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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

PubMedJournal of International Society of Preventive & Community Dentistry2026-07-25

A Comparative Evaluation of Serum and Salivary Antioxidant Levels in Healthy Controls, Gingivitis, and Periodontitis Patients.

Dsouza Teena Sheethal TS, Ashwini Konchady K, Roopashree Padmanabha Poojary PP, Acharya Ranjitha R

Periodontitis is a chronic inflammatory disorder that gives rise to tissue damage and loss due to the complex interaction between pathogenic bacteria and the host's immune response. The aim of this study is to determine the lipid peroxidation, total antioxidant (AO) capacity (TAC), and superoxide dismutase (SOD) levels in patients diagnosed with chronic gingivitis and chronic periodontitis and in periodontally healthy control subjects. The subjects were divided into three groups. Blood sample and saliva were collected. TAC, MDA, and SOD levels were estimated by spectrophotometric methods. SOD in the saliva samples was analyzed by using the enzyme-linked immunosorbent assay (ELISA) kit method. The mean age of the study population in the control group was 45.21 ± 13.12, which in the gingivitis group was 44.12 ± 9.10 and in the periodontitis group was 42.19 ± 12.11. TAC and SOD levels were significantly reduced in both serum and saliva in the periodontitis compared to control and the gingivitis group. MDA levels were significantly increased in the serum and the saliva of the periodontitis compared to control and the gingivitis group. Oxidative stress, or the imbalance between oxidants and AO, is a major factor in the development and course of periodontitis.

PMID 42500370
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PubMedJournal of environmental sciences (China)2026-07-25

Assessment of Salvinia molesta for phytoremediation potential of copper and lead in contaminated water: Their impact on morpho-physio-cytological status.

Pal Nandita N, Sukul Soma S

This study evaluates the phytotoxic and cytogenetic effects of copper (Cu) and lead (Pb) on the aquatic fern Salvinia molesta, with emphasis on its potential for phytoremediation of heavy metal-contaminated water. Plants were exposed to graded concentrations (20, 40, 120 and 200 µmol/L) of Cu and Pb for 15 days. Pb exposure induced visible morphological alterations, while Cu had minimal structural impact. Both metals caused a dose-dependent reduction in chlorophyll (up to 60.82 % by Pb at 200 µmol/L) and protein content, accompanied by increased proline accumulation and elevated antioxidant enzyme activity, such as Superoxide dismutase, Catalase and Peroxidase, indicating oxidative stress responses. Cytological analysis revealed a significant decrease in mitotic index and increased chromosomal abnormalities, including c-mitosis, stickiness, laggards, and anaphase bridges, suggesting genotoxicity. Metal accumulation studies confirmed substantial uptake, with maximum tissue concentrations of 3755.47 mg/kg dry weight (dw) for Cu and 2362 mg/kg dw for Pb at 200 µmol/L. S. molesta exhibited extraction coefficients > 1 and a translocation factor > 1 for Cu, highlighting its effective submerged leaf-to-shoot metal transport. These findings underscore the potential of S. molesta as a sustainable, low-cost bioindicator and phytoremediator for Cu and Pb in aquatic ecosystems.

PMID 42498400
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PubMedJournal of environmental sciences (China)2026-07-25

Size- and polymer-dependent toxicity of microplastics on Achromobacter-mediated polychlorinated biphenyl biodegradation: Gene suppression, oxidative stress, and morphological responses.

Yang Yingying Y, Fei Sijia S, Yang Mengting M, Sun Faqian F et al.

The ubiquitous presence of microplastics (MPs) in polychlorinated biphenyl (PCB)-contaminated environments may hinder microbial bioremediation through adsorption and toxicity effects; however, their specific effects on PCB-degrading bacteria remain unclear. In this study, the effects of polyethylene (PE), polypropylene (PP), polystyrene (PS), and polyvinyl chloride (PVC), each at particle sizes of 25 μm and 250 μm, on the growth and Aroclor 1242-degrading capability of the resuscitated strain Achromobacter sp. HR2 were systematically evaluated. In addition, MP-induced alterations in the expression of functional genes, antioxidant enzyme activity, and morphological and physiological characteristics were assessed. The results revealed that MPs significantly inhibited microbial growth and PCB degradation in a size-dependent manner, with PS25 causing the greatest inhibition. Transcriptional analysis showed significant downregulation of key degradation genes (bphB, bphD, pobA, pcaGH, and pcaB) in MP-amended groups, with PS25 eliciting the most pronounced repression. MPs also induced elevated levels of intracellular reactive oxygen species and malondialdehyde, accompanied by enhanced activities of superoxide dismutase and catalase, indicating activation of the bacterial antioxidant defense system. Morphological and physiological disturbances were more pronounced with smaller (25 μm) MPs. This study provides valuable insights into the evaluation of microbial bioremediation performance in environments co-contaminated with MPs and PCBs.

PMID 42498405
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PubMedBiomaterials2026-07-25

Cascade-catalytic microneedles convert the tumor cholesterol shield into an oxidative spear for self-amplifying ferroptosis-driven cancer immunotherapy.

Yang Rongjie R, Zhang Yu Y, Dong Yushu Y, Chen Shuiling S et al.

Ferroptosis holds great promise for cancer immunotherapy, yet elevated cholesterol levels in tumor cells impose substantial structural and functional barriers to ferroptosis. Here, a cascade-catalytic nanocomposite microneedle platform (CSMZC MNs) is developed to convert this tumor-intrinsic cholesterol shield into an oxidative spear for ferroptosis-amplified cancer immunotherapy. By integrating superoxide dismutase (SOD) and cholesterol oxidase (COD) within Mn-doped zeolitic imidazolate framework nanoparticles and embedding them into dissolvable poly(γ-glutamic acid) microneedles, the platform enables localized intratumoral delivery and coordinated catalytic activation. After tumor cell internalization, the SOD-COD-Mn2+ cascade rewires redox metabolism and membrane lipid homeostasis by depleting cholesterol and 7-dehydrocholesterol, thereby dismantling tumor resistance to ferroptosis while amplifying reactive oxygen species generation and lipid peroxidation. This self-reinforcing oxidative amplification induces ferroptosis-associated immunogenic cell death and promotes cytosolic accumulation of nuclear and mitochondrial DNA, resulting in endogenous cGAS-STING activation. Meanwhile, Mn2+ enhances cGAS sensitivity to cytosolic DNA and amplifies type I interferon-mediated innate immune signaling. Through catalytic amplification and immune remodeling, CSMZC MNs reshape the immunosuppressive tumor microenvironment and elicit systemic T cell-mediated antitumor immunity against both primary and distant tumors. This work establishes an agonist-free immunometabolic strategy for converting tumor-protective cholesterol metabolism into a therapeutic vulnerability for tumor immunotherapy.

PMID 42497773
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PubMedPlant physiology and biochemistry : PPB2026-07-25

Priming-induced drought memory in rapeseed and cotton: A meta-analytic assessment.

Hashemi Amenehsadat A, Faghani Elham E, Roitsch Thomas Georg TG

Seed priming is increasingly used to enhance crop resilience to drought, yet whether it induces functional stress memory, and how this varies across crops, remains unclear. We conducted a global meta-analysis of 28 studies comprising 761 effect sizes to evaluate priming-induced drought memory in two major crops, rapeseed (Brassica napus) and cotton (Gossypium hirsutum). Effect sizes were calculated as standardized mean differences (Hedges' g) and synthesized using a random-effects model. Responses were evaluated across physiological, biochemical, and yield-related traits, while drought intensity and priming type were tested as key moderators to explain variation among studies. Priming significantly improved drought tolerance in both crops, but through divergent strategies: rapeseed responses were generally consistent with enhanced cellular protection via robust antioxidant activation (superoxide dismutase, catalase, ascorbate peroxidase) and reduced oxidative damage (malondialdehyde and hydrogen peroxide), particularly under moderate drought stress. In contrast, cotton may reflect a reproductive assurance strategy, sustaining leaf water status (RWC), accumulating proline, and significantly enhancing seed and boll yield, even when antioxidant responses were non-significant. Nutrient/mineral and microbial priming were most effective in cotton, whereas nutrient/mineral and hormonal/biochemical priming excelled in rapeseed. High heterogeneity in cotton (I2 = 90.99%) indicates that priming responses are strongly influenced by experimental context, including drought severity and priming treatment. Overall, our findings are compatible with a functional, phenotypic interpretation of stress-memory-related responses rather than direct evidence of epigenetic memory, and highlight the potential value of crop-tailored priming strategies for improving drought resilience and supporting climate-smart agricultural production under increasingly water-limited conditions.

PMID 42497668
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PubMedBiochemical pharmacology2026-07-25

Mitochondria-targeted reactive species scavenger JP4-039 protects against disturbances of redox homeostasis, mitochondrial quality control, and glucose metabolism in brains of glutaryl-CoA dehydrogenase-deficient mice: A potential new therapeutic strategy for glutaric acidemia type 1.

de Britto Renata R, Moura Alvorcem Leonardo de L, Marcuzzo Manuela Bianchin MB, Ribeiro Rafael T RT et al.

Glutaric aciduria type 1 (GA1) is a cerebral organic aciduria caused by deficient activity of glutaryl-CoA dehydrogenase (GCDH). Patients present with acute striatal degeneration and develop progressive cortical leukodystrophy whose pathophysiology is only partially known. As treatment for GA1 is limited, we evaluated the impact of JP4-039, a mitochondria-targeted reactive oxygen species (ROS) and electron scavenger, on redox homeostasis, mitochondrial quality control, and glucose metabolism in the cortical and striatal brain tissues of GCDH-deficient (Gcdh-/-) mice. Both tissues exhibited increases in lipid peroxidation, ROS levels, and the activities of superoxide dismutase, catalase, and glutathione S-transferase. Furthermore, glutathione reductase activity was increased, and glutathione peroxidase was reduced in the striatum, while Nrf2 mRNA levels were elevated in the cortex. Notably, most of these altered endpoints of redox homeostasis were prevented by treatment with JP4-039. Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1α) expression was reduced in the cortex of Gcdh-/- mice, whereas voltage-dependent anion channel (VDAC) and dynamin-related protein 1 (DRP1) expression were increased in the striatum, signaling a disturbance of mitochondrial quality control. JP4-039 mitigated the DRP1 change. The cerebral cortex displayed reduced glucose metabolism, increased lactate levels, and elevated activities of hexokinase, pyruvate kinase, and lactate dehydrogenase (LDH), which JP4-039 mitigated. GLUT3 expression was reduced in the cerebral cortex, but JP4-039 did not change this effect. Our data suggest that redox imbalance and dysregulated mitochondrial quality control and of the glycolytic pathway contribute to the pathophysiology of GA1, and that JP4-039 may offer therapeutic benefit.

PMID 42498157
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