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gemigliptin + dapagliflozin (LR 19051 / LR19051)

✓ Approved

LG Chem Ltd. · DPP4 · 小分子

什么是 gemigliptin + dapagliflozin？

gemigliptin + dapagliflozin 是一种小分子，由LG Chem Ltd.研发。该药已获批，用于治疗相关适应症，给药途径：Unknown。

药物档案

商品名LR 19051, LR19051
公司LG Chem Ltd.
药物类别小分子
分子靶点DPP4, SLC5A2
给药途径Unknown
状态Approved
来源： ClinicalTrials.gov, LG Chem Ltd.

作用机制

分子靶点

gemigliptin + dapagliflozin 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

gemigliptin + dapagliflozin 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

PubMedCase reports in critical care2026-10-26

Euglycemic SGLT2 Inhibitor-Associated Ketoacidosis in a Nondiabetic Patient: A Case Report.

Zinnato Carmelo C, Roatta Teresa T, Berta Giacomo G, Penso Roberto R et al.

We present the case of a 62-year-old nondiabetic woman receiving dapagliflozin for dilated cardiomyopathy presenting to the emergency department with severe hypoxemic respiratory failure because of suspected cardiogenic pulmonary edema. Despite treatment, she remained symptomatic and required intubation and intensive care admission. After intubation, high-anion-gap metabolic acidosis was unmasked. After exclusion of other common causes, SGLT2 inhibitor-associated ketoacidosis due to dapagliflozin was suspected. Marked ketonuria confirmed the diagnosis despite the absence of hyperglycemia. Dapagliflozin was discontinued, and intravenous insulin, glucose infusion, and early enteral nutrition were initiated. Metabolic acidosis resolved completely within 24 h. The patient was successfully extubated and discharged from the intensive care unit 48 h later. SGLT2 inhibitor-associated ketoacidosis should be considered in patients receiving sodium-glucose cotransporter-2 inhibitors who develop otherwise unexplained high-anion-gap metabolic acidosis, irrespective of diabetic status or blood glucose concentration. Fasting and acute illness are relevant precipitating factors; prompt drug withdrawal, carbohydrate administration, insulin therapy, and nutritional support can lead to rapid resolution.

PMID 42928725
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PubMedBritish journal of clinical pharmacology2026-10-26

Cardiovascular outcomes of SGLT2 inhibitors across the spectrum of myocardial infarction: A systematic review and meta-analysis.

Elazab Ahmed A, Elbataa Ahmed A, Mansour Ahmed A, Abouzid Mohamed M et al.

Sodium-glucose cotransporter-2 inhibitors (SGLT2i) help in heart failure (HF), but their benefit after acute myocardial infarction is unclear. This meta-analysis assesses their impact on mortality and heart failure hospitalization post-acute myocardial infarction (AMI) and identifies which patients benefit most. Four databases were searched through August 2025 for randomized controlled trials (RCTs) and matched studies comparing SGLT2i with control post-AMI. all-cause death and hospitalization for heart failure (HHF); secondary: major adverse cardiovascular events (MACE), cardiovascular (CV) death, stroke and recurrent myocardial infarction (MI). Subgroups and meta-regression examined timing, diabetes, follow-up, design, SGLT2i type and baseline HF/diabetes. Fifteen studies including 117 096 patients (58 613 SGLT2i vs. 58 483 control) were included. A total of 117 096 patients contributed to the all-cause mortality analysis (OR 0.78, 95% CI 0.67-0.90), whereas 116 992 patients across 14 studies contributed to the HHF analysis (OR 0.74, 95% CI 0.63-0.88). All-cause mortality was significantly lower in PSM observational studies (OR 0.64, 95% CI 0.61-0.67), whereas the reduction did not reach statistical significance in RCTs (OR 0.87, 95% CI 0.76-1.01), with a significant interaction by study design. HHF reduction occurred with both early and delayed initiation; dapagliflozin and empagliflozin were similarly effective. MACE was significantly lower with SGLT2i, but CV death, recurrent MI and stroke did not differ. Baseline HF or diabetes showed no association with primary outcomes. SGLT2i reduced HHF after MI, but this benefit should be interpreted cautiously because of small-study effects and possible publication bias. The all-cause mortality benefit is driven by observational studies; RCTs show a favourable but nonsignificant trend.

PMID 42928993
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PubMedRomanian journal of internal medicine = Revue roumaine de medecine interne2026-10-25

Same Class, Different Risk? Dapagliflozin versus Empagliflozin and Genitourinary Safety in Heart Failure with Preserved Ejection Fraction: A Retrospective Comparative Cohort Study.

Danau Razvan Alexandru RA, Munteanu Madalina Andreea MA, Muraru Minerva M, Nicolae Camelia C et al.

Sodium-glucose cotransporter 2 inhibitors are guideline-directed therapy for heart failure with preserved ejection fraction (HFpEF), but comparative genitourinary safety data for dapagliflozin and empagliflozin in HFpEF-treated populations remain limited. To compare 6-month symptomatic urinary tract infection (UTI), asymptomatic bacteriuria, and other genitourinary adverse events among patients newly initiated on dapagliflozin or empagliflozin for HFpEF. This retrospective, single-centre comparative cohort study included 239 adults with physician-documented HFpEF retained after a requirement for at least 6 months of continuous follow-up: 113 received dapagliflozin 10 mg once daily and 126 received empagliflozin 10 mg once daily. The original outcome of any documented bacteriuria/UTI was separated into symptomatic UTI and asymptomatic bacteriuria. Risk differences and 95% confidence intervals were calculated; a multivariable logistic model of the original documented bacteriuria/UTI composite adjusted for age, sex, and baseline estimated glomerular filtration rate (eGFR). Any documented bacteriuria/UTI occurred in 21/113 (18.6%) dapagliflozin-treated participants and 25/126 (19.8%) empagliflozin-treated participants. Symptomatic UTI occurred in 4/113 (3.5%) and 5/126 (4.0%), respectively; 17/113 (15.0%) and 20/126 (15.9%) had documented asymptomatic bacteriuria. The risk difference for the composite, calculated as empagliflozin minus dapagliflozin, was 1.3 percentage points (95% CI -8.9 to 11.2). The adjusted odds ratio was 1.62 (95% CI 0.76-3.45; p = 0.208). Other genitourinary events were uncommon and estimates were imprecise. No statistically detectable between-group difference was found in symptomatic UTI, asymptomatic bacteriuria, or the original composite outcome. Confidence intervals were wide and compatible with clinically meaningful differences in either direction. These exploratory findings require confirmation in prospective multicentre studies with standardized culture ascertainment and complete follow-up.

PMID 42927657
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PubMedAmerican journal of translational research2026-10-25

SGLT-2 inhibitor dapagliflozin improves left ventricular diastolic function and reduces circulating inflammatory markers in HFpEF patients: a retrospective cohort study.

Ye Jian-Feng JF, Zhang Jian J, Wang Xu X, Yang Guang-Quan GQ et al.

This study sought to evaluate the efficacy of sodium-glucose cotransporter 2 (SGLT-2) inhibitor Dapagliflozin in ameliorating left ventricular diastolic function (LVDF) and attenuating systemic inflammatory biomarkers in patients with heart failure with preserved ejection fraction (HFpEF). A total of 114 patients diagnosed with HFpEF were retrospectively enrolled and allocated into either the SGLT-2 inhibitor group (Dapagliflozin combined with standard guideline-directed therapy; n = 58) or the Control group (standard guideline-directed therapy alone; n = 56). Echocardiographic parameters at baseline and 6-month follow-up were measured, including early diastolic transmitral flow velocity/early diastolic mitral annular velocity ratio (E/e') and left atrial volume index (LAVI). Circulating inflammatory markers comprising high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α) were examined. In addition, N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels and Minnesota Living with Heart Failure Questionnaire (MLHFQ) scores were collected for functional and symptomatic assessments. After six months of treatment, the SGLT-2 inhibitor group exhibited significant improvements in cardiac diastolic parameters. E/e' ratio decreased significantly from 14.8 ± 3.2 to 12.1 ± 2.7 (P < 0.001), and LAVI decreased from 38.6 ± 8.4 to 34.2 ± 7.1 mL/m2 (P = 0.003). Consistently, systemic inflammation was markedly alleviated. hs-CRP decreased from 4.82 ± 1.73 to 2.94 ± 1.28 mg/L (P < 0.001), IL-6 decreased from 8.46 ± 2.91 to 5.73 ± 2.14 pg/mL (P = 0.002), and TNF-α decreased from 12.8 ± 4.6 to 9.4 ± 3.8 pg/mL (P = 0.011). Moreover, NT-proBNP levels in the SGLT-2 inhibitor group exhibited a substantial 28.4% reduction, which was significantly greater than the 8.7% reduction observed in the Control group (P = 0.004). There was also a striking reduction in MLHFQ scores in the SGLT-2 inhibitor group (average reduction: -8.6 ± 4.2 points, P < 0.001), demonstrating significant symptomatic improvement. SGLT-2 inhibitor Dapagliflozin effectively improved LVDF and reduced systemic inflammatory burden in patients with HFpEF. These findings support the role of Dapagliflozin as a promising disease-modifying therapeutic agent for HFpEF.

PMID 42923614
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PubMedEchocardiography (Mount Kisco, N.Y.)2026-10-25

DAPAgliflozin-Related Cardiac REverse Remodeling by 2D and 3D Echocardiography in OptiMally Treated HFrEF Patients: The DAPA-REM Study.

Amelotti Nicola N, Mantegazza Valentina V, Garlaschè Anna A, Salvioni Elisabetta E et al.

Sodium-glucose cotransporter-2 inhibitors promote cardiac reverse remodeling in heart failure (HF), yet data integrating two-dimensional and three-dimensional echocardiography (2DE and 3DE, respectively) in optimally treated HFrEF populations are limited. This study aimed to evaluate heart chambers size and function by 2D/3DE after dapagliflozin initiation, and to explore whether baseline estimated glomerular filtration rate (eGFR) or myocardial fibrosis on cardiac magnetic resonance (CMR) influence reverse remodeling. Seventy-five patients with LVEF ≤40% on guideline-directed therapy were prospectively enrolled. Echocardiographic and clinical data were collected at baseline and 6-month follow-up (6MFU) after introduction of dapagliflozin 10 mg daily. Sub-analyses were performed according to eGFR (<45 vs. ≥45 mL/min/1.73 m2) and extent of late gadolinium enhancement (LGE) on CMR. After 6MFU, left ventricular (LV) end-diastolic and end-systolic volumes reduced, and LVEF increased as assessed by both 2DE (respectively: 88[72-122] vs. 92[79-122]mL/m2, 58[42-80] vs. 57[48-88]mL/m2, 36.6±8.8 vs. 34.5±7.7%; p < 0.001) and 3DE (respectively: 100[79-140] vs. 108[90-136]mL/m2, 64[46-82] vs. 69[55-93]mL/m2, 37.4±8.7 vs. 34.4±7.9%; p < 0.001). No significant association between eGFR and the magnitude of LV reverse remodeling was detected, while CMR analyses suggested a possible inverse correlation between LGE burden and improvement in 2D LVEF. LV diastolic function improved (grade≥2 diastolic dysfunction: 4.7% vs. 18.7%; p = 0.015), along with systolic pulmonary artery pressure (25[23-29] vs. 27[24-29]mmHg; p = 0.037). In optimally treated HFrEF patients, LV size and systolic and diastolic function significantly improved during the 6MFU following dapagliflozin initiation. No significant differences in the magnitude of LV reverse remodeling were detected according to eGFR or LGE burden. NCT05770167. What is already know Sodium-glucose cotransporter-2 inhibitors improve clinical outcomes in heart failure across a wide spectrum of left ventricular ejection fraction, with evidence of cardiac reverse remodeling. Dapagliflozin has been shown to reduce left ventricular and left atrial volumes, improve biventricular systolic function, and lower filling pressures, independent of diabetes status and baseline renal function. What this study adds In clinically stable HFrEF patients on fully optimized guideline-directed medical therapy, significant left ventricular reverse remodeling and improvement in systolic and diastolic function within 6 months after introduction of dapagliflozin was observed, as consistently demonstrated by both 2D and 3D echocardiography. A proportion of patients with baseline LVEF ≤35% crossed the 35% threshold at 6-month follow-up. This observation is hypothesis-generating and may warrant further investigation regarding the potential implications of reverse remodeling for subsequent device-therapy assessment. Exploratory analyses did not detect a statistically significant association between baseline renal function and the magnitude of cardiac reverse remodeling. In the CMR subgroup, preliminary data suggest that the extent of LGE burden might inversely correlate with improvement in 2D LVEF.

PMID 42927625
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PubMedCureus2026-10-25

Graves' Disease and the Heart: Severe Reversible Left Ventricular Systolic Dysfunction With Apical Thrombus in a Young Woman With Relapsed Thyrotoxicosis.

Joseph Jomol J, Sarkar Chandranath C, Boda Sai Aditya SA

Graves' disease is a common cause of autoimmune hyperthyroidism and is frequently associated with cardiovascular manifestations, including sinus tachycardia, atrial fibrillation and high-output heart failure. Severe left ventricular (LV) systolic dysfunction complicated by LV thrombus is an uncommon presentation. Recognition may be challenging when concurrent illness and antithyroid treatment complicate the interpretation of thyroid function tests. A 27-year-old woman with Graves' disease diagnosed in 2021 presented in March 2025 with progressive dyspnoea, orthopnoea, profound lethargy, jaundice and generalised oedema. Following relapse in September 2024, carbimazole had been recommenced, but adherence was suboptimal, and heart failure symptoms had developed over several months. Examination revealed sinus tachycardia, diffuse goitre, exophthalmos, hepatomegaly and marked anasarca. Community-acquired pneumonia was also diagnosed. Admission free thyroxine was 8.5 pmol/L (reference range: 8.9-17.3), thyroid-stimulating hormone (TSH) was 0.48 mIU/L (0.30-4.40), and free triiodothyronine was unavailable. This biochemical pattern was interpreted in the clinical context as consistent with non-thyroidal illness. N-terminal pro-B-type natriuretic peptide (NT-proBNP) was elevated at 9,326 ng/L. Electrocardiography demonstrated sinus tachycardia, and transthoracic echocardiography showed LV dilatation with severe global systolic dysfunction and an estimated LV ejection fraction (LVEF) of approximately 10%. Contrast-enhanced computed tomography demonstrated an LV apical thrombus and hepatic congestion. Graves' disease-associated myocardial dysfunction was considered an important contributor; however, tachycardia-mediated dysfunction, myocarditis and critical illness-related myocardial dysfunction remained potential contributing causes. Management included adjustment of carbimazole, diuresis, bisoprolol, valsartan, spironolactone and dapagliflozin, alongside treatment of pneumonia. Therapeutic anticoagulation was initiated with enoxaparin, followed by intravenous unfractionated heparin and bridging to warfarin. Clinical improvement was accompanied by recovery of LVEF to 36% during admission, approximately 40% in June 2025 and 52%-54% on echocardiography in September 2025. Cardiac magnetic resonance imaging during the same time confirmed normal biventricular size and systolic function, with an LVEF of 54% and no residual intracardiac thrombus. A small area of nonspecific non-infarct-pattern fibrosis could represent previous myocarditis. Definitive thyroidectomy was planned. This case highlights severe but reversible LV systolic dysfunction with apical thrombus in a young woman with relapsed Graves' disease and suboptimal treatment adherence. Although the clinical course suggests a thyroid-related contribution, the myocardial dysfunction may have been multifactorial. The reduction in thyroid-stimulating immunoglobulins (TSIs) alongside cardiac recovery represents a temporal association and does not establish causation. Careful clinical assessment and cardiac imaging are essential to recognising significant cardiac involvement when thyroid biochemistry is complicated by concurrent illness.

PMID 42924373
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