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Last update 09 Sep 2026

Pioglitazone Hydrochloride

Last update 09 Sep 2026

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

+ [40]

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 SLActavis Group PTC ehf

+ [8]

Inactive Organization

Vaia S.A.

Krka dd Novo Mesto

Strekin AG

+ [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

623

Clinical Trials associated with Pioglitazone Hydrochloride

CTR20263060

/ Active, not recruitingNot Applicable

北京太洋药业股份有限公司提供的盐酸吡格列酮片（规格：30 mg）与武？テバ薬品株式会社持证的盐酸吡格列酮片（商品名：ACTOS®，规格：30 mg）在中国健康试验参与者中进行的空腹状态下的生物等效性试验

[Translation] A bioequivalence study was conducted in Chinese healthy participants on pioglitazone hydrochloride tablets (30 mg) supplied by Beijing Taiyang Pharmaceutical Co., Ltd., and pioglitazone hydrochloride tablets (trade name: ACTOS®, 30 mg) certified by Takeya Pharmaceutical Co., Ltd., in a fasting state.

以北京太洋药业股份有限公司提供的盐酸吡格列酮片（规格：30 mg）为受试制剂，武？テバ薬品株式会社持证的盐酸吡格列酮片（商品名：ACTOS®，规格：30 mg）为参比制剂，考察两制剂在空腹状态下单次给药的药代动力学参数及相对生物利用度，评价两制剂是否具有生物等效性；并评价盐酸吡格列酮片在健康试验参与者中的安全性。

[Translation]

Using pioglitazone hydrochloride tablets (30 mg) provided by Beijing Taiyang Pharmaceutical Co., Ltd. as the test formulation and pioglitazone hydrochloride tablets (trade name: ACTOS®, 30 mg) certified by Takeya Pharmaceutical Co., Ltd. as the reference formulation, the pharmacokinetic parameters and relative bioavailability of the two formulations under fasting conditions after a single dose were investigated to evaluate whether the two formulations are bioequivalent; and the safety of pioglitazone hydrochloride tablets in healthy trial participants was evaluated.

Start Date21 Aug 2026

Sponsor / Collaborator

Beijing Taiyang Pharmaceutical Co. Ltd.

JPRN-jRCTs051260025

/ RecruitingNot Applicable

Pioglitazone MASH Trial: Efficacy and Safety of Pioglitazone (Actos(R)) on Liver Fibrosis and Hepatic Reserve After Hepatectomy for MASH-Related Hepatocellular Carcinoma: A Single-Arm Interventional Study (PMASH Trial)

Start Date21 Jul 2026

Sponsor / Collaborator-

NCT07056699

/ 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 T1D.

Start Date01 Jul 2026

Sponsor / Collaborator

University of Texas Health Science Center At San Antonio

[+1]

100 Clinical Results associated with Pioglitazone Hydrochloride

100 Translational Medicine associated with Pioglitazone Hydrochloride

100 Patents (Medical) associated with Pioglitazone Hydrochloride

5,857

Literatures (Medical) associated with Pioglitazone Hydrochloride

01 Feb 2027·TISSUE & CELL

Dapagliflozin uncouples the anti-inflammatory and lipogenic effects of pioglitazone in valproic acid-induced steatohepatitis in rats: Lipid-sensing nuclear receptors (LXRα and PPARγ) as the molecular nexus between hepatoprotection and lipogenesis

Article

Author: Hassan, Hend M ; Elshenawy, Dina S ; Elkatary, Rania G ; Hammad, Maha O ; Saad, Somaya

Valproic acid (VPA) is a foundation antiepileptic medication, implicated in dose-dependent hepatotoxicity via mitochondrial dysfunction, progression of oxidative-inflammatory cascade, and steatosis. LXRα/PPARγ are crucial regulators of hepatic lipogenesis, representing a pertinent therapeutic target. Dapagliflozin, a SGLT2 inhibitor and pioglitazone, a PPARγ agonist, are emerging therapies for metabolic hepatic steatosis; however, while pioglitazone confers notable anti-inflammatory benefits, its hepatic PPARγ signaling remains a recognized concern. The current study targets the individual or combined modulatory effects of both drugs on the hepatic LXRα and PPARγ pathways in VPA-induced steatohepatitis in rats. Forty male Sprague-Dawley rats were randomized into five groups: Control, VPA (500 mg/kg/d given orally), PIO + VPA (10 mg/kg/d pioglitazone), DAPA + VPA (1 mg/kg/d dapagliflozin), and COMB (1 mg/kg/d dapagliflozin and 10 mg/kg/d pioglitazone). All prophylactic treatments were orally given 1 h prior to VPA. Spectrophotometry, RT-PCR, histopathological and immunohistochemical parameters were used to assess hepatic injury across groups. The results indicated that hepatocytes are nudged toward increased lipogenesis in the VPA group via activation of hepatic PPARγ (P < 0.001), LXRα (P < 0.01), SREBP1c (P < 0.001), and perilipin 2 (P < 0.05). VPA was associated with impaired LFTs, dyslipidemia, altered MDA/GSH equilibrium, and intense NF-κB immunoreactivity (all P < 0.001), besides significant fibrosis (P < 0.001) and elevated histopathology scores (P < 0.01). Relative to VPA, PIO + VPA exhibited significant hepatic anti-inflammatory and antioxidative benefits, restoring LFTs (P < 0.001) and MDA/GSH equilibrium (P < 0.001), alongside inhibiting NF-κB immunoreactivity (P < 0.001), however; it failed to significantly improve histopathological scores or lipogenic effectors (P > 0.05). Relative to VPA, DAPA + VPA and COMB groups showed a downregulation of hepatic lipogenic effectors (PPARγ at P < 0.001, LXRα at P < 0.01, SREBP1c at P < 0.001, and perilipin 2 at P < 0.05), with additional improvement of histopathological scores (P < 0.05), fibrosis (P < 0.001), and lipid profiles (P < 0.001) while simultaneously restoring LFTs and hepatic redox status (P < 0.001). Within the scope of the available literature, this study is the first to elucidate the divergent effects of pioglitazone and dapagliflozin on VPA-induced steatosis through the intricate hepatic LXRα/PPARγ signaling, underscoring the pronounced hepatoprotective capacity of dapagliflozin, effectively rescuing pioglitazone's pro-steatotic signaling.

31 Dec 2026·ANNALS OF MEDICINE

Pioglitazone mitigates early brain injury by suppressing neuroinflammation and oxidative stress after subarachnoid hemorrhage: a rodent model study

Article

Author: Özates, Mehmet Özgür ; Kullukçu, Hümeyra ; Kazancı, Atilla ; Deveci Bulut, Tuba Saadet ; Gürcan, Oktay ; Cetinkaya, Kadir ; Ünsal, Yasar ; Önder, Evrim ; Gürcay, Ahmet Gürhan

OBJECTIVE:

Subarachnoid haemorrhage (SAH) is a devastating neurovascular emergency where outcomes are largely driven by early brain injury (EBI). Neuroinflammation and oxidative stress are central to EBI pathogenesis. This study experimentally evaluated whether pioglitazone attenuates inflammatory and oxidative responses in the early phase after SAH.

MATERIALS AND METHODS:

Thirty-two adult male Sprague-Dawley rats were randomly allocated to four groups (n = 8/group): Sham, SAH, SAH+pioglitazone (PIO), and SAH+vehicle (VEH). SAH was induced by autologous blood injection into the cisterna magna. Pioglitazone (10 mg/kg, intraperitoneally) was administered 1 h post-SAH. Serum interleukin-6 (IL-6), interleukin-1β (IL-1β), and malondialdehyde (MDA) levels were quantified by Enzyme-Linked Immunosorbent Assay (ELISA) at 24 h. Hippocampal neuronal injury was assessed using semi-quantitative histopathological analysis of haematoxylin-eosin-stained sections. Acute-phase biochemical and histopathological effects were evaluated; long-term functional outcomes were not assessed.

RESULTS:

IL-6, IL-1β, and MDA levels were significantly elevated in all SAH groups compared with sham (p < 0.001). Pioglitazone significantly reduced IL-6 compared with SAH (p = 0.032) and VEH (p = 0.049), though levels remained higher than sham. Conversely, IL-1β and MDA levels in the PIO group were significantly lower than in SAH and VEH (p = 0.001 and p = 0.002, respectively) and were comparable to sham. Histopathological analysis demonstrated significantly lower hippocampal neuronal degeneration scores in the pioglitazone-treated group (p < 0.05).

CONCLUSION:

Early post-SAH administration of pioglitazone suppresses systemic inflammation and lipid peroxidation while mitigating hippocampal neuronal injury. These findings support a potential neuroprotective role of pioglitazone in EBI after SAH, likely mediated via peroxisome proliferator-activated receptor-γ (PPAR-γ) activation.

31 Dec 2026·ANNALS OF MEDICINE

Targeted activation of PPARG or AKT1 alleviates liver injury in mice with type 2 diabetes and sepsis by modulating inflammatory and metabolic pathways

Article

Author: Ma, Jie ; De, Tianyu ; Liu, Mei ; Ma, Tian ; Feng, Xiaoli ; Li, Wendi ; Qi, Xin ; Li, Huifang ; Ma, Junbai ; Ma, Hongmei ; Ma, Gang ; Man, Jia ; Li, Shan ; Liu, Jian ; Li, Jinyu ; Wang, Hao ; Gao, Jun

BACKGROUND:

The simultaneous presence of sepsis and type 2 diabetic mellitus (T2DM) has a synergistic effect on hepatic damage. Although the activation of peroxisome proliferator-activate receptor gamma (PPARG) and AKT serine/threonine kinase 1 (AKT1) have been shown to confer protection alone in isolated models of sepsis or T2DM. The present study was designed to systematically assess the effects of PPARG or AKT1 activation on inflammatory responses and glucose and lipid metabolism as well as intestinal barrier function in a murine model of T2DM and sepsis (T2DM/sepsis), and understand the molecular pathways involved.

METHODS:

Mice were treated with either the PPARG agonist pioglitazone or the AKT1 activator SC79 and we then evaluated survival, inflammatory indicators, metabolic changes, tissue pathology, intestinal barrier integrity, and gut microbiota composition. Mechanistic studies focused on the PPARG/AMPK and PI3K/AKT1/mTOR signaling pathways.

RESULTS:

Activation of either PPARG or AKT1 was associated with significantly increased survival rates, reduced systemic and hepatic levels of pro-inflammatory cytokines, increased the expression of anti-inflammatory mediators, ameliorated the abnormalities of the glucose and lipid metabolism, and partially improved hepatic, pulmonary, and intestinal injury. Mechanistically, PPARG activation mainly activated the PPARG/AMPK pathway and AKT1 activation enhanced the PI3K/AKT1/mTOR pathway. Furthermore, the intestinal barrier integrity and gut microbiota composition was partially improved.

CONCLUSION:

These results suggest that targeting PPARG or AKT1 is associated with protection against sepsis-associated liver injury in mice with T2DM by modulating the PPARG/AMPK axis or the PI3K/AKT1/mTOR pathway, respectively, which may collectively contribute to anti-inflammatogenic, metabolic, and gut-barrier protective mechanisms.

112

News (Medical) associated with Pioglitazone Hydrochloride

28 Aug 2026

·www.fiercebiotech.com

Why Roche is 'really excited' about a UCN2 analog for obesity after seeing preclinical data

Roche has decided to pay $190 million upfront for an unusual obesity mechanism after viewing preclinical data that “clearly suggests” the modality can reduce weight while preserving lean muscle, Fierce has learned. The Swiss pharma’s Genentech unit stumped up the cash last week for rights outside South Korea to HM17321, a corticotropin-releasing factor 2 (CRF2) receptor-selective urocortin-2 (UCN2) analog developed by South Korea’s Hanmi Pharm. Researchers have known for decades that activating the CRF2 receptor with UCN2 can protect against muscle atrophy in animal models. Roche is betting that attribute could prove useful in weight loss. “The [preclinical] data clearly suggests that through a non-incretin mechanism, you can still have weight loss—but more importantly, have weight loss through the preservation of lean mass, without losing muscle mass,” Manu Chakravarthy, M.D., Ph.D., global head of cardiovascular, renal and metabolism product development at Roche, told Fierce. Preclinical studies also suggest the drug could improve muscle function, another feature that has caught Roche’s attention. “So what we’re really excited about is the potential for improvement in muscle function and overall enhancing metabolic function as well,” Chakravarthy said. The first clinical data will come from a phase 1 study that Hanmi is already overseeing. Chakravarthy wasn’t able to provide a timeline for that readout because the study is being run by Hanmi, but said Roche is keen for Genentech to take over and start a phase 2 trial “as quickly as possible.” Roche remains cautiously optimistic about the preclinical findings, Chakravarthy said, while recognizing that not everything seen in animal studies will carry over to humans. “Having done this for a few decades, I can tell you that translation ... doesn't always happen,” Chakravarthy said. “That's why, as much as I’m excited about the preclinical data that we've seen, we have to await the clinical data.” The licensing of HM17321 follows a ramp-up in Roche’s obesity strategy last year, which included a bold goal of becoming one of the “top three” companies in the weight loss space. The pharma’s weight loss pipeline includes enicepatide, the dual GLP-1/GIP receptor agonist brought over in the buyout of Carmot Therapeutics that Roche has previously said it hopes to take to market by 2030. There’s also another Carmot asset in phase 2, the oral GLP-1 receptor agonist CT-996, as well as petrelintide, the long-acting amylin analog Roche is developing with Zealand Pharma. Chakravarthy said incretins, which include enicepatide and CT-996, and amylins are each a “foundational pillar” of Roche’s obesity strategy. A “third pillar” is FGF21 analogs, which Roche added when it acquired 89bio last year and which could help address obesity-related comorbidities such as MASH. Even with this varied portfolio, Roche saw other unmet needs that required a more “holistic” approach, Chakravarthy said. “You can certainly have agents that reduce weight, but how do you maintain that over some period of time?” he said. “And importantly, how do you do that while maintaining lean mass preservation as well? Because lean mass does go down, particularly in those that are vulnerable, like the elderly, those that are predisposed to falls, or even just having a predisposition to fractures.” HM17321’s mechanism also has the potential to improve insulin sensitivity, Chakravarthy said. Insulin resistance is a fundamental feature of many metabolic diseases, making that potential particularly interesting to Roche. “If you have an insulin sensitizer that can reset that core pathophysiological defect, that becomes very exciting, because now you're really able to go after the core defect, plus also maybe address some of the comorbidities of obesity, which also is one of our core anchors of our strategy,” Chakravarthy said. Eli Lilly previously explored UCN2 in heart failure before scrapping a phase 1 UCN2 peptide program in 2019. Roche’s deal, however, represents a move into a largely unexplored use of the mechanism for obesity. Does Chakravarthy expect others to follow? “I wouldn't be surprised,” he told Fierce. “You know, usually, this is how it all typically happens—they look for a ‘validation event,’ and then things might happen.” Despite pushing its obesity strategy into this underexplored area, Chakravarthy said Roche is “absolutely not done” looking for other mechanisms. The company's search for new approaches is driven by where the science is heading, he said. “We always follow the science to see where it is breaking, where it is making an impact, and how we can translate that science to the benefit of patients,” Chakravarthy added.

Phase 2AcquisitionPhase 1

24 Jun 2026

·www.prnewswire.com

CIR-0602K Begins Dosing in Breakthrough T1D-Supported Phase 2 in Type 1 Diabetes

Randomized placebo-controlled study Assessing 3 months of CIR-0602K for increasing glucose time-in-range, reducing HbA1c and total daily insulin dose, and improving cardiovascular biomarkers and vascular function Supported by Breakthrough T1D and ongoing at University of Virginia School of Medicine Topline data expected in the second half of 2027 GRAND RAPIDS, Mich., June 24, 2026 /PRNewswire/ -- Cirius Therapeutics, Inc., a developer of innovative therapies for people suffering from diseases caused by mitochondrial dysfunction and insulin resistance, today announced enrollment and dosing has begun in a Phase 2 clinical study (CTI-0602K-201A, NCT07186660) evaluating CIR-0602K in adults with type 1 diabetes (T1D) treating their T1D with automated insulin delivery (AID). The randomized, double-blind, placebo-controlled study is actively recruiting and will enroll approximately 34 participants to receive either CIR-0602K or placebo tablets daily for three months. It is a signal-finding study powered to show improved glucose time-in-range and supported by a research award from Breakthrough T1D. "Beginning treatment in these first participants marked an important milestone for this study and for our broader effort to address a major unmet need across diabetes," said Robert A. Beardsley, Ph.D., President and Chief Executive Officer of Cirius. "We are also developing CIR-0602K for treatment of type 2 diabetes (T2D), as well as our recently announced initiative to prevent T2D in women who experienced gestational diabetes during their pregnancies, supported with funding from the Gates Foundation. By treating insulin resistance, potentially preserving pancreatic beta cell function, and, more broadly, correcting mitochondrial dysfunction, we believe CIR-0602K can offer significant contributions to treating T1D, T2D and other cardiometabolic disease." Automated insulin delivery systems have significantly improved glycemic control in T1D, yet many patients continue to require high insulin doses and fail to consistently achieve target glucose ranges. For this study, glucose time-in-range (70-180 mg/dL) via continuous glucose monitoring is the primary endpoint. Key secondary and exploratory endpoints include HbA1c, total daily insulin dose, insulin sensitivity (by euglycemic insulin clamp), markers of vascular function and other cardiometabolic biomarkers. Insulin resistance in people with T1D contributes to suboptimal glycemic control and higher total daily insulin requirements. These factors, along with related mitochondrial dysfunction, are linked to systemic inflammation, vascular dysfunction and long-term cardiovascular risk. CIR-0602K is designed to improve insulin sensitivity – and mitochondrial dysfunction – by targeting mitochondrial metabolism. In prior clinical studies in people living with T2D, CIR-0602K simultaneously improved glycemic control and reduced insulin resistance by approximately 50%. In addition, it reduced systemic inflammation and other biomarkers of cardiometabolic disease. The study will test whether this is also true in people living with T1D, and whether it can help reduce the related cardiovascular dysfunctions. If successful, this study will help accelerate development of CIR-0602K across diabetes. "In T1D, unresolved mitochondrial dysfunction contributes to insulin resistance and cardiovascular complications," said Dr. Jerry Colca, Ph.D., Chief Scientific Officer of Cirius. "In addition, while exogenous insulin is essential for people with T1D, it is now known that requirements for higher insulin levels can interfere with the ability to control glucose in the optimal range and impact cardiovascular function. CIR-0602K offers a potential solution by correcting insulin resistance and the underlying mitochondrial dysfunction, leading to better glycemic control with less insulin and potentially improving cardiovascular outcomes." This Phase 2 study is being conducted at the University of Virginia School of Medicine. "Closed-loop systems have meaningfully improved glycemic management in T1D, but they do not address underlying intrinsic insulin resistance," said Dr. William B. Horton, M.D., Associate Professor of Medicine in the University of Virginia School of Medicine's Division of Endocrinology and Metabolism and Principal Investigator for the study. "Even with the latest automated insulin delivery, insulin resistance and the accompanying cardio-metabolic derangements associated with T1D lead to a risk of cardiovascular and other complications more than twice that of non-diabetics. The high level of interest in participating in this study reflects the desire of people living with T1D to address this." Topline data is expected in the second half of 2027. About Cirius Cirius is a clinical-stage pharmaceutical company focusing on metabolic health via targeting mitochondrial pyruvate carrier (MPC), addressing the mitochondrial dysfunction that causes insulin resistance and the organ pathologies associated with type 2 diabetes (T2D), type 1 diabetes (T1D) and obesity/overweight. Its lead product candidate, CIR-0602K, is a potential best-in-class novel 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 diabetes, body composition in obesity, liver function and fibrosis in metabolic dysfunction-associated steatohepatitis (MASH), and outcomes in cardiometabolic disorders. About CIR-0602K CIR-0602K has completed 7 US clinical trials including a 52-week placebo-controlled Phase 2b study in 392 participants with MASH with and without T2D, and a 28-day placebo-controlled Phase 2a study in 129 participants with T2D. In those clinical studies it lowered HbA1c and insulin levels, and reduced liver injury and MASH – including on top of existing GLP-1 therapy. A pilot clinical study also showed CIR-0602K markedly reduces HbA1c, insulin levels and fat in muscle, and increases muscle metabolic function in people with obesity & T2D. A Phase 2a study in people with type 1 diabetes (T1D) and supported by Breakthrough T1D has begun dosing. Cirius also recently announced that the Gates Foundation is providing a grant to initiate clinical studies as a potential postpartum therapeutic for women with a history of gestational diabetes mellitus (GDM). Preclinical studies also demonstrate increased lean muscle mass, strength and metabolic function, together with metabolically beneficial shifts in adipose tissue phenotype ("bad fat" to "good fat"), both alone and on top of GLP-1 and GLP-1/GIP agonists. In combination with GLP-1/GIP dual agonist tirzepatide, the synergistic transformation of subcutaneous adipose tissue includes dramatic reduction in adipocyte size and increase in "beiging." Selectively targeting MPC – while avoiding PPAR-γ activation – CIR-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, CIR-0602K has the potential to become a cornerstone of therapy. Coupling this potent pharmacology with that of the GLP-1s could particularly benefit people with T2D, T1D, obesity/overweight, MASH and other cardiometabolic diseases. Media Contact: [email protected] SOURCE Cirius Therapeutics 21% more press release views with Request a Demo

Phase 2

01 Jun 2026

·www.prnewswire.com

Cirius Therapeutics Announces Presentation on CIR-0602K as Novel Diabetes Treatment at the American Diabetes Association's 2026 Scientific Sessions

GRAND RAPIDS, Mich., June 1, 2026 /PRNewswire/ -- Cirius Therapeutics, Inc., a developer of innovative therapies for people suffering from diseases caused by mitochondrial dysfunction and insulin resistance, today announced that clinical data on the treatment of type 2 diabetes (T2D) with investigational drug CIR-0602K will be highlighted in a poster presentation at the upcoming American Diabetes Association (ADA) 86th Scientific Sessions, June 5-8, in New Orleans, LA. The presentation, "New Insulin Sensitizer CIR-0602K Potential to Expand Treatment Options to Manage Diabetes," will discuss emerging evidence supporting CIR-0602K as a novel therapeutic approach to directly treat insulin resistance and bring more persons with T2D to their HbA1c goals. Recent population-based studies suggest that even as new classes of drugs have become available to treat T2D, the proportion of people meeting the HbA1 goal of <7% has markedly declined.1 One reason for this is ineffective treatment of intrinsic insulin resistance in many, even those who are successful in overcoming other factors, such as obesity / overweight.2 By targeting mitochondrial dysfunction, CIR-0602K directly addresses intrinsic insulin resistance in these persons with T2D. "Unresolved intrinsic insulin resistance is preventing patients from achieving optimal HbA1c goals. Even with the use of modern therapies, over half of people with type 2 diabetes in the U.S, still do not reach the minimally acceptable level of 7% in a real-world setting," said Jerry Colca, Ph.D., Chief Scientific Officer of Cirius. "The clinical data we're presenting support the potential for CIR-0602K to complement existing therapies, including GLP-1 agents, and enable more of them to achieve their HbA1c goals and hopefully live longer, healthier lives. Furthermore, addressing intrinsic insulin resistance with this mechanism can work synergistically with weight loss therapies." CIR-0602K is a next-generation insulin sensitizer inhibiting mitochondrial pyruvate carrier (MPC), a mechanism which reduces mitochondrial dysfunction, metabolic inflammation and insulin resistance without the side effects associated with 1st generation insulin sensitizers. The resulting ability to reduce HbA1c, while also reducing plasma insulin levels is particularly attractive for treating diabetes mellitus in its many forms. "T2D is the single largest diabetes segment, afflicting an estimated 35 million American, and the data to be presented suggest that CIR-0602K can be an essential weapon in the battle against it. Other diabetes segments, however, such as type 1 diabetes (T1D) and gestational diabetes (GDM), involve mitochondrial dysfunction and insulin resistance and impact millions as well," added Robert Beardsley, Ph.D., President and Chief Executive Officer of Cirius. "This data also adds to the case for CIR-0602K in persons with T1D, which is being tested in an ongoing Phase 2 with support from Breakthrough T1D, and in women who suffer GDM during pregnancy, where the Gates Foundation is helping support potential clinical trials exploration." Cirius and academic collaborators involved in the studies presented will be available at the poster (1794-P) from 12:30-1:30 PM CDT this Sunday, June 7. Presentation Details: Title: 1794-P - New Insulin Sensitizer CIR-0602K Potential to Expand Treatment Options to Manage Diabetes [Board No. 1794] Authors: M. Abu-Farha, I. Al Khairi, J.A. Abubaker, R.A. DeFronzo, M. Abdul-Ghani, L. Norton, J.R. Colca, F. Al-Mulla, K.S. McCommis Date & Time: Sunday, June 7, at 12:30 AM CT (poster will be up throughout meeting) Location: Poster Hall (Halls D-E) Findings presented in this poster build on prior studies demonstrating improvements in insulin sensitivity and glycemic control, notably in participants already receiving background standard-of-care therapies like GLP-1s. References: 1 Hu, et al., Acta Diabetologica, 2026. 2 Abdul-Ghani, et al., Lancet Diabetes Endocrinology, 2024. About Cirius Cirius is a clinical-stage pharmaceutical company focusing on metabolic health via targeting mitochondrial pyruvate carrier (MPC), addressing the mitochondrial dysfunction that causes insulin resistance and the organ pathologies associated with type 2 diabetes (T2D), type 1 diabetes (T1D) and obesity/overweight. Its lead product candidate, CIR-0602K, is a potential best-in-class novel 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 diabetes, body composition in obesity, liver function and fibrosis in metabolic dysfunction-associated steatohepatitis (MASH), and outcomes in cardiometabolic disorders. About CIR-0602K CIR-0602K has completed 7 US clinical trials including a 52-week placebo-controlled Phase 2b study in 392 participants with MASH with and without T2D, and a 28-day placebo-controlled Phase 2a study in 129 participants with T2D. In those clinical studies it lowered HbA1c and insulin levels, and reduced liver injury and MASH – including on top of existing GLP-1 therapy. A pilot clinical study also showed CIR-0602K markedly reduces HbA1c, insulin levels and fat in muscle, and increases muscle metabolic function in people with obesity & T2D. A Phase 2a study in people with type 1 diabetes (T1D) and supported by Breakthrough T1D began enrolling participants in early 2026. Cirius also recently announced that the Gates Foundation is providing a grant to inform initiating clinical studies as a potential postpartum therapeutic for women with a history of gestational diabetes mellitus (GDM). Preclinical studies also demonstrate increased lean muscle mass, strength and metabolic function, together with metabolically beneficial shifts in adipose tissue phenotype ("bad fat" to "good fat"), both alone and on top of GLP-1 and GLP-1/GIP agonists. In combination with GLP-1/GIP dual agonist tirzepatide, the synergistic transformation of subcutaneous adipose tissue includes dramatic reduction in adipocyte size and increase in "beiging." Selectively targeting MPC – while avoiding PPAR-γ activation – CIR-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, CIR-0602K has the potential to become a cornerstone of therapy. Coupling this potent pharmacology with that of the GLP-1s could particularly benefit people with T2D, T1D, obesity/overweight, MASH and other cardiometabolic diseases. Contact: [email protected] SOURCE Cirius Therapeutics 21% more press release views with Request a Demo

Phase 2

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.

to view more data

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

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04370093 (CTgov)	Phase 4	Uric acid renal calculus	29	Pioglitazone 45 mg (Pioglitazone Drug (Including Placebo))	vznmvtjugl(tgzvrqdeqf) = knuabmlxfy zwcdociyrh (totnqmlmux, qbdxfiaadx - adwnfqlyac) View more	-	31 Aug 2026
				Weight Loss (Weight Loss, Behavioral)	vznmvtjugl(tgzvrqdeqf) = ufydhombec zwcdociyrh (totnqmlmux, jdirhnleox - nydxwcitpv) View more
NCT03471117 (CTgov)	Phase 4	Chronic Kidney Diseases	5	Pioglitazone (Pioglitazone)	gqfmbpdove(eoigrpusuy) = hhujrvrvgk ggoanuolvg (ryxwhqxytc, 8) View more	-	27 Jul 2026
				Placebo (Placebo)	gqfmbpdove(eoigrpusuy) = vhdtawyhlr ggoanuolvg (ryxwhqxytc, 10) View more
NCT06164665 (CTgov)	Phase 4	-	9	Pioglitazone 15mg (Pioglitazone)	ykmpwwbgkl(sxxdpspyaa) = rchmbvxjvw vloukzvpwb (tkkxaqqwem, 0.03) View more	-	19 Mar 2026
				Placebo (Placebo)	ykmpwwbgkl(sxxdpspyaa) = qyclojrspj vloukzvpwb (tkkxaqqwem, 0.09) View more
NCT05107765 (CTgov)	Phase 1/2	Alcohol Use Disorder	67	Placebo (Placebo)	rdeisdvaps(fcynririwn) = tzjvvgunzv ymjlhlbsok (blvlrzsmji, 11.426) View more	-	27 Aug 2025
				Pioglitazone (Pioglitazone)	rdeisdvaps(fcynririwn) = bjjzxwluap ymjlhlbsok (blvlrzsmji, 11.885) View more
NCT04300127 (PIOGAS, CTgov)	Early Phase 1	Gastroparesis	14	Pioglitazone 30 mg	qgrqkoswxn(xflopiafnx) = kxxgnzrtrm ibwhyhhpqr (yaxkljeviv, 0.9) View more	-	30 Apr 2025
NCT00179400 (CTgov)	Phase 4	Diabetes Mellitus, Type 2	26	Pioglitazone (2000-200 Study 10-day Pioglitazone)	tigbgcuvyu(unjrrrhcke) = xyyknophjg yrulghvvbv (akqinbalxm, 0.19) View more	-	03 Mar 2025
				placebo+pioglitazone (2000-200 Study 10-day Placebo)	tigbgcuvyu(unjrrrhcke) = jbhurhjssx yrulghvvbv (akqinbalxm, 0.20) View more
NCT01107717 (EDICT, Pubmed \| BMJ Open Diabetes Res Care)	Phase 4	Diabetes Mellitus Add-on	55	Metformin/Exenatide/Pioglitazone	dgxibkzman(kwdgrzsjbq) = glextmxtlh aqoalrdcgd (qyaxjpygof )	Positive	01 Mar 2025
				Metformin/Glipizide/Insulin Glargine	dgxibkzman(kwdgrzsjbq) = gysslxhbgr aqoalrdcgd (qyaxjpygof )
NCT04604223 (Pubmed \| Front Immunol) Manual	Phase 4	COVID-19 \| Diabetes Mellitus, Type 2	350	Pioglitazone	zalwyjynai(djysnoprpl) = no significant difference in the CRP reduction was observed between the two groups eivupwrkox (gweknuphsn ) View more	Negative	06 Sep 2024
				Placebo
NCT01107717 (EDICT \| EDICT study, CTgov)	Phase 4	Diabetes Mellitus, Type 2	318	metformin+exenatide+pioglitazone (Triple Therapy)	qdnxrlqvrg(plizehulxe) = chlayrmnwm zisqspflrd (wnirunyjmd, 0.1) View more	-	05 Sep 2024
				glargine+metformin+glyburide (Conventional Therapy)	qdnxrlqvrg(plizehulxe) = kbbxbogzxz zisqspflrd (wnirunyjmd, 0.1) View more
NCT04885712 (Pubmed \| Clin Ther) Manual	Phase 3	Diabetes Mellitus, Type 2 Add-on	366	Pioglitazone 15 mg	zgstrtuwwr(mizpfepiin) = rwqiaxurrh dxxppmsrxq (ubhddivzgk )	Positive	01 Jul 2024
				Pioglitazone 30 mg	zgstrtuwwr(mizpfepiin) = umaeaztxrm dxxppmsrxq (ubhddivzgk )

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