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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

Related Research Articles

PubMedArchives of toxicology2026-11-09

CYP450 quantification and metabolic activation capacity of rat and hamster liver S9 fractions: implications for nitrosamine mutagenicity testing.

Dieckhoff Jessica J, Bringezu Frank F, Singh Jasjot J, Moniot Sébastien S et al.

N-nitrosamine impurities are a major concern in the pharmaceutical industry and public safety. The assessment of this chemically diverse group using conventional regulatory test batteries, including the Ames test (OECD TG 471), remains challenging. Consequently, refined strategies such as the Enhanced Ames Test (EAT) have been developed and recommended by regulatory authorities, requiring 30% induced rat and hamster S9. Recently, we showed that hamster S9 metabolizes short-chain N-nitrosamines more efficiently than rat S9, likely due to differences in the induction pattern of metabolizing enzymes. Metabolic activation by cytochrome P450 isoenzymes (CYP) is a critical step in the bioactivation of N-nitrosamines. Building on our previous publication, the present work focusses on key CYPs and sets the proteome data into perspective with in vitro mutagenicity data for selected N-nitrosamines. Targeted proteomics quantified CYP1A2, 2A6, 2C8/9/19, 2D6, 2E1, and 3A4 of rat and hamster orthologs in uninduced, Aroclor 1254-, and PB/NF-induced rat and hamster liver S9. In rat S9, induction markedly increased CYP1A2 and CYP3A1 (> 40-fold). For the selected set of CYPs, most protein levels in hamster S9 decreased or increased only slightly (< 6-fold) following induction, although baseline levels were higher than those in uninduced rat S9. Nevertheless, induced hamster S9 generated the strongest Ames responses for NDBA and 1-CPNP, indicating that induction enhances CYP activity beyond protein quantity alone. N-nitroso-atenolol was negative under all rat S9 conditions but positive in TA1535 only with induced hamster S9, indicating that larger NDSRIs require elevated metabolic activity for detection. These findings provide a mechanistic basis for species- and induction-specific differences in mutagenicity detection and contribute to a better understanding of the metabolic activation capacity of S9.

PMID 43002211
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PubMedCureus2026-11-01

Reported Life-Threatening Polymorphic Ventricular Arrhythmia With Torsade-Like Morphology in a Patient With Gordon Syndrome and Hyperkalaemia.

Kayani Laiba L, Emam Ayman A, Nair Rithima R, Elmahadi Saba S

Gordon's syndrome (pseudohypoaldosteronism type II) is a rare, inherited tubulopathy characterised by salt-sensitive hypertension, hyperkalaemia, and metabolic acidosis despite preserved renal function. Pathogenic variants affecting the with-no-lysine (K) signalling pathway include WNK1, WNK4, KLHL3, and CUL3. We report the case of a 37-year-old woman with genetically confirmed CUL3-related Gordon's syndrome who developed hyperkalaemia after a three-week interruption of bendroflumethiazide. During pre-hospital assessment, ambulance clinicians documented a self-terminating rhythm that they identified as torsade de pointes. The original recording cannot be retrieved; consequently, the rhythm classification, preceding QT interval, and possible alternative rhythm or artefact could not be independently assessed. Point-of-care venous blood gas potassium was 4.8 mmol/L, whereas formal laboratory potassium was 6.1 mmol/L. The sampling and processing information available did not establish the cause of this discrepancy. Subsequent echocardiography, computed tomography coronary angiography, cardiac magnetic resonance imaging, ambulatory monitoring, exercise testing, and additional electrical assessment did not identify a definitive alternative substrate, although an intermittent electrical disorder could not be excluded. Following treatment of hyperkalaemia and multidisciplinary cardiology and electrophysiology review, an extravascular implantable cardioverter-defibrillator was implanted. Bendroflumethiazide was resumed, with subsequent improvement in potassium control. This case highlights the importance of uninterrupted thiazide therapy in Gordon's syndrome, assessment of discordant potassium measurements, and careful interpretation of a reported serious rhythm event when its original tracing is unavailable. The temporal association with hyperkalaemia does not establish that it caused torsade de pointes.

PMID 42967171
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PubMedCureus2026-10-23

Newly Diagnosed Graves' Disease Followed by the Discovery of a Cavernous Internal Carotid Artery Aneurysm Causing Panhypopituitarism: A Case Report.

Touffaha Ibrahim M IM, Elhomsy Georges G

Sellar and parasellar vascular lesions are rare causes of pituitary dysfunction and may mimic pituitary adenomas or other sellar masses. Cavernous internal carotid artery (ICA) aneurysms can cause hypopituitarism through compression of the pituitary gland or stalk, but diagnosis may be delayed when symptoms are initially attributed to a more common endocrine disorder. We report a 37-year-old man who presented with six weeks of unintentional weight loss, fatigue, heat intolerance, excessive sweating, anxiety, tremor, and tachycardia. Initial evaluation showed suppressed thyroid-stimulating hormone (TSH), elevated total triiodothyronine (T3), positive thyrotropin receptor antibody, positive thyroid-stimulating immunoglobulin, and a hypervascular thyroid gland on ultrasound, consistent with Graves' disease. He was started on methimazole and atenolol. Although thyroid function tests improved, he developed persistent neck discomfort, prompting contrast-enhanced computed tomography (CT), which revealed an enhancing sellar mass. Magnetic resonance imaging (MRI) showed a T2-hypointense sellar lesion with internal flow artifact, and CT angiography confirmed a saccular aneurysm of the cavernous segment of the right ICA. Pituitary hormone evaluation demonstrated secondary adrenal insufficiency, central hypothyroidism, hypogonadotropic hypogonadism, growth hormone (GH) deficiency, and mild hyperprolactinemia, consistent with panhypopituitarism from pituitary compression. The patient was started on prednisone and levothyroxine, and atenolol and prednisone were subsequently discontinued before endovascular embolization was performed. At follow-up, symptoms improved, but panhypopituitarism persisted. This case highlights the importance of reassessing patients when endocrine symptoms evolve despite an initially appropriate diagnosis.

PMID 42910339
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PubMedBriefings in bioinformatics2026-10-19

Metabolomics workbench: data-driven classification and correlation analysis between metabolite classes, biomarkers, and drugs.

Khandokhin Mikhail M MM, Sokolov Aleksandr A, Oskolkov Nikolay N, Fredriksson Robert R et al.

Public repositories now accumulate an unprecedented amount of metabolomics data. Despite the opportunities for large-scale meta-analyses opened by these repositories, the deposited data rarely becomes systematically re-analyzed. We conducted a systematic metadata-based re-analysis of all human blood metabolomics studies in the Metabolomics Workbench performed using Orbitrap or QTOF mass spectrometry, encompassing 44 165 samples. After harmonizing metabolites with PubChem identifiers and embedding them using SMILES representations, we generated a map of 6752 blood metabolites forming 25 structural clusters, and subsequently performed correlation analysis between these clusters, biomarkers, and drugs. Analysis of 337 120 metabolite pairs detected in at least 10 studies showed that structurally related clusters display correlated abundances (ρ up to 0.6). Correlation patterns among established clinical biomarkers revealed candidate metabolic correlates, several with ρ > 0.7. We also developed open-source software enabling similar analyses for any metabolite across the Workbench data explored. Additionally, curating drug-containing datasets enabled meta-analyses for compounds such as acetaminophen, metoprolol, and atenolol, identifying both known and novel metabolic signatures. Besides the biological insights, we have found that Orbitrap and QTOF tend to detect different metabolites, but they give quantitatively coherent results on overlapping compounds. Overall, the present study provides the methodology and software to perform large-scale mining of public metabolomics data enabling its re-analysis to obtain novel biomedical insights.

PMID 42894388
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PubMedInternational journal of molecular sciences2026-10-16

A Mechanistic Map of the Phenotypic Complexity in Recessive Dystrophic Epidermolysis Bullosa Provides Basis for Therapeutic Target Discovery and Drug Repurposing.

Herráiz-Gil Sara S, Payá-Milans Miriam M, de Arriba María Del Carmen MDC, Martínez-Santamaría Lucía L et al.

Recessive dystrophic epidermolysis bullosa (RDEB) is a genodermatosis caused by loss-of-function mutations in the COL7A1 gene, producing a complex and heterogeneous phenotype. Clinical manifestations include skin fragility, local and systemic inflammation, impaired wound healing, dysbiosis, pain, and pruritus, increasing the risk of skin cancer. This work aimed to develop an actionable model of RDEB's molecular mechanisms to identify and prioritize therapeutic targets for drug repurposing. Transcriptomic data of skin biopsies from pediatric RDEB patients and unaffected individuals were used to build the mechanistic map of the disease. This model, combined with machine learning, made it possible to infer actionable targets from the map circuits and identify candidate drugs capable of reversing the transcriptomic alterations. The resulting map is defined by 13 altered signaling circuits and 10 effector proteins which were linked to disease hallmarks including inflammation, fibrosis, and tumor progression. Analysis of the map identified 66 actionable targets with 74 drug candidates. Among them, overrepresentation analysis showed enrichment of phosphodiesterases and antineoplastic and immunomodulating agents. Finally, 16 drugs were prioritized for their potential to revert circuit alterations without potentiating unintended effects, with bendroflumethiazide and ibutilide showing the highest impact. This mechanistic model delivers the first functional disease map of RDEB and reveals promising therapeutic candidates targeted by approved drugs.

PMID 42883687
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PubMedCase reports in urology2026-10-13

Catecholamine-Secreting Retroperitoneal Paraganglioma: A Case Report and Literature Review.

Felício Eduardo E, Gião Nuno N, Bernardo Guilherme G, Barcelos André A et al.

Paragangliomas are rare neuroendocrine tumors arising from autonomic paraganglia. These tumors have metastatic potential, and histopathological findings alone cannot reliably predict their biological behavior. Clinical manifestations range from the classic triad of headache, diaphoresis, and palpitations to incidental findings in asymptomatic patients. A 75-year-old man was incidentally found to have a 5 cm retroperitoneal mass adjacent to the right renal hilum. Biochemical testing confirmed marked catecholamine hypersecretion, and 18F-FDOPA PET/CT demonstrated isolated uptake within the lesion without additional disease. Preoperative preparation included progressive alpha-adrenergic blockade with doxazosin for approximately 1 month, followed by atenolol for heart rate control. An open approach through a right subcostal hemichevron incision was selected because the tumor was located between the right renal artery and vein and lateral to the inferior vena cava. During dissection, an iatrogenic renal artery injury with intraoperative hemorrhage occurred, necessitating en bloc removal of the tumor, right kidney, and right adrenal gland. Histopathological examination confirmed a paraganglioma with a Ki-67 proliferation index below 1%, focal nuclear atypia, no mitotic figures, no tumor necrosis, no vascular invasion, and microscopic margin involvement. Immunohistochemistry was positive for Chromogranin A, synaptophysin, GATA-3, and S100. Germline testing using a 14-gene pheochromocytoma-paraganglioma panel identified no reported pathogenic or likely pathogenic variants. At 6 months, contrast-enhanced thoracoabdominopelvic computed tomography showed no evidence of local recurrence or metastatic disease, and plasma and urinary metanephrines had normalized, consistent with postoperative biochemical remission. The patient remains under joint endocrinology and urology follow-up with lifelong annual clinical and biochemical surveillance. This case highlights the diagnostic and surgical challenges of a functioning perihilar retroperitoneal paraganglioma. Careful endocrine preparation, vascular planning, multidisciplinary management, and lifelong surveillance are essential, particularly when the surgical margin is microscopically involved.

PMID 42865698
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