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

PubMedDermatology (Basel, Switzerland)2026-11-06

Dipeptidyl Peptidase-4 Inhibitors and Bullous Pemphigoid: A Danish Nationwide Case-Control Study.

Ahle Erichsen Philip P, Heerfordt Ida M IM, Huan Olsen Rasmus R, Mogensen Mette M et al.

Anti-diabetic dipeptidyl peptidase-4 inhibitors (DPP-4i) are associated with an increased risk of bullous pemphigoid (BP), but Danish population-based data, including product specific estimates, are lacking. We conducted a nationwide matched case-control study in Denmark of incident BP cases diagnosed between 2007 and 2024. BP cases were matched 1:100 to population controls using risk set sampling based on age, sex, and index date. DPP-4i exposure was defined as at least one redeemed prescription before the index date (ever use) or during the preceding three months (current use). In a specificity analysis, we compared DPP-4i users and users of other type 2 antidiabetics without DPP-4i use with non-users of type 2 diabetes medications. Odds ratios (ORs) with 95% CIs were estimated using conditional logistic regression. We identified 2,497 incident BP cases and 249,700 controls (median age 78 years). DPP-4i exposure was more common among BP cases for both ever use (OR: 3.81, 95% CI: 3.31-4.40) and current use (OR: 5.59, 95% CI: 4.70-6.63). For current use, the highest odds ratios were observed for vildagliptin (OR: 10.82, 95% CI: 6.73-17.41) and linagliptin (OR: 9.86, 95% CI: 7.33-13.25), whereas the estimate for sitagliptin was lower (OR: 2.46, 95% CI: 1.65-3.66). In the specificity analysis, other antidiabetic therapies did not show a similarly increased risk of BP. In the Danish population there was a strong association between DPP-4i use and incident BP. This was most pronounced for vildagliptin and linagliptin while the signal was weaker for sitagliptin.

PMID 42993181
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PubMedSAR and QSAR in environmental research2026-10-29

Integrating QSAR, molecular dynamics and MM-GBSA to re-rank natural product-derived DPP4 candidates from virtual screening.

Aktaş E E

Dipeptidyl peptidase-4 (DPP4) is a validated target for type 2 diabetes, and virtual screening of natural product libraries is a common route to new chemotypes. We asked whether a top docking rank survives independent scrutiny. From COCONUT, 85,600 compounds were filtered to 32,008 and docked against DPP4; 873 outscored the crystallographic ligand N7F (-10.01 kcal/mol), with Lig_771 first at -12.5 kcal/mol. Across four 300 ns simulations (two replicas per complex, 1.2 μs) Lig_771 stayed bound but never reproduced the gliptin recognition motif: the control held its salt bridges to Glu205 and Glu206 in over 93% of frames, whereas Lig_771 formed no persistent hydrogen bond to these residues and sampled two distinct poses. MM-GBSA gave -15.6 kcal/mol for Lig_771 against -23.9 for the control. A QSAR model built on 4327 measured DPP4 inhibitors (scaffold-based external R2 = 0.415; random split 0.669) predicted a pIC50 of 6.59 for Lig_771, below linagliptin (8.29), sitagliptin (7.39) and vildagliptin (6.96). None of the three analyses corroborated the docking ranking. The study is computational and does not establish DPP4 inhibition. Lig_771 occupies largely unexplored chemical space (maximum Tanimoto similarity 0.316) and merits testing, but selecting hits on docking score alone would have been misleading here.

PMID 42954798
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PubMedJournal of molecular histology2026-10-21

Effects of topical vildagliptin versus triamcinolone acetonide on experimentally induced hypertrophic scars in a rabbit model.

Nasser Zaynab Ali ZA, Jaafar Farrah Rasool FR

The present study aimed to evaluate the effects of topical vildagliptin on experimentally induced hypertrophic scars (HTSs) in a rabbit model. A total of 40 healthy male albino rabbits were randomly assigned to five groups (n = 8): healthy control (CTRL), untreated induced HTS model (HTS model), vehicle-received (VEH), 0.1% triamcinolone acetonide-treated (TAC), and 3% vildagliptin-treated (VIL). On day 0, four full-thickness wounds extending to the cartilage were created on the ventral surface of each rabbit ear using an 8-mm biopsy punch. On day 30, topical treatment was initiated on the newly formed scars and continued twice daily for 21 days. Samples were collected on day 51 post-wounding. Outcome measures included molecular quantification of collagen type 1 (Col I), collagen type 3 (Col III), transforming growth factor-beta 1 (TGF-β1), interleukin 6 (IL-6), histopathological examination, and alpha-smooth muscle actin (α-SMA) immunoreactivity. Vildagliptin significantly reduced Col I, Col III, TGF-β1, and IL-6 compared with the HTS model group (p < 0.001). Histopathological analysis revealed a marked improvement in scar architecture, as evidenced by lower histopathological scores and a reduced scar elevation index. Masson's trichrome (MT) staining demonstrated a significant reduction in collagen deposition, accompanied by partial restoration of normal collagen fiber organization. Immunohistochemical analysis revealed no significant change in α-SMA immunoreactivity. This more likely reflects a potential incomplete suppression of myofibroblasts. Overall, these findings suggest that topical vildagliptin may represent a promising therapeutic approach for the treatment of HTSs.

PMID 42902087
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PubMedFrontiers in immunology2026-10-20

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, where they were also cytotoxic. 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 without affecting islet viability. 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 42898311
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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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