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anagliptin + metformin (SK 1501 / Metoana / SK1501)

✓ Approved

Sanwa Kagaku Kenkyusho Co., Ltd. · DPP4 · Small Molecule

What is anagliptin + metformin?

anagliptin + metformin is a small molecule developed by Sanwa Kagaku Kenkyusho Co., Ltd.. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesSK 1501, Metoana, SK1501
CompanySanwa Kagaku Kenkyusho Co., Ltd.
Drug ClassSmall Molecule
Molecular TargetDPP4
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Sanwa Kagaku Kenkyusho Co., Ltd.

Mechanism of Action

Molecular Targets

anagliptin + metformin acts on 1 molecular target:

DPP4dipeptidyl peptidase 4 (CD26, DPPIV)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

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

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersType 2 diabetes mellitus✓ Approved

Related Research Articles

PubMedJournal of applied oral science : revista FOB2026-11-12

Metformin alleviates LPS-induced inflammation via suppression of the MAPK/AP-1 pathway in human dental pulp cells.

Park Sam-Young SY, Kim Won-Jae WJ, Park Hyo-Seon HS, Lim Hoi-Soon HS et al.

Metformin, a first-line antidiabetic drug, has been increasingly recognized for its anti-inflammatory actions beyond glycemic control. This study investigated whether metformin modulates lipopolysaccharide (LPS)-induced inflammatory responses in human dental pulp cells (HDPCs) and explored the underlying signaling mechanisms. In HDPCs stimulated with Escherichia coli LPS in the presence or absence of metformin, cell viability, inflammatory mediator expression, mitogen-activated protein kinase (MAPK)/activator protein-1 (AP-1) signaling, and autophagy-related LC3 conversion were examined. Metformin and LPS treatment did not significantly affect HDPC viability at the tested concentrations. LPS stimulation increased the expression of pro-inflammatory mediators, including interleukin-6 and cyclooxygenase-2, whereas metformin significantly attenuated these responses. Mechanistically, metformin suppressed LPS-induced phosphorylation of p38, c-Jun N-terminal kinase, extracellular signal-regulated kinase, and AP-1. Pharmacological inhibition of MAPK signaling also reduced AP-1 phosphorylation and interleukin-6 expression in LPS-stimulated HDPCs, supporting the involvement of MAPK-dependent AP-1 activation in the inflammatory response. Additionally, LPS enhanced LC3-I to LC3-II conversion, whereas metformin attenuated this autophagy-associated response. These findings suggest that metformin attenuates LPS-induced inflammatory responses in HDPCs, at least in part, by suppressing MAPK/AP-1 signaling and modulating autophagy-associated signaling. Metformin may therefore have biological relevance as a host-modulatory agent in pulpal inflammation.

PMID 43017961
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PubMedAnais da Academia Brasileira de Ciencias2026-11-12

Effects of caloric restriction and metformin in LDL receptor knockout mice: visceral fat reduction with limited benefits in dyslipidemia and cognition.

Braga Sara P SP, Dezanetti Talissa T, Oliveira Vanessa Ecléa DE VE, Delanogare Eslen E et al.

Familial hypercholesterolemia is a genetic disorder characterized by chronically elevated low-density lipoprotein cholesterol levels and an increased risk of metabolic and cognitive dysfunction. Mice lacking low-density lipoprotein receptors (LDLr-KO) serve as a well-established model of the homozygous form of familial hypercholesterolemia, showing lifelong hypercholesterolemia and neurobehavioral impairments. In this study, we investigated whether a 30% caloric restriction (CR) regimen, alone or combined with metformin in drinking water, could ameliorate metabolic and behavioral alterations in middle-aged female LDLr-KO mice. Control subjects were C57Bl/6 mice with normal lipid profiles. CR significantly reduced body mass gain and visceral adiposity, particularly when combined with metformin. However, neither intervention normalized plasma cholesterol, triglycerides, or glucose levels measured after a 6-hour fasting period. CR also attenuated the hyperlocomotor activity observed in LDLr-KO mice during the T-maze test. In contrast, recognition memory and anxiety-like behavior remained impaired across all intervention groups. Interestingly, combined CR and metformin modestly improved short-term aversive memory in the step-down task. Interleukin-1 beta levels in the hippocampus and prefrontal cortex did not differ significantly between groups. These findings indicate that CR and metformin reduce adiposity and partially modulate behavior. However, their effects on dyslipidemia and cognitive deficits in LDLr-KO mice were limited.

PMID 43017939
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PubMedFrontiers in pharmacology2026-11-12

Metformin promotes apoptosis of senescent chondrocytes by disrupting the Bcl-xL/Mcl-1-Bak interaction.

Feng Biying B, Liu Longzhou L, Lin Yueyang Y, Wu Guihao G

The accumulation of senescent chondrocytes (SEC) beyond the body's tolerance capacity is a key contributor to osteoarthritis (OA) pathogenesis. Metformin (Met), a first-line oral medication for type 2 diabetes, has shown therapeutic potential in various diseases. This study aims to explore the therapeutic effects and underlying mechanisms of Met in OA. Cellular senescence was induced in immortalized human chondrocytes using doxorubicin (Dox), confirmed by β-galactosidase staining and western blotting. The effects of Met on SEC viability, mitochondrial membrane potential, and apoptosis were assessed. Protein expression and interactions were analyzed by western blot and live-cell fluorescence resonance energy transfer (FRET) analysis. Met promoted death of SEC and reduced mitochondrial membrane potential, inducing caspase- and reactive oxygen species (ROS)-dependent apoptosis. Met upregulated Bak and Bim expression, downregulated Mcl-1, and activated Caspase-3, Caspase-8, and Caspase-9, leading to PARP cleavage. FRET analysis revealed that Met disrupted Mcl-1/Bak and Bcl-xL/Bak binding while facilitating Bim-Bak interaction, promoting Bak dimerization. This study provides the first evidence that Met induces apoptosis of SEC by reducing Mcl-1-Bak and Bcl-xL-Bak interactions while enhancing Bim-Bak binding, suggesting a novel therapeutic strategy for OA by targeting senescent chondrocytes through mitochondrial apoptosis pathways.

PMID 43017451
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PubMedClinical endocrinology2026-11-12

Prevalence, Incidence, Clinical Presentation, and Treatment of Polyendocrine Metabolic Ovarian Syndrome in Primary Care in the United Kingdom Between 1998 and 2025.

Shapiro Samantha B SB, Yu Oriana H Y OHY, Dahan Michael H MH, Azoulay Laurent L

Polyendocrine metabolic ovarian syndrome (PMOS) is a multisystemic disorder with a wide range of health consequences. We sought to describe temporal trends in the prevalence and incidence of PMOS and to characterize its clinical presentation, comorbidity burden, and pharmacological management in primary care in the United Kingdom (UK) between 1998 and 2025. Population-based matched cohort study using primary care records from the UK Clinical Practice Research Datalink. Females newly diagnosed with PMOS between the ages of 15 and 49 matched on age, general practice, calendar year of cohort entry, and duration of medical history to population controls without PMOS. Annual prevalence and incidence of diagnosed PMOS; baseline prevalence and incidence of cardinal PMOS features and various comorbidities; and pre- and post-cohort entry prevalence of hormonal contraceptive, anti-androgen, ovulation-inducing drug, and metformin use. The prevalence of diagnosed PMOS increased from < 0.1% in 1998 to 2.0% in 2025, with incidence rising from 0.1 to 3.6 per 1,000 person-years over the same period. Among 125,482 patients with newly diagnosed PMOS matched with an equal number of controls, patients with PMOS had higher baseline prevalence and incidence of cardinal features of PMOS, as well as diabetes, dyslipidemia, hypertension, cardiovascular and cerebrovascular disease, sleep apnea, thyroid disorders, endometriosis, uterine fibroids, chronic pain, depression, and anxiety. Use of anti-androgens, ovulation-inducing drugs, and metformin was substantially higher in patients with PMOS, especially in the year following diagnosis. PMOS is increasingly diagnosed in UK primary care and is associated with substantial multimorbidity and pharmacotherapy.

PMID 43016113
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PubMedFrontiers in nutrition2026-11-12

Colon-targeting potential and metabolic effects of sodium butyrate-loaded CPC microspheres in type 2 diabetic mice.

Zhang Qinqin Q, Yao Gaiqi G

Oral sodium butyrate (SB) is rapidly absorbed in the proximal small intestine, limiting its colonic availability and local metabolic effects. We evaluated the in vitro release characteristics of chitosan-protocatechualdehyde/calcium alginate microspheres loaded with SB (CPC/SB), together with metabolic and microbial outcomes in mice with high-fat diet/streptozotocin-induced diabetes. CPC/SB release was measured in separate simulated gastric, intestinal, and colonic fluids. Thirty-five male C57BL/6J mice were assigned to seven groups: normal control and six diabetic groups receiving vehicle, unloaded CPC, free SB, CPC/SB, metformin, or metformin plus CPC/SB for 4 weeks (34 completed). Endpoints included gastrointestinal and fecal butyrate; blood glucose, homeostasis model assessment of insulin resistance (HOMA-IR), low-density lipoprotein cholesterol (LDL-C), and interleukin-6 (IL-6); and fecal microbiota assessed by 16S rRNA gene sequencing and PICRUSt2. Relative butyrate release was 0.91%, 8.53%, and 94.17% in simulated gastric, intestinal, and colonic fluids, respectively. After CPC/SB administration, colonic butyrate exceeded gastric and small-intestinal levels, and fecal butyrate increased versus the model group (0.0523 ± 0.0121 vs. 0.0180 ± 0.0068 μg/mg; p < 0.0001). Random blood glucose decreased to 18.64 mmol/L at week 4 (p < 0.0001 vs. baseline and model). CPC/SB also reduced HOMA-IR (3.14 ± 0.43 vs. 4.81 ± 1.30; p = 0.046) and serum IL-6 (85.82 ± 1.90 vs. 93.55 ± 4.10 pg./mL; p = 0.008); LDL-C and α-diversity were unchanged. Exploratory 16S analyses suggested taxonomic and predicted pathway differences, but none survived Benjamini-Hochberg correction. At the tested dose, CPC/SB increased fecal butyrate, improved glycemic indices, and reduced serum IL-6 relative to the diabetic model group. SB, carrier, and delivery-related effects could not be separated, and in vivo targeting efficiency was not demonstrated.

PMID 43017592
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PubMedThe European journal of general practice2026-11-12

Canadian guidelines for post COVID-19 condition (CAN-PCC): A summary for general practitioners.

Aloosh Mehdi M, Hopkins Jessica P JP, Nieuwlaat Robby R, Darzi Andrea J AJ et al.

Post COVID-19 condition (PCC), also known as Long COVID is associated with a substantial global burden. The Canadian Guidelines for Post COVID-19 Condition (CAN-PCC), developed by the CAN-PCC Collaborative, led by McMaster University's Cochrane Canada and GRADE Centres with support from the Public Health Agency of Canada, synthesised over 100 recommendations across prevention, diagnosis, clinical interventions and individualised care, neurological and psychiatric care, paediatric considerations, and health system supports. This summary highlights key, actionable recommendations for general practitioners and outlines their relevance across diverse healthcare contexts. We extracted recommendations from the CAN‑PCC guidelines and organized them into four domains. Across the four domains, several priority recommendations for general practitioners were identified: [1] testing, identification and diagnosis (conditional recommendation for symptom‑guided work‑up; strong recommendation to screen adults for depression); [2] clinical interventions (conditional recommendation for patient‑centred goals, functional recovery, targeted pharmacotherapy, and non-pharmacological strategies); [3] prevention (conditional recommendation for vaccination, masking, indoor air quality improvement, early outpatient pharmacotherapy where indicated, including metformin and nirmatrelvir/ritonavir); and [4] paediatric considerations (conditional recommendation for vaccination and mental‑health screening; strong recommendation against cannabidiol/CBD). As evidence evolves, the CAN‑PCC guidelines provide a comprehensive, patient‑centred framework to support general practitioners in the prevention, identification, and management of PCC. Its recommendations can be adapted across varied healthcare settings to support consistent, safe, and effective care delivery.

PMID 43016329
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