Drug Database
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remogliflozin etabonate + vildagliptin (Remozen V / Remo V)

✓ Approved

Glenmark Pharmaceuticals Limited · DPP4 · Small Molecule

What is remogliflozin etabonate + vildagliptin?

remogliflozin etabonate + vildagliptin is a small molecule developed by Glenmark Pharmaceuticals Limited. It is approved for therapeutic indications via oral (po).

Drug Profile

Brand NamesRemozen V, Remo V
CompanyGlenmark Pharmaceuticals Limited
Drug ClassSmall Molecule
Molecular TargetDPP4, SLC5A2
RouteOral (PO)
StatusApproved
Sources: ClinicalTrials.gov, Glenmark Pharmaceuticals Limited

Mechanism of Action

Molecular Targets

remogliflozin etabonate + vildagliptin acts on 2 molecular targets:

DPP4dipeptidyl peptidase 4 (CD26, DPPIV)
SLC5A2solute carrier family 5 member 2 (SGLT2)
Want deeper analysis?Noah AI can explain complex mechanisms and compare to similar drugs.

Therapeutic Indications

remogliflozin etabonate + vildagliptin is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersType 2 diabetes mellitus✓ Approved

Related Research Articles

PubMedImmunopharmacology and immunotoxicology2026-10-11

Vildagliptin attenuates thioacetamide-induced hepatic fibrosis in rats: associations with AMPK/SIRT1/Nrf2 and STAT3/TGF-β1 signaling.

Almikhlafi Mohannad A MA, Alsayb May A MA, Almadani Sara A SA, Saeedi Tahani T et al.

Liver fibrosis is a progressive consequence of chronic injury with limited treatment options. Vildagliptin (Vilda), a dipeptidyl peptidase-4 inhibitor, possesses antioxidant and anti-inflammatory properties, but its effects on thioacetamide (TAA)-induced liver fibrosis are not fully characterized. This study evaluated Vilda in TAA-treated male rats by assessing hepatic function, oxidative stress, and signaling markers. Rats received TAA (100 mg/kg, i.p., twice weekly for 6 weeks) alone or with Vilda (10 or 20 mg/kg, p.o., daily during weeks 3-6). Serum biochemistry, hepatic antioxidants, and specific protein concentrations (AMPK, p-AMPK, SIRT1, Nrf2, STAT3, p-STAT3, TGF-β1, and AFP) were measured. Liver sections were assessed via H&E, qualitative Masson's trichrome, and immunohistochemistry for p-AKT and SIRT1. TAA impaired liver function, altered lipid profiles, increased oxidative stress, and induced histopathological injury with collagen deposition. These changes coincided with altered hepatic AMPK/SIRT1/Nrf2 and STAT3/TGF-β1-associated markers, alongside PGC-1α and KEAP1 mRNA expression. Vilda treatment was associated with dose-dependent improvements in biochemical, oxidative-stress, and histopathological findings, alongside shifts in inflammation- and fibrosis-associated markers. Vilda was also associated with increased SIRT1 and reduced p-AKT immunoreactivity. Vilda treatment was associated with attenuation of TAA-induced hepatic injury and fibrotic changes in parallel with modulation of AMPK/SIRT1/Nrf2 and STAT3/TGF-β1-related markers. Because quantitative collagen morphometry and pathway-intervention experiments were not performed, these findings represent associations rather than confirmed causal mechanisms. Further studies are required to define the precise molecular interactions and translational potential of Vilda as an antifibrotic agent.

PMID 42858114
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PubMedNaunyn-Schmiedeberg's archives of pharmacology2026-10-01

Vildagliptin attenuates the development of CCl₄-induced liver fibrosis: associations with gut-liver axis modulation and LPS/notch-related signaling.

Eid Aya M AM, El-Gendy Ahmed O AO, Ewees Mohamed Gamal El-Din MGE

Liver fibrosis is a progressive pathological condition closely linked to gut microbiota dysbiosis and impaired intestinal barrier integrity. Vildagliptin, a dipeptidyl peptidase-4 inhibitor used in type 2 diabetes, exhibits pleiotropic anti-inflammatory and antioxidant properties; however, its impact on the gut-liver axis during hepatic fibrogenesis remains insufficiently defined. This experimental study investigated whether concomitant vildagliptin administration attenuates the development of CCl₄-induced liver fibrosis and whether this effect is associated with alteration in gut microbial composition, intestinal barrier-related markers, and circulating lipopolysaccharide (LPS), and hepatic fibrosis-associated molecular changes. Male rats were allocated to five groups: normal control, Vildagliptin alone (20 mg/kg/day), CCl₄-fibrosis, and CCl₄ + Vildagliptin (10 or 20 mg/kg/day). Liver fibrosis was induced by CCl₄ administration for six weeks, with concomitant daily oral Vildagliptin in the treatment groups. Liver function indices, fibrotic markers, oxidative stress parameters, and serum LPS were assessed. Intestinal barrier-related changes were assessed by measuring colonic ZO-1 and occludin levels, while circulating LPS was quantified as a marker of systemic endotoxemia. Hepatic ADAM17, Notch-1, DNMT3A, and Smad7 protein levels and β-Klotho mRNA expression were assessed. Liver and colon histopathology was examined, and gut microbiota composition was profiled using 16S rRNA gene amplicon sequencing. Vildagliptin significantly ameliorated CCl₄-induced liver injury and fibrosis, evidenced by improved biochemical parameters, reduced collagen deposition and hydroxyproline, and attenuation of hepatic stellate cell activation. These effects were accompanied by increased colonic ZO-1 and occludin levels, reduced circulating LPS, decreased hepatic ADAM17, Notch-1, and DNMT3A protein levels, increased β-Klotho mRNA expression and Smad7 protein levels, and alterations in gut microbiota composition. Collectively, concomitant vildagliptin administration attenuated the development of CCl₄-induced liver fibrosis and was associated with modulation of gut-liver axis -related changes and alterations in LPS- and Notch-related molecular markers.

PMID 42820991
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PubMedJournal of the ASEAN Federation of Endocrine Societies2026-09-28

Cost-Effectiveness Analysis of Triple Oral Antidiabetic Drug Combination in Patients With Type 2 Diabetes Mellitus: An Outpatient Study in Indonesia.

Hanifiyah Izzatu Al IA, Nita Yunita Y, Libriansyah, Ridwan Achmad A et al.

Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent hyperglycemia. Initial therapy for type 2 diabetes typically starts with metformin monotherapy, but because of its progressive nature, combination therapy is often required to achieve glycemic targets. However, research on combination therapy with three oral antidiabetic drugs is currently limited. This study assessed direct medical costs and the cost-effectiveness of a combination of triple oral antidiabetics with first-line metformin combined with glimepiride, pioglitazone, and DPP-4 inhibitors (sitagliptin/vildagliptin), among type 2 DM patients treated in the outpatient clinic of Dr. Ramelan Central Naval Hospital, Surabaya, Indonesia. A retrospective cross-sectional analysis was conducted from the hospital perspective using medical records and cost data from January to December 2024. Eligible patients had type 2 DM, received a combination of triple oral antidiabetics with metformin as first-line treatment combined with glimepiride, pioglitazone, and DPP-4 inhibitors (sitagliptin/vildagliptin), attended monthly follow-ups, had at least two HbA1c measurements, and had complete clinical and cost data. Direct medical costs included doctor services, drug acquisition costs, and laboratory monitoring costs. A total of 79 patients were included, 60.8% male, with an average (SD) age of 54.9 (9.26) years, and 69.6% with comorbidities. Compared with the combination of metformin + glimepiride + pioglitazone, the combination of metformin + sitagliptin/vildagliptin + glimepiride and metformin + sitagliptin/vildagliptin + pioglitazone was more cost-effective, with ICER values of IDR -162,119.77; IDR 845,655.5, respectively. Both ICER values were below the willingness-to-pay (WTP) threshold. One-way sensitivity analysis showed that the model results were relatively robust to parameter variations of ±20%. In the combination of metformin + sitagliptin/vildagliptin + glimepiride vs metformin + glimepiride + pioglitazone, laboratory monitoring costs had the greatest influence on the ICER value. Meanwhile, the combination comparison metformin + sitagliptin/vildagliptin + pioglitazone vs metformin + glimepiride + pioglitazone was most sensitive to changes in effectiveness (ΔHbA1c). Metformin + sitagliptin/vildagliptin + glimepiride and metformin + sitagliptin/vildagliptin + pioglitazone are both more cost-effective compared to metformin + glimepiride + pioglitazone in this setting.

PMID 42802796
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PubMedToxicology mechanisms and methods2026-09-28

Remogliflozin attenuates cyclophosphamide-associated peripheral neurotoxicity in rats: concomitant changes in redox, inflammatory, neurotrophic, and apoptosis-related markers.

Almarghalani Daniyah A DA, Qadri Marwa M, Alarifi Abdulaziz A, Fayed Hany M HM et al.

Peripheral neurotoxicity represents a debilitating complication of cancer chemotherapy. Although cyclophosphamide (CP) is an alkylating agent with lower clinical propensity for classic peripheral neuropathy than platinum compounds or taxanes, its reactive metabolites provoke significant neurotoxic injury in experimental settings. This study investigated whether remogliflozin (Remo), a sodium-glucose cotransporter-2 inhibitor (SGLT2) with pleiotropic antioxidant and anti-inflammatory properties, attenuates CP-associated peripheral neurotoxicity in an experimental rat model. Twenty-four male Wistar rats were divided into four groups: control, CP alone (100 mg/kg intraperitoneally once weekly), CP plus Remo 25 mg/kg/day orally, and CP plus Remo 50 mg/kg/day orally, all for one month. Behavioral assessments revealed that CP treatment was associated with altered motor coordination and nociceptive responses, which showed dose-related numerical improvements with Remo treatment. Biochemically, Remo treatment was associated with a favorable shift in redox markers, evidenced by higher Nrf2, glutathione, and superoxide dismutase levels, alongside reduced malondialdehyde. Remo treatment was associated with lower concentrations of inflammatory markers, including NF-κB, MCP-1, TNF-α, IL-6, and IL-1β. Furthermore, Remo treatment was associated with increased BDNF and CREB concentrations, PI3K, and total/phosphorylated Akt (with an improved p-Akt/total Akt ratio), along with lower concentrations of caspase-3 and BAX, and higher BCL-2. Histopathological and immunohistochemical analyses demonstrated that Remo was associated with preserved nerve structural integrity, attenuated myelin loss, and elevated Nrf2 and p-Akt immunoreactivity. These findings suggest that Remo is associated with attenuation of CP-induced peripheral neurotoxicity in rats, presenting a phenotypically consistent biomarker profile that warrants further causal and mechanistic evaluation.

PMID 42805919
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PubMedInternational journal of molecular sciences2026-09-26

Effects of DPP4 Inhibition on Inflammation and Oxidative Stress in Experimental Gestational Diabetes Mellitus.

Tufan Akarslan Öznur Ö, Er Ayşe A

Gestational diabetes mellitus (GDM) is a common pregnancy complication, with inflammation and oxidative stress playing a significant role in its pathogenesis. Therefore, this study evaluated the effects of vildagliptin on metabolic, hormonal, inflammatory, and oxidative stress parameters in an STZ-induced GDM model. Rats were divided into five groups: control, GDM, GDM + V10, GDM + V20 and GDM + V30. High blood glucose levels were observed in the GDM group, while a slight decrease was observed in the vildagliptin groups. While GLP-1 levels decreased in the GDM group, they increased in the GDM + V20 and GDM + V30 groups. Overall, an increase in pro-inflammatory cytokines and a decrease in anti-inflammatory cytokines were observed in the GDM group, while vildagliptin administration reversed these effects. Among the vildagliptin groups, IL-10 was found to be lowest and IL-6 highest in the GDM + V20 group. Although fluctuations were generally observed in oxidative stress markers, the highest MDA levels and the lowest GSH levels were found in the GDM + V20 group. In the GDM group, FW and PE were lower, and PW was higher. In contrast, FW and PE were higher, and PW was lower in the GDM + V30 group than in the GDM group. The best results were obtained at a dose of 30 mg/kg; however, further research is needed to confirm this effect.

PMID 42794730
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PubMedClinical ophthalmology (Auckland, N.Z.)2026-09-19

Longitudinal Changes in Corneal Epithelial and Central Corneal Thickness in Type 2 Diabetes Assessed by AS-OCT: A Real-World Study.

Boyacı İhsan İ, Demirci Göktuğ G

To evaluate longitudinal changes in central corneal epithelial thickness (CCET) and central corneal thickness (CCT) using anterior segment optical coherence tomography (AS-OCT) over 12 months in adults with type 2 diabetes receiving one of two routinely prescribed oral antidiabetic regimens, and to explore their association with glycemic changes. In this retrospective observational cohort study, 40 adults with type 2 diabetes receiving one of two routinely prescribed treatment regimens (vildagliptin-metformin, n=19; empagliflozin-metformin, n=21) underwent AS-OCT at baseline, 3 months, and 12 months. Glycated hemoglobin and fasting plasma glucose were assessed at each visit. Precision analysis indicated detectable between-group differences of 4.7 µm for CCT and 6.1 µm for CCET. Both groups showed significant within-group glycated hemoglobin improvement (mean reduction: -2.28% and -2.88% in the vildagliptin-metformin and empagliflozin-metformin groups, respectively; p<0.05) without between-group differences. CCT and CCET showed no statistically detectable longitudinal change over 12 months, with no significant differences in longitudinal change between groups. Glycated hemoglobin change showed a modest independent association with CCT change (β = 0.81 µm per 1% glycated hemoglobin; 95% CI 0.20-1.42; p=0.011; n=32). Corneal structural parameters showed no statistically detectable longitudinal change or between-group difference over 12 months. Given the modest sample size and observational design, these findings should be considered hypothesis-generating and require confirmation in larger prospective studies.

PMID 42761673
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