A Phase 2 Trial to Evaluate Safety, Tolerability, and Efficacy of Bardoxolone Methyl in Patients With Chronic Kidney Disease at Risk of Rapid Progression

This multi-center, randomized, double-blind, placebo-controlled, Phase 2 trial will study the safety, tolerability, and efficacy of bardoxolone methyl in qualified patients with CKD due to multiple etiologies at risk of rapid disease progression. Approximately 70 patients will be enrolled and randomized 1:1 to either bardoxolone methyl or placebo. Patients with CKD secondary to varying etiologies will be enrolled from age 18-70 years with eGFR ≥ 20 to < 60 mL/min/1.73 m2, and other risk factors for rapid progression of kidney disease.
The maximum target dose will be determined by baseline proteinuria status. Patients with baseline urine albumin to creatinine ratio (UACR) ≤ 300 mg/g will be titrated to a maximum dose of 20 mg, and patients with baseline UACR > 300 mg/g will be titrated to a maximum dose of 30 mg. Qualified patients will be randomized 1:1 to receive either bardoxolone methyl or placebo once daily (preferably in the morning) throughout a 12-week dosing period.
Patients in the study will follow the same visit and assessment schedule. Patients will be assessed during treatment at Day 1, Weeks 1, 2, 4, 6, 8, and 12 and by telephone contact on Days 3, 10, 21, 31, 35, and 45. Date of last dose and the end-of-treatment assessments mark the end of the treatment period. Patients will not receive study drug during a 5-week off-treatment period between Weeks 12 and 17. The off-treatment (OT) period includes 5 visits requiring various assessments to characterize eGFR from the time of study drug discontinuation through Day 35 off-treatment.

Start Date09 Feb 2021

Sponsor / Collaborator

Biogen, Inc.

NCT04494646

/ CompletedPhase 2IIT

BARCONA: A Phase II, Randomized, Double-blind, Placebo-controlled, Multi-center Study of the Effects of Bardoxolone Methyl in Participants With SARS-Corona Virus-2 (COVID-19)

This multi-center, double-blind, placebo-controlled, randomized Phase 2 trial will study the safety, tolerability, and efficacy of bardoxolone methyl in patients hospitalized with confirmed COVID-19. The trial will include approximately 40 patients and is designed to provide an early interim analysis of safety. Patients will be randomized using permuted block randomization in a 1:1 fashion to either once-daily administration of bardoxolone methyl (20 mg) or matching placebo and treatment will be administered for the duration of hospitalization (until recovery), with a maximum treatment duration of 29 days.

Start Date08 Sep 2020

Sponsor / Collaborator

NYU Langone Health

[+1]

100 Clinical Results associated with Bardoxolone Methyl

100 Translational Medicine associated with Bardoxolone Methyl

100 Patents (Medical) associated with Bardoxolone Methyl

528

Literatures (Medical) associated with Bardoxolone Methyl

08 Jan 2026·KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY

Interleukin-1β-induced arthritis involves chondrocyte oxiapoptophagy

Article

Author: Kim, Jae-Sung ; Seo, Jeong-Yeon ; Lim, HyangI ; Oh, Ji-Su ; Kim, Do Kyung ; Kang, Kyeong-Rok ; Chun, Hong Sung

Pro-inflammatory cytokine-induced chondrocyte death contributes to various types of arthritis, including osteoarthritis and rheumatoid arthritis. Recent studies have indicated that oxysterols induce oxiapoptophagy, a form of cell death characterized by oxidative stress, apoptosis, and autophagy. This study aimed to determine whether interleukin-1β (IL-1β)-induced articular cartilage degeneration is associated with chondrocyte oxiapoptophagy. Intra-articular injection of IL-1β into the knee joints of experimental animals induced progressive articular cartilage degeneration and promoted the expression of cholesterol-25-hydroxylase (CH25H), 25-hydroxycholesterol 7α-hydroxylase (CYP7B1), caspase-3, cyclooxygenase-2 (COX-2), and beclin-1. Consistently, IL-1β-stimulated cartilage explants showed proteoglycan loss, and chondrocytes exhibited increased expression and activation of matrix metalloproteinases (MMP-1, MMP-3, MMP-13). IL-1β upregulated the expression of CH25H and CYP7B1, thereby increasing 25-HC production in chondrocytes. Sequentially, IL-1β promoted chondrocyte apoptosis by triggering the caspase cascade, while levels of oxidative stress-related molecules, including reactive oxygen species (ROS), inducible nitric oxide synthase, COX-2, nitric oxide, and prostaglandin E₂, were elevated in chondrocytes. Additionally, IL-1β increased autophagosome formation and the expression of autophagy biomarkers, including beclin-1 and microtubule-associated protein 1A/1B-light chain 3, by increasing p53 and decreasing the phosphorylation of Akt and mTOR in chondrocytes. Furthermore, IL-1β increased the phosphorylation of NF-κB, which subsequently translocated from the cytosol to the nucleus in chondrocytes. CDDO-Me, an inhibitor of the NF-κB pathway, suppressed the IL-1β-induced expression of CH25H, CYP7B1, caspase-3, and beclin-1, as well as ROS production in chondrocytes. Collectively, these findings consistently indicate that IL-1β-induced articular cartilage degeneration is associated with chondrocyte oxiapoptophagy via the NF-κB signaling pathway.

01 Jan 2026·BRAIN RESEARCH BULLETIN

Treadmill Exercise Attenuates CUMS-Induced Depressive Behaviors by Modulating the UPRmt via the Nrf2/Keap1 Pathway

Article

Author: Wang, Jingfeng ; Lei, Siyun ; Peng, Mingshi ; Zhou, Tongxi ; Wang, Yang ; Li, Li ; Si, Juncheng ; Shangguan, Yuwen

INTRODUCTION:

Depression is a very common brain disorder worldwide. It is associated with damaging behaviors such as self-harm and suicide that hurt the brain and body. Mitochondrial dysfunction and dysregulation of the mitochondrial unfolded protein response (UPRmt) are increasingly seen as playing a key role in chronic stress-induced pathophysiology of depression. Aerobic exercise is a very effective non-pharmacological intervention, however, the specific mechanisms of how it modifies hippocampal UPRmt is poorly understood. This effect may be attributed to the Nrf2/Keap1 pathway, a master regulator of cellular antioxidant defense that mediates exercise-induced neuroprotection. This study aimed to investigate whether treadmill exercise modulates UPRmt dysregulation in CUMS-induced depressive mice by activating the hippocampal Nrf2/Keap1 signaling pathway, thereby ameliorating mitochondrial dysfunction and depression-like behaviors.

METHODS:

Male C57BL/6J mice were subjected to a chronic unpredictable model of stress for the induction of a depression model which through exercise on a treadmill for 6 weeks was tested for therapeutic effects. Behaviors consistent with a model of depressive behavior were assessed by OFT, SPT, and TST. Hippocampal mitochondrial function was assessed by transmission electron microscopy, flow cytometry, biochemical, and ELISA. Oxidative stress markers were assessed with biochemical kits and ELISA. The mRNA and protein levels of key markers in the Nrf2/Keap1 pathway and UPRmt were analyzed using RT-qPCR, Western blotting, and immunofluorescence. Pathway dependence was determined using the Nrf2 inhibitor, ML385 and the Nrf2 activator Bardoxolone methyl.

RESULTS:

The six-week treadmill exercise program significantly reduced depression-like behaviors (e.g., anxiety-like behaviors, anhedonia, and behavioral despair), restored mitochondrial functions (mitochondrial cristae morphology, Δψm, ATP, and ROS levels) and eliminated oxidative stress (SOD, T-AOC, and MDA levels). Moreover, treadmill exercise significantly increased the expression of proteins in the Nrf2/Keap1 pathway (Nrf2, Keap1, NQO1, and HO-1), which attenuated CUMS-induced UPRmt markers (HSP60, ClpP, HSP70, LONP1, and ATF5) and the associated stress transcription factor CHOP.

CONCLUSION:

The treadmill exercise activates the Nrf2/Keap1 pathway in the hippocampus, thereby reducing CUMS-induced excessive and dysregulated endoplasmic reticulum stress (UPRmt) in an Nrf2-dependent manner, which leads to a recovery of mitochondrial function, suppression of oxidative stress, and improvement of depressive-like behaviors.

01 Jan 2026·TOXICOLOGY

Deciphering the quantitative relationship between NRF2 and SRXN1 through semi-mechanistic computational modeling

Article

Author: White, Andrew ; Niemeijer, Marije ; Middleton, Alistair M ; Ter Braak, Bas ; Sharma, Raju Prasad ; van de Water, Bob ; Loonstra-Wolters, Liesanne ; Beltman, Joost B

Nuclear factor erythroid 2-related factor 2 (NRF2) plays a vital role in the regulation of various antioxidant response element (ARE) genes, which control physiological processes such as oxidative stress, autophagy, proliferation and apoptosis to maintain cellular homeostasis. It is not understood in detail how the NRF2 program acquires its flexibility with respect to regulation of its downstream targets. Various NRF2 binding partners and cofactors specific to ARE genes are involved in this regulation, and are potentially condition-specific (e.g., type of stressor) and dependent on non-canonical signaling pathways (i.e., crosstalk). Here, we explored the quantitative relationship between NRF2 and sulfiredoxin 1 (SRXN1), a bona fide key NRF2 target gene. We developed a semi-mechanistic mathematical model based on time course experimental data of NRF2 and SRXN1 protein expression in HepG2 cells following single or repeated exposure to NRF2 activating soft electrophiles (sulforaphane, andrographolide, ethacrynic acid or CDDO-me) at a wide concentration range. We showed that a nonlinear mixed effect modeling approach with partially hierarchical parameters accurately captures the observed experimental dynamics. Our analysis highlights that NRF2 requires a cofactor or post-translational modification to regulate its activity as a transcription factor. Moreover, this modulation of the transcription factor activity of NRF2 is time-, compound- and exposure scenario specific. We conclude that a complete understanding of NRF2-mediated ARE genes activation requires detailed dynamic information on NRF2 binding partners and cofactors.

News (Medical) associated with Bardoxolone Methyl

08 Dec 2023

·synapse.patsnap.com

What are Nrf2 inhibitors and how do you quickly get the latest development progress?

Nrf2, or nuclear factor erythroid 2-related factor 2, is a transcription factor that plays a crucial role in the human body's defense against oxidative stress and inflammation. It regulates the expression of various antioxidant and detoxification genes, promoting cellular protection and maintaining redox homeostasis. Nrf2 activation is essential for combating harmful free radicals and reactive oxygen species, which can lead to various diseases, including cancer, neurodegenerative disorders, and cardiovascular conditions. Understanding and harnessing the potential of Nrf2 signaling pathways have become a significant focus in pharmaceutical research, aiming to develop novel therapeutic interventions for oxidative stress-related diseases. Due to the biological characteristics of tumors, multidrug resistance (MDR) is a major cause of chemotherapy failure. Studies have shown that high expression of Nrf2 is found in different types of cancer cells (bladder cancer, lung cancer, pancreatic cancer, liver cancer, and head and neck cancer). Nrf2 can activate the transcription of more than 500 genes in the human genome, most of which have cell protective functions, enhancing the detoxification and excretion of harmful substances and toxic metals, thereby leading to tumor resistance to chemotherapy drugs. Therefore, the development of Nrf2 inhibitors is considered an important strategy to overcome chemotherapy drug resistance. The use of Nrf2 inhibitors as sensitizers in combination with anticancer drugs will reverse tumor resistance and significantly improve the efficacy of chemotherapy drugs. The analysis of the target Nrf2 in the pharmaceutical industry reveals a competitive landscape with companies like Biogen, Inc., Reata Pharmaceuticals, Inc., and Teva Pharmaceutical Industries Ltd. leading the way in R&D progress. Multiple drugs targeting Nrf2 have been approved for indications such as Multiple Sclerosis and Friedreich Ataxia. Small molecule drugs are progressing rapidly, with biosimilars indicating intense competition. The United States is at the forefront of development, followed by the European Union, China, and other countries. The future development of target Nrf2 holds promise for the treatment of various indications and requires continued research and investment in innovative drug development. How do they work?Nrf2 inhibitors are a class of compounds or drugs that specifically target and inhibit the activity of the nuclear factor erythroid 2-related factor 2 (Nrf2). Nrf2 is a transcription factor that plays a crucial role in regulating the expression of genes involved in antioxidant response and cellular defense against oxidative stress. From a biomedical perspective, Nrf2 inhibitors are of interest because they have the potential to modulate the Nrf2 pathway and alter the cellular response to oxidative stress. By inhibiting Nrf2, these compounds can prevent the activation of antioxidant genes and disrupt the cellular defense mechanisms against oxidative damage. Nrf2 inhibitors have been studied in various biomedical contexts, including cancer research. In some cancer cells, Nrf2 is overexpressed, leading to increased antioxidant capacity and resistance to chemotherapy or radiation therapy. By inhibiting Nrf2, researchers aim to sensitize cancer cells to treatment and enhance the effectiveness of anticancer therapies. Moreover, Nrf2 inhibitors have also been investigated as potential therapeutic agents for other conditions associated with oxidative stress, such as neurodegenerative diseases, cardiovascular diseases, and inflammatory disorders. By modulating the Nrf2 pathway, these inhibitors may offer a way to restore redox balance and mitigate the detrimental effects of oxidative stress in these conditions. It is important to note that the development and use of Nrf2 inhibitors require careful consideration of their potential side effects and impact on normal cellular functions. While inhibiting Nrf2 may be beneficial in certain disease contexts, it may also disrupt the physiological antioxidant defense mechanisms and have unintended consequences. Therefore, further research and clinical trials are necessary to fully understand the therapeutic potential and safety profile of Nrf2 inhibitors. List of Nrf2 InhibitorsThe currently marketed Nrf2 inhibitors include: OmaveloxoloneMonomethyl fumarateDiroximel fumarateDimethyl fumarateBardoxolone MethylOltipraz10-Nitrooleic acidALZ-001ALZ-002APPAFor more information, please click on the image below. What are Nrf2 inhibitors used for?Nrf2 inhibitors have been studied in various biomedical contexts, including cancer research. For more information, please click on the image below to log in and search. How to obtain the latest development progress of Nrf2 inhibitors?In the Synapse database, you can keep abreast of the latest research and development advances of Nrf2 inhibitors 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!

10 May 2023

·www.fiercebiotech.com

Reata, Kyowa Kirin's bardoxolone faces the music after ph. 3 flop, ending 13-year saga

Kyowa Kiryin and Reata have worked together on bardoxolone for more than 13 years. Reata and Kyowa Kirin are burying bardoxolone methyl after new phase 3 data laid bare the dwindling—if not non-existent—potential of the kidney disease treatment. The two companies said that while the treatment hit the primary and secondary endpoints in a phase 3 trial testing bardoxolone in patients with diabetic kidney disease, there was no difference in the time to end-stage renal disease between treated patients and placebo. That was the nail in the coffin, with Kyowa and Reata saying Wednesday that they’ll end development of bardoxolone as a treatment for chronic kidney disease. Investors punished Reata for the disappointing conclusion, with shares down roughly 23% an hour after the market opened, from $105.37 down to $81. Thus ends an incredibly tumultuous saga for bardoxolone that’s extended some 13 years and spanned three different partnerships. Reata first handed over commercialization rights to certain markets to both Kyowa Kirin and Abbott (now AbbVie) back in 2009 and 2010, respectively, when bardoxolone was in phase 2 development for patients with diabetes who had chronic kidney disease. AbbVie double dipped a year later, offering up another $400 million to jointly develop and commercialize other Reata projects aimed at kidney and autoimmune diseases. But the wheels slowly, but surely, began to come off, beginning in 2012 when a phase 3 trial was halted after treated patients were experiencing higher rates of heart-related side effects, including hospitalizations and death. The company swiftly pivoted to aiming the treatment at patients with pulmonary arterial hypertension. Reata couldn’t just step away from the kidney ambitions, however, launching additional studies including one testing bardoxolone in patients with chronic kidney disease caused by Alport syndrome. AbbVie had enough, backing out in 2019 and recouping $330 million out of the original $850 million it handed over across the two deals. FDA advisors told Reata to go back to the drawing board two years later when they unanimously voted against the risk-benefit profile of bardoxolone kidney disease treatment in patients with Alport syndrome. The FDA formally rejected the med last year. Kyowa Kirin has dutifully held on throughout, launching a phase 3 study five years ago testing bardoxolone in diabetic patients with chronic kidney disease. But after the latest readout, the Japanese pharma said it no longer sees a viable regulatory route. The axed development plan has forced Reata to address a $350 million investment from Blackstone in 2020 to help develop bardoxolone, the majority of which was to be paid from royalties on the treatment. Reata says Blackstone will now receive single-digit royalties on Skyclarys (omaveloxolone), which was approved in March as a treatment for Friedreich’s ataxia and is one of two assets remaining in the company's pipeline. Reata's attention is now on the commercialization effort for Skyclarys. The company says it has received approximately 500 patient start forms since approval but doesn’t expect to be in specialty pharmacies until mid-August while the FDA reviews an NDA supplement submitted by Reata asking for an increase in drug substance specification. The company says approval of the supplement is required before the drug can be sent to pharmacies. Reata is also working on RTA 901 treatment for diabetic peripheral neuropathic pain, completing a phase 1 single ascending and multiple ascending dose study. The company planned to launch a phase 2 study in the second half of 2022 but it’s unclear if that’s happened. A phase 2 clinical trial record was not found on clinicaltrials.gov.

Phase 3Phase 2Drug ApprovalNDAPhase 1

10 May 2023

·endpts.com

Reata culls bardoxolone, ending decade of R&D on troubled kidney disease drug

Reata’s long and winding road with bardoxolone appears to be over. The Plano, TX-based biotech and partner Kyowa Kirin said Wednesday morning that they are scrapping development of the asset in chronic kidney disease programs, which include CKD caused by Alport syndrome, people with diabetic CKD and a rare, hereditary form of the disease. With that, Reata expects to save more than $100 million previously set aside for the drug, a move that will push runway to the end of 2026, the company said in a presentation. Reata also disclosed a non-dilutive $275 million debt facility as part of its first-quarter update .

100 Deals associated with Bardoxolone Methyl

External Link

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D09585	Bardoxolone Methyl	-	DB05983

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Indication	Highest Phase	Country/Location	Organization	Date
Nephritis, Hereditary	NDA/BLA	European Union	Reata Pharmaceuticals, Inc.	27 Oct 2021
Kidney Failure, Chronic	Phase 3	United States	Biogen, Inc.	08 Mar 2019
Kidney Failure, Chronic	Phase 3	Japan	Biogen, Inc.	08 Mar 2019
Kidney Failure, Chronic	Phase 3	Australia	Biogen, Inc.	08 Mar 2019
Kidney Failure, Chronic	Phase 3	France	Biogen, Inc.	08 Mar 2019
Kidney Failure, Chronic	Phase 3	Spain	Biogen, Inc.	08 Mar 2019
Polycystic Kidney, Autosomal Dominant	Phase 3	United States	Biogen, Inc.	08 Mar 2019
Polycystic Kidney, Autosomal Dominant	Phase 3	Japan	Biogen, Inc.	08 Mar 2019
Polycystic Kidney, Autosomal Dominant	Phase 3	Australia	Biogen, Inc.	08 Mar 2019
Polycystic Kidney, Autosomal Dominant	Phase 3	France	Biogen, Inc.	08 Mar 2019

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT03918447 (FALCON, CTgov)	Phase 3	Polycystic Kidney, Autosomal Dominant	667	Placebo oral capsule	dnorvayxgt(qqfmdsnpuu) = xktwszzvxz cewnwktkfj (gchjolqxzh, 0.769) View more	-	11 Jun 2024
NCT03749447 (EAGLE, CTgov)	Phase 3	Polycystic Kidney, Autosomal Dominant \| Kidney Failure, Chronic \| Nephritis, Hereditary ... View more	270	Placebo+Bardoxolone Methyl (Prior Placebo to Bardoxolone Methyl)	cnniaubvzp = aqufxtiffc kwmydyvjal (agfoojuiar, spgbshhhiv - siawfiakcf) View more	-	19 Mar 2024
				Bardoxolone Methyl (Prior Bardoxolone Methyl to Bardoxolone Methyl)	cnniaubvzp = nynkvbpzqi kwmydyvjal (agfoojuiar, hcdhpmzvop - ryfasxfhcq) View more
NCT03068130 (RANGER, CTgov)	Phase 3	Hypertension, Pulmonary	261	Bardoxolone Methyl	abgnogstkn = xpwbngadni aaxiayhhzc (fomdcooqid, gikblnsmop - bzymxrpmgz) View more	-	12 Oct 2023
NCT03019185 (CARDINAL, CTgov)	Phase 2/3	Nephritis, Hereditary	187	Bardoxolone Methyl (Phase 2 Bardoxolone Methyl)	lkzuzvxfxg(godivkkoax) = nzwuughuwc xlaxiadytk (ujundsskak, 1.4111) View more	-	11 Oct 2023
				Placebo Oral Capsule (Phase 3 Placebo)	gxcohotmbo(nnvmgxgzjb) = wwvbejckzi zgjupsoydg (vgojiqluqd, 1.248) View more
NCT02657356 (CTgov)	Phase 3	Connective Tissue Diseases \| Pulmonary arterial hypertension associated with connective tissue disease	202	Placebo capsules (Placebo Capsules)	ajmxehmdri(uafhguflrp) = gxvpgywgqz sagnbyivyl (aixpxkpkuw, 4.954) View more	-	19 May 2023
				Bardoxolone methyl capsules (Bardoxolone Methyl Capsules)	ajmxehmdri(uafhguflrp) = iqghkapoqy sagnbyivyl (aixpxkpkuw, 4.952) View more
NCT04702997 (MERLIN, CTgov)	Phase 2	Chronic Kidney Diseases	81	Bardoxolone methyl oral capsule (Bardoxolone Methyl)	oriwkaiqti(hnkxkghhly) = gzlgxcavkk xgrmoqcxuv (dqxmuyrrco, 0.925) View more	-	01 Dec 2022
				Placebo oral capsule (Placebo)	oriwkaiqti(hnkxkghhly) = rbekkoyzxz xgrmoqcxuv (dqxmuyrrco, 0.868) View more
NCT03019185 (CARDINAL, Pubmed) Manual	Phase 2/3	Nephritis, Hereditary	157	Bardoxolone Methyl	nocnjhtute(swmljemeoc) = jawfenfzqp crppqdcwxa (ccpsmexhpa ) View more	Positive	21 Nov 2022
				Placebo	nocnjhtute(swmljemeoc) = pbesugpapf crppqdcwxa (ccpsmexhpa ) View more
NCT03749447 (EAGLE, ISN WCN2022)	Phase 3	Nephritis, Hereditary	112	Bardoxolone methyl 5 mg	fwbkzuwvcm(nwbpvumwwg) = bhboaqtovj jayhutbbku (myqanwmbdl, 11.1)	Positive	01 Feb 2022
NCT03366337 (PHOENIX, CTgov)	Phase 2	Polycystic Kidney, Autosomal Dominant \| Type 1 diabetes mellitus with established diabetic nephropathy \| Glomerulosclerosis, Focal Segmental ... View more	103	Bardoxolone methyl capsules (Bardoxolone Methyl - ADPKD)	tonxvducdz(uxmzmtvkch) = faeeiibfaf eaxidskjrn (wolsvqkvxg, 1.3743) View more	-	18 Jan 2022
				Bardoxolone methyl capsules (Bardoxolone Methyl - IgAN)	tonxvducdz(uxmzmtvkch) = rihqklqvgl eaxidskjrn (wolsvqkvxg, 1.5700) View more
NCT04494646 (CTgov)	Phase 2	COVID-19	40	Bardoxolone Methyl (Bardoxolone Methyl)	mzysnkluwe = wzqvfjcsfk ovvjninyyw (mnhxoricnq, hjfrdsgkab - adxbtvdfmx) View more	-	12 Jan 2022
				Placebo (Placebo)	mzysnkluwe = gtbsmnjzvp ovvjninyyw (mnhxoricnq, ajfxtsuqoq - hqyngchcbn) View more

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