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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

PubMedFood microbiology2026-05-30

Biochemical, transcriptomics, and metabolomics analyses reveal coordinated antioxidant responses in Penicillium digitatum under MAP-simulated gas conditions.

Wang Zhengli Z, Liu Shihao S, Xu Huihui H, Ji Nana N et al.

Antioxidant metabolism plays a key role in maintaining redox balance and enhancing adaptive capacity in postharvest fungal pathogens. However, the mechanism by which Penicillium digitatum adapts under modified atmosphere packaging (MAP) conditions remains unclear. To investigate this, integrated biochemical, transcriptomic, and metabolomic analyses were conducted on P. digitatum exposed to Air, controlled atmosphere (CA), and MAP treatments for three days. Transcriptomic profiling on day 3, identified 75 differentially expressed genes (DEGs) associated with antioxidant pathways, while metabolomic analysis revealed 4 differentially accumulated metabolites. Under both CA and MAP treatments, enhanced fatty acid β-oxidation was associated with increased reactive oxygen species (ROS), specifically hydrogen peroxide (H2O2) and superoxide anion. Moreover, MAP-adapted P. digitatum efficiently scavenged H2O2, as supported by biochemical assays showing increases in catalase (CAT) activity and moderate elevation of superoxide dismutase activity. MAP treatment was associated with transcriptional reprogramming of the HOG-MAPK signaling pathway and downregulated the transcription factor Sko1, which was correlated with CAT expression and activity. Additionally, MAP promoted ascorbic acid biosynthesis via upregulation of D-glucarate dehydratase and L-gulonate dehydrogenase, and strengthened the glutathione cycle through upregulation of glutathione reductase and glutathione peroxidase. Inhibition of CAT of pathogen by 3-amino-1,2,4-triazole under MAP conditions suppressed fungal growth, suggesting its critical role in adaptive antioxidant defense. Finally, qRT-PCR validation of eight key DEGs confirmed the transcriptomic patterns. In conclusion, these coordinated responses under MAP conditions were associated with enhanced ROS scavenging and alleviated oxidative damage and provided new insights into the adaptive antioxidant mechanism of P. digitatum.

PMID 42215221
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PubMedScientific reports2026-05-30

Impact of alpha-ketoglutarate treatment on enhancing vase life of chrysanthemum by enhancing antioxidant systems and suppressing ethylene biosynthesis.

Malekzadeh Parviz P, Samadi Soheila S, Ghasemifar Elham E

Chrysanthemum is a globally valued cut flower with substantial commercial importance; however, its postharvest longevity is often limited by rapid senescence. This study investigated the application of alpha-ketoglutarate (AKG), a cost-effective and environmentally friendly metabolic intermediate, for extending the vase life of cut chrysanthemum flowers. The effects of 5 mM AKG (compared to a 0 mM control) on vase performance, physiological traits, biochemical composition, and the molecular regulation of ethylene biosynthesis were systematically evaluated. Our results demonstrated that 5 mM AKG significantly prolonged vase life by improving water balance and enhancing flower hydration through increased water uptake. The treatment effectively reinforced the antioxidant defense system by increasing the contents of glutathione, ascorbic acid, total phenolics, and flavonoids, while stimulating the activities of catalase (CAT) and superoxide dismutase (SOD). Consequently, AKG inhibited the accumulation of reactive oxygen species (ROS), leading to a marked reduction in malondialdehyde (MDA) levels, electrolyte leakage (EL), and lipoxygenase (LOX) activity. Furthermore, AKG application suppressed ethylene (ETH) production by downregulating the activities of 1-aminocyclopropane-1-carboxylic acid synthase (ACS) and oxidase (ACO), which was further confirmed by the reduced expression of CmACS1 and CmACO1 genes. Collectively, these findings demonstrate that 5 mM AKG represents a sustainable and eco-friendly strategy for enhancing the postharvest quality and longevity of cut chrysanthemums by integrating metabolic stability with hormonal regulation.

PMID 42215683
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PubMedEuropean journal of pharmacology2026-05-30

SGLT2 inhibitors ameliorate myocardial hypertrophy in rats via AMPK/Nrf2-mediated ferroptosis suppression and antioxidant response.

Wang Jiao J, Zhang Wen-Qiong WQ, Zhang Lu-Lu LL, Shi Hong-Tao HT

This study investigated whether dapagliflozin, a sodium-glucose cotransporter 2 inhibitor, alleviates myocardial hypertrophy by modulating the AMP-activated protein kinase (AMPK)/nuclear factor E2-related factor 2 (Nrf2) signalling pathway, thereby reducing oxidative stress and ferroptosis. A rat model of myocardial hypertrophy was created using abdominal aortic stenosis. Rats were divided into blank, sham, surgery (Abdominal Aortic Coarctation, AAC), and dapagliflozin-treated groups (n=4), with evaluations at 2, 4, 8, and 12 weeks post-surgery. In vitro, an isoproterenol-induced hypertrophic model in H9C2 cardiomyocytes was used, involving control, ISO, dapagliflozin intervention, and separate or combined intervention groups with AMPK and Nrf2 inhibitors.Dapagliflozin treatment significantly improved cardiac function in pressure-overloaded rats, reduced myocardial hypertrophy and fibrosis, and lowered myocardial hypertrophy marker expression. It also enhanced superoxide dismutase activity, decreased malondialdehyde levels and myocardial iron deposition, and improved mitochondrial ultrastructural integrity, indicative of reduced ferroptosis. Mechanistic studies showed that dapagliflozin activates AMPK phosphorylation, promotes Nrf2 nuclear translocation, and upregulates downstream proteins. This protective effect was nullified when either AMPK or Nrf2 was specifically inhibited. Further, changes in expression levels following separate inhibition of AMPK and Nrf2 confirmed AMPK's regulatory role over Nrf2.In conclusion, dapagliflozin mitigates stress-induced myocardial hypertrophy by activating the AMPK/Nrf2 signalling pathway at least in the early stages, boosting myocardial antioxidant defence, and inhibiting ferroptosis. This study identifies the AMPK/Nrf2 pathway as a crucial mechanism in dapagliflozin's cardiovascular protective effects.

PMID 42214780
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PubMedBMC pharmacology & toxicology2026-05-30

Lycopene ameliorates acrylamide-induced reproductive toxicity through enhancement in testicular antioxidant status and upregulation of androgen receptor expression in male Wistar rats.

Adebodun Great Oluwamayokun GO, Obabolujo Tirenimioluwa Blessings TB, Adesope Praise Ebunoluwa PE, Onyeacholem Emmanuella E et al.

Acrylamide (ACR), a food contaminant, has been reported to exert adverse effects on the male reproductive system through increased oxidative stress and hormonal imbalance. This study aimed to investigate the ameliorative potentials of lycopene on reproductive parameters, oxidative stress, and expression of androgen receptors in acrylamide-induced reproductive toxicity in male Wistar rats. Thirty-five male Wistar rats were randomly divided into seven groups (n = 5). Groups I-VII were orally administered distilled water, olive oil, acrylamide (10 mg/kg), lycopene (5 mg/kg), lycopene (20 mg/kg), acrylamide+lycopene (5 mg/kg), and acrylamide+lycopene (20 mg/kg), respectively, for 8 weeks. Following the end of the experiment, the animals were fasted overnight, weighed, and euthanized. Blood was collected, centrifuged, and serum obtained. The testes were collected and used for sperm, biochemical, and immunohistochemical analyses. The results revealed that acrylamide administration decreased sperm quality, resulted in oxidative stress, hormonal imbalance, and reduced testicular androgen expression. However, lycopene significantly increased sperm count, viability, motility, serum testosterone, follicle-stimulating hormone (FSH), and luteinizing hormone levels. Also, reduced testicular oxidative stress markers, decreased malondialdehyde (MDA), and enhanced antioxidant enzymes, increased superoxide dismutase (SOD) and catalase activities were observed following lycopene administration. Treatment with lycopene upregulated the expression of testicular androgen receptors. These findings demonstrated the ameliorative potential of lycopene in acrylamide-induced reproductive toxicity by improving testicular antioxidant status, hormonal balance, spermatogenesis, and testicular androgen receptor expression in male Wistar rats.

PMID 42216064
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PubMedMedicine2026-05-30

Network toxicology-driven insights on nitrogen-based flame retardant-induced hepatotoxicity: Computational prediction and experimental validation.

Qu Yueyu Y, Li Guanyin G, Wang Hai H, Peng Yong Y

Nitrogen-based flame retardants (NBFRs) are widely used in various products, and their long-term exposure may cause liver damage in humans. However, the underlying mechanism remains unclear. This study systematically investigated the mechanisms of NBFR-induced liver injury by integrating network toxicology, molecular docking, and Mendelian randomization analyses. The potential target genes of NBFR and liver injury-related genes were obtained from multiple databases. A protein-protein interaction network was constructed, followed by functional enrichment analysis. The core genes were validated using 2 liver injury-related transcriptomic datasets. Subsequently, molecular docking was performed to simulate the binding interactions between NBFR and the core proteins. Toxicological assessment revealed that NBFRs had significant hepatotoxic potential. The intersection analysis identified 41 genes related to both NBFR exposure and liver injury. Cross-validation using 2 transcriptomic datasets confirmed that superoxide dismutase 2 (SOD2) was a core target gene. Molecular docking results showed that all 4 NBFR compounds exhibited stable binding to SOD2. NBFR treatment significantly reduced telomerase-immortalized human liver epithelial-2 cell viability in a time-dependent manner, as determined by the Cell Counting Kit-8 assay. Moreover, quantitative polymerase chain reaction analysis revealed a marked downregulation of SOD2 mRNA levels, whereas western blot analysis confirmed a corresponding decrease in SOD2 protein expression. This study identified SOD2 as a key molecular target mediating liver injury induced by NBFR, although further experimental validation is required to confirm its mechanisms and clinical relevance.

PMID 42216319
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PubMedJournal of integrative neuroscience2026-05-30

Lactobacillus mucosae Reduces Neuronal Oxidative Stress in Alzheimer's Disease via the Regulation of CB2 Signaling.

Kong Yu Y, Lv Xinhuang X, Yang Yao Y, Li Qiyao Q et al.

The probiotic Lactobacillus mucosae has been widely shown to have many positive effects. However, its neuroprotective effects and underlying mechanism in Alzheimer's disease (AD) remain elusive. Male APP/PS1 mice were treated for 4 weeks with L. mucosae WMU007, followed by the evaluation of cognitive function, neuronal damage, amyloid-β (Aβ) deposition, and Tau phosphorylation. RNA-seq coupled with Gene Ontology (GO) enrichment analysis implicated L. mucosae WMU007 in modulating oxidative stress in this AD model. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and qPCR were performed to identify the specific mechanism by which this probiotic suppresses oxidative stress in the pathogenesis of AD. In addition, we quantified the levels of classical oxidative stress markers, such as superoxide dismutase 2 (SOD2) and glutathione peroxidase 4 (GPX4). We also examined the expression of cannabinoid receptor type 2 (CB2) and its key downstream regulators in the redox pathway, namely nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1), in both animal and cellular models. Our results showed that treatment with L. mucosae WMU007 significantly decreased cognitive impairment, neuronal damage, Aβ deposits, and Tau phosphorylation in APP/PS1 mice. Activation of CB2 was identified as the key mechanism by which L. mucosae WMU007 reduces oxidative stress in AD. In addition, L. mucosae WMU007 reduced oxidative stress and increased the levels of CB2 pathway-related proteins in vivo and in vitro. These results indicate that L. mucosae WMU007 confers neuroprotection in AD by targeting CB2-mediated oxidative pathways, highlighting its therapeutic potential as a novel probiotic intervention.

PMID 42216640
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