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

PubMedJournal of clinical medicine2026-07-15

Evaluating Lacrimal Punctum Size as a Clinical Indicator of Dry Eye Disease Severity in a Real-World Lebanese Cohort.

Tlaiss Yehya Y, Warrak John J, Warrak Elias E

Background/Objectives: To investigate the relationship between lacrimal punctum size and the severity of dry eye disease (DED) in a clinically refractory, real-world patient cohort from a tertiary ophthalmology center in Lebanon. Methods: A retrospective observational study was conducted at Advanced Eye Care Center, Beirut, Lebanon (2016-2024). A total of 312 eyes from 156 patients with moderate-to-severe DED unresponsive to topical artificial tears, loteprednol etabonate, and cyclosporine (0.05% ophthalmic emulsion) were included. All eyes subsequently underwent lower lacrimal punctum plug insertion as part of clinical management. Lacrimal punctal diameter was estimated by the largest silicone plug (0.5 mm, 0.6 mm, or 0.7 mm) inserted nonforcefully into the lower punctum under slit-lamp visualization. Tear film stability was assessed by Tear Break-Up Time (TBUT). Group differences were analyzed using the Kruskal-Wallis H test with post hoc Mann-Whitney U tests (Bonferroni correction), and Spearman's rank correlation was calculated to quantify the monotonic association. Results: Eyes were distributed across punctal diameter categories as follows: 0.5 mm (n = 15, 4.8%), 0.6 mm (n = 204, 65.4%), and 0.7 mm (n = 93, 29.8%). Median TBUT values were 5.55 s [IQR 5.51-5.77], 5.06 s [IQR 4.80-5.37], and 4.51 s [IQR 4.23-4.71] for the 0.5 mm, 0.6 mm, and 0.7 mm groups, respectively. Kruskal-Wallis analysis confirmed significant inter-group differences (H = 140.1, p < 0.001). All post hoc pairwise comparisons remained significant after Bonferroni correction (p < 0.001). Spearman's rank correlation demonstrated a significant negative association between lacrimal punctal diameter and TBUT (ρ = -0.70, p < 0.000001). All analyses were conducted at the eye level and do not account for within-patient correlation (bilateral design, 156 patients); p-values should be interpreted accordingly. Conclusions: In this treatment-refractory cohort, larger lacrimal punctal diameter was significantly associated with greater tear film instability. These findings suggest that lacrimal punctal diameter estimation during therapeutic plug insertion may serve as a practical, cost-free adjunct to standard DED evaluation. Prospective multimodal studies are needed to validate punctal diameter as an independent clinical indicator of DED severity.

PMID 42452448
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PubMedBMC pregnancy and childbirth2026-07-14

Comparison of the permeability of DPP-4 inhibitors-sitagliptin, vildagliptin, linagliptin, and alogliptin-in placental barrier cell models and exploration of their transport mechanisms by LC-MS/MS.

Bai Mengru M, Shen Qian Q, Wu Yong Y, Chen Mingyang M et al.

Uncontrolled hyperglycemia in pregnancy poses risks to both mother and fetus, but treatment options are limited. Sitagliptin, vildagliptin, linagliptin, and alogliptin are dipeptidyl peptidase-4 (DPP-4) inhibitors effective in type 2 diabetes. However, data on their placental transfer and safety in pregnant women is lacking. Therefore, this study compared the permeability of these drugs in multiple placental cell models, including BeWo, HTR-8/SVneo, and primary human trophoblast cells, and attempted to explore their transport mechanisms. A cost-effective liquid chromatography-tandem mass spectrometry method was developed and validated to quantify the four DPP-4 inhibitors. The accumulation of these drugs in placental cell models was compared, and the BeWo Transwell transport assay was conducted to assess transport rates. Transporter inhibitors, siRNA knockdown, and transporter overexpression cell models were used to explore the transmembrane transport mechanism of these drugs. Linagliptin had the highest accumulation in placental cells, followed by alogliptin, sitagliptin, and vildagliptin. The apparent permeability coefficient of linagliptin, alogliptin and sitagliptin was similar in BeWo cells, while vildagliptin was the lowest. The accumulation of linagliptin, alogliptin, sitagliptin and vildagliptin in BeWo cells at 37 °C were significantly higher than those at 4 °C, indicating the presence of carrier-mediated uptake. However, studies using transporter inhibitors, siRNA knockdown, and transporter overexpression cell models showed that equilibrative nucleoside transporters (ENTs), concentrative nucleoside transporters (CNTs), and organic anion transporter (OAT) 4 do not facilitate the placental transfer of linagliptin, alogliptin, sitagliptin, and vildagliptin. Vildagliptin had the lowest accumulation and permeability in placental cells among the four DPP-4 inhibitors. There might be carrier-mediated transmembrane transport of linagliptin, alogliptin, sitagliptin and vildagliptin, but ENTs, CNTs and OAT4 were not involved in. This study provides a basis for future research on their safety during pregnancy.

PMID 42443801
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PubMedChemistry & biodiversity2026-06-30

Structure-Based De Novo Design of Novel Dual DPP IV and PTP 1B Inhibitors (DDPI's).

Singh Yogesh Y, Thareja Suresh S

Inhibition of DPP IV and PTP 1B constitutes a legitimate approach in modulating glucose homeostasis, thereby representing a viable therapeutic strategy for managing T2DM. This study employed a novel structure-based de novo design approach for developing dual DPP IV and PTP 1B inhibitors (DDPI's) with synergistic anti-hyperglycemic potential to effectively manage T2DM. By leveraging high-resolution protein structures, a specialized ligand library was designed employing a de novo approach to perform virtual screening. Molecular docking studies revealed four promising lead candidates, that is, YS-3, YS-5, YS-14, and YS-15 (>-138.26 kcal/mol in DPP IV while >-150.29 kcal/mol in PTP1B), with higher binding affinities as compared to clinical standard inhibitors, Vildagliptin (-103.46 kcal/mol; DPP IV) and Ertiprotafib (-141.91 kcal/mol; PTP 1B). Further, molecular dynamics (MD) and MM-GBSA analyses were performed to comprehend the thermodynamic stability of these leads. Analysis of 100 ns trajectories, integrating depth-based PCA, FEL, and DSSP, enabled identification of key intermolecular contacts responsible for the dual inhibitory behavior. DFT-based electronic profiling and ADMET predictions confirmed the biological viability and drug-like properties. These findings provide a robust structural blueprint for DDPI's with improved affinity, along with a better understanding of the inhibitory mechanisms.

PMID 42378400
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PubMedScientific reports2026-06-26

Simple and cost-effective UV spectrophotometric platforms integrating advanced green and blue metrics for concurrent analysis of dapagliflozin and vildagliptin in diabetes therapy.

Darweish Eman E, Hashem Hisham A HA, Nasr Rawan R, Bahgat Eman A EA

The co-administration of dapagliflozin (DPF) and vildagliptin (VLT) in tablet dosage forms is a clinically established strategy for managing of type 2 diabetes mellitus and has demonstrated favorable therapeutic outcomes. Nevertheless, the simultaneous quantitative determination of both drugs remains challenging because of the severe overlap in their UV absorption spectra, with λmax values at 224 nm for DPF and 214 nm for VLT. In this study, novel eco-friendly UV spectrophotometric methods were developed and validated for the accurate determination of DPF and VLT in their combined pharmaceutical formulations. The proposed methods include Fourier deconvolution, mean centering, dual wavelength, and induced dual wavelength techniques, which allow precise, reliable, and sensitive analysis without the need for prior separation. These approaches are simple, minimize noise in ratio spectra, and require limited mathematical manipulation, thereby reducing analysis time. DPF and VLT showed linear responses over concentration ranges of 2-24 µg/mL and 10-100 µg/mL, respectively. The limits of detection ranged from 0.00486 to 0.7979 µg/mL for DPF and from 0.0185 to 0.8690 µg/mL for VLT. Method greenness was evaluated using Eco-scale, GAPI, MoGAPI, CaFRI, and blueness assessment, while CACI was applied to assess overall analytical performance. Statistical comparison between the methods showed no significant differences.

PMID 42350572
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PubMedACS pharmacology & translational science2026-06-18

Phosphatidylinositol-3-kinase/Protein Kinase B (PI3K/AKT) and Nucleotide-Binding Oligomerization Domain-like Receptor Family Pyrin Domain Containing 3 (NLRP3) Inflammasome Modulation Underlies the Neuroprotective Effects of Vildagliptin in a Rotenone-Induced Mouse Model of Parkinson's Disease.

Patel Dishank D, Soni Ritu R, Bhogal Inderjeet I, Roy Sudeep S et al.

Parkinson's disease (PD) is a chronic neurodegenerative disorder marked by the gradual loss of dopaminergic neurons. Mitochondrial impairment, neuroinflammation, oxidative stress, and abnormal aggregation of α-synuclein are the most prominent features of the pathology. Current therapeutic approaches lack disease-modifying abilities and render only symptomatic relief. It has been observed that increased risk of PD is somehow linked to type 2 diabetes mellitus, and these pathologies share some common signaling cascades. Hence, repurposing hypoglycemic agents targeting specific molecular signaling pathways that mediate α-synuclein aggregation and neuroinflammation can be an effective disease-modifying strategy for PD treatment. This study investigated the neuroprotective potential of the DPP-4 inhibitor, vildagliptin, in a mouse model of chemically induced PD. In silico analyses, including molecular docking as well as molecular dynamics simulation, demonstrate good binding affinity as well as stable interaction of vildagliptin with PI3K (4YKN) and NLRP3 (7ALV) proteins in comparison to other DPP-4 inhibitors (sitagliptin, saxagliptin, linagliptin, and alogliptin). In in vivo studies, it was observed that vildagliptin improved motor coordination, muscle strength, and cognitive abilities. Biochemical assays show a reduction in MDA and restoration of GSH, indicating alleviation of oxidative stress. Moreover, at the molecular level, vildagliptin upregulated neuroprotective markers like PI3K, AKT, CREB, BDNF, and TH and downregulated pathological and inflammatory markers like NLRP3, IL-1β, caspase-1, gasdermin D, and α-syn. Histopathological and immunohistochemistry studies also demonstrate preservation of dopaminergic neurons. These findings collectively suggest that vildagliptin rendered neuroprotection by PI3K/AKT activation and inhibition of NLRP3-mediated neuroinflammation and apoptosis. In conclusion, we can say that vildagliptin possesses definitive neuroprotective potential as a disease-modifying therapy that warrants further clinical exploration.

PMID 42312164
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PubMedCureus2026-06-15

Dipeptidyl Peptidase-4 Inhibitor-Associated Bullous Pemphigoid in an Elderly Woman With Type 2 Diabetes Mellitus: A Case Report.

Roa Alvarez Guillermo G, Shuchleib Cukiert Mario M, Hernández Altamirano Felix R FR, Berumen Glinz Cristina C et al.

Bullous pemphigoid (BP) is the most common autoimmune subepidermal blistering disease and predominantly affects older adults. In recent years, dipeptidyl peptidase-4 inhibitors (DPP-4i), widely prescribed for type 2 diabetes mellitus, have emerged as important pharmacologic triggers of BP. DPP-4 inhibitors as a class have been associated with BP, with the strongest evidence reported for vildagliptin, although cases involving linagliptin have also been documented. Linagliptin has also been increasingly recognized as a potential trigger of drug-associated disease. We report the case of an 81-year-old woman with long-standing type 2 diabetes mellitus treated with metformin and linagliptin who developed a generalized pruritic vesiculobullous eruption. Dermatologic examination demonstrated multiple tense bullae, erosions, crusted plaques, and post-inflammatory hyperpigmented lesions involving the trunk, extremities, and intertriginous regions. Histopathologic examination revealed a subepidermal blister with prominent eosinophilic infiltration. Direct immunofluorescence demonstrated linear C3 and IgG deposition along the basement membrane zone, while indirect immunofluorescence localized immunoreactants to the roof of the split, confirming the diagnosis of BP. The temporal association with linagliptin exposure and the absence of alternative triggers supported the diagnosis of DPP-4 inhibitor-associated BP. Linagliptin was discontinued, and treatment with prednisone was initiated, resulting in progressive improvement and complete cessation of new blister formation at follow-up. This case highlights the importance of recognizing medication-induced BP in older diabetic patients and reviews current evidence regarding the epidemiology, pathogenesis, clinical presentation, diagnosis, and management of DPP-4 inhibitor-associated BP.

PMID 42292723
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