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(S)-amlodipine + (S)-atenolol

✓ Approved

Emcure Pharmaceuticals · ADRB1 · Small Molecule

What is (S)-amlodipine + (S)-atenolol?

(S)-amlodipine + (S)-atenolol is a small molecule developed by Emcure Pharmaceuticals. It is approved for therapeutic indications via oral (po).

Drug Profile

CompanyEmcure Pharmaceuticals
Drug ClassSmall Molecule
Molecular TargetADRB1, CACNA1C
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Emcure Pharmaceuticals

Mechanism of Action

Molecular Targets

(S)-amlodipine + (S)-atenolol 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

(S)-amlodipine + (S)-atenolol is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Cardiac disordersAngina pectoris✓ Approved
Vascular disordersHypertension✓ Approved

Related Research Articles

PubMedEuropean spine journal : official publication of the European Spine Society, the European Spinal Deformity Society, and the European Section of the Cervical Spine Research Society2026-10-15

Subarachnoid-subarachnoid bypass versus extradural decompression for adhesive syringomyelia: experimental and early clinical evaluation.

Zhang Can C, Yuan Chenghua C, Bai Jun J, Cui Shengyu S et al.

Adhesive syringomyelia (SM) is associated with cerebrospinal fluid (CSF) obstruction in the spinal subarachnoid space (SAS). Recurrent obstruction after decompression or arachnoidolysis may limit surgical efficacy, making the durable surgical management of adhesive SM an important challenge in neurosurgery. Rats with MRI-confirmed SM were allocated to S-S bypass, extradural decompression, or vehicle treatment; sham-operated rats served as additional controls. Outcomes included MRI, blinded behavioral assessment, histology, and CT and fluorescent tracer studies. A prospective uncontrolled series of 14 selected patients evaluated technical feasibility, short-term safety, and clinical and radiological changes. In the rat model, S-S bypass was associated with greater syrinx regression and more favorable behavioral and histological outcomes than extradural decompression. Distal tracer passage was also improved, whereas scar-associated tissue and recurrent SAS narrowing were observed after extradural decompression. Clinically, all 14 procedures were completed without major complications. At final follow-up, 13 patients were descriptively classified as improved and one as stable, accompanied by modest increases in ASIA sensory and motor scores. In this rat model, S-S bypass produced more favorable structural and functional outcomes than extradural decompression by providing an alternative pathway across the obstructed segment. The preliminary clinical series supports the technical feasibility and short-term safety of the procedure, but its clinical effectiveness requires confirmation in larger controlled studies.

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PubMedFrontiers in cellular and infection microbiology2026-10-15

MerR-type regulator ZccR links zinc homeostasis to biofilm formation and interspecies competition in Streptococcus mutans.

Pan Yangyang Y, Xu Zhaonan Z, Wang Shuyu S, Xu Muxin M et al.

Zinc is widely present in the oral microenvironment and can influence the growth of oral bacteria. ZccR is a MerR-type transcriptional regulator that controls zinc efflux in Streptococcus mutans (S. mutans), but its role in biofilm virulence and interspecies competition with oral commensals remains unclear. This study aimed to investigate the role of ZccR in the formation of single-species biofilms of S. mutans and dual-species biofilms with oral commensal streptococci, and its underlying regulatory mechanisms. We constructed an in-frame zccR knockout mutant of S. mutans. The growth curve, crystal violet staining, anthrone method, scanning electron microscopy, fluorescence in situ hybridization, and deferred antagonism assay were used to assess growth, biofilm development, dual-species biofilm composition, and interspecies competitive capacity. RNA-seq was employed to identify genome-wide transcriptional alterations, and promoter-lacZ reporter strains were constructed to confirm the transcriptional regulation mode of ZccR on zccE and on itself. The deletion of zccR significantly suppressed biofilm formation and water-insoluble exopolysaccharide production of S. mutans at 150 μM Zn2+, a concentration that only modestly affected planktonic growth. In dual-species biofilms containing Streptococcus gordonii (S. gordonii), the mutant exhibited reduced oxidative stress tolerance and weaker inhibition of S. gordonii, despite upregulation of bacteriocin genes. RNA-sequencing identified 89 differentially expressed genes (67 upregulated and 22 downregulated), including downregulation of the mutanobactin cluster and FAD-dependent oxidoreductases, upregulation of iron-uptake genes, induction of HomR-tcy-linked cystine-uptake pathways, glutamine biosynthesis, and CRISPR-Cas genes, and a shift from sucrose import (scrA/msmX) toward lac-dependent lactose/galactose metabolism. Most of these shifts tracked intracellular zinc accumulation rather than direct ZccR control. Promoter-lacZ assays revealed that ZccR activates zccE and represses its own promoter, and zinc acts on these promoters through ZccR-dependent and ZccR-independent routes. ZccR links zinc homeostasis with biofilm formation and oral interspecies ecology of S. mutans, thus offering a future intervention point for cariogenic biofilm control.

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PubMedEuropean psychiatry : the journal of the Association of European Psychiatrists2026-10-15

Shared genetic architecture between premenstrual disorder symptoms and major psychiatric disorders suggests a role for calcium signaling.

Jaholkowski Piotr P, Hysaj Elgeta E, Parker Nadine N, Wiström Erik David ED et al.

Major psychiatric disorders (MPDs) and premenstrual disorders (PMDs) are often comorbid, with indications of shared genetic architecture. However, the specific genetic variants underlying this comorbidity remain elusive. The aim of this study was to identify genomic loci shared between MPDs and PMDs, and to assess the functional characteristics of genes mapped to these loci. We used genome-wide association data for symptoms of PMDs (S-PMD, n = 67 068) from the Norwegian Mother, Father and Child Cohort Study (MoBa), and for MPDs (schizophrenia, n = 130 644; bipolar disorder, n = 827 335; major depression, n = 1 918 432) from the Psychiatric Genomic Consortium. Shared genetic loci were identified with the conjunctional false discovery rate (conjFDR). Genes mapped to the identified loci were included in functional and pharmacological gene-set enrichment analyses (GSEAs). We identified 20 loci shared between S-PMD and the MPDs, including 19 novel loci for S-PMD (conjFDR<0.05). GSEA revealed genes involved in calcium signaling and neuronal projection pathways. The drug enrichment analysis identified 36 drugs, including riluzole and mianserin, significantly associated with the identified molecular pathways. We identified 20 genetic loci shared between the S-PMD and MPDs, implicating calcium transmission in the pathogenesis of PMDs. Together with the drug enrichment results, this provides a biological basis for repurposing existing drugs in the treatment of PMD.

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PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-10-15

Loss of Intestinal MSTN Promotes GLP-1 Secretion Through SGLT1 Palmitoylation.

Han Sheng-Zhong SZ, Chang Shuang-Yan SY, Luo Zhaobo Z, Sun Ke K et al.

Intestinal glucagon-like peptide-1 (GLP-1) is secreted by intestinal L cells in a glucose-dependent manner. The localization and surface abundance of glucose-sensing proteins on the cell membrane affect the response to glucose, but the regulatory mechanism remains poorly understood. Here, we show that S-palmitoylation is required for stable plasma membrane enrichment of SGLT1 and for SGLT1-mediated GLP-1 secretion. Notably, myostatin (MSTN) was identified as a key upstream regulator of this modification. Intestinal MSTN deficiency markedly enhanced SGLT1 palmitoylation, increased its plasma membrane abundance, and thereby promoted glucose-stimulated GLP-1 secretion. Importantly, simvastatin induced intestinal MSTN upregulation and impaired glucose homeostasis, whereas MSTN deficiency largely alleviated these effects. Mechanistically, MSTN regulated the expression of the palmitoyl acyltransferase ZDHHC20, which catalyzed SGLT1 S-palmitoylation at Cys301. Blocking SGLT1 palmitoylation attenuated SGLT1 membrane enrichment and markedly suppressed the induction of GLP-1 secretion caused by MSTN deficiency. Collectively, our research results have revealed a new mechanism by which MSTN regulates intestinal endocrine function and S-palmitoylation modification promotes GLP-1 secretion, providing potential targets for regulating endogenous GLP-1 secretion in the intestine and treating metabolic diseases related to glucose imbalance.

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PubMedSoft matter2026-10-15

The roles of elasticity and dimension in liquid-gel phase separation.

Wang Shichen S, Olmsted Peter D PD

We compare seven elastic models for polymer networks in the context of phase separation within a gel, including a new model that combines the finite extensible Arruda-Boyce model and the slip tube model for entangled chains. We study incompressible uniaxial stretch and compression, and three volume-changing constrained-dimension deformations, in which the material can only deform in the designated dimension(s), while the constrained direction(s) remain(s) the same. Each model responds differently to large deformations, and our proposed model successfully describes both strain softening and strain hardening, which are both present in well-entangled elastomers. When considering phase separation, we show that the commonly used neo-Hookean model fails to admit a common tangent construction for phase coexistence for 3D deformations. This can be resolved by using a model with finite extension, such as the Arruda-Boyce model. In constrained-dimension deformations, where the gel's volume is allowed to change, for elastic models in which phase coexistence is possible, the critical temperature increases and the critical concentration decreases with increasing deformation dimensions. This strong dependence of the phase diagram on spatial dimension and geometry distinguishes phase separation in elastic media from conventional liquid-liquid phase separation.

PMID 42876437
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PubMedTransport in porous media2026-10-15

Adaptive Time-Stepping and Machine Learning Approach for Pore-Scale Reactive Transport Simulations.

Baur Micha P MP, Churakov Sergey V SV, Prasianakis Nikolaos I NI

Pore-scale reactive transport simulations are typically computationally very expensive, which limits their application to complex heterogeneous systems. To solve the computational bottleneck, an adaptive time-stepping algorithm is developed and combined with machine learning-derived surrogate models for geochemical calculations. The time-step is adapted by monitoring the evolution of the diffusion field and the precipitation reactions and by exploiting intermediate stationary states of the system. The algorithm is benchmarked on a system relevant to cement-claystone interaction with the geochemical reaction being the precipitation of Calcium-Silicate-Hydrates (C-S-H) in the pore space of a claystone. The precipitation of C-S-H is modeled as a solid solution, and it is possible to calculate and trace the local Ca/Si ratio of C-S-H, as well as the local amount of gel porosity. In the reactive transport simulations presented here, the geochemical surrogate models alone lead to acceleration factors of up to two orders of magnitude. The adaptive time-stepping algorithm leads to an additional acceleration of three to five orders of magnitude maintaining the relative deviation below 2%. The overall combined acceleration is demonstrated to be six to seven orders of magnitude having a profound impact and opening new computational avenues. The online version contains supplementary material available at https://doi.org/10.1007/s11242-026-02287-4.

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