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anagliptin + metformin (SK 1501 / Metoana / SK1501)

✓ Approved

Sanwa Kagaku Kenkyusho Co., Ltd. · DPP4 · 小分子

什么是 anagliptin + metformin？

anagliptin + metformin 是一种小分子，由Sanwa Kagaku Kenkyusho Co., Ltd.研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名SK 1501, Metoana, SK1501
公司Sanwa Kagaku Kenkyusho Co., Ltd.
药物类别小分子
分子靶点DPP4
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Sanwa Kagaku Kenkyusho Co., Ltd.

作用机制

分子靶点

anagliptin + metformin 作用于 1 个分子靶点：

DPP4dipeptidyl peptidase 4 (CD26, DPPIV)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

anagliptin + metformin 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Metabolism and nutrition disordersType 2 diabetes mellitus✓ Approved

相关研究文献

PubMedPharmaceuticals (Basel, Switzerland)2026-10-27

Multi-Omics Analysis Identifies Gut-Associated Metabolic Signatures Associated with Metformin-Mediated Protection Against LPS-Induced Lung Injury.

Cheng Meihui M, Zhang Mi M, Wang Wei W, Jia Xianxian X et al.

Background/Objectives: Lipopolysaccharide (LPS)-induced lung injury involves pulmonary inflammation, metabolic disturbance, and intestinal dysregulation. This study investigated whether metformin attenuates LPS-induced lung and colonic injury and characterized associated gut microbiota-metabolite changes. Methods: Male C57BL/6J mice were assigned to control (CON), LPS, metformin 200 mg/kg (MET 200 mg/kg), and metformin 400 mg/kg (MET 400 mg/kg) groups. Metformin was administered by gavage for 7 days before intranasal LPS challenge. Lung and colon injury were assessed by histology, immunostaining, ELISA, and RT-qPCR. Untargeted serum metabolomics, colonic-content metabolomics, and colonic-content shotgun metagenomics were performed in the CON, LPS, and MET 400 mg/kg groups. Differential-feature, pathway-enrichment, and exploratory Spearman correlation analyses were conducted. Results: Metformin reduced LPS-induced lung injury, inflammatory cytokine production, F4/80- and MPO-positive immune-cell infiltration, and colonic inflammatory and barrier-related abnormalities. Serum metabolomics identified 468 differential features in LPS versus CON and 286 in MET versus LPS, with 218 overlapping features. Colonic-content metabolomics identified 1000 and 554 differential features, respectively, with 328 overlapping features. Eight metabolites showed metformin-associated directional shifts toward control levels in both serum and colonic contents. Metagenomics showed metformin-associated remodeling of gut microbial composition and predicted gene-content functional potential. Exploratory integrated analyses linked metformin-responsive genera and shared metabolites with pulmonary inflammatory indicators. Conclusions: Metformin was associated with attenuated LPS-induced lung and colonic injury and coordinated gut-associated microbiota-metabolite remodeling. Because the study did not include a metformin-only group or causal perturbation experiments, these findings identify candidate associations rather than demonstrating a causal gut microbiota-metabolite-lung mechanism.

PMID 42943340
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PubMedAdvances in drug and alcohol research2026-10-27

Acute metformin treatment increased social sniffing in male but not female BTBR mice.

Greene Susan M SM, Alcala Gloria-Andrea GA, Bordas Blanka B, Vu Vy V et al.

Autism spectrum disorders (ASDs) are characterized by social deficits and restrictive-repetitive behaviors. Metformin has recently been investigated for its potential behavioral effects in ASD models. This study examined the acute effects of metformin on social interaction preferences and marble burying in male and female BTBR T + Itpr3tf/J (BTBR) mice, with C57BL/6J and 129S1/SvImJ mice included as strain controls. The mice received a single intraperitoneal injection of metformin (0 mg, 75 mg, or 150 mg/kg), and the effects were compared using three-chamber social preference and marble burying tests. Acute metformin increased not only social interaction preferences, as determined by differences in time spent in chambers, but also by differences in social sniffing time in male BTBR mice at 150 mg/kg. Surprisingly, it did not alter sociability preferences in BTBR females or in C57BL/6J or 129S1/SvImJ mice. In C57BL/6J females, metformin reduced chamber entries and marble burying, whereas males were unaffected. Progesterone and corticosterone levels were measured in BTBR and C57BL/6J serum collected after behavioral testing, and their levels were unaffected by metformin treatment. These findings indicate that metformin acutely produces modest, beneficial behavioral effects in male BTBR mice, which otherwise exhibit social interaction deficits that are translationally relevant to ASD.

PMID 42935953
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PubMedDiabetes, obesity & metabolism2026-10-27

Metformin Use During Pregnancy and Early-Life Nutritional Status: A Systematic Review of Randomized Clinical Trials.

Perichart-Perera Otilia O, Hernández-Hernández Larissa L, Rodríguez-Cano Ameyalli M AM

Metformin is increasingly used to treat gestational diabetes mellitus and other insulin-resistant conditions during pregnancy. Because it crosses the placenta, concerns remain regarding its potential effects on offspring growth and metabolic programming. This systematic review evaluated the effects of prenatal metformin exposure on infant nutritional status and adiposity during the first year of life. PubMed and Scopus were searched from inception through May 2026 for randomized controlled trials comparing metformin with placebo or standard care during pregnancy. Eligible studies reported infant nutritional status or adiposity-related outcomes from birth to 12 months. Risk of bias was assessed, and results were synthesized narratively. Eight publications from six randomized controlled trials were included. Birthweight and birth size classifications were the most frequently reported outcomes. Metformin was not consistently associated with differences in birthweight or other anthropometric measures. One trial reported lower birthweight, while two reported fewer large-for-gestational-age or macrosomic infants. No study assessed direct measures of infant adiposity. Current evidence does not consistently support an effect of prenatal metformin exposure on early infant anthropometry. Limited postnatal data and absent adiposity measures limit conclusions regarding postnatal growth and early metabolic programming and support standardized longitudinal body composition assessment.

PMID 42935209
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PubMedJournal of clinical medicine2026-10-27

Comparative Effects of Myo-Inositol, Metformin, Berberine, and Combination Therapy on Metabolic, Anthropometric and Hormonal Parameters in Women with Polycystic Ovary Syndrome: A 6-Month Observational Cohort Study.

Yanachkova Vesselina V, Yordanov Angel A, Yaneva Antonia A, Lebanova Hristina H et al.

Background: Polycystic ovary syndrome (PCOS) is the most prevalent endocrine condition among women of reproductive age. It is marked by metabolic and reproductive irregularities and is often linked to insulin resistance, dyslipidemia, and obesity. Diverse methods of treatment are employed to enhance metabolic and hormonal parameters, including inositol-based supplements, metformin, and novel compounds such as berberine. Objective: To describe changes observed over six months in anthropometric, metabolic, lipid, and hormonal metrics among women with PCOS undergoing myo-inositol, metformin, berberine, or a combination of metformin and berberine in standard clinical settings, and to investigate if disparities among treatment groups remained after controlling for initial characteristics. Materials and Methods: This retrospective observational cohort study included 148 women with PCOS diagnosed according to the Rotterdam criteria who completed six months of treatment with myo-inositol (n = 38), metformin (n = 52), berberine (n = 28), or combined metformin-berberine therapy (n = 30). Anthropometric, metabolic, lipid, and androgen parameters were assessed at baseline and after six months. Within-group changes were evaluated with correction for multiple testing using the Holm method. Given the non-random treatment allocation and baseline differences among groups, supplementary baseline-adjusted analyses were performed for the continuous outcomes. Results: Treatment groups differed significantly in several baseline metabolic variables including body mass index (BMI), fasting plasma glucose (FPG), fasting insulin and homeostatic model assessment of insulin resistance (HOMA-IR). After Holm correction for multiple testing, the metformin group showed significant reductions in BMI, FPG, markers of insulin resistance, lipid parameters, and androgen-related hormonal parameters, together with an increase in high-density lipoprotein cholesterol (HDL-C). In the myo-inositol group, significant reductions were observed in fasting insulin, HOMA-IR, total cholesterol, low-density lipoprotein cholesterol (LDL-C), triglycerides, androstenedione, and dehydroepiandrosterone sulfate (DHEAS). In the berberine group, significant reductions were observed in BMI, fasting insulin, HOMA-IR, total cholesterol, triglycerides, and androstenedione. In the combined metformin-berberine group, significant reductions were observed in BMI, fasting insulin, HOMA-IR, total cholesterol, LDL-C, triglycerides, testosterone, androstenedione, DHEAS, and 17-hydroxyprogesterone, together with an increase in HDL-C. In the baseline-adjusted analyses, no significant overall treatment-group effects remained for the principal metabolic outcomes after correction for multiple testing, whereas significant overall treatment-group effects were observed for DHEAS and 17-hydroxyprogesterone. Conclusions: In this real-world observational cohort, six months of treatment with metformin, myo-inositol, berberine, or combined metformin-berberine therapy was associated with changes in several metabolic and hormonal parameters. However, substantial baseline differences among the clinically selected treatment groups and the absence of significant baseline-adjusted between-group effects for the principal metabolic outcomes preclude conclusions regarding comparative treatment efficacy. The observed between-group differences in selected hormonal outcomes warrant further investigation in prospective comparative studies.

PMID 42941281
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PubMedLife (Basel, Switzerland)2026-10-27

Next-Generation Pharmacotherapy for Uterine Leiomyomas: Combining Metformin and Ulipristal Acetate as Neoadjuvant and Adjuvant Interventions to Minimally Invasive Procedures.

Rozmurat Nuray N, Aimagambetova Gulzhanat G, Terzic Sanja S, Zhao Peng P et al.

Uterine fibroids (leiomyomas) are the most common benign tumors of the myometrium in women of reproductive age. They are a major cause of heavy menstrual bleeding, pelvic pressure and pain, and reduced fertility in women of reproductive age. This scoping review aims to examine the potential of two existing medications, metformin and ulipristal acetate (UPA), to treat fibroids individually and in combination with current minimally invasive procedures. Studies published between January 2016 and May 2026 were identified from four databases: PubMed, Scopus, EBSCO, and Google Scholar. Of the 2583 papers identified, 23 studies met the inclusion criteria for this review. Ulipristal acetate (UPA) has been shown to decrease heavy menstrual bleeding and uterine fibroid volume in several clinical studies. However, its use as a treatment for uterine fibroids has been severely restricted in several countries because of the rare occurrence of idiosyncratic drug-induced liver injury. Metformin acts on multiple pathways reported to be involved in the pathogenesis of leiomyomas, including activation of the energy sensor AMP-activated protein kinase (AMPK), inhibition of the mammalian target of rapamycin (mTOR) signaling pathway, modulation of steroidogenesis, suppression of angiogenesis, and induction of apoptosis. The complementary molecular mechanisms of action of metformin and UPA provide a theoretical basis for investigating combination therapy. However, there is currently a lack of direct evidence regarding the potential for synergistic reduction in fibroid volume or regression with combination treatment, and no clinical trials have investigated the use of metformin in conjunction with UPA for the treatment of uterine fibroids in humans. Future studies of metformin and UPA may also benefit from the development of targeted intrauterine and intralesional delivery systems to increase local drug exposure. However, the pharmacokinetics, tissue penetration, hepatic safety, and clinical efficacy of such systems remain to be established. Therefore, while the available evidence supports further investigation of metformin and UPA individually as potential therapeutic agents for uterine fibroids, their combined use, as well as their use in conjunction with current minimally invasive procedures for fibroid treatment, should be regarded as investigational and requires further preclinical and prospective clinical evaluation.

PMID 42942262
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PubMedJournal of clinical medicine2026-10-27

Effects of Metformin Treatment on Liver Glucose Metabolism-Related Enzyme Levels in Streptozotocin-Induced Diabetic Rats.

Gül Cihan C, Kelle Mustafa M, Kayhan Kaya Hacer H, Bulduk Bahattin B et al.

Background: Diabetes mellitus (DM) disrupts hepatic glucose handling and alters pathways involved in glycogen metabolism, glycolysis, the pentose phosphate pathway, and gluconeogenesis. This study examined hepatic glycogen content and glucose metabolism-related enzyme levels at defined stages of streptozotocin (STZ)-induced diabetes and evaluated the effect of metformin at week 8. Methods: Sixty-three adult male Wistar Albino rats were initially allocated to nine groups (n = 7/group): four time-matched control groups (C1-C4), four untreated diabetic groups (D1-D4), and one metformin-treated diabetic group (T). Diabetes was induced with a single intraperitoneal dose of STZ (35 mg/kg). D1/C1, D2/C2, D3/C3, and D4/C4 were evaluated at weeks 1, 3, 6, and 8, respectively; T received metformin (100 mg/kg/day) in drinking water and was evaluated at week 8. One animal each in D3, D4, and T died spontaneously before the scheduled endpoint, leaving 60 animals for final analyses. Hepatic glycogen and glucose metabolism-related enzyme levels were measured by rat-specific sandwich ELISA. Results: Time-matched comparisons showed significant diabetes-associated differences in hepatic glycogen and all measured enzyme levels at weeks 1, 3, 6, and 8. At week 8, metformin shifted glycogen, glycogen synthase (GS), glycogen phosphorylase (GP), lactate dehydrogenase (LDH), pyruvate kinase (PK), hexokinase (HK), glucose-6-phosphatase (G6Pase), glucose-6-phosphate dehydrogenase (G6PD), and fructose-1,6-bisphosphatase (FBP1) toward control values compared with untreated diabetic rats (Holm-adjusted p = 0.0035 for each comparison). However, T remained significantly different from C4 for every hepatic parameter, and final fasting blood glucose did not differ significantly between T and D4. Conclusions: STZ-induced diabetes was associated with marked alterations in hepatic glycogen and glucose metabolism-related enzyme levels. Metformin partially ameliorated these hepatic changes at week 8 despite persistent severe hyperglycemia, but it did not normalize the measured hepatic profile.

PMID 42941621
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