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

PubMedToxicology mechanisms and methods2026-08-13

Remogliflozin attenuates thioacetamide-induced nephrotoxicity: association with Nrf2/HO-1, SIRT1/AMPK, and TLR4/NF-κB pathway modulation.

Qadri Marwa M, Almarghalani Daniyah A DA, Alarifi Abdulaziz A, Mohamed Bassim M S A BMSA et al.

Thioacetamide (TAA) induces renal injury via oxidative stress and inflammation. Remogliflozin (Remo), an SGLT2 inhibitor, was evaluated for potential renoprotection. Twenty-four male Wistar rats were assigned to control, TAA (100 mg/kg IP twice weekly), TAA + Remo 25 mg/kg, or TAA + Remo 50 mg/kg (oral daily). Outcomes included renal function, oxidative stress (GSH, SOD, MDA), antioxidant biomarkers (Nrf2, HO-1), inflammatory mediators (TLR4/NF-κB, TNF-α, IL-1β), metabolic/kinase biomarkers (SIRT1, AMPK, PI3K, AKT), and histopathology/immunohistochemistry (mTOR, MYD88, Nrf2). Remogliflozin was associated with lower serum creatinine, urea, and uric acid, with endpoint-specific differences between doses. Remo was associated with higher renal Nrf2, HO-1, SIRT1, and p-AMPK, and lower MDA, TLR4, NF-κB, TNF-α, IL-1β, PI3K, and AKT. Histopathology and IHC showed associations with reduced tissue injury, lower mTOR and MYD88 immunoreactivity, and increased Nrf2 staining. While the 50 mg/kg group showed changes in more markers, this does not establish uniform dose superiority or a formal dose-response relationship; at 25 mg/kg, effects differed among AMPK-related endpoints. Direct 25-versus-50 mg/kg comparisons were included in the Tukey-Kramer analysis for each endpoint. No pharmacokinetic measurements or formal dose-response analyses were performed. In this exploratory model, remogliflozin was associated with attenuation of TAA-induced renal injury and modulation of related biomarkers. Causal mechanisms remain to be confirmed by targeted intervention studies. Findings are limited to young male Wistar rats and should not be generalized to other populations or clinical settings. Remogliflozin warrants further preclinical investigation in TAA-associated renal injury.

PMID 42590936
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PubMedCureus2026-08-02

Probable Vildagliptin-Associated Acute Pancreatitis in a Patient With Well-Controlled Type 2 Diabetes Mellitus: A Case Report.

Aung Kyaw Zin KZ, Saw Naw Eh Law NEL

Drug-induced acute pancreatitis (DIAP) is rare, accounting for approximately 0.1%-5% of all cases, and the association between dipeptidyl peptidase-4 (DPP-4) inhibitors and pancreatitis remains controversial despite postmarketing safety signals. We report the case of a 46-year-old man with well-controlled type 2 diabetes mellitus who presented with severe epigastric pain radiating to the back after six months of therapy with vildagliptin and metformin. Laboratory evaluation showed markedly elevated serum amylase (1,220 U/L) and lipase (2,334 U/L), exceeding three times the upper limit of normal, while contrast-enhanced CT demonstrated acute interstitial edematous pancreatitis without evidence of necrosis. A systematic evaluation excluded common etiologies, including gallstones, alcohol use, hypertriglyceridemia, hypercalcemia, pancreaticobiliary obstruction, and structural abnormalities. Vildagliptin was promptly discontinued, and the patient received supportive management, with complete clinical recovery. The temporal association, exclusion of alternative causes, and improvement following drug withdrawal (positive dechallenge), together with a Naranjo Adverse Drug Reaction Probability Scale score of 7, support a probable drug-related association, with vildagliptin considered the most likely causative agent. Clinicians should remain aware of this rare but potential adverse effect when evaluating patients receiving DPP-4 inhibitors who present with acute pancreatitis after exclusion of more common causes.

PMID 42539684
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PubMedbioRxiv : the preprint server for biology2026-07-29

Effect of Immunosuppressive Drugs on Glucose-Stimulated Insulin Secretion: Concentration-Response Studies in Dynamic Perifusion Assays.

Chuang Sung-Ting ST, Watts Brandon B, Alcazar Oscar O, Buchwald Peter P

Immunosuppressive drugs, which are required to maintain graft function in transplant recipients, are associated with many unavoidable side effects including posttransplant diabetes mellitus (PTDM) that involves both peripheral insulin resistance and impairment of insulin secretion. To characterize in detail the concentration-dependency of the effect of well-known immunosuppressive drugs on glucose-stimulated insulin secretion (GSIS), we performed dynamic perifusion studies with human pancreatic islets. The effect on the time-profile of GSIS has been assessed over a wide concentration range for several clinically relevant immunomodulatory therapies, including small-molecule drugs (cyclosporine, sirolimus, tacrolimus, prednisolone acetate, and loteprednol etabonate) and biologics (abatacept and anti-CD40L), plus a prospective β-cell proliferation-inducing agent (harmine). While biologics showed no significant detrimental effects after one-day treatment even at relatively high concentrations (5 μM), all small-molecule drugs inhibited insulin secretion in a concentration-dependent manner, although glucocorticoids showed a distinct response pattern. Calcineurin and mTOR inhibitors preserved GSIS within their therapeutic ranges but progressively distorted its time-profile at higher concentrations and completely suppressed secretion at the highest levels. Cyclosporine exhibited the least, only about 35-fold, separation between its therapeutic target (C targ) and half-maximal GSIS inhibitory (IC50) concentrations. Glucocorticoids did not alter the shape of the time-profile but inhibited overall insulin secretion even at therapeutic levels. Their inhibitory effect only increased slowly with concentration and did not follow a classic sigmoid pattern that has unity Hill slope. These findings establish quantitative benchmarks for immunosuppressant-induced β-cell toxicity and provide a framework for optimizing immunosuppressive regimens to reduce the risk of PTDM.

PMID 42523260
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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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