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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

PubMedCancers2026-10-16

Metformin as an Adjunct to Fertility-Sparing Treatment in Atypical Endometrial Hyperplasia and Early-Stage Endometrioid Endometrial Cancer: Narrative Review.

Yordanov Angel A, Tsoneva Eva E, Kostov Stoyan S, Yanachkova Vesselina V et al.

Objective: This study aims to evaluate the potential role of metformin as an adjunct to fertility-sparing treatment strategies for women with atypical endometrial hyperplasia/endometrial intraepithelial neoplasia (AEH/EIN) and early-stage endometrioid endometrial cancer (EEC), with particular emphasis on oncologic and reproductive outcomes. Methods: A systematic search of PubMed/MEDLINE, Embase, Scopus, Web of Science, and the Cochrane Library was conducted from database inception through May 2026. Eligible studies included randomized controlled trials, prospective studies, and retrospective cohort studies evaluating metformin-containing fertility-sparing treatment regimens in women with AEH/EIN or early-stage EEC. Owing to substantial clinical and methodological heterogeneity in study design, treatment protocols, metformin dosage, follow-up duration, and outcome reporting, a quantitative meta-analysis was considered inappropriate, and the findings were synthesized narratively. Results: Eight publications represented approximately 795 unique patients after accounting for overlapping cohorts. Complete response was reported in 63/92 patients overall (69%) in Acosta-Torres et al., including 23/34 (68%) receiving progestin plus metformin, and in 61/63 (97%) receiving medroxyprogesterone acetate plus metformin in Mitsuhashi et al. Reported recurrence rates ranged from 13.1% to 34.2%. Live births occurred in 2/34 (6%) metformin-treated patients in Acosta-Torres et al., 14/31 (45%) women wished to conceive in Mitsuhashi et al., and 29/79 (36.7%) patients overall in Jing et al. Differences in populations, assessment times, and reproductive denominators limited direct comparisons and attribution of benefit to metformin. Conclusions: Current evidence suggests that metformin may have a promising adjunctive role in fertility-sparing treatment for women with AEH/EIN and early-stage EEC, particularly among patients with obesity, insulin resistance, polycystic ovary syndrome, or other metabolic risk factors. Nevertheless, the overall body of evidence should be interpreted with caution because of substantial heterogeneity across studies, the predominance of retrospective designs, and the limited number of prospective randomized trials. Well-designed multicenter randomized controlled trials are required to define the optimal role of metformin, identify the patients most likely to benefit, and establish standardized treatment strategies before routine incorporation into clinical practice can be recommended.

PMID 42882834
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PubMedJournal of clinical medicine2026-10-16

Effects of Metformin on Clinical Outcomes After Acute Ischemic Stroke in Patients with Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis.

Chen Ting-Yen TY, Su Yu-Chi YC, Lin Yu-Ching YC

Objective: This study investigated the effects of metformin on clinical outcomes after acute ischemic stroke in patients with type 2 diabetes mellitus (T2DM). Methods: PubMed, Embase, Web of Science, and the Cochrane Library were systematically searched for relevant English articles published from database inception to 6 April 2026. Moreover, the reference lists of eligible articles were searched. Studies were included if they focused on patients with T2DM and acute ischemic stroke, indicated whether the patients used metformin before stroke onset, and reported the patients' modified Rankin Scale (mRS) scores after stroke onset. Studies lacking adequate outcome data were excluded. Two reviewers independently extracted relevant data-for example, study details, clinicodemographic characteristics, and poststroke outcomes (mRS scores, National Institutes of Health Stroke Scale [NIHSS] scores, symptomatic intracranial hemorrhage [sICH], and mortality). A senior reviewer was consulted in cases of between-reviewer disagreements. The primary outcome was poststroke mRS score (functional outcome), and the secondary outcomes were poststroke NIHSS scores (neurological severity), sICH, and mortality. Results: Eleven studies met the inclusion criteria. Most studies reported better functional outcomes (mRS scores) and lower NIHSS scores for metformin users than for nonusers. Some studies indicated reduced rates of sICH and mortality among metformin users than among nonusers. Sensitivity analyses generally supported the benefits of metformin. Caution should be exercised when interpreting these findings because the results might have been influenced by variations in study designs, stroke classifications, and renal function reporting. Conclusions: In patients with T2DM, metformin may reduce stroke severity and improve poststroke functional outcomes. To the best of our knowledge, this meta-analysis is the first to investigate the association between metformin use and neurological severity, estimate adjusted ORs for favorable functional outcomes, and highlight publication bias on this topic.

PMID 42881994
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PubMedInternational journal of molecular sciences2026-10-16

Correction: Yang et al. Molecular Mechanism of Metformin Regulating the Regeneration of Planarian Dugesia japonica Through miR-27b. Int. J. Mol. Sci. 2025, 26, 7092.

Yang Kexin K, Feng Minmin M, Zhang Chunmei C, Zhao Zelong Z et al.

In the original publication [...].

PMID 42884187
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PubMedOncotarget2026-10-16

WIN-MTB-2024002 - WIN International Molecular Tumor Board: A 52-year-old female with unmeasurable Stage IIIc colon cancer.

El-Deiry Wafik S WS, Hernando-Calvo Alberto A, Magidi Shai S, Bresson Catherine C et al.

Copyright: © 2026 El-Deiry et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Colorectal cancer (CRC) is a leading cause of cancer-related mortality, with a complex molecular profile that impacts tumor behavior and treatment response. This case report discusses a 52-year-old female diagnosed with Stage IIIc colon cancer, exhibiting KRAS, TP53, IDH1, and APC mutations, as well as a tumor microenvironment with high PD-L1 expression and elevated VEGFR1 and VEGFR3. Despite surgical resection and adjuvant treatment which included FOLFOX, FOLFIRI with bevacizumab and local radiation, the patient’s disease was difficult to track due to small, non-FDG-avid lymph nodes in the aortocaval region and persistent circulating tumor DNA (ctDNA). Following a review by an international Molecular Tumor Board (MTB), maintenance therapy options were discussed, including the personalized combinations of regorafenib, sulindac, and metformin, or fruquintinib, sulindac, and metformin, based on the patient’s molecular alterations. Alternatively, 5-FU with or without bevacizumab was suggested. In the event of relapse, the MTB recommended the combination of regorafenib, sulindac, and metformin, with the addition of trametinib and ivosidenib. The combination of regorafenib, ipilimumab, and nivolumab (RIN) was also considered due to the patient’s high PD-L1 expression. Further clinical trial options, such as pan-RAF inhibitors, NK cell agonists, and TAS-102 with bevacizumab, were also discussed. Additionally, the potential combination of PD-1 and TGFβ inhibitors was explored. This case underscores the critical role of molecular profiling in tailoring personalized treatment strategies for advanced CRC, providing novel avenues for managing recurrent disease, even in the absence of measurable disease.

PMID 42885719
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PubMedCells2026-10-16

Dexamethasone Modulates Global DNA Methylation and Oxidative DNA Damage in Glioblastoma Cell Lines.

Barciszewska Anna-Maria AM, Belter Agnieszka A, Barciszewski Jakub F JF, Perrigue Patrick M PM et al.

Glioblastoma remains one of the most aggressive primary brain tumors, characterized by rapid progression, therapeutic resistance, and poor prognosis. Dexamethasone is routinely administered to patients with glioblastoma to reduce peritumoral edema and improve neurological symptoms. However, its broader molecular effects on tumor-cell biology and treatment response remain incompletely understood. This study examined the effects of dexamethasone alone and in combination with temozolomide, valproic acid, or metformin on glioblastoma cell viability, real-time proliferation, senescence-associated β-galactosidase activity, cell-cycle distribution, global DNA methylation, and oxidative DNA damage. Dexamethasone induced concentration- and time-dependent changes in global DNA methylation in glioma cells. In T98G cells, shorter exposure increased 5-methylcytosine, whereas longer incubation or selected combined treatment conditions reduced methylation, suggesting dynamic epigenetic remodeling. Low dexamethasone concentrations were associated with increased 5-methylcytosine content, also in temozolomide-containing conditions. In contrast, higher dexamethasone concentrations reduced global methylation. That effect was cell-line dependent. In SW1783 cells, high-dose dexamethasone caused a reduction in 5-methylcytosine amount as well as an increase in 8-oxo-2'-deoxyguanosine level. Dexamethasone also reduced real-time T98G cell proliferation after prolonged exposure, while temozolomide was the main compound associated with cell-cycle changes in T98G cells. Metformin displayed comparatively limited cytotoxicity under the tested conditions. Beyond dexamethasone's well-established anti-edematous and anti-inflammatory role, it may also modify glioma redox and epigenetic states and influence cellular responses to temozolomide, valproic acid, and metformin. When considering these findings it is necessary to take into account a number of limitations. The upper limits of the DEX, TMZ, and MF concentration ranges were one to three orders of magnitude higher than the brain or CSF exposure levels that have been reported, and the experiments were carried out at standard culture oxygen concentrations (about 18-21% O2), which are much higher than the oxygen levels found in brain tissue (about 2-6% O2). Furthermore, the conclusions drawn from the T98G experiments only apply to this cell line and cannot be applied to glioblastoma without first being verified in other models.

PMID 42882443
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PubMedBMC endocrine disorders2026-10-16

Effects of SGLT-2 inhibitors on thyroid-stimulating hormone and systemic immune-inflammation index in type 2 diabetes: a retrospective study.

Bayram Seyit Murat SM, Demirci Hüseyin H, Üçgül Enes E, Canlar Şule Ş et al.

This retrospective study examined whether long-term SGLT-2i use is associated with differences in thyroid-stimulating hormone (TSH) and the systemic immune-inflammation index (SII) in patients with type 2 diabetes mellitus (T2DM) without known thyroid disease. The neutrophil-to-lymphocyte ratio (NLR), renal function (eGFR), diabetes duration, and metformin use were also evaluated as potential covariates. This was a single-center, retrospective observational study. Adults with T2DM who had used empagliflozin or dapagliflozin for at least six months were compared with an age- and sex-matched control group of patients with T2DM not using SGLT-2i, drawn from the same outpatient clinics. Key exclusion criteria included known thyroid disease, known positivity for thyroid autoantibodies, active inflammatory or autoimmune processes, advanced organ failure, and immunomodulatory treatment. TSH, SII, and NLR were measured. Statistical analyses included intergroup comparisons, correlation, multivariate linear regression, post-hoc power calculation, and multicollinearity diagnostics (variance inflation factor, VIF). The study included 330 patients across the empagliflozin (n = 139), dapagliflozin (n = 85), and control (n = 106) groups. Median TSH (1.6, 1.8, and 1.9 µIU/mL; p = 0.338) and SII (481, 531, and 468.5; p = 0.509) did not differ significantly between groups. SII and NLR were significantly correlated (r = 0.467, p < 0.001). In multivariate regression, female sex (B = 0.161, p = 0.015) and eGFR (B=-0.0043, p = 0.037) were independent predictors of log-transformed TSH; SGLT-2i use, SII, NLR, age, metformin use, and diabetes duration were not. The study had 80% power to detect a Cohen's f of 0.17 or greater; observed effect sizes were substantially below this threshold (f = 0.02 for TSH, f ≈ 0.00 for SII). Long-term SGLT-2i use was not associated with significant changes in TSH or SII in patients with T2DM without known thyroid disease, and the achieved effect sizes suggest that any true effect, if present, is likely small. Renal function emerged as an independent correlate of TSH, suggesting that the relationship between the hypothalamic-pituitary-thyroid axis and renal physiology merits further attention in this population, independent of SGLT-2i exposure. Prospective, multicenter studies incorporating free thyroxine and triiodothyronine measurements are warranted to further clarify these relationships. This study is retrospective and does not involve a clinical trial registration.

PMID 42881387
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