Drug Database
SU

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

PubMedBMC plant biology2026-11-11

Complementary protective effects of autophagy and antioxidative activity on salt tolerance in Suaeda salsa seedlings.

Deng Lina L, Feng Yanya Y, Cheng Hai H, Liu Changqing C et al.

Soil salinity is a major concern for agricultural productivity worldwide. The halophyte Suaeda salsa can survive in saline environments, and the timely removal of reactive oxygen species (ROS) by plants is critical for enhancing salt tolerance. However, the mechanisms underlying salt tolerance in S. salsa remain unclear. In this study, we investigated the relationships among autophagy, antioxidant enzyme activity, and ROS accumulation in S. salsa under salt stress. The root/shoot ratio of S. salsa desreased as salt concentration increased, whereas dry weight and polysaccharide content remained relatively high under saline conditions. Under 200 mM sodium chloride treatment, S. salsa exhibited the strongest superoxide anion radical and hydroxyl radical scavenging capacities, along with the lowest H2O2 content. Transmission electron microscopy revealed basal autophagy under 200 mM sodium chlorid. Superoxide dismutase activity remained high under salt stress, while the activities of catalase and peroxidase were highest in the salt-free control. Transcriptome analysis showed that the expression profiles of key genes were broadly consistent with changes in enzyme activity and autophagy. Correlation analysis further indicated that both antioxidant enzyme activity and autophagy were associated with free radical scavenging. Superoxide anion radical scavenging ability was negatively correlated with Atg8, Pod, and Cat; hydroxyl radical scavenging ability was positively correlated with Sod, and H2O2 content was positively correlated with Cwm. Our findings suggest that autophagy and antioxidative enzymes act in a coorrdinated protective network during S. salsa adaptation to salt stress, providing a theoretical foundation for future work on regulating salt tolerance.

PMID 43009794
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PubMedNano letters2026-11-11

ROS-Responsive Selenocysteine-Releasing Nanozyme for Targeted Ferroptosis Suppression and Pancreatic β-Cell Protection in Type 2 Diabetes.

Zhang Juncai J, Li Yuqi Y, Xie Yingying Y, Wang Runqi R et al.

Pancreatic β-cell ferroptosis, driven by oxidative stress and impaired glutathione peroxidase 4 (GPX4) activity, has emerged as an important contributor to the progression of type 2 diabetes mellitus (T2DM). However, persistent reactive oxygen species (ROS) accumulation and insufficient selenocysteine (Sec) availability limit GPX4-dependent antioxidant defense, making effective ferroptosis intervention challenging. Here, we engineered a ROS-responsive Sec-loaded copper-based single-atom nanozyme (Se@CuSAzyme) that combines catalytic ROS scavenging with Sec supplementation. Benefiting from its intrinsic superoxide dismutase- and catalase-like activities, Se@CuSAzyme efficiently eliminated excessive ROS, while oxidative stress-triggered Sec release enhanced GPX4 expression. As a result, Se@CuSAzyme markedly suppressed high glucose and erastin-induced ferroptosis, reduced lipid peroxidation, and preserved mitochondrial integrity in pancreatic β-cells. In high-fat diet/streptozotocin-induced diabetic mice, Se@CuSAzyme demonstrated therapeutic efficacy comparable to that of metformin in ameliorating hyperglycemia, alleviating insulin resistance, and increasing energy expenditure. Importantly, Se@CuSAzyme outperformed metformin in protecting against hepatic steatosis and glycolipid metabolic dysfunction.

PMID 43012594
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PubMedInternational journal of immunopathology and pharmacology2026-11-11

Ayanin attenuates thioacetamide-induced liver toxicity in vivo: Modulation of oxidative stress, inflammation, and apoptosis.

Ibrahim Alsharif Hanan H, Jabbar Ahmed A J AAJ

BackgroundAyanin is an O-methylated flavonol isolated from many plant species recognized for its in vitro antioxidant and anti-inflammatory properties. However, studies on its toxicity profile and hepatoprotective effects are scarce.ObjectiveTherefore, this study investigates the acute toxicity and hepatoprotective effects of ayanin in thioacetamide (TAA)-induced hepatotoxicity in rats, along with its association with the regulation of cellular processes.DesignAcute toxicity evaluation included a single oral delivery of 250 and 500 mg/kg Ayanin to rats, which were observed regularly for 14 days. In a hepatoprotective experiment, rats were treated (p.o.) with 50 mg/kg silymarin, 20 mg/kg Ayanin, or 40mg/kg Ayanin p. o. daily, along with 200 mg/kg TAA (2 injections/week, i.p.) for two months.ResultsThe results indicated non-toxic effect of up to 500 mg/kg Ayanin, and a noticeable hepatoprotective effect of Ayanin (20 and 40 mg/kg), preserving body weight/liver weight index and liver histoarchitecture (lowering liver fibrosis phenotypes, including hemorrhage, reduced splenic congestion/necrosis, and collagen generation). These effects aligned with its antioxidant(up-regulating superoxide dismutase, catalase, and reducing malondialdehyde levels) and anti-inflammatory effects (reducing tumour necrosis factor-α and interleukin-6). The anti-apoptotic effects of Ayanin (20 and 40 mg/kg) were confirmed by significant (p<0.001) lowering of Bax by 10.20% and 34.04%; lessening caspase-3 by 26.02 and 47.74%; while increasing Bcl-2 concentration by 107.51 and 122.55%, respectively, which ultimately improved the liver's function.ConclusionThe results suggest that Ayanin exhibits anti-fibrotic action, attributable to orchestrated pathways associated with oxidative stress, inflammation, and apoptosis.

PMID 43010865
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PubMedNutrition & diabetes2026-11-11

Effectiveness of bitter almond (Amygdalus communis L. var. Amara) gum as a prebiotic on glycemic indices, oxidative stress, and antioxidant biomarkers in women with type 2 diabetes mellitus: a randomized, placebo-controlled trial.

Rafiei Zahra Z, Yagin Neda Lotfi NL, Dehghan Parvin P, Aliasgharzadeh Soghra S et al.

Type 2 diabetes mellitus (T2DM) is marked by hyperglycemia, oxidative stress, and systemic inflammation. Prebiotics, such as bitter almond gum (Amygdalus communis L. var. amara), have the potential to influence gut microbiota and metabolic parameters, suggesting their role as dietary interventions for enhancing glycemic control in the management of T2DM. This study evaluated the effects of bitter almond gum on glycemic indices, oxidative stress, and oxidant biomarkers in individuals with T2DM. This randomized, triple-blinded, placebo-controlled, clinical trial included 44 women with T2DM. They were assigned to either the intervention (n = 22) or control (n = 22) groups receiving 5 g per day of bitter almond gum or maltodextrin, respectively, for a duration of 8 weeks. Various outcomes, including glycemic indices, lipopolysaccharide (LPS) levels, oxidative stress markers, and antioxidant biomarkers, were measured at baseline and again after 8 weeks. Bitter almond gum supplementation significantly reduced insulin levels (-1.23 mg/dL; 95% CI, [-2.40, -0.03]), LPS ( - 6.32 mg/dL; 95% CI, [-9.51, -3.09]), pentosidine (-38.02 mg/dL; 95% CI, [-55.18, -20.71]), and oxidative stress index (OSI) (-5.59 mg/dL; 95% CI, [-10.81, -0.30]), and increased McAuley_index (0.20 mg/dL; 95% CI, [0.14, 0.32]), total antioxidant capacity (TAC) (0.18 mg/dL; 95% CI, [0.07, 0.26]), superoxide dismutase (SOD) (180.20 mg/dL; 95% CI, [65.27, 295.14]), and glutathione peroxidase (GSH-Px) (2.21 mg/dL; 95% CI, [0.78, 3.62]) compared with the placebo group (P < 0.05, ANCOVA adjusted for baseline and confounding factors). Bitter almond gum supplementation for 8 weeks led to improvements in glycemic control, a reduction in oxidative stress, and an enhancement of antioxidant defenses in women with T2DM. These findings indicate its potential as a complementary functional food for managing diabetes.

PMID 43009479
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PubMedFrontiers in cell and developmental biology2026-11-11

Diosbulbin B aggravates doxorubicin-induced hepatotoxicity with PI3K/AKT signaling and redox-inflammatory stress responses.

Xie Xinran X, Xing Yudi Y, Liu Xiaoyue X, Zhai Jinghui J et al.

This study evaluated whether diosbulbin B (DB) affects doxorubicin (DOX)-induced hepatotoxicity. It further characterized the associated changes in redox-related biochemical indices, mitochondrial membrane potential, inflammatory stress-related proteins, and DNA damage-response-related proteins. ICR mice were treated with DOX and/or DB to assess liver injury and serum biochemical changes. LO2 hepatocyte-like cells were used as a simplified in vitro model to evaluate cell viability, nuclear morphology, lactate dehydrogenase release, and mitochondrial membrane potential. Bulk RNA sequencing and Western blotting were performed to characterize transcriptomic and protein-expression changes associated with combined DB and DOX exposure. DB co-administration was associated with lower body weight, comparable hepatic histopathological alterations, and higher serum alanine aminotransferase and aspartate aminotransferase activities in DOX-treated mice. Redox-related biochemical indices showed a non-classical pattern, including increased glutathione levels, decreased malondialdehyde levels, and reduced superoxide dismutase activity in the treatment groups. These changes are indicative of altered redox-related biochemical status rather than direct evidence of a specific oxidative cell-death mechanism. In LO2 cells, DB further reduced cell viability, increased lactate dehydrogenase release, altered nuclear morphology, and enhanced mitochondrial membrane depolarization during DOX exposure. Comparison of the DOX + DB and DOX groups identified 1,221 differentially expressed genes, including 130 upregulated and 1,091 downregulated genes. Enrichment analyses showed terms and pathways related to DNA repair, cell-cycle regulation, chromatin organization, and stress-response processes. Combined treatment was also associated with increased phospho-PI3K/PI3K, phospho-AKT/AKT, p38, TXNIP, IL-6, and IL-8 levels, as well as reduced p53 and GADD45A levels. DB co-treatment was associated with enhanced DOX-related hepatotoxicity and cytotoxic changes in LO2 cells. Combined exposure was accompanied by mitochondrial membrane depolarization, non-classical redox-related biochemical alterations, increased inflammatory and stress-related protein expression, and reduced p53 and GADD45A abundance. Because direct assays of lipid peroxidation-dependent cell death, ferroptosis, oxytosis, necroptosis, and DNA damage were not performed, the present data do not establish a specific oxidative cell-death mechanism.

PMID 43011381
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PubMedApplied and environmental microbiology2026-11-11

Integrated physiological and multiomic analyses reveal the multilayered aluminum tolerance mechanisms of acidophilic alga Coccomyxa sp. A2.

Yang Jinru J, Banda Joseph Frazer JF, Yu Na N, Hao Chunbo C et al.

Acid mine drainage (AMD) is a pervasive global environmental challenge, and algal-based bioremediation represents one of the most robust strategies for its treatment. However, the mechanisms by which algae survive in metal-rich AMD remain largely unclear. Here, we integrated physiological, transcriptomic, and proteomic analyses to explore the tolerance mechanisms of the acidophilic alga Coccomyxa sp. A2 to aluminum (Al), a metal prevalent in AMD. The results demonstrated that A2 exhibited substantially higher Al tolerance than the model alga Chlamydomonas reinhardtii under their respective optimal pH conditions. Upon Al exposure, A2 significantly increased the extracellular levels of three strong organic acids (oxalic, citric, and tartaric acids), thereby facilitating chelation of free Al3+ present in the acidic environment. In the near-neutral cytosol, A2 accumulated a broader array of organic acids at higher concentrations to sequester Al despite severe extracellular H+ stress. To restrict Al influx, A2 enhanced the synthesis of cellulose, hemicellulose, and proteins across the distinct layers of its cell wall, increasing cell wall dry weight by 66%. This remodeling was probably supported by starch degradation, enhanced gluconeogenesis, and Calvin cycle activation, which together supplied sufficient monosaccharide precursors for polysaccharide synthesis. Concurrently, the upregulation of glycosyltransferases facilitated rapid polysaccharide chain elongation. To scavenge ROS, the alga likely initiated a temporally coordinated, biphasic antioxidant response, in which non-enzymatic ascorbic acid pools compensated for lagging superoxide dismutase activity during the early acute phase of stress. Calcium, abscisic acid, and jasmonic acid coordinated these defense mechanisms, with calcium serving as the primary signaling hub.IMPORTANCEThe conventional treatment method for acid mine drainage (AMD) involves neutralization with lime, which is costly and generates large amounts of sludge that is difficult to manage. The application of sulfate-reducing bacteria (SRB) presents a promising alternative by eliminating secondary pollution and enabling metal sulfide recovery. However, a key challenge of this approach is ensuring an affordable and sustainable organic carbon source for SRB since AMD is oligotrophic. A potential solution is the in-situ cultivation of acidophilic algae. Given the high metal concentrations in AMD, investigating the metal tolerance mechanisms of acidophilic algae is vital for producing sufficient biomass to support SRB. Meanwhile, about 40% of the world's arable soils are acidic, and these soils typically contain high concentrations of aluminum (Al), which is a major factor limiting crop production. Therefore, research on the exceptional Al tolerance mechanisms of acidophilic algae can provide insights into improving crop metal resistance through genetic engineering techniques.

PMID 43012561
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