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gemigliptin + dapagliflozin (LR 19051 / LR19051)

✓ Approved

LG Chem Ltd. · DPP4 · Small Molecule

What is gemigliptin + dapagliflozin?

gemigliptin + dapagliflozin is a small molecule developed by LG Chem Ltd.. It is approved for therapeutic indications via unknown.

Drug Profile

Brand NamesLR 19051, LR19051
CompanyLG Chem Ltd.
Drug ClassSmall Molecule
Molecular TargetDPP4, SLC5A2
RouteUnknown
StatusApproved
Sources: ClinicalTrials.gov, LG Chem Ltd.

Mechanism of Action

Molecular Targets

gemigliptin + dapagliflozin 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

gemigliptin + dapagliflozin is developed for 1 unique indication across 1 therapeutic area.

Therapeutic AreaConditionPhase
Metabolism and nutrition disordersType 2 diabetes mellitus✓ Approved

Related Research Articles

PubMedFrontiers in pharmacology2026-08-25

Metabolic remodeling and cardiac functional adaptation mediated by dapagliflozin in patients with acute heart failure: a retrospective cohort study.

Liu Feng F, Liu Xingjun X, He Yuping Y, Liu Guobin G et al.

Grounded in the "myocardial metabolic starvation" hypothesis, this study evaluated the pharmacological effects of dapagliflozin on serum metabolic profiles, ventricular remodeling, and cardiac function in patients hospitalized with acute heart failure (AHF), and explored the associations between circulating metabolic alterations, ventricular remodeling, and cardiac functional parameters. This single-center retrospective cohort study included 50 AHF patients (25 pairs) after 1:1 propensity score matching. The dapagliflozin group received standard care plus dapagliflozin 10 mg once daily for 6 months, while the control group received standard care alone. Changes in circulating metabolic parameters, including fasting blood glucose, lactic acid, free fatty acids, and ketone-related metabolites (β-hydroxybutyrate and acetoacetic acid), as well as glycolytic enzyme activity (pyruvate kinase), were compared between groups. Echocardiographic parameters, 6-min walk test (6 MWT) distance, B-type natriuretic peptide (BNP), and major adverse cardiovascular events (MACE) were also assessed. The dapagliflozin group showed greater reductions in circulating metabolic parameters, particularly fasting plasma glucose, free fatty acids, β-hydroxybutyrate, and acetoacetic acid, compared with controls (all P < 0.05). Left ventricular end-systolic diameter (37.29 ± 4.07 vs. 43.16 ± 4.41 mm) and end-diastolic diameter (45.17 ± 5.02 vs. 52.63 ± 6.20 mm) improved more markedly in the dapagliflozin group (both P < 0.001). left ventricular ejection fraction (48.36% ± 4.88% vs. 43.85% ± 4.90%, P = 0.002), BNP (116.45 ± 12.15 vs. 214.50 ± 20.36 pg mL-1, P < 0.001), and 6 MWT distance (385.56 ± 51.42 vs. 314.78 ± 42.17 m, P < 0.001) were also significantly superior in the dapagliflozin group. FFA reduction correlated positively with LVEDD reduction (r = 0.638, P < 0.001). Multiple regression analysis identified ΔFFA (β = -0.412, P = 0.008) and Δβ-HB (β = -0.385, P = 0.012) as independent predictors of ΔLVEF improvement. MACE incidence was numerically lower in the dapagliflozin group (8.0% vs. 32.0%, P = 0.076). In this small retrospective cohort, early in-hospital initiation of dapagliflozin was associated with favorable changes in circulating metabolic profiles, ventricular remodeling, and cardiac function in patients with acute heart failure. These findings suggest potential therapeutic benefits for ventricular remodeling, but require confirmation in larger prospective studies.

PMID 42638832
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PubMedFrontiers in genetics2026-08-24

A novel TRPC6 variant (c.131C>T, p.(Pro44Leu)) associated with focal segmental glomerulosclerosis: a case report.

Yang Fan F, Wang Xiaoqi X, Li Yan Y, Su Kaijie K et al.

Pathogenic variants in the transient receptor potential cation channel subfamily C member 6 (TRPC6) cause autosomal dominant focal segmental glomerulosclerosis (FSGS). We report a patient with early-onset FSGS carrying a novel TRPC6 variant not previously described. A 21-year-old Chinese male presented with proteinuria (3.17g/24h) and mild renal insufficiency (Cr 103 μmol/L). Renal biopsy confirmed FSGS, not otherwise specified (NOS). Genetic testing was initially declined due to cost concerns. He received losartan, dapagliflozin, strict salt restriction, and ambrisentan, achieving proteinuria reduction to 0.7g/24h without immunosuppression. Two years later, genetic testing identified a novel TRPC6 variant: c.131C>T p.(Pro44Leu), extremely rare in public databases and classified as a variant of uncertain significance. This is the first report of the TRPC6 p.Pro44Leu variant, expanding the variant spectrum of TRPC6-associated FSGS. The clinical decision to withhold immunosuppression was guided primarily by the patient's phenotype (young age, sub-nephrotic proteinuria, FSGS-NOS, and no secondary causes); the TRPC6 variant, although classified as a VUS, provided supportive evidence for a genetic etiology and reinforced this management approach. This case demonstrates that genetic testing can guide personalized management in young patients with FSGS, offering a practical framework for avoiding unnecessary treatment-related morbidity. This case also illustrates that cost and psychological barriers can delay genetic diagnosis and highlights the value of early supportive therapy in genetic FSGS.

PMID 42634699
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PubMedAmerican journal of translational research2026-08-22

Sacubitril/valsartan plus dapagliflozin improves cardiac function and reduces MACE and rehospitalization in hFrEF: a retrospective study.

Lu Nimin N, Li Jinzhao J, Li Tianzhu T

To evaluate the efficacy and safety of sacubitril/valsartan combined with dapagliflozin in heart failure with reduced ejection fraction (HFrEF). A retrospective study included 400 HFrEF patients (control group: sacubitril valsartan, n=200; observation group: add dapagliflozin, n=200) treated for 6 months. Cardiac function, NT-proBNP, 6MWT, MACE, readmission rate, and adverse reactions were compared. After treatment, LVEF increased in both groups (control: 32.5 ± 5.6% to 38.6 ± 6.2%; observation: 32.8 ± 5.4% to 42.3 ± 6.5%, P<0.05), with greater improvement observed in observation group. LVEDD, LVESD, and NT-proBNP decreased, while 6MWT increased in both groups (all P<0.05), with superior changes in observation group. Readmission rate (8.5% vs. 16.0%, P=0.022) and MACE (6.0% vs. 9.5%, P=0.040) were significantly lower in observation group. No significant differences in adverse reactions between groups (all P>0.05). Sacubitril valsartan combined with dapagliflozin improves cardiac function, reduces NT-proBNP, enhances exercise tolerance, and lowers readmission and MACE rates without increasing adverse reactions, offering better clinical net benefit than sacubitril valsartan alone.

PMID 42630636
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PubMedBiochemical pharmacology2026-08-21

Dapagliflozin attenuates cellular senescence and mitochondrial dysfunction in diabetic kidney disease: potential involvement of AMPK/Sirt3 signaling.

Tong Xin X, Wang Bin B, Gao Fenfei F, Zhong Ailing A et al.

Cellular senescence contributes to the pathology of diabetic kidney disease (DKD). Besides, mitochondrial dysfunction and cellular senescence are closely associated pathological processes that may influence one another during kidney injury progression. Dapagliflozin has demonstrated its renal protective benefits independent of the glucose-lowering effects, yet whether it acts via modulating cellular senescence is poorly understood. The design of our study is to explore the potential renal protective mechanism of dapagliflozin, focusing on cellular senescence and mitochondrial function. The streptozotocin-induced diabetic mice and high glucose-treated human renal tubular epithelial (HK-2) cells were used to achieve the purpose. We also employed Compound C and Sirt3 knockdown by small interfering RNA transfection to examine dapagliflozin's effect on AMPK/Sirt3 signalling pathway in HK-2 cell experiments. Dapagliflozin reduced the expression of renal senescence markers in both in vivo and in vitro experiments. Concurrently, dapagliflozin improved mitochondrial function, with evidence in mitochondrial membrane potential restoration, mitochondrial dynamics, and mitochondrial reactive oxygen species reduction, and lowered the levels of senescence-associated secretory phenotypes. Mechanistically, AMPK phosphorylation and Sirt3 expression level were attenuated by AMPK inhibitor compound C, which consequently attenuated dapagliflozin-mediated protective effects. Knockdown of Sirt3 in HK-2 cells substantially reduced dapagliflozin's improvements on mitochondrial function and its protective effects against cellular senescence, thereby reversing its alleviation of kidney function. Dapagliflozin treatment attenuated renal cellular senescence and improved mitochondrial function in DKD. Our findings support the involvement of AMPK/Sirt3 signaling in these renoprotective effects, as evidenced by the attenuation of dapagliflozin-mediated protection following AMPK inhibition and knockdown of Sirt3.

PMID 42628756
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PubMedWorld journal of nephrology2026-08-21

Efficacy of finerenone in reducing proteinuria in diabetic kidney disease on dapagliflozin and telmisartan: A disease-modifying approach.

Jose Antresa A, Kamrul-Hasan Abul Bashar Mohammad ABM, Fernandez Cornelius J CJ, Pappachan Joseph M JM

With the alarming rise in the global prevalence of the disease, type 2 diabetes mellitus (T2DM) has recently become the leading cause of chronic kidney disease (CKD) worldwide. Proteinuria, the earliest and common indicator of diabetic kidney disease (DKD), not only increases the risk of progression of CKD to end-stage renal disease (ESRD) but also multiplies the risk of cardiovascular (CV) disease in patients with diabetes. Medications such as angiotensin-converting enzyme inhibitors (ACEis), angiotensin II receptor blockers (ARBs), sodium-glucose cotransporter-2 inhibitors (SGLT-2is), and mineralocorticoid receptor antagonists (MRAs) have been shown to reduce proteinuria and therefore possess disease-modifying properties in patients with DKD. Clinical trials have demonstrated the efficacy of finerenone, a highly selective, non-steroidal MRA, in reducing renal and CV outcomes in patients with long-standing T2DM. The benefits of various SGLT-2is have also been observed in multiple studies. Therefore, a combination of these medications, with independent but complementary mechanisms of action, could provide superior benefits as add-on therapies to ACEis/ARBs rather than using either alone. This Opinion Review explores disease-modifying strategies in patients with DKD based on the most up-to-date evidence.

PMID 42626011
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PubMedWorld journal of nephrology2026-08-21

From kidney to liver: Are sodium-glucose cotransporter-2 inhibitors emerging as metabolic disease modifiers?

Mpisa Sydney S, Soldera Jonathan J

Sodium-glucose cotransporter-2 (SGLT2) inhibitors are increasingly recognized for benefits beyond glycaemic control, with established roles in renal and cardiovascular protection. In diabetic kidney disease (DKD), dapagliflozin-based strategies target persistent proteinuria, while emerging data suggest potential effects on hepatic outcomes, including hepatocellular carcinoma (HCC), in metabolic dysfunction-associated steatotic liver disease (MASLD). To evaluate the association between SGLT2 inhibitor use and HCC incidence in MASLD. A systematic review and meta-analysis was conducted following PRISMA 2020 guidelines and registered in PROSPERO (CRD1003646). Studies including adults with MASLD comparing SGLT2 inhibitors with other oral hypoglycemic agents and reporting HCC incidence were identified through searches of PubMed, EMBASE, Scopus, and Web of Science up to April 12, 2025. Pooled risk ratios (RRs) were calculated using a random-effects model, and heterogeneity was assessed using the I 2 statistic. Three retrospective cohort studies comprising 352890 individuals with MASLD were included. SGLT2 inhibitor use was associated with a significantly lower risk of HCC (RR = 0.60, 95%CI: 0.52-0.70; P < 0.0001), corresponding to an approximate 40% relative risk reduction, with low heterogeneity (I 2 = 14.1%). Sensitivity analyses yielded consistent results. SGLT2 inhibitor use is associated with a reduced incidence of HCC in MASLD, although findings are derived from observational data. These results, together with established renal and cardiovascular benefits, support a broader role for SGLT2 inhibitors as modifiers of metabolic disease across organ systems.

PMID 42626005
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