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remogliflozin etabonate + vildagliptin (Remozen V / Remo V)

✓ Approved

Glenmark Pharmaceuticals Limited · DPP4 · 小分子

什么是 remogliflozin etabonate + vildagliptin？

remogliflozin etabonate + vildagliptin 是一种小分子，由Glenmark Pharmaceuticals Limited研发。该药已获批，用于治疗相关适应症，给药途径：Oral (PO)。

药物档案

商品名Remozen V, Remo V
公司Glenmark Pharmaceuticals Limited
药物类别小分子
分子靶点DPP4, SLC5A2
给药途径Oral (PO)
状态Approved
来源： ClinicalTrials.gov, Glenmark Pharmaceuticals Limited

作用机制

分子靶点

remogliflozin etabonate + vildagliptin 作用于 2 个分子靶点：

DPP4dipeptidyl peptidase 4 (CD26, DPPIV)
SLC5A2solute carrier family 5 member 2 (SGLT2)
需要更深入的分析？Noah AI 可解释复杂机制并与同类药物比较。

治疗适应症

remogliflozin etabonate + vildagliptin 针对 1 个适应症，涉及 1 个治疗领域。

治疗领域疾病/病症分期
Metabolism and nutrition disordersType 2 diabetes mellitus✓ Approved

相关研究文献

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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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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