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superoxide dismutase (bSOD, OXIS / Orgotase / Peroxinorm)

✓ Approved

GT Biopharma, Inc. · therapeutic agent

What is superoxide dismutase?

superoxide dismutase is a therapeutic agent developed by GT Biopharma, Inc.. It is approved for therapeutic indications.

Drug Profile

Brand NamesbSOD, OXIS, Orgotase, Peroxinorm
CompanyGT Biopharma, Inc.
StatusApproved
Sources: ClinicalTrials.gov, GT Biopharma, Inc.

Therapeutic Indications

superoxide dismutase is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Nervous system disordersAmyotrophic lateral sclerosis✓ Approved
Musculoskeletal and connective tissue disordersArthritis✓ Approved

Related Research Articles

PubMedAdvanced science (Weinheim, Baden-Wurttemberg, Germany)2026-08-30

An Injectable ROS-Responsive Nanozyme Hydrogel Regulates the Uterine Microenvironment to Prevent Intrauterine Adhesions.

Cheng Peixian P, Song Jian J, Li Yuxin Y, Chen Ming M et al.

Intrauterine injury triggers a self-reinforcing cycle of inflammation, oxidative stress, and fibrosis that culminates in intrauterine adhesions (IUA), severely impairing women's reproductive health. Current treatments, including hysteroscopic adhesiolysis combined with hormonal therapy or physical barriers, show high recurrence and cannot simultaneously target these interconnected pathways. Here, we developed an injectable ROS-responsive hydrogel (GPP) loaded with cerium-tannic acid metal-phenolic nanozymes (CeTA) that exhibit superoxide dismutase (SOD)- and catalase (CAT)-mimetic activities. Unlike passive barriers, its boronate ester-crosslinked network remains stable under physiological conditions but is selectively cleaved in ROS-rich inflammatory microenvironments, enabling on-demand, lesion-localized CeTA delivery. In vitro, by scavenging excess superoxide and hydrogen peroxide, CeTA alleviated oxidative stress, restored mitochondrial membrane potential, promoted macrophage repolarization from the pro-inflammatory M1 to the anti-inflammatory M2 phenotype, and reversed TGF-β1-induced fibrosis in endometrial stromal cells. In a rat IUA model, CeTA@GPP hydrogel restored uterine antioxidant enzyme activity, suppressed TGF-β1 expression and myofibroblast activation, and enhanced cell proliferation and angiogenesis; transcriptomic profiling confirmed coordinated down-regulation of the inflammation, oxidative stress, and fibrosis pathways. Accordingly, CeTA@GPP hydrogel promoted structural and functional endometrial regeneration and improved endometrial receptivity. By integrating minimally invasive injectability, physical barrier protection, and intelligent ROS-responsive multi-target bioactivity, CeTA@GPP hydrogel provides a promising strategy for IUA.

PMID 42669616
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PubMedPakistan journal of medical sciences2026-08-30

Evaluation of serum antioxidant markers and calcium levels in women with Arthritis.

Rehman Abdul A, Jamil Muhammad M, Farhan Maham M, Khan Amna Saleem AS et al.

Osteoarthritis (OA) and Rheumatoid Arthritis (RA) are chronic, degenerative and inflammatory joint diseases, aggravated by reactive oxygen species (ROS) and impaired antioxidant defense system. However, gender based oxidative stress analysis remain under-examined, despite increasing evidence points towards sex-based biochemical changes in arthritis patients. The study aimed to measure the antioxidant activities of enzymes including superoxide dismutase (SOD), Glutathione reductase (GR) alongside reduced glutathione (GSH), and catalase (CAT) in female arthritis patients. Calcium balance is also estimated in order to analyze the bone demineralization. The case-control study was designed and conducted at the Orthopedic Department of a Dr. Ruth K. M. Pfau, Civil hospital, Karachi. Serum levels of GSH, GR, SOD, CAT, and calcium were evaluated in 42 arthritis patients and 16 age matched healthy female controls by using standard spectrophotometric and biochemical assays. Data was expressed as mean ± SD and analyzed statistically to compare both the groups. Arthritis patients in comparison with healthy controls showed significant decrease in GSH (p < 0.001) and GR (p < 0.01) levels, while SOD and CAT levels were slightly reduced but non-significant. Similarly, slightly higher calcium levels were also observed, suggesting altered mineral homeostasis associated with inflammatory conditions. The simultaneous decrease in antioxidant enzyme activities suggests the impaired redox homeostasis in female patients. The study highlights an altered antioxidant status and disturbed calcium homeostasis in female patients. These alterations in biochemical system suggest the therapeutic potential of antioxidant and calcium modulating interventions as effective treatment for managing and slowing disease progression in females.

PMID 42668919
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PubMedComparative biochemistry and physiology. Toxicology & pharmacology : CBP2026-08-30

Combined exposure to cypermethrin and sulfamethoxazole is associated with muscle injury in grass carp through oxidative stress, endoplasmic reticulum stress, MAPK activation, autophagy, and apoptosis.

Yin Yutong Y, Zhang Xin X, Lu Hongmin H, Ma Yingjie Y et al.

The co-occurrence of pesticides and antibiotics in aquatic environments has raised increasing concern because of their potential effects on aquatic organisms. Cypermethrin (CMN) and sulfamethoxazole (SMZ) are representative pyrethroid pesticides and sulfonamide antibiotics, respectively, but their combined effects on fish muscle remain poorly understood. In this study, grass carp (Ctenopharyngodon idella) were exposed to CMN (0.65 μg/L), SMZ (0.30 μg/L), or their combination for 42 days. Network toxicology, histopathology, oxidative stress assays, Western blotting, protein-protein interaction analysis, and molecular docking were used to investigate muscle injury and related molecular responses. The MIX group showed more severe pathological alterations than the single-exposure groups, including extensive myofiber disruption, fragmentation, nuclear condensation, and nuclear displacement. It also increased malondialdehyde levels, decreased total superoxide dismutase activity, and markedly altered proteins associated with endoplasmic reticulum stress. Phosphorylation of P38, JNK, and ERK was elevated, indicating enhanced MAPK signaling. Suppression of the PI3K-AKT-mTOR pathway was accompanied by increased Beclin-1 expression, an elevated LC3-II/LC3-I ratio, and decreased P62 expression, suggesting enhanced autophagy-related responses. In addition, Bax, Caspase-9, and Caspase-3 expression increased, whereas Bcl-2 expression decreased, indicating enhanced mitochondria-associated apoptotic signaling. Network analysis and molecular docking identified HSP90, HSP70, and Caspase-3 as potential core targets. These findings show that combined CMN and SMZ exposure induces severe muscle injury in grass carp, with the MIX group exhibiting the most pronounced changes in oxidative stress, endoplasmic reticulum stress, MAPK activation, autophagy, and apoptosis.

PMID 42669390
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PubMedImmunobiology2026-08-30

The Sesn2/Nrf2 axis suppresses oxidative stress and pyroptosis-associated signaling in LPS/nigericin-challenged alveolar macrophages.

Zhang Qiong Q, Zhou Guanlin G, Gao Chunming C, Jia Sen S et al.

Pyroptosis is a key mechanism driving immune imbalance in sepsis, while the stress-induced protein Sestrin 2 (Sesn2) and Nuclear factor E2-related factor 2 (Nrf2) are core regulators of antioxidant defense. No existing studies have clarified the interactive regulatory effect of the Sesn2/Nrf2 axis on pyroptosis in alveolar macrophages. Therefore, this study aims to investigate the regulatory mechanism of the Sesn2/Nrf2 axis on pyroptosis and oxidative stress in LPS/nigericin-challenged alveolar macrophages, providing a theoretical basis for further understanding of sepsis. Bioinformatics analysis involved screening differentially expressed genes in sepsis from the Gene Expression Omnibus dataset GSE185263, intersecting them with genes related to pyroptosis and ferroptosis, constructing a protein-protein interaction network, and identifying core genes. An inflammatory injury model was established in the mouse alveolar macrophage cell line MH-S by stimulating cells with LPS and nigericin. Interventions were performed using siRNA to knock down Sesn2 and plasmids to overexpress Nrf2. Cell viability, oxidative stress markers, expression of pyroptosis-related molecules, and secretion of inflammatory cytokines were measured. SESN2 as a key gene common to sepsis, pyroptosis, and ferroptosis. The Sesn2/Nrf2 signaling axis significantly enhanced the cell viability of MH-S cells after inflammatory injury, increased Superoxide Dismutase activity and Glutathione levels, and reduced reactive oxygen species and Lactate Dehydrogenase levels. Simultaneously, this axis suppressed the expression of pyroptosis-related inflammasomes (NOD-like receptor thermal protein domain associated protein 3, Absent in melanoma 2) and key execution proteins (Gasdermin D, Cleaved Caspase-1, Caspase-4), and reduced the secretion of inflammatory cytokines IL-1β, IL-18, and TNF-α. Sesn2 and Nrf2 exhibited mutual positive regulation in macrophages following inflammatory injury. In vitro cell model studies indicate that the Sesn2/Nrf2 axis synergistically suppresses oxidative stress and pyroptosis-associated signaling in LPS/nigericin-challenged alveolar macrophages, suggesting that this axis may represent a potential target warranting further investigation in in vivo models.

PMID 42669253
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PubMedEnvironmental technology2026-08-30

Preparation and catalytic degradation performance of cobalt ferrite based on the recycling of retired lithium-ion battery cathode materials.

Shuai Hui H, Tang Ping P, Yu Yezhe Y

In response to dual demands of advanced oxidation of organic pollutants and recycling of retired lithium-ion batteries, this research proposed a high-value recycling method to convert cobalt resources from retired lithium-ion batteries into high-performance cobalt ferrite (CoFe2O4) catalysts. Cobalt leaching and cobalt ferrite synthesis were coupled into an integrated process to achieve efficient cobalt leaching (> 98%). By optimising the sol-gel process, optimal conditions were identified: tartaric acid-to-total metal ion molar ratio 2:1, pH = 7.0, and calcination at 500°C for 2 h. The spinel-type cobalt ferrite particles obtained under these conditions are well-structured, with high catalytic activity, and stable magnetic properties. The cobalt ferrite material catalyzed the degradation of rhodamine B (RhB) by activated peroxymonosulfate (PMS) with excellent performance. Under the optimised reaction conditions (PMS concentration of 0.50 mmol/L, cobalt ferrite concentration of 75 mg/L, initial pH = 7, RhB concentration of 20 mg/L, and reaction time of 90 min), the degradation rate of RhB could reach 99.46%, with an apparent rate constant of 0.0387 min-1. The quenching experiments showed that sulfate radical (SO4-·) was the main reactive oxygen species for the degradation of RhB, while hydroxyl radical (·OH) and superoxide radical (·O2-) also promoted the activation of PMS. Moreover, the cobalt ferrite catalyst could maintain high catalytic activity after multiple cycles, with the degradation rate of RhB remaining above 81%, demonstrating favourable cycling stability. This research offers a novel approach for retired lithium-ion battery valorisation and theoretical support for advanced heterogeneous catalyst development.

PMID 42669456
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PubMedFood microbiology2026-08-29

Molecular mechanisms of the VBNC state induced by polyhexamethylene guanidine in biofilm-associated Staphylococcusaureus.

Zeng Shuhao S, Ma Tianzheng T, Lu Yuxuan Y, Duan Menghua M et al.

Polyhexamethylene guanidine (PHMG) is widely used to eliminate biofilms in the dairy industry; however, sublethal chemical stress inadvertently forces pathogens into a viable but non-culturable (VBNC) state. This study examined PHMG-induced VBNC formation in biofilm-associated Staphylococcus aureus under laboratory and food-relevant conditions. PHMG at 4.0 mg/mL (0.4%) eliminated culturability within 3 h, whereas flow cytometry detected a viable fraction of 25.70 ± 3.83% in TSB-grown biofilms at 25 °C. This shift was primarily driven by acute oxidative stress, marked by a 1.56-fold accumulation of intracellular ROS levels and compensatory increases in catalase and superoxide dismutase activities. Concurrently, the cells underwent severe metabolic shutdown, characterized by intracellular ATP depletion, membrane depolarization, and cell shrinkage. Transcriptional profiling of energy- and virulence-related genes confirmed this systemic reprogramming, revealing altered expression in key energy metabolism and stress survival pathways. Crucially, this dormant state was highly unstable in food environments. When transferred back to milk, the VBNC cells rapidly resuscitated within 4 h and successfully resumed hemolysin production. Ultimately, these findings highlight the urgent need for the dairy industry to re-evaluate current PHMG disinfection strategies and closely monitor hidden VBNC risks to ensure food safety.

PMID 42668194
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