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glimepiride + metformin SR (Amaryl Mex / Amaryl M SR)

✓ Approved

Sanofi S.A · KCNJ11 · Small Molecule

What is glimepiride + metformin SR?

glimepiride + metformin SR is a small molecule developed by Sanofi S.A. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesAmaryl Mex, Amaryl M SR
CompanySanofi S.A
Drug ClassSmall Molecule
Molecular TargetKCNJ11, ABCC8
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Sanofi S.A

Mechanism of Action

Molecular Targets

glimepiride + metformin SR acts on 2 molecular targets:

KCNJ11potassium inwardly rectifying channel subfamily J member 11 (BIR, HHF2)
ABCC8ATP binding cassette subfamily C member 8 (MRP8, SUR1delta2)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

glimepiride + metformin SR is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersType 2 diabetes mellitus✓ Approved

Related Research Articles

PubMedInternational immunopharmacology2026-08-30

Targeting the macrophage-NLRP3 inflammasome-pyroptosis axis: Metformin-capped silver nanoparticles as a novel therapy for premature ovarian insufficiency.

Feng Sifang S, Zhao Juan J, Li Peixuan P, Yang Ting T et al.

The paracrine crosstalk between macrophages and granulosa cells, forming a "macrophage M1 polarization-inflammation-pyroptosis" vicious cycle in the ovarian immune microenvironment, promotes premature ovarian insufficiency (POI) progression. This study aimed to investigate the therapeutic potential of metformin-capped silver nanoparticles (Met-AgNPs) in disrupting pathological paracrine signaling axis and restoring ovarian function. Met-AgNPs and control AgNPs were synthesized and physicochemically characterized. Dynamic light scattering (DLS) was conducted to evaluate the hydrodynamic diameter, polydispersity index (PDI), and zeta potential of the nanoparticles in different dispersion media (deionized H2O, PBS, DMEM). The in vitro release kinetics and in vivo biodistribution were also evaluated. THP-1-derived macrophages were induced to M1 polarization and treated with Met-AgNPs, AgNPs, or metformin, followed by assessment of macrophage polarization states. The conditioned medium (CM) from these macrophages was then applied to human granulosa KGN cells to evaluate its effects on NLRP3 inflammasome activation and pyroptosis. A cyclophosphamide (CTX)-induced POI rat model was established and treated with Met-AgNPs, AgNPs, or metformin. Ovarian function was evaluated via estrous cycle, hormone levels, follicle counting, and fertility assessment. Ovarian histopathology, macrophage polarization, inflammation, and NLRP3-driven pyroptosis were assessed. Met-AgNPs exhibited a spherical morphology, smaller hydrodynamic diameter, and enhanced colloidal stability compared to AgNPs. Crucially, Met-AgNPs demonstrated sustained drug release and achieved targeted accumulation with localized retention in inflamed ovaries. In vitro, treatment with Met-AgNPs, AgNPs, or metformin all reprogrammed M1 macrophages towards M2 phenotype, accompanied by decreased pro-inflammatory cytokine secretion and increased anti-inflammatory cytokine secretion. The CM from all treated macrophages inhibited NLRP3 inflammasome activation and pyroptosis in KGN cells. Notably, Met-AgNPs demonstrated superior efficacy among all treatment groups. In POI rats, Met-AgNPs treatment restored estrous cycles, serum hormone levels, and healthy follicle count, and improved fertility. These improvements were mechanistically associated with the inhibition of M1 macrophage infiltration and NLRP3-driven pyroptosis within the ovarian tissues. Met-AgNPs ameliorated POI by reprogramming macrophage polarization from M1 to M2 phenotype and then inhibiting NLRP3-dependent pyroptosis in granulosa cells. Our findings propose Met-AgNPs as a promising nanotherapeutic strategy for alleviating ovarian inflammation and restoring fertility in POI.

PMID 42669281
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PubMedEuropean archives of psychiatry and clinical neuroscience2026-08-30

Untargeted plasma metabolomics identifies metabolite signatures associated with suicidality status in chronic schizophrenia.

Wang Lijun L, Lu Chenghao C, Sun Xiaochun X, Sun Wenjie W et al.

Suicide contributes substantially to mortality in schizophrenia, yet metabolic signatures associated with suicidality remain poorly understood. We applied untargeted plasma metabolomics with multivariate modeling to identify plasma metabolic signatures associated with suicidality status and clinical features. We enrolled 146 frequency-matched psychiatric inpatients with chronic schizophrenia: 73 in the suicide-risk (SR) group, defined by current suicidal ideation or suicidal behavior/attempt history at admission, and 73 in the non-suicide-risk (NSR) group. Plasma samples underwent untargeted metabolomic profiling. Discriminating metabolites were identified using orthogonal partial least squares discriminant analysis (OPLS-DA) and Benjamini-Hochberg-adjusted Mann-Whitney U testing (variable importance in projection [VIP] >1.0 and adjusted p <0.05). Stepwise logistic regression with forced clinical covariates generated an exploratory metabolite-based classification model, and Spearman correlations examined associations with Positive and Negative Syndrome Scale (PANSS) and Repeatable Battery for the Assessment of Neuropsychological Status (RBANS) scores. OPLS-DA identified 70 discriminating metabolites (R2Y = 0.938, Q2Y = 0.650), with nominal enrichment of lysine degradation, glutathione metabolism, phenylalanine/tyrosine/tryptophan biosynthesis, and sphingolipid metabolism. Stepwise regression retained six metabolites associated with SR status (area under the curve [AUC] = 0.774): Sphingosine, 3-OH-TML, Ile-Leu+Leu-Ile, TML, Taurine, and 12-HETE. Gamma-Glu-Thr showed the highest VIP (5.003) and broad clinical correlations. Plasma metabolic differences involving sphingolipid, lysine/carnitine, neuroinflammatory, amino-acid, and glutathione-related pathways were associated with suicidality status in chronic schizophrenia. These exploratory cross-sectional findings require validation in larger longitudinal cohorts using dedicated suicidality assessments.

PMID 42669098
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PubMedClinical & experimental optometry2026-08-30

Clinical validation of a multifunction ocular biometer in children.

Lin Rui R, Li Yong Y, Yang Yong Y, Qian Chaoxu C

Reliable ocular biometry and refraction measurements are essential for monitoring paediatric myopia in routine practice and school screening. Integrated instruments may improve clinical workflow, but measurement differences between devices can influence longitudinal interpretation. Accurate assessment of biometric and refractive parameters is essential for paediatric myopia management. The aim was to evaluate the agreement and repeatability of a multifunctional ocular biometer, the SW-9000ARK, compared with established instruments for ocular biometry and refraction. This prospective cross-sectional study included 361 children (mean age 10.7 ± 2.5 years; 49.0% girls). All subjects underwent non-cycloplegic measurements with the SW-9000ARK, IOLMaster 700, and Topcon KR-800 in random order, followed by subjective refraction (SR). Agreement was assessed using Bland-Altman analysis. Repeatability in 211 right eyes was assessed using within-subject standard deviation, test-retest repeatability, coefficient of variation and intraclass correlation coefficient (ICC). The SW-9000ARK showed excellent agreement with the IOLMaster 700 for axial length (mean difference -0.01 mm; 95% LoA -0.08 to +0.05 mm), central corneal thickness (+5.19 µm; 95% LoA -9.57 to +19.96 µm), anterior chamber depth (-0.03 mm; 95% LoA -0.11 to +0.05 mm), lens thickness, and keratometry, with ICC values ≥ 0.96. Spherical equivalent exhibited strong agreement with the Topcon KR-800 (+0.08D; 95% LoA -0.65 to +0.81D) and SR (+0.35D; 95% LoA -0.43 to +1.13D). Repeatability was high across all parameters (Sw = 0.018 mm for AL; ICC ≥0.94). The SW-9000ARK provides highly agreeable and repeatable measurements of ocular biometry and non-cycloplegic refraction in paediatric ametropia, supporting its use as a reliable single-platform tool for myopia management and large-scale screening.

PMID 42669424
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PubMedInternational journal of biological macromolecules2026-08-30

Targeted delivery of antimicrobial peptide LL-37 via ferritin fusion improves antibacterial and anti-inflammatory outcomes in a murine sepsis model.

Pan Wangyao W, Tian Changhao C, Ding Yang Y, Pei Zejun Z et al.

The antimicrobial peptide LL-37 holds considerable therapeutic potential for treating infection and inflammation; however, its clinical application is often limited by poor stability, susceptibility to proteolytic degradation, and insufficient targeting capability. In this study, we engineered a targeted fusion protein (designated as FL) based on ferritin light chain (FTL) by genetically fusing the LL-37 peptide to the C-terminus of FTL, thereby markedly enhancing the structural stability and proteolytic resistance of LL-37. This design further exploits the specific recognition of FTL by scavenger receptor A (SR-A), which is highly expressed on the macrophage surface, to achieve targeted delivery to inflammatory lesions. Both in vitro and in vivo experiments demonstrated that FL not only retained the antimicrobial activity of LL-37, but also exhibited certain anti-inflammatory capacity. In a murine sepsis model, FL exerted superior antibacterial and anti-inflammatory efficacy compared with free LL-37, and partially alleviated structural and functional damage in multiple organs. Moreover, safety evaluations confirmed that FL showed no significant hemolytic activity, immunogenicity or tissue toxicity, indicating good biocompatibility. This study presents a novel protein formulation that integrates enhanced stability, inflammation-targeting capability, and multiple biological activities, thereby providing a promising translational candidate strategy for the precise treatment of infection- and inflammation-related diseases.

PMID 42669340
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PubMedFrontiers in oncology2026-08-29

Metformin modulates the phenotypes of tumor-associated macrophages in glioblastoma in a context-dependent manner by promoting the homeostasis of macrophages.

Das Ashish A, Mahfooz Sadaf S, Wang Fei F, Guan Bingjie B et al.

Glioblastoma (GBM) remains the most aggressive primary adult brain cancer attributed to its immunosuppressive nature. Radiation therapy (RT) and concurrent temozolomide chemotherapy are the standard treatments for GBM. Emerging evidence indicates that metformin has potential as an anti-tumor agent that can reshape the immune landscape across various malignancies. We thus postulate that metformin may enhance the anti-tumor effect of RT by modulating the immunosuppressive milieu in GBM. We first explore multiple in vitro conditions, with or without pre-induction, and mimicked a tumor microenvironment to demonstrate a highly context-dependent effect of metformin on the polarization of bone marrow-derived macrophages (BMDMs). We then investigated the antitumor activity and immune-modulatory effects of metformin in combination with RT in GBM-bearing mice. The in vitro experiment showed that metformin inhibited the immunosuppressive effects of IL-4/IL-13 but also the immunostimulatory effects of Lipopolysaccharide (LPS) on BMDMs, demonstrating bidirectional immunomodulatory properties that depend on the baseline inflammatory stimulus. In tumor cell co-culture environment, metformin exhibited context-dependent immunoregulatory effects, predominantly promoting M1-associated activation. Notably, concurrent metformin treatment counteracted M2 polarization typically induced by the tumor microenvironment. In a high m-MCSF inducted M2-dominated condition, metformin preferentially shifted the highly polarized M2 phenotype toward an M1-like state in a time and dose-dependent manner but with limited promotion of M1 subtype maturation. RNAseq results on BMDM treated with metformin showed increased homeostasis. Metformin showed dose-dependent immunomodulatory effects when combined with RT in vitro. In syngeneic GBM mouse models, concurrent metformin + RT significantly prolonged survival and reduced tumor burden by reprogramming tumor-associated macrophages (TAMs), elevating intratumoral CD8+ T-cell infiltration and the CD8+/Treg ratio, increasing circulating CD8+ T cells, reversing RT-induced expansion of monocytic myeloid-derived suppressor cells (mMDSCs), and expanding CD4+ and CD8+ effector memory populations in peripheral blood. Metformin demonstrates inhibitory effects on M2 phenotype of macrophages. However, it is not a simple M2 inhibitor; instead, it functions primarily as a neutralizer of highly polarized macrophage states by promoting transcriptomic homeostasis. This context-dependent activity enables metformin to relieve the profoundly immunosuppressive TME of GBM to potentiate the anti-tumor effects of RT and by enhancing systemic immune memory.

PMID 42666173
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PubMedNeurosurgery practice2026-08-29

Outcomes of Laser Interstitial Thermal Therapy-Augmented Surgery in the Management of Subcortical Glioblastoma.

Chen Hsien-Chung HC, Yekula Anudeep A, Weimar Marcus W MW, Wong Eric T ET et al.

Subcortical glioblastomas present surgical challenges owing to their proximity to critical anatomy. In this study, we assessed the utility of laser interstitial thermal therapy (LITT) in the management of subcortical glioblastomas. Clinical outcomes were evaluated in 80 consecutive patients with subcortical glioblastoma (isocitrate dehydrogenase wild-type, H3K27 nonmutant) treated surgically between 2017 and 2025. During this time period, LITT was increasingly incorporated into stereotactic needle biopsy (SNB) and surgical resection (SR) workflows, enabling comparisons between SNB vs SNB + LITT and between SR only vs planned subtotal resection (STR) + LITT. Among 46 treatments involving SNB, 24 underwent SNB only and 22 SNB + LITT. Lesion size was similar between these groups (1.72 ± 0.38 vs 1.92 ± 0.36 cm, P = .07), with comparable procedural morbidity (4.2% vs 4.5%, P = 1.0). In newly diagnosed glioblastoma, SNB + LITT was associated with improved overall survival compared with SNB alone (median 375 vs 162 days, P = .0012). Thirty-four patients underwent resections (18 SR, 16 STR + LITT). Lesion size was comparable between these cohorts (3.77 ± 0.68 vs 3.74 ± 0.83 cm, P = .9) as was the extent of cytoreduction (77.8% vs 93.8%, P = .34), but STR + LITT was associated with fewer permanent postoperative deficits (0% vs 27.8%, P = .047). Survival did not differ between STR + LITT and SR (median 368 vs 289 days, P = .43). Across all patients, postoperative motor deficits were associated with worse survival (112 vs 254 days, P < .001). Our results support incorporating LITT as a staged procedure into planned STR or in conjunction with SNB in the management of subcortical glioblastoma. Postoperative motor deficit is associated with poor survival outcomes.

PMID 42667011
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