiazide is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Vascular disordersHypertension✓ Approved
Renal and urinary disordersRenal failure✓ Approved

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Genetic Bone Diseases: A Scoping Review of Pathology, Symptoms, Diagnosis, Treatment, and New Horizons.

Jones Colin C, Jayasuriya Ambalangodage C AC

Genetic bone diseases are a rare group of afflictions suffered by the general population. However, their rarity should not diminish research efforts to help patients understand and treat their diseases. This review summarizes the pathology, symptoms, diagnosis, and treatment insight into six well-known genetic bone diseases. Only six bone diseases are included due to the relatively low prevalence of them as whole limiting our scope to ensure accurate information and attention is provided for each disease individually. A literature search of PubMed is conducted, including studies published within the past five years (January 2020-December 2025). Thirty-six studies met inclusion criteria, and no significant risk of bias is identified among the selected articles. Study findings are synthesized into disease overview, clinical and radiographic features, and diagnostic and treatment approaches. Actively developing or novel therapies relevant to each disease are also included. These treatments include: fresolimumab for osteogenesis imperfecta, small interfering ribonucleic acid (RNA) therapy for Osteopetrosis, denosumab for Paget's disease of bone, vosoritide/recifercept/infigratinib for achondroplasia, mesenchymal stem cell therapy for craniosynostosis, and combination losartan and atenolol therapy for Marfan syndrome. These treatments are generally more recently acknowledged in literature and are either actively undergoing research or require further research to determine their efficacy.

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PubMedJACC. Clinical electrophysiology2026-07-10

Beta-Blockers and Exercise Performance in Children with Long QT Syndrome.

Webster Gregory G, Gill Nathan N, Carberry Thomas T, Chandler Stephanie F SF et al.

Young people taking beta-blockers for long QT syndrome (LQTS) have concerns about exercise performance. This study sought to determine whether objective measures of cardiopulmonary fitness are influenced by beta-blocker dose in LQTS. In a retrospective chart review of treadmill cardiopulmonary exercise tests (CPETs), we measured peak oxygen consumption (Vo2), respiratory exchange ratio (RER), blood pressure, and percent predicted heart rate at peak exertion (%PHR), each analyzed with a linear mixed-effects model. We analyzed nadolol data (noncardioselective) as our primary analysis, then analyzed a validation cohort of atenolol data (cardioselective). We evaluated 220 CPETs in 93 patients with LQTS. The mean age at first CPET was 12 ± 3.9 years. In multivariable analysis, %PHR decreased by 13% for every 1 mg/kg/d increase in beta-blocker dose, demonstrating physiologic beta-blocker effects. However, we identified no correlation between nadolol dose and measures of cardiopulmonary fitness. Neither peak Vo2 nor peak RER was correlated with nadolol dose. Only mild blood pressure changes were observed (<9 mm Hg decrease at peak exertion per 1 mg/kg increase in nadolol dose). Increased atenolol dose was also associated with stable peak Vo2 and peak RER. In children with LQTS, we did not observe any relationship between higher nadolol doses and objective measures of effort (peak RER) or cardiopulmonary fitness (peak Vo2), despite a linear dose-response between nadolol dose and %PHR. These results suggest that treatment with nadolol for LQTS does not affect most patients' peak exercise performance. These data were validated in patients from an earlier era who had been prescribed atenolol.

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PubMedWater research2026-07-09

Metagenomic insights into microbial drivers of organic micropollutant removal in wastewater-impacted riverbank filtration.

Zhai Yujia Y, Wang Xun X, Deng Xuhan X, Li Xiaoming X et al.

Organic micropollutants (OMPs) in wastewater treatment plant (WWTP) effluent pose persistent risks to aquatic ecosystems and drinking water sources. Riverbank filtration (RBF) is a nature-based treatment process, yet the compartment-specific roles of riverbed sediment and downstream soil in OMP attenuation remain poorly resolved under wastewater-impacted conditions. Here, we combined targeted chemical analysis, OMP property compilation, shotgun metagenomics, EnviPath-based biotransformation annotation, and exploratory network analysis to investigate OMP attenuation in a laboratory-scale RBF system treating real WWTP effluent for 10 months. Nineteen OMPs were monitored along a sequential sediment-soil filtration pathway. Sediment preferentially attenuated hydrophilic or charged compounds, including lidocaine, amantadine, and sotalol, whereas soil contributed more strongly to the attenuation of naproxen, atenolol, and losartan. Metagenomic profiling revealed distinct microbial communities and functional gene repertoires between sediment and soil after long-term operation. Sediment harbored higher relative abundances of genes associated with oxidative xenobiotic transformation, including cytochrome P450-related enzymes, demethylases, dehydrogenases, oxidases, and aromatic compound degradation pathways. An exploratory Spearman network further identified associations among microbial genera, EnviPath-annotated candidate biotransformation genes, and OMP removal rates, including 17 KO-OMP links supported by both correlation and pathway annotation. These findings indicate that sediment and soil develop complementary microbial functional potentials that may support compound-specific OMP attenuation. This study provides a mechanistic basis for optimizing sediment-soil configurations in wastewater-impacted RBF systems and for improving nature-based barriers against diverse OMP mixtures.

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PubMedScientific reports2026-07-09

Decoding cytokine interactions for psoriasis therapy through computational repurposing of antihypertensive drugs.

Chakith M R Sai MRS, Pradeep Sushma S, Raj Ranjith R, Reddy Pruthvish P et al.

Psoriasis is a chronic, immune-mediated skin disorder characterized by excessive inflammation and the overexpression of pro-inflammatory cytokines, including IL-6, IL-1β, IL-17 A, and IFN-γ. Despite the availability of targeted therapies, current treatments often entail high costs, limited accessibility, and adverse side effects. Drug repurposing-utilizing approved medications for novel indications-offers a cost-effective strategy to accelerate the development of alternative therapies with established safety profiles. Twelve FDA-approved antihypertensive drugs-including ACE inhibitors, angiotensin receptor blockers, beta-blockers, and calcium channel blockers-were computationally evaluated for anti-inflammatory potential in psoriasis. Target cytokines were identified using network analysis via STRING and Cytoscape. Molecular docking was performed against IL-6, IL-1β, IL-17 A, and IFN-γ. The top-performing ligands underwent further analysis using ADMET prediction, BOILED-Egg visualization, Density Functional Theory (DFT) calculations, and molecular dynamics (MD) simulations to assess pharmacokinetics, electronic properties, and protein-ligand complex stability. Apremilast, a clinically approved anti-psoriatic agent, served as the reference drug. Lisinopril, Ramipril, Amlodipine, and Atenolol emerged as top candidates based on docking scores and pharmacokinetic profiles. Among them, Lisinopril exhibited the strongest binding affinity across all four cytokines, comparable to or exceeding that of Apremilast. Amlodipine demonstrated the highest electronic reactivity, and all selected drugs showed favorable ADMET properties. MD simulations over 200 ns confirmed the dynamic stability of the Lisinopril-IL-6 complex. Lisinopril has shown potential as a molecular candidate through detailed computational analysis of cytokine interactions. However, these results are purely predictions and should be viewed with caution, especially considering reports of potential ACE inhibitor-related psoriasis worsening. Further thorough laboratory, animal, and clinical studies are necessary to assess its practical application and safety in treating psoriasis.

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PubMedScientific reports2026-07-06

Development and validation of a green dispersive liquid-liquid microextraction-LC-MS/MS method for sotalol quantification in human plasma using central composite design optimization and pharmacokinetic application.

Serag Ahmed A, Abduljabbar Maram H MH, Alosaimi Manal E ME, Baryyan Alaa O AO et al.

An LC-MS/MS method coupled with central composite design (CCD)-optimized dispersive liquid-liquid microextraction (DLLME) was developed and validated for sotalol quantification in human plasma according to ICH M10 guidelines. CCD with response surface methodology systematically evaluated four DLLME parameters - disperser solvent volume, extraction solvent volume, sample pH, and centrifugation time - identifying extraction solvent volume, pH, and disperser volume as dominant factors governing extraction efficiency. Optimal conditions of disperser volume 1200 µL, extraction solvent 300 µL, pH 10.0, and centrifugation time 3 min yielded predicted recovery of 95.29%, experimentally confirmed at 99-103%, with organic solvent consumption of 1.5 mL per sample representing a reduction compared to conventional SPE and LLE approaches. Chromatographic separation was achieved on a Poroshell 120 EC-C18 column (100 × 2.1 mm, 2.7 μm) with 4-min isocratic elution, and quantification employed MRM transitions m/z 273.1→255.1 for sotalol and m/z 267.2→145.1 for atenolol internal standard in positive ESI mode. The method demonstrated excellent linearity (1-1200 ng/mL, r² = 0.9994), sensitivity (LLOQ 1 ng/mL), acceptable accuracy and precision, and comprehensive stability under multiple storage conditions, in full compliance with ICH M10 acceptance criteria. Preliminary pharmacokinetic application in healthy volunteers following single oral 80 mg sotalol administration yielded Cmax 701 ± 53.8 ng/mL, t½ 10.1 ± 1.0 h, and AUC0→∞ 11,713 ± 1,345 ng·h/mL, broadly consistent with published literature values, supporting method applicability for therapeutic drug monitoring. Multi-metric sustainability assessment encompassing AGSA-prep (64/100), AGSA (65.28/100), CaFRI (69/100), BAGI (75.0/100), CACI (69/100), AMRI (71/100), and WECA (81%) demonstrated improved environmental performance relative to conventional extraction approaches, providing comprehensive sustainability characterization of the developed method.

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PubMedCell biochemistry and function2026-07-02

Identification of PRKCB, NLRC4, and TNFSF10 as Key Regulators of the Lipid Metabolism-Autophagy Network in Atherosclerosis.

Li Min M, Sun Yanjun Y, Sun Yanyi Y, Chen Zhenyue Z

The occurrence and development of atherosclerosis (AS) are closely related to disorders of lipid metabolism and dysfunction of autophagy. However, the key regulatory genes and immune microenvironment characteristics require further exploration. This study integrated the bulk transcriptome and single-cell RNA sequencing data, and utilized bioinformatics methods to screen the differentially expressed genes (DEGs) of AS. The weighted gene co-expression network analysis (WGCNA) was used to identify the key gene modules related to lipid metabolism and autophagy. The core regulatory genes were further screened based on the machine learning algorithm (LASSO regression). The enrichment scores of 28 immune cell subtypes were calculated by ssGSEA, and the correlation between the immune infiltration characteristics and the expression levels of the three core genes (PRKCB, NLRC4, and TNFSF10) was analyzed by Spearman correlation analysis. The single-cell transcriptome data analysis was performed to determine the cell subtype distribution characteristics of the core genes and to compare the expression differences in lipid metabolism-autophagy-related gene expression across distinct cell subtypes. In addition, we screened potential drugs targeting the key genes from the public drug database, and simulated the binding mode of approved drugs with the active site of PRKCB by molecular docking technology. Ultimately, the expression of target factors in mouse aortic tissues was determined by quantitative real-time PCR (RT-qPCR), Western blotting, and immunohistochemical (IHC) analysis. Concurrently, the levels of TNFSF10 in mouse plasma were confirmed through enzyme-linked immunosorbent assay (ELISA). Three lipid metabolism-autophagy core regulatory genes, PRKCB, NLRC4, and TNFSF10, were identified. These genes were significantly associated with the immune microenvironment of AS plaques and exhibited different cell subpopulation distribution patterns. The macrophage subpopulations showed higher lipid metabolism-autophagy regulatory activity. Molecular docking revealed that the anti-atherosclerotic drugs quercetin and atenolol can stably bind to the active site of PRKCB (with docking energies of -8.3 kcal/mol and -6.2 kcal/mol, respectively), a finding that identifies PRKCB as a candidate target worthy of further attention. Experimental evidence confirmed that the expression of these three key factors was significantly elevated in atherosclerotic plaque tissue, and the levels of TNFSF10 in the plasma of atherosclerotic mice were also significantly higher than those in the control group. This study identifies PRKCB, NLRC4, and TNFSF10 as key hub genes that link lipid metabolism and autophagy in AS, and highlights their potential as diagnostic biomarkers and therapeutic targets.

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