Prospective, Open-label, Randomized, Parallel-group, Multicenter, Investigator, Initiated Phase 4 Clinical Trial to Evaluate the Glycemic Lowering Effects of Adding SGLT2 Inhibitor Monotherapy, TZD Monotherapy, or SGLT2 Inhibitor/TZD Combination Therapy in Patients With Type 2 Diabetes on DPP4 Inhibitors

This clinical trial investigates the effects of adding different diabetes medications to patients with type 2 diabetes who are currently being treated with DPP4 inhibitors. The study evaluates three treatment strategies: SGLT2 inhibitor monotherapy, TZD monotherapy, and a combination of both SGLT2 inhibitor and TZD. Participants will be randomly assigned to one of four groups, including a control group continuing DPP4 inhibitor alone.
The primary objective is to assess changes in blood sugar control, specifically HbA1c levels, after 12 and 24 weeks of treatment. Secondary outcomes include changes in fasting and postprandial glucose, insulin, C-peptide, lipid profiles (total cholesterol, triglycerides, HDL-C, LDL-C), body composition (muscle mass, visceral fat, subcutaneous fat), and insulin resistance indicators such as HOMA-IR, HOMA-beta, and Insulinogenic Index.
Eligible participants are adults aged 19 to 75 years with type 2 diabetes who have been on stable doses of DPP4 inhibitors, with or without metformin or sulfonylurea, for at least 8 weeks. Individuals with recent use of SGLT2 inhibitors or TZDs, significant organ dysfunction, or other exclusion criteria will not be enrolled.
The study is open-label and multicenter, conducted at four hospitals in Korea. All medications used in the trial are provided by the sponsor. Participants will receive lifestyle counseling throughout the study period, including guidance on diet and exercise. Safety monitoring will be conducted regularly, and adverse events will be documented and managed according to protocol.

Start Date01 Sep 2025

Sponsor / Collaborator

Yonsei University

NCT07056517

/ CompletedPhase 1

A Single-Dose, Open-label, Pharmacokinetics Study of Lobeglitazone From M107 ODT and Duvie® Under Fasted and Fed Conditions in Healthy Adults

Phase 1 study evaluating the safety, tolerability, and pharmacokinetics of lobeglitazone administered as M107 Orally Disintegrating Tablet and Duvie tablet in healthy adult participants under fasted and fed conditions.

Start Date11 Jul 2025

Sponsor / Collaborator

Aclipse Two Inc.

CTRI/2024/12/078217

/ Not yet recruitingPhase 4

A Comparative Study of Lobeglitazone Versus Pioglitazone on Urinary Albumin to Creatinine Ratio (UACR) In Normotensive and Hypertensive Type 2 Diabetes Mellitus Patients - NIL

Start Date30 Dec 2024

Sponsor / Collaborator-

100 Clinical Results associated with Lobeglitazone Sulfate

100 Translational Medicine associated with Lobeglitazone Sulfate

100 Patents (Medical) associated with Lobeglitazone Sulfate

Literatures (Medical) associated with Lobeglitazone Sulfate

01 Mar 2026·BMJ Open

Lobeglitazone and the risk of renal progression in Korean patients with type 2 diabetes mellitus: a retrospective cohort study

Article

Author: Hong, Young Sun ; Lee, Hyejin ; Jung, Hyein ; Kim, Min-ho ; Hong, So-hyeon ; Sung, Yeon-Ah ; Lee, So-young ; Song, Do Kyeong

Objective:

To evaluate the effect of lobeglitazone on renal disease progression in patients with type 2 diabetes mellitus using longitudinal real-world data.

Design:

Retrospective cohort study.

Setting:

Hospital-based Common Data Model database.

Participants:

A total of 14 712 adults with type 2 diabetes mellitus who visited the Diabetes Center of Ewha Womans University Mokdong Hospital between 2013 and 2019 were identified. A 1:2 propensity score matching was performed to compare patients treated with lobeglitazone plus metformin with those receiving metformin monotherapy, sulfonylurea plus metformin, or a dipeptidyl peptidase-4 (DPP4) inhibitor plus metformin.

Interventions:

Treatment with lobeglitazone plus metformin compared with metformin monotherapy, sulfonylurea plus metformin or DPP4 inhibitor plus metformin.

Primary outcome measures:

Renal progression, defined as initiation of renal replacement therapy, a sustained ≥30% decline in estimated glomerular filtration rate (eGFR) from baseline, or doubling of serum creatinine with a concurrent eGFR ≤45 mL/min/1.73 m².

Results:

The HR of renal progression was 0.84 (95% CI 0.58 to 1.21) in the lobeglitazone plus metformin compared with metformin monotherapy, 1.00 (95% CI 0.79 to 1.27) compared with sulfonylurea plus metformin group, 1.10 (95% CI 0.84 to 1.44) compared with DPP4 inhibitor plus metformin group after adjusting for multiple variables. Subgroup analyses demonstrated significant interactions by sex in the comparison with metformin monotherapy (P for interaction=0.0179) and by glycaemic control in the comparisons with sulfonylurea plus metformin (P for interaction=0.0161) and DPP4 inhibitor plus metformin (P for interaction=0.0006), suggesting potential heterogeneity in treatment effects.

Conclusions:

Lobeglitazone showed renal outcomes comparable to those of other antidiabetic medications, with a possible heterogeneity in treatment effects according to sex and glycaemic control.

01 Mar 2026·DIABETES OBESITY & METABOLISM

Sodium‐glucose cotransporter 2 inhibitor ameliorates thiazolidinedione‐induced fluid retention through vascular leakage reduction in white adipose tissue

Article

Author: Kim, Dong‐Hoon ; Kim, Nam Hoon ; Lee, Hye‐Jin ; Lee, Ah Hyeon ; Kim, Ji Yoon ; Kim, Sin Gon ; Jang, Hye‐Min

Abstract:

Aim:

Thiazolidinediones (TZDs) are effective insulin sensitisers; however, their use is restricted owing to adverse effects such as fluid retention. Previous research has linked increased vascular permeability in white adipose tissue (WAT) to TZD‐induced fluid retention. We explore the potential of sodium‐glucose cotransporter 2 inhibitors (SGLT2is) to counteract this side effect and elucidate the underlying mechanisms.

Materials and Methods:

High‐fat‐diet‐induced obese mice (C57BL/6) were assigned to three groups: (1) lobeglitazone 0.5 mg/kg (TZD monotherapy); (2) a combination of lobeglitazone 0.5 mg/kg plus empagliflozin 10 mg/kg with 0.16 mg/mL in drinking water (TZD + SGLT2i combination therapy); and (3) distilled water (control). After 6 weeks of treatment, body composition and water content in multiple tissues were measured. The expression of proteins and mRNA related to vascular permeability, renal sodium and water channels was investigated. Additionally, in vivo and in vitro experiments (the latter in human umbilical vein endothelial cells) using anti‐VEGF agents were conducted.

Results:

TZD treatment escalated vascular leakage and fluid retention in WAT, which was associated with diminished VE‐cadherin expression and compromised vascular integrity. Co‐treatment with the SGLT2i mitigated these adverse effects, reinstating VE‐cadherin expression, reducing vascular permeability and normalizing tissue water content. Empagliflozin was found to inhibit the VEGF‐A/VEGFR2 signalling pathway, thereby reducing VE‐cadherin internalisation and degradation. In vitro studies reinforced these findings, emphasizing the interplay between VEGF and VE‐cadherin in maintaining endothelial junction stability.

Conclusions:

Our results suggest that SGLT2is protect against TZD‐induced fluid retention by preserving vascular integrity in WAT, providing a viable therapeutic strategy to minimise TZD‐associated side effects.

01 Jan 2026·DIABETES OBESITY & METABOLISM

Lobeglitazone improves glycaemic control as add‐on therapy to empagliflozin plus metformin in patients with type 2 diabetes mellitus: A double‐blind, randomised, placebo‐controlled trial

Article

Author: Min, Kyung Wan ; Kim, Sang Yong ; Sohn, Ho Sang ; Kim, So Hun ; Cha, Bong‐Soo ; Park, Cheol‐Young ; Seo, Da Hea ; Yoon, Kun‐Ho ; Jeong, In‐Kyung

Abstract:

Aims:

This study aimed to evaluate the efficacy and safety of triple therapy with lobeglitazone 0.5 mg as an add‐on treatment compared with placebo in patients with type 2 diabetes mellitus (T2DM) inadequately controlled with metformin and empagliflozin.

Materials and Methods:

In this Phase 3, multicentre, double‐blind, randomised trial, patients with T2DM who had an insufficient response to metformin (≥1000 mg/day) and empagliflozin 10 mg/day (Study 1) or 25 mg/day (Study 2) were randomised to receive either lobeglitazone 0.5 mg/day, or placebo once daily for 24 weeks. Participants then entered an open‐label extension phase for an additional 28 weeks, bringing the total treatment duration to 52 weeks. The primary endpoint was the change from baseline in glycated haemoglobin ( HbA1c ) at 24 weeks.

Results:

At 24 weeks, the mean change in HbA1c was significantly greater with lobeglitazone than with placebo, regardless of the background empagliflozin dose (−0.71%; 95% confidence interval, −0.88 to −0.55; p < 0.001 in Study 1 and −0.62%; −0.79 to −0.45; p < 0.001 in Study 2). A higher proportion of patients achieved HbA1c levels <7% with lobeglitazone compared to placebo (48.7% vs. 13.4% in Study 1, and 44.4% vs. 13.0% in Study 2; p < 0.001). Although the incidence of adverse events was numerically different between groups, no statistically significant differences were observed, indicating a generally comparable profile for the triple combination therapy with metformin, empagliflozin, and lobeglitazone.

Conclusions:

Lobeglitazone as an add‐on to empagliflozin and metformin significantly improved glycaemic control in patients with T2DM inadequately controlled on metformin and empagliflozin dual therapy. The treatment was well tolerated, with a low incidence of adverse events.

News (Medical) associated with Lobeglitazone Sulfate

24 Sep 2026

·www.biospace.com

Aclipse Therapeutics and Cypress BioPharma Announce Agreement to Launch Phase 2 Study in Childhood Nephrotic Syndrome and Expand Renal Development Capabilities

Aclipse plans to expand M107 (lobeglitazone), a best-in-class PPARγ activator, into nephrotic syndrome in children, including steroid-dependent and frequently relapsing disease, where it could become the first non-immunosuppressive treatment option for these children. The planned renal trial will run in parallel with the ongoing Mayo Clinic-sponsored Phase 2 LOGAST trial in gastroparesis, delivering dual-track M107 Phase 2 proof-of-concept readouts. Aclipse raising a Series B preferred equity financing to advance its expanded pipeline. KING OF PRUSSIA, Pa.--(BUSINESS WIRE)--Aclipse Therapeutics ("Aclipse"), a clinical-stage biopharmaceutical company developing best-in-class therapies for chronic, rare, and severe diseases, today announced an agreement that provides Aclipse the option to acquire Cypress BioPharma ("Cypress"), a developer of novel therapies for rare kidney diseases. Upon completion, the transaction would establish parallel renal (M107R) and gastrointestinal (M107G) development programs for the Aclipse M107 molecule, creating two Phase 2 clinical readouts, while adding renal development expertise and additional early-stage renal assets. Completion of the transaction is subject to specified closing conditions. Nephrotic syndrome in children is a serious kidney disorder affecting thousands of children in the United States. In severe or treatment-resistant cases, the disease can progress to chronic kidney disease and end-stage kidney disease requiring dialysis or kidney transplantation. Corticosteroids are the standard initial therapy, but recurrent, steroid-dependent, or treatment-resistant disease can require additional immunosuppressive therapy that can be associated with substantial treatment burden and toxicity. The planned M107R Phase 2 LOKID (LObeglitazone for the treatment of KIDney disease in kids) clinical trial will evaluate its potential to induce and maintain long-term remission of nephrotic syndrome. Patients and caregivers need better treatment options, including therapies that may reduce steroid exposure and address underlying disease biology. "I am proud of our team's progress with Mayo Clinic in preparing for the M107G Phase 2 LOGAST (LObeglitazone for the treatment of idiopathic GASTroparesis) clinical trial. We now look forward to working with the Cypress BioPharma team to expand the M107 molecule into the childhood nephrotic syndrome (M107R) program, where it may offer a potential disease-modifying and steroid-sparing treatment option for children with this serious kidney disease. The proposed transaction would establish parallel renal and GI development programs for the M107 molecule, add experienced renal development expertise, and add two early-stage kidney drug candidates into the Aclipse pipeline," said Raymond K. Houck, Aclipse CEO. Despite recent advances in treatments for IgA nephropathy (IgAN) and focal segmental glomerulosclerosis (FSGS), and the FDA's acceptance of new surrogate endpoints, children with nephrotic syndrome are still treated largely with old immunosuppressive agents, such as prednisone, which carry substantial toxicity. "Cypress was founded on the pioneering work of Dr. William E. Smoyer at Nationwide Children's Hospital, which showed that PPARγ agonists act directly on podocytes to protect them from injury. Podocytes comprise a key component of the kidney’s glomerular filtration barrier and are the key target cell of injury in nephrotic syndrome. Notably, PPARγ agonist–induced podocyte protection and proteinuria reduction, may be achieved without added steroids or other immunosuppressive drugs. The transaction with Aclipse will allow us to advance the M107 molecule, a best-in-class PPARγ activator, into childhood nephrotic syndrome and other glomerular diseases, while combining the Cypress renal development expertise with the Aclipse clinical-stage development capabilities," said Michelle Higgin, PhD, Cypress CEO. Aclipse is initiating a Series B financing to advance the two Phase 2 development programs for M107: the Mayo Clinic-sponsored M107G Phase 2 LOGAST trial in idiopathic gastroparesis, which is undergoing final study-start-up activities; and the M107R Phase 2 LOKID trial in childhood nephrotic syndrome, planned to begin next year. The M107G and M107R programs will evaluate the potential for the M107 molecule to provide a disease-modifying treatment approach through macrophage rebalancing and cytoprotection and builds on the extensive M107 clinical safety database. About Aclipse Therapeutics: Aclipse Therapeutics is a clinical-stage biopharmaceutical company developing disease-modifying therapies for chronic and severe diseases. Its lead program, M107G, is a best-in-class PPARγ activator in development for gastroparesis, a chronic gastrointestinal disorder characterized by nausea, vomiting, abdominal pain and delayed gastric emptying. In parallel, the Aclipse M107R program is in development for childhood nephrotic syndrome, a serious kidney disorder that can lead to progressive kidney dysfunction and, in severe cases, end-stage kidney disease requiring dialysis or kidney transplantation. Aclipse is also developing M102, an NRF2 and HSF1 activator, for amyotrophic lateral sclerosis (ALS) and traumatic brain injury (TBI) entering Phase 1, and M228 for cystinuria, a rare kidney disease. About Cypress BioPharma: Cypress BioPharma, a spin-out from Nationwide Children’s Hospital, develops therapies for rare pediatric kidney diseases, including childhood nephrotic syndrome, focal segmental glomerulosclerosis (FSGS), and cystinuria. Cypress has built a specialized renal development team with expertise spanning regulatory, preclinical, and clinical development. Contacts For more information, contact Michael Kranda, Chief Business Officer, at mkranda@aclipsetherapeutics.com O r visit

Phase 2Acquisition

17 Nov 2025

·www.businesswire.com

Aclipse Therapeutics to Collaborate with Mayo Clinic on Phase 2 Clinical Development of M107 for the Treatment of Gastroparesis

KING OF PRUSSIA, Pa.--(BUSINESS WIRE)--Aclipse Therapeutics LLC (“Aclipse” or “the Company”) today announced that it has entered into a clinical collaboration and Know-How Agreement with Mayo Clinic for the Phase 2 clinical development of M107, the Company’s novel small molecule drug candidate being advanced as a potential disease modifying treatment for gastroparesis (i.e., stomach paralysis). The collaboration leverages the combined scientific and clinical expertise of both organizations to target macrophage related inflammation and seeks to address the biological cause of gastroparesis, a chronic and debilitating disease affecting stomach nerves and muscles resulting in stomach paralysis and delayed stomach emptying. “We are proud to announce this collaboration with Mayo Clinic to bring this potential new treatment to patients,” stated Raymond K. Houck, Chief Executive Officer of Aclipse Therapeutics. Houck continued “M107 is an orally available small molecule drug with anti-inflammatory benefits and a clinically favorable safety profile that has been shown to promote increased expression of M2 macrophages and decreased expression of M1 macrophages, thereby addressing macrophage dysregulation and highlighting its disease-modifying potential in gastroparesis.” The M107 Phase 2 study, Lobeglitazone for the treatment of idiopathic gastroparesis (the LOGAST trial), is to be conducted under the direction of Principal Investigator Dr. Pankaj Jay Pasricha, MBSS, MD, Chair, Department of Internal Medicine, Mayo Clinic Arizona. The LOGAST trial, expected to begin enrollment during the first quarter of 2026, is slated to involve approximately 10 clinical investigators at three Mayo clinical and research campuses: Rochester, MN, Phoenix, AZ, and Jacksonville, FL. The study is an investigator initiated clinical trial sponsored by Mayo Clinic and supported through a research grant from Aclipse Therapeutics. Mayo Clinic has a financial interest in the technology referenced in this press release. Mayo Clinic will use any revenue it receives to support its not-for-profit mission in patient care, education, and research. About Aclipse Therapeutics Aclipse Therapeutics develops novel and highly differentiated immunological and anti-inflammatory therapeutics to treat life-threatening and severe diseases. Aclipse focuses on molecular pathways that regulate cellular stress, protein misfolding and inflammation in neuromuscular diseases that are strongly impacted by these molecular pathways. In addition to our M107 program, we are initiating a Phase 1 trial of M102, our NRF2 and HSF1 motor neuron protectant for the treatment of ALS (also known as Lou Gerhig’s or Motor Neuron Disease) in collaboration with the Sheffield Institute for Translational Neuroscience at the University of Sheffield, UK. For more information about Aclipse Therapeutics, visit the website at https://www.aclipsetherapeutics.com or email info@aclipsetherapeutics.com.

Phase 2Phase 1

05 Jan 2024

·synapse.patsnap.com

Demystifying PPAR agonists: A Comprehensive Guide and How to Keep Up with the Latest Developments

PPAR, or peroxisome proliferator-activated receptor, is a group of nuclear receptor proteins found in the human body. These receptors play a crucial role in regulating various physiological processes, including metabolism, inflammation, and cell differentiation. PPARs act as transcription factors, meaning they can influence gene expression by binding to specific DNA sequences. They are involved in lipid and glucose metabolism, making them important targets for pharmaceutical interventions in conditions like diabetes, obesity, and cardiovascular diseases. PPARs also have anti-inflammatory properties and are implicated in regulating immune responses. Understanding the role of PPARs is essential for developing drugs that can modulate these receptors and potentially treat various diseases. PPAR agonists play a crucial role in metabolic regulation and have significant medicinal properties. Many PPAR agonists have been synthesized for the treatment of metabolic diseases, particularly dyslipidemia and type 2 diabetes mellitus (T2DM). For instance, selective PPARα agonists like bezafibrate, in combination with statins, are used to treat atherosclerotic hyperlipidemia and hypertriglyceridemia. Thiazolidinediones (TZDs) are effective PPARγ activators used as insulin sensitizers to treat T2DM patients. Given the clear lipid-lowering activity of PPARα agonists and the insulin-sensitizing effect of PPARγ agonists, successful clinical studies of bezafibrate and TZDs have not only promoted the development of various PPARα/γ agonists but also triggered the formulation of novel PPAR modulators, including selective PPARβ/δ activators, dual PPAR agonists, and pan-PPAR agonists. Besides dyslipidemia and T2DM, PPAR has profound effects on other aspects of metabolic syndrome (MetS), such as diabetic complications, non-alcoholic fatty liver disease (NAFLD), and non-metabolic diseases including neurodegenerative diseases, cancer, and inflammatory diseases. Therefore, research on PPAR agonists in various diseases and complications has attracted widespread interest. The analysis of the target PPAR reveals a competitive landscape with multiple companies actively developing drugs. Takeda Pharmaceutical Co., Ltd., Viatris Inc., GSK Plc, CHEPLAPHARM Arzneimittel GmbH, and Pfizer Inc. are among the companies with the highest phase of development. The approved indications for target PPAR drugs primarily focus on hyperlipidemias and diabetes mellitus type 2. Small molecule drugs dominate the drug types being developed, indicating intense competition. China, the European Union, Japan, and the United States are leading in the development of target PPAR drugs. Overall, the target PPAR market shows promising growth potential, with a focus on lipid-related disorders and diabetes. How do they work?PPAR agonists are a class of drugs that activate peroxisome proliferator-activated receptors (PPARs) in the body. PPARs are a group of nuclear receptors that play a crucial role in regulating gene expression and controlling various metabolic processes. There are three subtypes of PPARs: PPAR-alpha, PPAR-gamma, and PPAR-delta. PPAR agonists bind to these receptors and modulate their activity, leading to specific physiological effects. PPAR-alpha agonists primarily target lipid metabolism and are used to treat dyslipidemia and reduce triglyceride levels. PPAR-gamma agonists mainly affect glucose metabolism and insulin sensitivity, making them useful in managing type 2 diabetes. PPAR-delta agonists are involved in regulating fatty acid oxidation and energy expenditure. By activating PPARs, these agonists can influence gene expression related to lipid metabolism, glucose homeostasis, inflammation, and other processes. This class of drugs has shown potential in treating metabolic disorders, such as dyslipidemia, insulin resistance, and obesity. However, it is important to note that the specific effects and applications of PPAR agonists can vary depending on the subtype targeted and the specific drug used. List of PPAR AgonistsThe currently marketed PPAR agonists include: Chiglitazar SodiumFenofibrate/Pitavastatin CalciumPemafibrateFenofibrate/SimvastatinLobeglitazone SulfateSaroglitazarPravastatin sodium/FenofibrateFenofibric acidCholine FenofibrateKetoprofen/OmeprazoleFor more information, please click on the image below. What are PPAR agonists used for?PPAR agonists are commonly used in managing type 2 diabetes. For more information, please click on the image below to log in and search. How to obtain the latest development progress of PPAR agonists?In the Synapse database, you can keep abreast of the latest research and development advances of PPAR agonists anywhere and anytime, daily or weekly, through the "Set Alert" function. Click on the image below to embark on a brand new journey of drug discovery!

100 Deals associated with Lobeglitazone Sulfate

External Link

KEGG	Wiki	ATC	Drug Bank
-	Lobeglitazone Sulfate	A10B	DB09198

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Diabetes Mellitus, Type 2	South Korea	Chong Kun Dang Pharmaceutical Corp.	04 Jul 2013

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Gastroparesis	Phase 1	-	Aclipse Therapeutics LLC	-

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


REFIND (Pubmed \| Diabetes Obes Metab) Manual	Phase 4	Diabetes Mellitus, Type 2	147	lobeglitazone (low-dose)	ninoqypiqs(rwtdjjhunc) = lrgjdiefjv durwhodvjv (wdiehbzzlg, 0.54) View more	Positive	17 May 2022
				lobeglitazone (standard-dose)	ninoqypiqs(rwtdjjhunc) = oljutcbuxp durwhodvjv (wdiehbzzlg, 0.46) View more
NCT01106131 (Pubmed \| Diabetes Ther)	Phase 3	Diabetes Mellitus, Type 2	253	Lobeglitazone	pfsbgormxu(cykalychsj) = qnyjxmgpcg ilfhzuxjzs (nwcxvnorps ) View more	-	01 Jan 2021
				Pioglitazone	tnamnlyjtf(qcvsdgwsub) = ucbbrfdbiu wxqqyoksbr (koyhqfxvkq ) View more
NCT02480465 (Pubmed) Manual	Phase 4	Metabolic Syndrome \| Diabetes Mellitus, Type 2	247	lobeglitazone	tfbqyxilkd(itcpnnswiq) = qjzfsxmqew mkmufmajcg (bluckxgfgk )	Positive	01 Oct 2020
				sitagliptin	tfbqyxilkd(itcpnnswiq) = ptemtqgufl mkmufmajcg (bluckxgfgk )
NCT02480465 (EASD2019)	Phase 4	Diabetes Mellitus, Type 2 \| Metabolic Syndrome Add-on	247	Lobeglitazone 0.5 mg	glnzuaismp(gbziorwwim) = demonstrating non-inferiority wkspxavrix (qoihropkhr ) View more	Positive	17 Sep 2019
				Sitagliptin 100 mg
NCT01106131 (Pubmed \| Diabetes Obes Metab) Manual	Phase 3	Diabetes Mellitus, Type 2	253	Lobeglitazone	jmljlqqpxh(pfxzdaqsji) = mzhulnztpq ulegsdbtai (sqnikvzvxj )	Non-inferior	01 Jun 2015
				pioglitazone	jmljlqqpxh(pfxzdaqsji) = sakubudoer ulegsdbtai (sqnikvzvxj )
NCT01330563 (Pubmed \| Clin Ther)	Phase 1	Diabetes Mellitus, Type 2	24	Lobeglitazone 0.5 mg	ekuyycjkhg(htmankagal) = dbznyvdyfj xxqxslursh (yizxtdfpeo ) View more	-	01 Jul 2014
				Lobeglitazone 0.5 mg + Ketoconazole	ekuyycjkhg(htmankagal) = vkmlibcpvi xxqxslursh (yizxtdfpeo ) View more
NCT01001611 (Pubmed \| PLoS One)	Phase 3	Diabetes Mellitus, Type 2	173	Lobeglitazone 0.5 mg	fvvideltsa(wuzkzltqvb) = digcytbuwo yqxuovmmoj (uxyrugpadr ) View more	Positive	01 Jan 2014
				Placebo	fvvideltsa(wuzkzltqvb) = toprzzzqef yqxuovmmoj (uxyrugpadr ) View more
NCT01001611 (EASD2013)	Phase 3	Diabetes Mellitus, Type 2	173	Lobeglitazone 0.5 mg (Group M)	eapvkwufei(otekibbsmc) = hdnchpysln kbgtnfitix (wbjgfassbj ) View more	Positive	25 Sep 2013
				Lobeglitazone 0.5 mg (Group S)	eapvkwufei(otekibbsmc) = fxxnwghwqd kbgtnfitix (wbjgfassbj ) View more

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