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Last update 25 Jul 2025

Pioglitazone Hydrochloride

Last update 25 Jul 2025

Overview

R&D Status

Clinical Result

Translational Medicine

Overview

Basic Info

Drug Type

Small molecule drug

Synonyms

(±)-5-((4-(2-(5-ethyl-2-pyridinyl)ethoxy)phenyl)methyl)-2,4-thiazolidinedione, 5-{4-[2-(5-ethylpyridin-2-yl)ethoxy]benzyl}-1,3-thiazolidine-2,4-dione, pioglitazone

+ [38]

Target

PPARγ

Action

agonists

Mechanism

PPARγ agonists(Peroxisome proliferator-activated receptor γ agonists)

Therapeutic Areas

Endocrinology and Metabolic Disease

Active Indication

Diabetes Mellitus, Type 2

Inactive Indication

Abdominal PainAlzheimer DiseaseAngina Pectoris+ [31]

Originator Organization

Takeda Pharmaceutical Co., Ltd.

Active Organization

Takeda Pharmaceuticals U.S.A., Inc.Accord Healthcare SLU

Celltrion, Inc.

+ [6]

Inactive Organization

Teva Pharmaceuticals Europe BVVaia S.A.

KRKA dd

+ [5]

License Organization

Celltrion, Inc.

Celltrion Healthcare Co., Ltd.

Eli Lilly & Co.

+ [3]

Drug Highest PhaseApproved

First Approval Date

United States (15 Jul 1999),

Diabetes Mellitus, Type 2

RegulationOrphan Drug (United States), Orphan Drug (European Union)

Structure/Sequence

Molecular FormulaC19H21ClN2O3S

InChIKeyGHUUBYQTCDQWRA-UHFFFAOYSA-N

CAS Registry112529-15-4

545

Clinical Trials associated with Pioglitazone Hydrochloride

NCT07053319

/ RecruitingPhase 1IIT

Protocol lV: SGLT2 Inhibitors, Pioglitazone and Ketone Production in Type 2 Diabetes Mellitus

To examine whether the empagliflozin-induced stimulation of EGP, lipolysis, and ketone production in T2D individuals can be blocked by pioglitazone (which has direct hepatic and adipose tissue effects).

Start Date01 Feb 2026

Sponsor / Collaborator

University of Texas Health Science Center At San Antonio

[+1]

NCT07056699

/ Not yet recruitingPhase 3IIT

Protocol V: San Antonio Site Sub Study: Can Pioglitazone Block SGLT2 Inhibitor-induced Stimulation of Lipolysis, Ketone Production and Liver Glucose Production in Type I Diabetic Patients

Participants are being asked to be in a research study. Scientists do research to answer important questions which might help change or improve treatment of participants disease in the future.
In patients with Type 1 Diabetes (T1D), Dapagliflozin a Selective Glucose Transporter 2 Inhibitor (SGLT2i) is known to increase production of glucose in the liver, increase breakdown of fats (lipolysis), and increase production of ketones (ketogenesis). Ketones are chemicals produced by the liver when the body breaks down fat for energy instead of glucose. When the level of ketones in the body becomes too high, a condition called ketoacidosis develops. In this study, the study team will investigate whether adding pioglitazone (a medication commonly used to treat type 2 diabetes), can reduce the Dapagliflozin - induced liver glucose production, fat break down (lipolysis) and ketone body production (ketogenesis) in patients with Type 1 Diabetes (T1D).

Start Date15 Oct 2025

Sponsor / Collaborator

University of Texas Health Science Center At San Antonio

[+1]

NCT07083401

/ RecruitingPhase 1

An Open-label, Randomized, Fed, Single-dose, 2-sequence, 2-period Crossover Study to Evaluate the Pharmacokinetics and Safety Between Single Oral Administration of "BR3006" and Co-administration of "BR3006A", "BR3006B" and "BR3006C" in Healthy Adult Volunteers

This was an open-label, randomized, fed, single-dose, 2-sequence, 2- period crossover study to evaluate the pharmacokinetics and safety between single oral administration of "BR3006" and co-administration of "BR3006A", "BR3006B," and "BR3006C" in healthy adult volunteers.

Start Date05 Jul 2025

Sponsor / Collaborator

Boryung Corp.

100 Clinical Results associated with Pioglitazone Hydrochloride

100 Translational Medicine associated with Pioglitazone Hydrochloride

100 Patents (Medical) associated with Pioglitazone Hydrochloride

6,996

Literatures (Medical) associated with Pioglitazone Hydrochloride

31 Dec 2025·ANNALS OF MEDICINE

PPAR-mediated reduction of lipid accumulation in hepatocytes involves the autophagy-lysosome-mitochondrion axis

Article

Author: Cetti, Federica ; Ossoli, Alice ; Gomaraschi, Monica ; Da Dalt, Lorenzo ; Garavaglia, Carola ; Norata, Giuseppe Danilo

BACKGROUND AND AIM:

Lipid accumulation in hepatocytes is reduced by the activation of the peroxisome proliferator-activated receptor (PPAR) α, which is associated with increased lysosomal acid lipase (LAL) activity, transcription factor EB (TFEB) expression, and mitochondrial β-oxidation.Aim of the study was to assess whether the three isoforms of PPAR, i.e. α, δ and γ, share the same ability to reduce lipid accumulation in hepatocytes and to clarify the involvement of autophagy activation, lysosomal hydrolysis, and mitochondrial β-oxidation in lipid clearance induced by PPARs.

METHODS:

HepG2 cells were treated with oleate/palmitate (O/P) to induce lipid accumulation and exposed to the PPARα agonist fenofibric acid, the γ agonist pioglitazone, the δ agonist seladelpar, or the dual α/γ agonist saroglitazar.

RESULTS:

The treatment of HepG2 cells with fenofibric acid, pioglitazone, seladelpar, or saroglitazar halved lipid accumulation induced by O/P. PPAR agonists increased TFEB, p62, and LC3 expression and rescued LAL impairment induced by O/P. Moreover, PPAR agonists significantly increased mitochondrial mass and the expression of genes involved in mitochondrial dynamics and fatty acid catabolism. Interestingly, PPAR agonists lost their ability to reduce lipid accumulation when autophagic flux, LAL activity, or fatty acid transport in the mitochondria were blocked by specific inhibitors.

CONCLUSION:

All PPAR agonists were able to promote the clearance of lipids in cells loaded with long-chain fatty acids. The key role of acid hydrolysis to generate fatty acids, which can be then catabolized in the mitochondria, and the ability of the PPAR system to sustain each phase of this clearing process were elucidated.

01 Dec 2025·INFLAMMATION RESEARCH

Peroxisome proliferator-activated receptor gamma prevents activation of RBL-2H3 cells by inhibiting FcεRI-mediated signal transduction

Article

Author: Xie, Yuhang ; Ruan, Suyu ; Wang, Weihua ; Zhang, Yu ; Rui, Xiaoqing ; Zhou, Jianjun

BACKGROUND:

Mast cells are essential contributors to the pathophysiology of allergic diseases. Peroxisome proliferator-activated receptor gamma (PPAR-γ) has recently been identified as being involved in the anti-inflammatory response by inhibiting mast cell activation.

METHOD:

In this study, the PPAR-γ agonist pioglitazone (PIO) was employed to evaluate the effects of PPAR-γ on the degranulation and production of pro-inflammatory mediators in RBL-2H3 cells. Meanwhile, differentially expressed genes (DEGs) were characterised in mast cells exposed to PIO, and pathway enrichment analysis were conducted. Furthermore, we conducted validation to confirm the involvement of PPAR-γ signaling pathways in the FcεRI-mediated signal transduction in mast cells.

RESULTS:

Administration of PIO significantly reduced the release of β-hexosaminidase and the mRNA expression levels of pro-inflammatory cytokines induced by the cross-linking of FcεRIs expressed on the surface of RBL-2H3 cells. A total of 24 DEGs were identified between RBL-2H3 cells treated with and without PIO, and there were 15 up-regulated and 9 down-regulated. GO and KEGG analyses revealed that the immune system, signal transduction, infectious disease, and signaling molecules and interactions were the most enriched annotations. According to PPI network analysis, most DEGs interacted with PPAR-γ. PPAR-γ agonist could activate PPAR-γ and NRF2 signaling pathways in resting RBL-2H3 cells. The protein expression levels of PPAR-γ, Cpt1a, and Acsl4 were greatly upregulated in activated RBL-2H3 cells mediated by FcεRI aggregation. Moreover, the suppressive effects of PPAR-γ agonist on degranulation and phosphorylation levels of FcεRI-mediated signaling molecules in RBL-2H3 cells were PPAR-γ-dependent.

CONCLUSION:

These data demonstrate that PPAR-γ inhibits FcεRI-mediated mast cell activation by modulating intracellular-specific signal transduction in a PPAR-γ-dependent manner.

01 Dec 2025·JOURNAL OF COMPUTER-AIDED MOLECULAR DESIGN

Computational investigation to identify multi-targeted anti-hyperglycemic potential of substituted 2-Mercaptobenzimidazole derivatives and synthesis of new α-glucosidase inhibitors

Article

Author: Ahmed, Madiha ; Zargaham, Muhammad Kazim ; Waseem, Tanya ; Rajput, Tausif Ahmed ; Nadeem, Humaira ; Amin, Adnan

One of the most widespread diseases recognized all over the world is diabetes, accounting for 1.5 million deaths each year. Recent studies have demonstrated benzimidazole derivatives as potential antidiabetic agents. Hence, the present study is focused on designing new derivatives of 2-mercaptobenzimidazole by C-S cross-coupling reaction and are subjected to computational screening to identify the most promising candidate. Molecular docking and MM-GBSA calculations were performed to ascertain the binding potential with different antidiabetic targets, including α-glucosidase, PPaR-γ, DPP-4, and AMPK. We observed somewhat moderate binding interactions of the synthesized compound against the α-glucosidase. Since binding affinities can be improved using synthetic chemistry approaches, synthesis of analogues (A-18a-c) by designing hybrids at sites such as the acidic functionality of A-18 was done. The analogue A-18a, with p-fluorobenzyl substitution, exhibited enhanced binding affinity (-4.339 Kcal/mol) with the α-glucosidase compared to the parent compound (-3.827 Kcal/mol). The synthesized analogues were also subjected to an in-vitro α-glucosidase inhibitory assay. Among them, A-18a exhibited the most significant inhibitory potential, with an IC₅₀ value of 0.521 ± 0.01 µM as compared to the standard drug Acarbose (IC₅₀ 21.0 ± 0.5 µM). This aligns with the computational study findings, where A-18a exhibited stronger binding interactions within the active site of the enzyme. Hence, a promising analogue of the designed compound was synthesized through a computationally guided approach as an anti-hyperglycaemic agent. Additionally, most of the designed compounds showed significantly greater binding affinity with PPaR-γ as compared to the standard pioglitazone. A-18 was successfully synthesized by S-arylation reaction using CuI in 89% yield and was subjected to MD-simulation against PPaR-γ, which revealed stable binding throughout the 200 ns run. Future studies will focus on exploring the activity of the designed drugs against PPaR-γ through in-vitro and in-vivo assays.

News (Medical) associated with Pioglitazone Hydrochloride

18 Jun 2025

·www.prnewswire.com

Wisner Baum: Ninth Circuit Affirms Actos RICO Class Action Certification Against Takeda and Eli Lilly

Appellate Court upholds decision in first-ever non-settlement national RICO class action lawsuit certified against a major pharmaceutical company, with potential damages exceeding $7 billion. SAN FRANCISCO, June 18, 2025 /PRNewswire/ -- The U.S. Court of Appeals for the Ninth Circuit affirmed a class certification order in Painters & Allied Trades District Council 82 Health Care Fund v. Takeda Pharmaceutical Company Limited, marking a watershed moment in a first-of-its-kind class action that is now in its eleventh year. The Ninth Circuit upheld the certification of a national class of third-party payers seeking damages under the Racketeer Influenced and Corrupt Organizations (RICO) Act against pharmaceutical giants Takeda Pharmaceutical Company and Eli Lilly and Company. The suit accuses both companies of conspiring to conceal the bladder cancer risks associated with the diabetes drug Actos (pioglitazone) for over a decade, exposing millions of vulnerable diabetics to a carcinogen without their consent. It is a legacy of fraud, attorneys say, and this ruling finally paves the way for a jury trial on this important case. The case is the first non-settlement national RICO class action lawsuit certified against a major pharmaceutical company. Legal experts estimate the total damages could exceed $7 billion. Important Legal Precedent The Ninth Circuit's affirmation comes despite opposition from the pharmaceutical defendants and industry amici, who challenged the district court's class certification on multiple grounds. In a detailed memorandum, the appellate court rejected each of the defendants' arguments, finding that the lower court "properly conducted a 'rigorous analysis,' as required to certify a class," and adding that it "did not abuse its discretion by finding the predominance requirement satisfied." The case stems from allegations that Takeda and Eli Lilly engaged in a decade-long conspiracy to conceal Actos's significant bladder cancer risks. Internal documents revealed Takeda and Lilly knew about the bladder cancer risk as early as 1999. After the FDA mandated a bladder cancer warning for Actos in 2011, drug sales dropped by 80%, demonstrating the material impact of the fraud. Plaintiffs allege the companies knew about the bladder cancer risks but chose to hide them to protect billions in annual sales, defrauding third-party payers who paid for the medication. Statement from Lead Counsel "We are in our eleventh year litigating this case and are eager to finally get this case to trial," said R. Brent Wisner, managing partner of Wisner Baum LLP and national class counsel. "The evidence in this case is crystal clear: The class was deceived into purchasing billions of dollars of Actos by Takeda and Lilly whose actions plainly violated civil RICO, and exposed millions of diabetics to a carcinogen without their consent or knowledge. It's been a long and hard-fought journey, but the magnitude of this precedent and the potential impact on all pharmaceutical manufacturers was worth it. It seems perseverance is the number one determinant of success in the end. We are ready to tell this story to a jury and recoup the billions Takeda and Lilly pilfered from our clients and all those similarly situated." What's Next With class certification affirmed, Wisner hopes that a trial date will be set for 2026. The class will seek to prove their allegations and recover treble damages under RICO's enhanced penalty provisions. Wisner Baum LLP, along with co-counsel Christopher L. Coffin of Pendley, Baudin & Coffin, LLP, serves as national class counsel. The case is Painters & Allied Trades District Council 82 Health Care Fund v. Takeda Pharmaceutical Company Limited, No. 23-55742 (9th Cir. 2025), District Court Case No. 2:17-cv-07223-JWH-AS (C.D. Cal.) Media Contact: Diana McKinley (310) 207 -3233 [email protected] The award-winning law firm of Wisner Baum has successfully litigated cases against many of the largest pharmaceutical companies in the world. Since 1985, the firm has earned a reputation for breaking new legal ground, holding corporations accountable, influencing public policy, and raising public awareness on important safety issues. Across all areas of practice, the firm has won more than $4 billion in settlements and verdicts. SOURCE Wisner Baum WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Patent Infringement

16 Jun 2025

·www.einpresswire.com

GenBio Addresses Maintaining Glucose Homeostasis

Hormonal and neural regulatory mechanisms that maintain blood glucose levels within a very narrow range Science is fun. Science is curiosity. We all have natural curiosity. Science is a process of investigating. It's posing questions and coming up with a method. It's delving in.” — Sally Ride ALISO VIEJO, CA, UNITED STATES, June 16, 2025 / EINPresswire.com / -- Glucose from a diet is the major energy source for humans and other mammals. Blood glucose concentrations increase rapidly after food intake and then decline as glucose is used or stored. Since nutrient intake is irregular but energy requirement is continuous, the body needs to store glucose, usually as glycogen, mainly in the muscles and liver. Two peptides produced by the pancreas, insulin and glucagon, control glucose storage by enhancing glucose uptake and glycogen breakdown, respectively. Persistent high blood glucose concentrations result from diminished insulin production as in type 1 diabetes or insulin resistance, a decreased cellular response to insulin as in type 2 diabetes . Type 2 diabetes is a chronic disease defined by hyperglycemia leading to microvascular and macrovascular damage. The prevalence of diabetes has been increasing globally since 1990, attributed to living environments and lifestyle leading to poorer nutrition and increased sedentary behaviour. The International Diabetes Federation estimates that 11.1% of the world’s adult population aged 20-79 years, around 452 million people, is living with diabetes, with 4 in 10 of these people unaware that they have the disease. Diabetes is more prevalent in people aged 65 years and older, including 122 million of this population of 652 million, or around 19%; further, prediabetes affects 48% of the 26 million older adults in the USA. The risk to these patients is increased by multiple comorbidities, increased incidence of hypoglycemia, increased dependence on care and worsening frailty. Cardiovascular disease remains the leading cause of death in type 2 diabetics, even though a marked decrease in all-cause mortality of 30–35% in diabetics in the USA and England has been related to decreases in mortality from cardiovascular disease. Cancer rates have remained unchanged in diabetes patients, but this is now an increased percentage of deaths while mortality rates from dementia and liver disease have increased. Lifestyle modifications, including nutrition and exercise, are the foundation for the management of type 2 diabetes. Drug treatment of diabetes now includes metformin, which lowers liver production of glucose, sulphonylureas such as glyburide, which stimulate insulin production, thiazolidinediones such as pioglitazone which increase glucose uptake into tissues, prompting insulin secretion and decreasing appetite with glucagon-like peptide-1 receptor agonists, including semiglutide, combined glucose-dependent insulinotropic polypeptide and glucagon-like peptide-1 receptor agonists such as tirzepatide and preventing the reabsorption of glucose in the kidneys by sodium-glucose cotransporter-2 inhibitors such as dapagliflozin and empagliflozin. Research is continuing, so potential clinical use of adiponectin and fibroblast growth factor 21 could allow personalized approaches to lower blood glucose concentrations. Healthy eating plans are essential for long-term control of diabetes. Preclinical trials with anthocyanin-containing foods have shown regulation of blood glucose concentrations, improved gut microbiota, reduced insulin resistance and inflammation, and changed adipocyte function. Large prospective cohort trials in people in the USA have shown an inverse relationship between a healthy plant-based diet and the risk of developing diabetes. Dietary anthocyanin intake was linked to a 15% lower incidence of type 2 diabetes in 8 cohort studies involving 394,913 participants. In a summary of 18 human trials in type 2 diabetes from the last 5 years, anthocyanins reduced blood glucose and HbA1c concentrations and improved insulin secretion and resistance, especially in at-risk groups. Further, diets containing polyphenols such as anthocyanins may reduce the risk of developing diabetes. The incidence of type 2 diabetes decreased by 5% when the intake of anthocyanins increased by 7.5 mg/day. As examples, plums such as the Queen Garnet, Illawarra and Davidson’s varieties may contain 250-500 mg anthocyanins per 100g fruit. Other important dietary sources of anthocyanins include raspberries, bilberries, chokeberries, mulberries, and saskatoon berries. These clinical investigations support the preclinical studies that anthocyanins simultaneously affect many targets associated with type 2 diabetes. These studies reinforce that improving nutritional status in people with diabetes by adding anthocyanin-containing fruit to current treatment regimens is likely to improve clinical outcomes. Nutrition, exercise, and treatment with antidiabetic medications remain the key approaches to the treatment of type 2 diabetes. Todd D. Sonoga GenBio Inc. +1 949-705-8021 email us here Visit us on social media: LinkedIn Facebook X GenBio Inc Elevator Pitch Legal Disclaimer: EIN Presswire provides this news content "as is" without warranty of any kind. We do not accept any responsibility or liability for the accuracy, content, images, videos, licenses, completeness, legality, or reliability of the information contained in this article. If you have any complaints or copyright issues related to this article, kindly contact the author above.

04 Jun 2025

·www.prnewswire.com

0602K + Tirzepatide Muscle Mass / Function and Adipose Transformation Data to be Presented at ADA Scientific Sessions

GRAND RAPIDS, Mich., June 4, 2025 /PRNewswire/ -- Cirius Therapeutics, Inc., developing innovative therapies for patients suffering from diseases caused by insulin resistance, including obesity/overweight and type 2 diabetes (T2D), today announced that new preclinical data combining lead candidate 0602K and tirzepatide as a late-breaking poster will be presented at the American Diabetes Association's (ADA) 85th Scientific Sessions, taking place June 20–23, 2025, at McCormick Place Convention Center in Chicago, Illinois. Presentation details: Title: 1982-LB - MPC-Directed Insulin Sensitizer MSDC-0602K Combines with Tirzepatide to Maintain Muscle Mass/Function and Restructure Adipose Tissue [Board No. 1982] Authors: M. Abu-Farha, J. Abubaker, F. Almulla, M. Abdul-Ghani, L. Norton , R.A. DeFronzo,J.R. Colca, K.S. McCommis Date & Time: Sunday, June 22, 2025, at 12:30 AM CT Location: Poster Hall (Hall F1) The abstract for this late-breaking poster will be available beginning Friday, June 20, 2025 at 6:30 PM CT. About Cirius Cirius is a clinical-stage pharmaceutical company focusing on mitochondrial pyruvate carrier (MPC), addressing the metabolic dysfunction that causes insulin resistance and the organ pathologies associated with type 2 diabetes (T2D) and obesity/overweight. Its lead product candidate, 0602K (azemiglitazone potassium), is a potential best-in-class small molecule being developed as a once-daily oral therapy designed to selectively inhibit the mitochondrial target MPC, which plays a central role in selecting mitochondrial energy substrates. MPC inhibition reprograms mitochondrial metabolism, reducing insulin resistance in cells and driving metabolic benefits in organs throughout the body. This markedly improves glycemic control in T2D, body composition in obesity, liver function and fibrosis in metabolic dysfunction-associated steatohepatitis (MASH), and outcomes in cardiometabolic disorders. About 0602K 0602K has completed 7 US clinical trials including a 52-week placebo-controlled Phase 2b study in 392 subjects with MASH with and without T2D, and a 28-day placebo-controlled Phase 2a study in 129 subjects with T2D. In those clinical studies it markedly lowered HbA1c and insulin levels, and reduced liver injury and MASH – including on top of existing GLP-1 therapy. Preclinical studies also demonstrate increased lean muscle mass and function, together with marked metabolically beneficial shifts in adipose tissue phenotype ("bad fat" to "good fat"), including increased brown adipose tissue ("brown fat"). Selectively targeting MPC – while avoiding PPAR-γ activation – 0602K harnesses the real-world proven efficacy of 1st generation insulin sensitizers, such as pioglitazone, but without their side effect concerns. Directly correcting a major underlying pathophysiology of chronic metabolic disease, 0602K has the potential to become a cornerstone of therapy. Coupling this potent pharmacology with that of the GLP-1s could particularly benefit patients with T2D, obesity/overweight and other diseases. SOURCE Cirius Therapeutics WANT YOUR COMPANY'S NEWS FEATURED ON PRNEWSWIRE.COM? 440k+ Newsrooms & Influencers 9k+ Digital Media Outlets 270k+ Journalists Opted In GET STARTED

Phase 2Clinical Result

100 Deals associated with Pioglitazone Hydrochloride

External Link

KEGG	Wiki	ATC	Drug Bank
D00945	Pioglitazone Hydrochloride	A10BG03	DB01132

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Diabetes Mellitus, Type 2	United States	Takeda Pharmaceuticals U.S.A., Inc.	15 Jul 1999

Developing

10 top R&D records.

to view more data

Indication	Highest Phase	Country/Location	Organization	Date
Hearing Loss, Sensorineural	Phase 3	Czechia	Strekin AG	24 Feb 2018
Hearing Loss, Sensorineural	Phase 3	Germany	Strekin AG	24 Feb 2018
Hearing Loss, Sensorineural	Phase 3	Switzerland	Strekin AG	24 Feb 2018
Alzheimer Disease	Phase 3	United States	Takeda Pharmaceutical Co., Ltd.	01 Aug 2013
Alzheimer Disease	Phase 3	Australia	Takeda Pharmaceutical Co., Ltd.	01 Aug 2013
Alzheimer Disease	Phase 3	Germany	Takeda Pharmaceutical Co., Ltd.	01 Aug 2013
Alzheimer Disease	Phase 3	Switzerland	Takeda Pharmaceutical Co., Ltd.	01 Aug 2013
Alzheimer Disease	Phase 3	United Kingdom	Takeda Pharmaceutical Co., Ltd.	01 Aug 2013
Mild cognitive disorder	Phase 3	United States	Takeda Pharmaceutical Co., Ltd.	01 Aug 2013
Mild cognitive disorder	Phase 3	Australia	Takeda Pharmaceutical Co., Ltd.	01 Aug 2013

Clinical Result

Indication

Phase

Evaluation

View All Results

Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04300127 (PIOGAS, CTgov)	Early Phase 1	Gastroparesis	14	Pioglitazone 30 mg	shmgyhrlaj(cptkmcbzsv) = ypalfrotjl hjvfxcdfdr (qxkzjjeytl, 0.9) View more	-	30 Apr 2025
NCT00179400 (CTgov)	Phase 4	Diabetes Mellitus, Type 2	26	Pioglitazone (2000-200 Study 10-day Pioglitazone)	brjuucvqlq(njaytjsxpe) = ipiuzhqagp kndfasgwtw (tocxhoqmiu, 0.19) View more	-	03 Mar 2025
				placebo+pioglitazone (2000-200 Study 10-day Placebo)	brjuucvqlq(njaytjsxpe) = vprwasniit kndfasgwtw (tocxhoqmiu, 0.20) View more
NCT04604223 (Pubmed \| Front Immunol) Manual	Phase 4	COVID-19 \| Diabetes Mellitus, Type 2	350	Pioglitazone	uqvbcraodp(loxnmksoxi) = no significant difference in the CRP reduction was observed between the two groups knwjwzdfbk (agzppumhxk ) View more	Negative	06 Sep 2024
				Placebo
NCT01107717 (EDICT \| EDICT study, CTgov)	Phase 4	Diabetes Mellitus, Type 2	318	exenatide+pioglitazone+metformin (Triple Therapy)	pddzmbgubx(aogbfpomfk) = onnejbrzht uufjcfrpge (jvvrysscgq, 0.1) View more	-	05 Sep 2024
				glargine+metformin+glyburide (Conventional Therapy)	pddzmbgubx(aogbfpomfk) = biilgmljpj uufjcfrpge (jvvrysscgq, 0.1) View more
NCT04885712 (Pubmed \| Clin Ther) Manual	Phase 3	Diabetes Mellitus, Type 2 Add-on	366	Pioglitazone 15 mg	micxbwnflb(ckfjfhnzfh) = wxzgtsohwc yvxsyqtubx (aemhhssnqp )	Positive	01 Jul 2024
				Pioglitazone 30 mg	micxbwnflb(ckfjfhnzfh) = ahscbfzbbb yvxsyqtubx (aemhhssnqp )
ADA2024	Not Applicable	Diabetes Mellitus, Type 1	-	Dapagliflozin 10 mg + Pioglitazone 45 mg	wxzwukwymh(xbjmefqusl) = xvtomcqany myhhofaxcd (ocsxaeiwnn, 0.18) View more	-	14 Jun 2024
				Dapagliflozin 10 mg + Placebo	wxzwukwymh(xbjmefqusl) = nuaivwdpsj myhhofaxcd (ocsxaeiwnn, 0.11) View more
ISRCTN45546616 \| ISRCTN29234515 \| ISRCTN11062950 (ISRCTN11062950;ISRCTN29234515;ISRCTN45546616, Pubmed)	Phase 3	Polycystic Ovary Syndrome HOTAIR rs1443512 genotype	65	pioglitazone	muhhuxkmqa(rdiwlhctrc) = anzyswhqmo iurogjnbep (wffwvnyhzc ) View more	-	01 Apr 2024
NCT05226897 (Pubmed) Manual	Phase 3	Diabetes Mellitus, Type 2	249	YYC405+Metformin+Dapagliflozin	luaqbzdxwu(jtfqnnjsjk) = Pioglitazone administration resulted in a significant reduction in HbA1c levels (from 7.80% ± 0.72% to 7.27% ± 0.82%) compared with placebo (from 7.79% ± 0.76% to 7.69% ± 0.86%, corrected mean difference: -0.42% ± 0.08%; p < 0.01). hfgarmnxvz (nrcslerxvn )	Positive	29 Feb 2024
				Placebo+Metformin+Dapagliflozin
NCT04604223 (EASD2023)	Phase 4	COVID-19	343	Pioglitazone	kcyayxyiag(wjoofmpcnf) = ntbgijkfms bwnlnbwnvi (jujuxjekqn )	Negative	04 Oct 2023
				Placebo	kcyayxyiag(wjoofmpcnf) = llojpzcprk bwnlnbwnvi (jujuxjekqn )
ISRCTN29234515 \| ISRCTN11062950 (ESPE2023)	Phase 3	Polycystic Ovary Syndrome HOTAIR rs1443512 genotype -	24	Pioglitazone 7.5 mg/d	wyaeoxchiw(aepcxcrpec) = xydythycbz zthrlzlnmw (danrmtzvyh, 0.4) View more	Positive	21 Sep 2023

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