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atenolol + nifedipine (nifedipine/atenolol / Bresben / Niften)

✓ Approved

AstraZeneca UK Limited · ADRB1 · Small Molecule

What is atenolol + nifedipine?

atenolol + nifedipine is a small molecule developed by AstraZeneca UK Limited. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand Namesnifedipine/atenolol, Bresben, Niften
CompanyAstraZeneca UK Limited
Drug ClassSmall Molecule
Molecular TargetADRB1, CACNA1C
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, AstraZeneca UK Limited

Mechanism of Action

Molecular Targets

atenolol + nifedipine acts on 2 molecular targets:

ADRB1adrenoceptor beta 1 (B1AR, RHR)
CACNA1Ccalcium voltage-gated channel subunit alpha1 C (CaV1.2, CACNL1A1)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

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

Therapeutic AreaConditionPhase
Cardiac disordersAngina pectoris✓ Approved
Vascular disordersHypertension✓ Approved

Related Research Articles

PubMedAnalytical chemistry2026-10-20

DES-Based Green Synthesis of 2D Fluorescent Molybdenum Disulfide for Highly Sensitive and Selective Detection of Nifedipine.

Ullah Rafee R, Rehman Shams Ur SU, Khan Adnan A, Wu Hui-Fen HF

Highly fluorescent 2D MoS2-x nanosheets exhibiting intense blue emission were synthesized using a green chemistry approach, utilizing DES as both the reaction medium and a surface passivating agent. The material was synthesized via a hydrothermal method, followed by ultrasonication-assisted exfoliation to yield ultrathin nanosheets with enhanced photoluminescence properties. The 2D MoS2-x nanosheets demonstrated strong fluorescence at λem = 420 nm when excited at λex = 330 nm. These nanosheets were employed as a fluorescence probe for the detection of the calcium channel blocker drug nifedipine (NIF) via a fluorescence quenching mechanism. Upon addition of NIF, the fluorescence of the 2D MoS2-x nanosheets was quenched due to electron transfer from the nanosheets to the electron-deficient NIF molecules, combined with the inner filter effect (IFE). The nanosheets enabled highly sensitive and selective detection of NIF, with photoluminescence spectroscopy revealing a broad linear detection range of 0.6-360 nM (R2 = 0.993) and an exceptionally low limit of detection (LOD) of 0.40 nM. The system showed high selectivity toward NIF over structurally similar compounds, drugs, and common metal ions. The sensor was effectively applied for the detection of NIF in urine and Lotus Pond water samples, highlighting its potential for practical pharmacological monitoring. This study presents a sustainable and effective approach for fabricating DES-assisted 2D nanosheets for trace-level analyte detection.

PMID 42899538
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PubMedAmerican journal of hypertension2026-10-19

Amlodipine and Nifedipine Associations with B-Type Natriuretic Peptide in Women with Hypertension and Heart Failure with Preserved Ejection Fraction.

Harada Eisaku E, Yamada Toshihiro T, Mizuno Yuji Y, Arima Yuichiro Y et al.

Calcium channel blockers (CCBs) are frequently prescribed to manage hypertension in patients with heart failure with preserved ejection fraction (HFpEF). However, whether individual dihydropyridine agents exert uniform class effects on myocardial wall stress remains unclear. This retrospective, single-center observational study analyzed 465 consecutive patients with hypertension and HFpEF (354 women and 111 men) evaluated at Kumamoto Kinoh Hospital between May 2012 and July 2018. Multivariable linear regression models assessed associations between individual dihydropyridine CCBs (amlodipine vs. nifedipine) and plasma log-transformed B-type natriuretic peptide (lnBNP) levels. In multiple imputation models among women, adjusted differences in lnBNP relative to no-CCB were 0.236 (95% CI, 0.031 to 0.441) for nifedipine and -0.118 (95% CI, -0.273 to 0.037) for amlodipine. Direct linear contrasts in women confirmed lower lnBNP levels with amlodipine than with nifedipine (adjusted difference, -0.355; 95% CI, -0.562 to - 0.147). In men, the corresponding amlodipine-versus-nifedipine difference was -0.051 (95% CI, -0.697 to 0.595; P=0.876). The formal sex-by-drug interaction contrast in complete-case analysis yielded an adjusted difference of - 0.424 (95% CI, -1.055 to 0.208; P = 0.188), with male precision constrained by sample size (7 male nifedipine users). In women with hypertension and heart failure with preserved ejection fraction, amlodipine use was associated with lower adjusted ln(BNP) levels than nifedipine use. These observational findings challenge the assumption of an interchangeable dihydropyridine class effect on myocardial wall stress, suggesting that individual pharmacological profiles-rather than uniform class-level equivalence-warrant attention in clinical evaluations.

PMID 42895302
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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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PubMedPharmacological research2026-10-18

Nifedipine-modulated gut microbiota attenuates hypertensive vascular injury through Bifidobacterium-associated inosine-Adora2b signaling.

Ren Xiaoyu X, Yan Xuefang X, Tang Ping P, Jin Jiajia J et al.

Although antihypertensive drugs mitigate hypertensive vascular injury, their vascular benefits are not fully explained by blood pressure reduction alone. Many cardiovascular drugs reshape the gut microbiota, which in turn influences their vascular pharmacology. We therefore investigated whether gut microbiota remodeling contributes to nifedipine-mediated vascular protection in high-salt hypertensive rats and a pilot patient cohort. Combining 16S rRNA sequencing, untargeted metabolomics, fecal microbiota transplantation, microbiota depletion, supplementation, and selective receptor antagonism, we found that nifedipine ameliorated gut dysbiosis. Transplantation of nifedipine-modulated microbiota improved intestinal barrier integrity and reduced vascular inflammation, oxidative stress, collagen deposition, and vascular smooth muscle cell (VSMC) phenotypic switching, while only marginally lowering blood pressure. Conversely, microbiota depletion markedly attenuated these vascular benefits despite preserving nifedipine-induced blood pressure lowering. These vascular benefits were associated with nifedipine-restored Bifidobacterium animalis subsp. lactis 420 (B420) and increased inosine availability. Supplementation with either recapitulated major vascular protective effects of nifedipine without statistically significant changes in blood pressure. In hypertensive patients, nifedipine treatment was associated with higher intestinal B420 abundance and inosine levels. In vitro, inosine modulated macrophages in an Adora2b- and Rap1-dependent manner, with accompanying changes in cAMP and KLF4, ameliorating VSMC dysfunction via paracrine signaling. In vivo, systemic Adora2b antagonism attenuated the vascular protective effects of both inosine and B420. Together, our findings support a gut microbiota-dependent component of nifedipine-mediated vascular protection that extends beyond blood pressure lowering, involving B420, increased inosine availability, and Adora2b signaling. We also nominate B420 and inosine as candidate adjuncts to calcium channel blocker therapy.

PMID 42892458
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PubMedWilderness & environmental medicine2026-10-15

Silent Hypoxemia in High-Altitude Pulmonary Edema: A Case Report.

Karki Iswor I, Thapa Sabitra S, Chapagain Subodh S

We report a case of a trekker who ascended to Tilicho Lake (4919 m) from Kathmandu (1400 m) in 3 days. On day 3, he descended to Shree Kharka (4045 m). The following day, he trekked to Yak Kharka (4025 m) where, although he had no symptoms, he measured his own oxygen saturation (SpO2) at 72% in ambient air. Overnight, his SpO2 ranged from 75-80% on oxygen 2L/min via nasal cannula. The next day his SpO2 dropped to 47% while still on oxygen. He descended on horseback to Manang (3500 m), where his SpO2 was 70% on room air. He was diagnosed with high-altitude pulmonary edema (HAPE). He was treated with oxygen, 4L by nasal cannula, and nifedipine. The following day, he flew to Kathmandu, where he made a full recovery. Trekkers may develop life-threatening HAPE without obvious symptoms or signs. Slow ascent can decrease the likelihood of developing HAPE, but trekkers do not always follow the recommended ascent rate. Early detection, by history and physical examination and with point-of-care ultrasound (POCUS), if available, is critical in resource-limited regions such as ours. The keys to managing HAPE are early recognition and management, including descending to a lower altitude as soon as possible.

PMID 42878551
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PubMedBeijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences2026-10-15

[Systemic sclerosis with anti-human neutrophil cytoplasm antibody associated vasculitis: A case report].

Yang Li L, Zou Jinmei J

Systemic sclerosis (SSc) is an autoimmune disease involving microvessels and a wide range of connective tissues. Anti-human neutrophil cytoplasm antibody-associated vasculitis (AAV) is a primary, systemic necrotizing small vasculitis. The coexistence of AAV and SSc is rare. We report a case of SSc combined with AAV complicated with alveolar hemorrhage, gastrointestinal hemorrhage, and cerebral hemorrhage. The patient was a 56-year-old woman with a 20-year history of Raynaud phenomenon, skin sclerosis on the fingertip and face. She developed dry cough for 1 year and shortness of breath after activity for 1month. Blood routine test showed moderate anemia, blood biochemistry showed renal function damage, and urine routine test showed positive urine protein and occult blood. Immunological examination showed that anti-topoisomerase Ⅰ (anti-SCL-70) antibody was positive. Lung CT showed interstitial fibrosis in both lower lungs. Systemic sclerosis and chronic renal injury were diagnosed and she was treated with low-dose prednisone and nifedipine. During the treatment, the patient developed rapidly progressive renal insufficiency, immunological indicator showed positive anti-myeloperoxidase antibody (MPO), and renal pathology suggested crescentic glomerulonephritis. The renal damage was considered to be caused by vasculitis, and the diagnosis was modified as systemic sclerosis complicated with AAV, with crescentic nephritis and interstitial lung disease. She was treated with methylprednisolone 500 mg. One day later, the patient developed hemoptysis, alveolar hemorrhage was considered, and treatment was adjusted to methylprednisolone 1 g for 3 days, plasma exchange and cyclophosphamide. Three days later, she had vomiting coffee-colored gastric contents and melena. Gastrointestinal hemorrhage was considered, and methylprednisolone was reduced to 80 mg. Plasma exchange and cyclophosphamide treatment were continued, supplemented by acid suppression. The patient's condition was finally controlled, improved and discharged. One month later, the patient developed cough and sputum, and lung CT showed pulmonary infection. During anti-infection treatment, the patient developed gastrointestinal hemorrhage again, accompanied by cerebral hemorrhage, and finally died. This case shows that the incidence of SSc combined with AAV is dangerous, mainly with kidney involvement, manifested as crescents glomerulonephritis. When combined with alveolar hemorrhage, cerebral hemorrhage, the mortality rate is high. Clinicians should pay attention to it, early diagnosis and active treatment should be taken seriously.

PMID 42880933
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