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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

PubMedBritish journal of pharmacology2026-08-27

Melatonin exerts dual, concentration-dependent effects on intestinal pacemaker networks via MT2 receptor activation and redox pathways.

Hossen Md Sajjad MS, Iwata Naoko N, Zhang Xin X, Nakayama Shinsuke S

Melatonin, primarily known for regulating circadian rhythms, also modulates gastrointestinal motility. However, its direct impact on network-forming interstitial cells of Cajal (ICCs), whose pacemaker activity enables flexible and coordinated gut movement, remains unclear. This study investigated the effect of melatonin on ICC electrical activity and micro-coordination in the murine ileum. Electrical activity was recorded from ileal musculature using a dialysis membrane-reinforced 8 × 8 microelectrode array (MEA), allowing visualisation of spatio-temporal coordination. Smooth muscle contraction and neuronal activity were suppressed using nifedipine and tetrodotoxin (TTX), respectively. RT-qPCR was used to assess melatonin receptor and antioxidant enzyme expression. Functionally relevant concentrations of melatonin (10-20 μM) increased the frequency of electrical slow waves without affecting amplitude or propagation patterns. This excitatory effect was blocked by the melatonin receptor antagonists, luzindole and 4P-PDOT, and was associated with MT2 receptor expression. In contrast, supraphysiological concentrations (500 μM-1 mM) suppressed both frequency and amplitude and increased the incidence of expanding activity patterns. This inhibitory effect was luzindole-insensitive but was mimicked by 3-indolepropionic acid (IPA), a gut microbiota-derived indole with antioxidant properties. High-dose melatonin also upregulated Nrf2 and its downstream antioxidant enzymes. Melatonin modulates ICC networks in a concentration-dependent manner: stimulation via MT2 signalling at functionally relevant levels and inhibition via antioxidant pathways at supraphysiological levels. These findings indicate that ICC networks contribute to melatonin responses and reveal distinct receptor-dependent and redox-dependent mechanisms regulating gastrointestinal pacemaker networks.

PMID 42655910
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PubMedNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2026-08-25

A novel CACNA1S variant associated with diltiazem-related worsening of hypokalemic periodic paralysis: a case report.

Sugiura Hidenori H, Watanabe Kazuki K, Furuhashi Kai K, Kawano Tatsuhiro T et al.

Hypokalemic periodic paralysis (HypoPP) is a skeletal muscle channelopathy characterized by recurrent episodes of transient paralysis associated with hypokalemia. Most cases are caused by heterozygous missense variants in CACNA1S, which encodes the α1 subunit of the skeletal muscle L-type calcium channel (CaV1.1). Known triggers include excessive carbohydrate intake, rest after strenuous exercise, and emotional stress; however, worsening potentially associated with the use of L-type calcium channel blockers (LTCCBs) has not been well documented. A 68-year-old man with HypoPP and a five-generation family history of the disease developed increased frequency of paralytic attacks and progressive muscle weakness after initiation of LTCCBs (nifedipine and diltiazem) for vasospastic angina. Exome sequencing and segregation analysis identified a novel heterozygous CACNA1S variant (NM_000069.3:c.4097T > G, p.(Met1366Arg)), which co-segregated with disease among genotyped affected family members and was classified as likely pathogenic. Despite continued nifedipine therapy, paralytic episodes ceased following discontinuation of diltiazem, and muscle strength improved. The p.(Met1366Arg) variant is located in the S6 segment of CaV1.1, outside the canonical S4 arginine residues implicated in most cases of CACNA1S-related HypoPP; nevertheless, strong intrafamilial segregation evidence supports its pathogenicity. Furthermore, its proximity to the diltiazem-binding site raises the possibility of altered drug-channel interactions. The observed diltiazem-associated worsening of HypoPP may be variant-specific rather than a class effect of LTCCBs. Nevertheless, careful monitoring may be warranted when prescribing these agents to patients with HypoPP.

PMID 42637926
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PubMedPediatric cardiology2026-08-25

Recurrent Cardiac Arrest in a Pediatric Patient with Hypertrophic Cardiomyopathy and a Myocardial Bridge: Player or Spectator?

Lodeiro Carlos A CA, Boyd Chelsea C, Menillo Alexandra A, Eilers Lindsay F LF et al.

Myocardial bridge (MB) is common in patients with hypertrophic cardiomyopathy (HCM), and can reduce coronary flow leading to myocardial ischemia, fibrosis, and malignant ventricular arrhythmias resulting in sudden cardiac arrest (SCA). However, MB has not been previously reported as an isolated, modifiable cause of recurrent SCA in pediatric HCM. To describe a case of HCM with recurrent SCA found to have left anterior descending (LAD) coronary artery MB, with resolution of recurrent SCA after MB unroofing. A 13-year-old male with HCM had an epicardial implantable cardioverter defibrillator (ICD) placed after his first SCA at age 8. Atenolol was started after his second SCA at age 12. After a third SCA he was transitioned to Nadolol and Mexiletine, and underwent transvenous ICD implantation due to delayed shock secondary to under-sensing on epicardial system. He had two additional episodes of SCA, for which he was started on Amiodarone and transferred to our institution for transplant evaluation in the setting of biventricular systolic dysfunction. During transplant evaluation, exercise stress test suggested the presence of ischemia. Cardiac catheterization revealed a 6 cm proximal LAD MB, with near occlusion during systole (Figure 1). He underwent LAD unroofing and remained asymptomatic at baseline activity level with no further episodes of SCA during the subsequent follow-up. MB can cause significant compression leading to compromised coronary flow and myocardial ischemia distinct from the intrinsic underlying cardiomyopathy in HCM. Modifiable causes should be considered in cases of recurrent SCA, as treatment may alter prognostic implications.

PMID 42640473
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PubMedAnalytical methods : advancing methods and applications2026-08-20

Analysis of real water samples with AQbD microextraction using thymol-based NADES: implications of uncontrolled hypertension risk in Egypt.

Elbalkiny Heba T HT, Nasry Elsaiad E, Nayer Marina M, Ahmed Sohaila S et al.

The global burden of hypertension and its severe form, resistant hypertension, affecting up to 20% of 1.4 billion adults worldwide, drives mass consumption of multiple drugs. Consequently, antihypertensive agents from different classes enter aquatic environments, yet simultaneous extraction of such chemically diverse drugs remains challenging. This work developed a green analytical method for the simultaneous determination of three model antihypertensive agents from distinct classes, namely, furosemide, atenolol, and lisinopril, in water samples. The method employed dispersive liquid-liquid microextraction using a thymol-based natural deep eutectic solvent selected for its superior hydrophobicity and tunability across varying analyte polarities and acid-base characteristics. Extraction was optimized via Box-Behnken design, followed by HPLC-UV analysis on a phenyl column with gradient elution (detection at 220 nm). The validated method showed good linearity (furosemide: 2-100 µg L-1, lisinopril: 5-100 µg L-1, and atenolol: 0.1-50 µg L-1) with LODs of 0.18, 0.66, and 0.031 µg L-1, respectively. The practical applicability of the developed method was evaluated by analyzing real water samples collected from multiple sites across Egypt. The results revealed detectable concentrations of the target pharmaceuticals in several samples, confirming the presence of these contaminants in Egyptian water systems. Specifically, furosemide was detected at 4.72 µg L-1, atenolol at 0.43 µg L-1, and lisinopril at 7.21 µg L-1 in samples collected from Giza. A comprehensive greenness assessment using the GAPI, AGREE, BAGI, and EVG tools confirmed strong alignment with sustainable chemistry principles. By enabling multi-class extraction of antihypertensive drugs with a low-ecological-footprint NADES-based protocol, this method addresses a critical gap as no prior NADES-based method exists for these three therapeutic classes together, supporting environmental monitoring and clean water objectives.

PMID 42621670
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PubMedSurgery2026-08-19

Impact of chronic beta-blocker versus renin-angiotensin inhibitor use on outcomes after blunt pelvic trauma.

Dhalla Zeyanna Z, Nunn Kaitlin K, Teoh Victoria V, Arellano Diana D

Chronic cardiovascular medications, including β-blockers and renin-angiotensin system inhibitors, may modify the physiologic response to trauma. The purpose of this study is to compare outcomes of pelvic fracture patients with preinjury β-blockers versus renin-angiotensin system inhibitor use after blunt pelvic trauma. A retrospective cohort study was conducted using TriNetX. Data was collected from 2015 to 2025, with a total sample size of n = 442,947 distributed across 16 comparison groups. Propensity score matching was applied to yield equitable cohorts based on medical comorbidities. Patient groups were mutually exclusive, such that individuals were classified as taking either a β-blocker or a renin-angiotensin system inhibitor, with exclusion of patients receiving both therapies or an antiplatelet treatment. Comparisons were made with outcomes that include hemorrhage, infections, pneumonia, sepsis, deep vein thrombosis, pulmonary embolism, respiratory ventilation, and mortality. The β-blocker group demonstrated higher rates of adverse events, including hemorrhage, infections, pneumonia, sepsis, deep vein thrombosis, pulmonary embolism, respiratory ventilation, and mortality, relative to the renin-angiotensin system inhibitor group. The differences were most pronounced when renin-angiotensin system inhibitors were compared with metoprolol and labetalol, where nearly all outcomes were significantly worse in the β-blocker cohorts. In contrast, no significant differences were observed when compared with carvedilol or atenolol. Prior use of β-blockers is correlated with significantly worse rates of hemorrhage, infection, and thromboembolic events after a traumatic pelvic fracture when compared with renin-angiotensin system inhibitors. This could be due to renin-angiotensin system inhibitors attenuating the post-traumatic inflammatory response system by blocking angiotensin II, which causes inflammation, oxidative stress, endothelial dysfunction, and vasoconstriction. These findings suggest that chronic cardiovascular therapy type may influence post-pelvic trauma outcomes, underscoring the need for further investigation.

PMID 42618398
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PubMedPregnancy (Hoboken, N.J.)2026-08-14

Hypertension-related morbidity after delivery discharge: A comparison of nifedipine versus labetalol.

Fabricant Sonya S, Cervantes Matthew M, Marshall Glenda G, Bello Natalie N et al.

To evaluate rates of hypertension-related morbidity after delivery discharge among individuals on nifedipine versus labetalol monotherapy. This was a retrospective cohort study of individuals who delivered at a level IV obstetric hospital from January 1, 2021 to January 20, 2024, had a hypertensive disorder of pregnancy, and were discharged on nifedipine or labetalol monotherapy. The primary outcome was hypertension-related post-discharge morbidity, defined as any of the following within 30 days of delivery discharge: severe hypertension, de novo preeclampsia lab abnormalities, or new-onset clinical morbidity (hemolysis, elevated liver enzymes and low platelets [HELLP] syndrome, eclampsia, pulmonary edema/acute heart failure, cerebrovascular disorders, myocardial infarction/cardiac arrest, liver hematoma, or acute renal failure). Secondary outcomes included hypertension-related hospital return and hospital return length of stay. Data were abstracted from the medical record. Logistic regression and bivariate analysis were used to compare groups. Multivariable logistic regression was used to adjust for baseline characteristics and readmission risk factors from the literature. Of 360 patients meeting inclusion criteria, 67.2% were discharged on nifedipine and 32.8% were discharged on labetalol. Nifedipine recipients had lower body mass index and were less likely to have chronic hypertension compared to labetalol recipients. Post-discharge morbidity occurred less frequently among individuals discharged on nifedipine compared to labetalol (1.7% vs. 10.2%; adjusted odds ratio [aOR], 0.1; 95% confidence interval [CI], 0.05-0.5). Individuals on nifedipine were less likely to return to the hospital in the 30 days following discharge (4.6% vs. 12.7%; aOR, 0.3; 95% CI, 0.1-0.7) and less likely to have a hospital return lasting ≥24 h (1.7% vs. 6.8%; OR, 0.2; 95% CI, 0.07-0.8). Among individuals on antihypertensive monotherapy at delivery discharge, nifedipine was associated with significantly reduced odds of post-discharge morbidity compared to labetalol.

PMID 42597114
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