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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

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

PubMedAntimicrobial agents and chemotherapy2026-08-06

The effect of metformin on the pharmacokinetics of rifampicin, isoniazid, and pyrazinamide in adults with tuberculosis.

Rossouw Jacques J, Wallis Robert R, Kornfeld Hardy H, Singhal Amit A et al.

Metformin is under investigation as adjunctive host-directed therapy for tuberculosis (TB), which might interact with first-line TB treatment. We used population pharmacokinetic modeling to assess whether metformin alters first-line TB-drug pharmacokinetics in HIV/TB-coinfected adults without diabetes. Rifampicin, isoniazid, and pyrazinamide pharmacokinetics were investigated in participants from a randomized clinical trial of adjunctive metformin (500 mg twice daily to week 12) in adults starting HIV-associated TB treatment. Antiretroviral therapy (ART)-naïve participants initiated dolutegravir-based ART within 8 weeks. Intensive and semi-intensive sampling was conducted at week 5; concentration-time data were analyzed using non-linear mixed-effects modeling. Data from 78 individuals (43 receiving metformin, median weight 60.8 kg, 62.8% male, 79.5% on ART) were analyzed. Rifampicin and pyrazinamide were described by one-compartment models with linear elimination; typical clearances were 15.8 L/h (95% CI: 13.5-18.7) and 3.88 L/h (95% CI: 3.54-4.08), respectively. Isoniazid followed a two-compartment model with a mixture model for acetylator status; clearance was 10.5 L/h (95% CI: 9.44-11.9) in slow acetylators and 28.8 L/h (95% CI: 25.6-31.0) in fast/intermediate acetylators. Metformin reduced isoniazid bioavailability by 15.6% (95% CI: 4.45-26.4%, P < 0.009) and rifampicin bioavailability by 24.0% (95% CI: 7.83-36.3%, P < 0.007), decreasing the area under the curve from 0 to 24 h from 18.2 to 15.6 mg·h/L and from 35.9 to 27.1 mg·h/L, respectively. No significant effect on pyrazinamide was detected. We found that non-diabetic patients on metformin had lower isoniazid and rifampicin bioavailability. Lowered rifampicin exposure might be clinically relevant; simulations suggest that this could be offset by a single 150 mg rifampicin dose.CLINICAL TRIALSThis study is registered with ClinicalTrials.gov as NCT04930744.

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PubMedFrontiers in medicine2026-08-06

Network meta-analysis of metformin, probiotics, krill oil, celecoxib, and glucosamine/chondroitin in the treatment of knee osteoarthritis.

Chen Keye K, Sun Yan Y, Cui Longkang L, Zhu Yuchen Y et al.

Knee osteoarthritis (KOA) creates a substantial global socioeconomic burden. Celecoxib remains a standard pharmacological treatment, but its long-term safety profile raises concerns. Several adjuvant therapies-probiotics, metformin, krill oil, and glucosamine/chondroitin (CS+GH)-have produced encouraging results in individual trials; however, direct head-to-head comparisons are absent. This network meta-analysis (NMA) compares the efficacy and safety of these five interventions to inform individualized treatment decisions in clinical practice. RCTs published from database inception through February 2026 were retrieved from PubMed, Web of Science, Embase, and the Cochrane Library. A random-effects NMA was conducted using Stata 18.0 and R (MetaInsight). Continuous outcomes were synthesized as mean differences (MD) and dichotomous safety endpoints as risk ratios (RR). Interventions were ranked by surface under the cumulative ranking curve (SUCRA), and evidence quality was assessed using the GRADE framework. Twenty-three RCTs met the inclusion criteria. No significant network inconsistency (P > 0.05) or publication bias was detected. For analgesic efficacy, celecoxib ranked highest on VAS pain improvement (MD = -0.48, 95% CI -0.78 to -0.17, SUCRA = 0.93) and WOMAC total scores (SUCRA = 0.912), followed by CS+GH (0.756). Probiotics (0.66) and metformin (0.63) showed potential efficacy, but the final network certainty for most of these auxiliary comparisons was low or very low, mainly due to severe imprecision and the absence of direct head-to-head trials. These SUCRA-based rankings should therefore be interpreted cautiously in clinical settings. On WOMAC subscales, celecoxib was associated with the largest improvements in pain and physical function; krill oil ranked highest on the pain subscale (SUCRA = 0.99), while probiotics and metformin had the most favorable safety profiles (SUCRA = 0.885 and 0.724, respectively). https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD420261345598, identifier: CRD420261345598.

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PubMedCancer treatment reviews2026-08-06

Pharmacological prevention of second primary cancers: From chemoprevention to precision cancer interception.

Wespiser Mylène M, Rochefort Pauline P, Gauduchon Thibault T, Coste Clio C et al.

The growing population of cancer survivors is increasingly exposed to the long-term risk of second primary cancers (SPCs), which represents a major source of morbidity and mortality. While current prevention mainly relies on surveillance and screening, pharmacological and immunological strategies may offer opportunities to reduce SPC incidence in selected high-risk populations. This narrative review synthesises current evidence on pharmacological prevention strategies for SPCs, including endocrine therapy, aspirin and non-steroidal anti-inflammatory drugs, PARP inhibitors, metformin, GLP-1 receptor agonists, statins, nicotinamide, immune checkpoint inhibitors, cancer vaccines, and microbiome modulation. Evidence from randomised trials, observational studies, translational research, and ongoing clinical trials was reviewed, with particular attention to SPC-specific endpoints, biological rationale, safety, and clinical applicability. The strongest evidence currently supports endocrine therapy for reducing contralateral breast cancer in patients with hormone receptor-positive breast cancer, and aspirin in selected populations such as Lynch syndrome carriers or patients with molecularly defined colorectal cancer. Other repurposed agents, including metformin, statins, GLP-1 receptor agonists, and nicotinamide, remain investigational, with most available data addressing incident cancer, recurrence, or surrogate endpoints rather than SPC prevention specifically. Immunological approaches are emerging as particularly promising strategies. Retrospective studies and exploratory analyses of randomised trials suggest that immune checkpoint inhibitors may reduce the occurrence of new malignancies, while neoantigen-based vaccines, especially in Lynch syndrome, provide an early proof of concept for cancer immunoprevention. Pharmacological prevention of SPCs is an expanding but remains a heterogeneous field. Current evidence supports a shift from broad chemoprevention toward biologically informed, risk-adapted prevention strategies. Future progress will depend on dedicated SPC-focused trials, biomarker-driven patient selection, long-term safety evaluation, and integration of pharmacological prevention into broader cancer interception programmes.

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PubMedInternational journal of cancer2026-08-06

Diabetes Increases Immunotherapy-Related Toxicity but Not Efficacy in Metastatic Non-Small Cell Lung Cancer: A Multicenter Retrospective Study.

Çakır Emre E, Divriklioğlu Didem D, Güven Deniz Can DC, Özel Gamze Serin GS et al.

This multicenter retrospective study evaluated the impact of type 2 diabetes mellitus (DM) on clinical outcomes and immune-related adverse events (irAEs) in 450 patients with metastatic non-small cell lung cancer (NSCLC) treated with second-line nivolumab at 17 centers between 2016 and 2024. Among these patients, 118 (26.2%) had DM. Baseline demographic and clinical characteristics, including age, sex, smoking status, ECOG performance status, histology, and PD-L1 expression, were similar between patients with and without DM. Nivolumab demonstrated similar antitumor activity in both groups, with no significant differences in median progression-free survival (PFS), overall survival (OS), or objective response rates. However, the incidence of Grade 3-4 irAEs was significantly higher in patients with DM. HbA1c levels were not associated with survival outcomes in univariate analyses, and metformin or insulin use did not affect PFS or OS among patients with DM. These findings indicate that DM does not compromise immunotherapy efficacy but is associated with a higher risk of severe toxicity. Clinicians should consider metabolic status and closely monitor patients with DM receiving immunotherapy. Further prospective studies are needed to clarify underlying mechanisms and optimize treatment strategies for this population.

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PubMedNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2026-08-06

Drug safety in patients with mitochondrial disease: an observational cohort study.

Järvinen Oskar O, Martikainen Mika H MH

Mitochondrial diseases are common inherited neurometabolic disorders and frequently involve the nervous system, yet their multisystem nature often necessitates complex pharmacological management. Many commonly prescribed medications have off-target effects on mitochondrial function, and patients with mitochondrial disease may be particularly vulnerable to such effects due to impaired energy metabolism. However, systematic data on medication safety in this patient group remain scarce. In this retrospective, single-centre, cohort-based study at Turku University Hospital (Turku, Finland), we reviewed the medication data from all hospital stays and outpatient prescriptions of 44 mostly adult (20 women; mean age 50 years, range 12-83 years) patients with genetically and clinically confirmed mitochondrial disease for years 2010-2022. We used the Anatomical Therapeutic Chemical system for drug classification. Potential drug-drug interactions and potential adverse drug reactions were investigated. Special focus was on potential mitochondrial toxicity of drugs and clinically relevant drug-drug interactions. Altogether ~ 1000 individual medication entries were reviewed. We identified several common drugs with potentially adverse effects on mitochondria, including metformin, beta-blockers, statins, ciprofloxacin, fluoxetine, ibuprofen, and certain anti-seizure drugs. Medications generally considered contraindicated in mitochondrial disease were not observed. No high-risk drug interactions were detected. Additional finding of clinical relevance was the frequent use of analgesics. Further research regarding mitochondrial safety of several drug classes is needed for more evidence-based safety evaluations. Pain in the context of mitochondrial disease merits increased attention.

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PubMedCancer reports (Hoboken, N.J.)2026-08-06

Harnessing Repurposed Drugs to Enhance Temozolomide Efficacy in Glioblastoma.

Nakhaei Ali A, Taghavi Atefeh A, Afshari Amir R AR, Davoudi Farzaneh F et al.

Glioblastoma (GB) is the most aggressive primary malignant brain tumor in adults and remains associated with poor survival despite surgical resection followed by radiotherapy and temozolomide (TMZ) chemotherapy. Intrinsic and acquired resistance to TMZ, including MGMT-dependent DNA repair and activation of pro-survival pathways, could decrease treatment efficacy. Drug repurposing offers an attractive strategy to identify agents that may enhance TMZ activity because these drugs already have known pharmacokinetic and safety profiles. This narrative review summarizes the available evidence on repurposed drugs investigated as potential modulators of TMZ response in GB. A range of repurposed agents, including chloroquine, valproic acid, levetiracetam, metformin, aspirin, amlodipine, atorvastatin, chlorpromazine, melatonin, disulfiram, bortezomib, and verteporfin, have been evaluated in GB models and selected clinical studies. Reported mechanisms include modulation of MGMT expression, autophagy, oxidative stress, apoptosis, DNA-damage responses, cancer stem-cell properties, and signaling pathways such as PI3K/AKT/mTOR, AMPK, EGFR, STAT3, ERK1/2, and NF-κB. Several agents have enhanced TMZ-associated cytotoxicity in cell culture and animal models. However, clinical evidence remains limited, and the results are inconsistent for some drugs. Blood-brain barrier penetration, achievable intratumoral drug exposure, toxicity, treatment scheduling, and molecular heterogeneity of GB remain major translational challenges. Repurposed drugs may provide useful candidates for improving TMZ-based therapy in GB. However, most evidence remains preclinical, and further studies are needed to clarify blood-brain barrier penetration, optimal dosing, toxicity, predictive biomarkers, and clinical efficacy. Well-designed prospective clinical trials are required before these combinations can be incorporated into routine GB treatment.

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