Drug Database
GE

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

PubMedNaunyn-Schmiedeberg's archives of pharmacology2026-10-20

Anti-inflammatory versus metabolic therapy in MASLD: a randomized clinical trial of aspirin and dapagliflozin using fibroscan outcomes.

Hamed Eman Mostafa EM, Hamza Eman E, Al-Dhelaan Reham A RA, Alsulami Fahad T FT et al.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a major hepatic consequence of metabolic dysfunction, yet evidence-based pharmacologic options remain limited. Repurposing widely available agents with metabolic and anti-inflammatory actions may offer a clinically meaningful benefit. To compare the effects of aspirin and dapagliflozin on hepatic steatosis, fibrosis, liver enzymes, and lipid profile in patients with MASLD. In this prospective randomized interventional study, 80 adults with confirmed MASLD were allocated (1:1) to aspirin 100 mg once daily or dapagliflozin 10 mg once daily for 6 months (n = 40 per group). Baseline and 6-month measurements included alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), triglycerides, high-density lipoprotein cholesterol (HDL-C), total cholesterol, and FibroScan-derived parameters, including controlled attenuation parameter (CAP; dB/m), which quantifies hepatic steatosis, and liver stiffness measurement (LSM; kPa), a surrogate marker of liver fibrosis. The primary endpoints included the between-group differences in changes in LSM, CAP, liver enzymes, and lipid profile from baseline to 6 months. Ethics approval was obtained (FMBSUREC/04032025). The trial was registered at ClinicalTrials.gov (NCT07338331) on 20 Dec 2025. Dapagliflozin significantly improved hepatic steatosis, reflected by lower CAP values compared to aspirin (260.35 ± 20.78 vs 271.48 ± 12.58 dB/m; p = 0.005), and reduced total cholesterol levels (138.87 ± 54.70 vs 192.48 ± 79.46 mg/dL; p = 0.003). In contrast, aspirin demonstrated a greater reduction in liver stiffness (LSM) (6.15 ± 2.55 vs 8.58 ± 4.13 kPa; p = 0.002) and alanine aminotransferase (ALT) percentage change (- 44.54% vs - 17.84%; p = 0.025). Other biochemical parameters showed no statistically significant between-group differences (all p > 0.05). Aspirin and dapagliflozin exert distinct and potentially complementary effects in MASLD, with dapagliflozin preferentially improving hepatic steatosis and aspirin showing a greater impact on fibrosis-related parameters. These findings support a dual-pathway therapeutic model targeting steatosis and fibrosis and underscore the need for larger trials evaluating combined strategies and histological outcomes.

PMID 42900372
Read full article →
PubMedAnatolian journal of cardiology2026-10-20

Early Changes in Left Atrial Mechanics During Sodium-Glucose Cotransporter-2 Inhibitor Therapy in Heart Failure with Preserved Ejection Fraction.

Altun Selen Cansu SC, Özyüncü Nil N, Akbulut Koyuncu İrem Müge İM, Tan Türkan Seda TS

Conventional echocardiographic improvements after sodium-glucose cotransporter-2 (SGLT2) inhibitor therapy have been reported in heart failure with preserved ejection fraction (HFpEF), but data on novel composite indices of atrial mechanics, particularly the left atrial (LA) stiffness index and the left atrioventricular coupling index (LACI), remain poorly characterized. The authors evaluated early changes in conventional diastolic parameters and atrial mechanics following initiation of SGLT2 inhibitor therapy. In this prospective, single-center observational cohort study, patients with HFpEF in sinus rhythm who were naive to SGLT2 inhibitors received empagliflozin or dapagliflozin. Clinical assessment, laboratory testing, and comprehensive echocardiography were performed at baseline and after 3 months. Echocardiographic evaluation included LA reservoir and pump strain, the LA stiffness index (E/e'/LA reservoir strain), and LACI (minimum LA volume/LV end-diastolic volume ×100). Fifty patients completed follow-up (70% women; mean age, 63.9 ± 8.1 years). New York Health Association functional class improved and N-terminal pro-brain natriuretic peptide levels decreased significantly (347 [134.8-524.8] vs. 257 [161.3-427.5] pg/mL; P = .007). Left atrial volume index and E/e' decreased significantly (34.6 ± 5.5 to 32.6 ± 5.7 mL/m2 and 12.1 ± 3.2 to 9.8 ± 2.8, respectively; both P < .001). Left atrial reservoir and pump strain increased, whereas the LA stiffness index and LACI decreased significantly (all P < .001). In this prospective observational cohort of patients with HFpEF, initiation of SGLT2 inhibitor therapy was associated with early changes in conventional diastolic parameters and LA mechanics. Composite atrial indices, particularly the LA stiffness index and LACI, changed in parallel with established clinical and echocardiographic markers, suggesting that they may provide complementary information for monitoring early atrial remodeling during SGLT2 inhibitor therapy.

PMID 42897925
Read full article →
PubMedRevista medica de Chile2026-10-20

Effectiveness of Weekly Semaglutide Treatment (0.5 or 1 mg) in Chilean Patients with Type 2 Diabetes Mellitus.

Estica Marcos M, Godoy Gonzalo G, Vargas Cecilia C, Elgueta Karina K et al.

Semaglutide is approved in Chile for the management of type 2 diabetes mellitus (T2DM), although it is generally not available in the public health system. Generating local evidence may aid in its incorporation into national guidelines and reduce the therapeutic gap with international standards. To evaluate the effectiveness and safety of adding weekly semaglutide to the standard treatment for T2DM in the public health system. A phase 4, multicenter, interventional study evaluated the weekly addition of 0.5 or 1 mg of subcutaneous semaglutide over 24 weeks, followed by a 5-week post-treatment monitoring period. n=104 (79.8% women; age: 58.3±9.3 years; 44.2% over 60 years of age; 35.6% with ≥1 complication of T2DM). Common comorbidities: hypertension: 71.2%; obesity: 71.2%; dyslipidemia: 51.9%. Most commonly used baseline treatments: metformin, 96.2%; NPH insulin, 65.4%; empagliflozin, 46.2%; regular insulin, 27.9%; insulin glargine, 22.1%; dapagliflozin, 21.2%. At 24 weeks, a reduction in glycosylated hemoglobin (HbA1c: 8.6±0.7% to 7±1%, difference: -1.6%), fasting blood glucose (160.3±49.3 to 133.7±54.8 mg/dL, difference: -26.2 mg/dL), and weight (89.3±20.2 to 85.3±20.4 kg; difference: -4 kg) were confirmed. Participants with HbA1c <7% increased from 0% to 56.4%. Thirty-one percent of patients receiving basal insulin reduced their dose (median: 6 IU). Gastrointestinal adverse events were the most frequent, consistent with the drug's safety profile. In people with inadequately controlled T2DM in the real world, the addition of a weekly dose of semaglutide was associated with improvement in HbA1c, fasting blood glucose, and weight, and a reduction in insulin dose, with an adequate safety profile. These results provide local evidence on the efficacy of semaglutide in improving various cardio-renal-metabolic risk factors in people with T2DM.

PMID 42899606
Read full article →
PubMedJournal of biochemical and molecular toxicology2026-10-18

Pharmacological Modulation of Catecholaminergic Brain Injury by Dapagliflozin and Its Nanovesicular Formulation in an Isoproterenol Model.

Bhat Faisal Ashraf FA, Haque Syed Ehtaishamul SE, Aqil Mohammed M, Akhtar Mohd M et al.

Sustained β-adrenergic stimulation represents a pharmacologically relevant stressor capable of inducing systemic oxidative and inflammatory injury that extends to the central nervous system. Isoproterenol (ISO), a synthetic catecholamine, is widely used to model catecholaminergic injury in experimental settings. Dapagliflozin, a sodium-glucose cotransporter-2 (SGLT2) inhibitor, exhibits pleiotropic antioxidant and anti-inflammatory properties; however, its effects on catecholamine-induced brain injury remain poorly defined. In the present study, we investigated the pharmacological effects of dapagliflozin and a bile salt-stabilized dapagliflozin-loaded nanovesicular formulation in an ISO-induced model of catecholaminergic brain injury in rats. ISO administration resulted in marked oxidative imbalance, neuroinflammatory activation, behavioral dysfunction, and structural alterations in hippocampal and cortical regions. These changes were accompanied by reduced expression of stress-responsive and neurotrophic proteins, including SIRT6, TRAP1, and BDNF, along with enhanced astroglial activation as indicated by increased GFAP immunoreactivity. Treatment with dapagliflozin attenuated these molecular, cellular, and functional alterations, while the nanovesicular formulation produced a more pronounced improvement of redox balance, suppression of inflammatory responses, normalization of protein expression, and preservation of neuronal architecture and behavior. Collectively, these findings demonstrate that dapagliflozin mitigates catecholaminergic brain injury through attenuation of oxidative and inflammatory stress, with enhanced efficacy achieved via formulation-assisted drug delivery, without implying a distinct pharmacodynamic mechanism.

PMID 42893416
Read full article →
PubMedLife sciences2026-10-18

Dapagliflozin alleviates CYH33-induced hyperglycemia and preserves antitumor immunity against ovarian cancer in type 1 diabetic mice.

Sun Jiaqi J, Xu Lan L, Qu Hui H, Zhang Xi X et al.

PI3K is frequently hyperactivated in ovarian cancer and has emerged as a promising therapeutic target. CYH33 is a novel PI3Kα-selective inhibitor that has been approved in Japan for the treatment of ovarian clear cell carcinoma harboring PIK3CA mutations. However, its on-target adverse effect of hyperglycemia limits its clinical application, particularly in patients susceptible to diabetes, underscoring the urgent need to optimize therapeutic strategies to improve both safety and efficacy. In this study, we employed an ID8 syngeneic murine ovarian cancer model and demonstrated that CYH33 significantly inhibited tumor growth with a modest effect on glucose homeostasis. We then established mouse models of type 1 (T1D) and type 2 diabetes (T2D) to expose hyperglycemia induced by PI3K inhibition and identified that dapagliflozin effectively alleviated CYH33-induced hyperglycemia while preserving its antitumor activity in T1D mice. Mechanistically, the combination of CYH33 and dapagliflozin may improve the immunosuppressive tumor microenvironment in T1D mice, as evidenced by upregulation gene sets involved in interferon-α and interferon-γ response, as well as significantly enhanced infiltration of CD8+ T-cell in ID8 tumors. Furthermore, this combination synergized with anti-PD-1 antibody to further enhance antitumor efficacy. These findings provide a potential strategy for optimizing the clinical use of PI3K inhibitors and shed light on metabolic interventions to modulate tumor immune microenvironment.

PMID 42892524
Read full article →
PubMedEuropean heart journal. Cardiovascular pharmacotherapy2026-10-17

Dapagliflozin in phenotypically stratified HFpEF without myocardial fibrosis: the STADIA-HFpEF randomized crossover trial.

Scheffer Mariëlle M, van Maarschalkerwaart Willemijn W, Dong Chaohui C, Landzaat Jochem W D JWD et al.

Heart failure with preserved ejection fraction(HFpEF) is characterized by increased diastolic left ventricular(LV) stiffness resulting from variable contributions of myocardial extracellular matrix(ECM) remodeling and titin-based cardiomyocyte stiffness. Sodium-glucose cotransporter-2 inhibitors(SGLT2i) improved cardiomyocyte distensibility, inflammation, and oxidative stress in experimental and human HFpEF myocardium. We investigated whether dapagliflozin improves LV distensibility in phenotypically stratified HFpEF patients without significant myocardial fibrosis. STADIA-HFpEF was a 34-week, randomized, double-blind, placebo-controlled crossover trial. HFpEF patients underwent multi-level phenotypic stratification including cardiac magnetic resonance imaging to exclude structural cardiomyopathies and significant myocardial ECM remodeling. Participants were randomized to dapagliflozin 10 mg or placebo for two 13-week treatment periods separated by an 8-week washout.The co-primary endpoints were changes in E/e'/LV end-diastolic volume index(LVEDVi) and mean LV e', reflecting LV distensibility and relaxation. Secondary endpoints included echocardiographic variables, quality of life, 6-minute walk distance, and inflammatory biomarkers. Between February 2020 and October 2022, 32 patients were randomized and 29 completed the study protocol. Median age was 73(68-76) years including 28 women(88%). Dapagliflozin did not significantly modify E/e'/LVEDVi compared with placebo 0.24 (0.20-0.32) to 0.26 (0.22-0.34) vs. 0.23 (0.22-0.29) to 0.25 (0.21-0.31); p=0.370 nor did it change mean LV e' 6.2 (5.6-7.5) to 6.2 (5.7-7.1) vs. 6.6 (5.6-7.4) to 6.7 (5.4-7.5); p=0.448. Most secondary outcomes were neutral. However, an isolated improvement in LA conduit strain and numerical reductions in inflammatory biomarkers were observed during dapagliflozin treatment. In phenotypically stratified HFpEF patients without significant myocardial fibrosis, dapagliflozin did not improve LV distensibility or relaxation. An isolated improvement in LA conduit strain and numerical reductions in inflammatory biomarkers were observed; however, these exploratory findings require confirmation in larger studies.

PMID 42888932
Read full article →

+4378 more articles available with a free account

Sign up free to view all articles →

Ask about gemigliptin + dapagliflozin