superoxide dismutase (bSOD, OXIS / Orgotase / Peroxinorm)

✓ Approved

什么是 superoxide dismutase？

superoxide dismutase 是一种治疗药物，由GT Biopharma, Inc.研发。该药已获批，用于治疗相关适应症。

药物档案

商品名	bSOD, OXIS, Orgotase, Peroxinorm
公司	GT Biopharma, Inc.
状态	Approved

来源： ClinicalTrials.gov, GT Biopharma, Inc.

治疗适应症

superoxide dismutase 针对 2 个适应症，涉及 2 个治疗领域。

治疗领域	疾病/病症	分期
Nervous system disorders	Amyotrophic lateral sclerosis	✓ Approved
Musculoskeletal and connective tissue disorders	Arthritis	✓ Approved

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PubMedColloids and surfaces. B, Biointerfaces2026-06-13

Magnolol nanoparticles combat MRSA by disrupting TCA cycle and arginine metabolism to induce oxidative stress.

Xu Hang H, Hao Muyi M, He Qizhi Q, Kuang Huifang H et al.

Plant-derived bioactive compounds are promising antimicrobial candidates due to their diverse bioactivities and low propensity for inducing bacterial resistance. However, the clinical translation of magnolol (MG) is hindered by its poor aqueous solubility, low bioavailability, and non-negligible cytotoxicity. Here, core-shell magnolol nanoparticles (MGs) were developed via self-assembly of MG, polyvinylpyrrolidone (PVP), and bovine serum albumin (BSA). This formulation significantly improved aqueous stability and sustained release, enhanced drug-bacteria interactions, while concomitantly reducing toxicity. In vitro, MGs exhibited enhanced antibacterial activity against Methicillin-Resistant Staphylococcus aureus (MRSA), with minimum inhibitory concentrations (MIC) and minimum bactericidal concentrations (MBC) values of 15.625 µg/mL and 31.25 µg/mL, approximately half of the values observed for free MG. In vivo studies further demonstrated superior therapeutic efficacy with improved biocompatibility. Mechanistically, MGs disrupted the tricarboxylic acid (TCA) cycle and arginine metabolism, promoted reactive oxygen species (ROS) accumulation, depleted superoxide dismutase (SOD) activity, and induced oxidative stress-mediated bacterial death. These findings highlight MGs as a promising strategy for treating drug-resistant infections through bacterial metabolic modulation.

PMID 42284961

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PubMedInternational journal of phytoremediation2026-06-13

Cold plasma treatment alleviates cadmium stress by optimizing growth, yield, and antioxidant defense mechanisms in wheat (Triticum aestivum L.).

Aslam Rimsha R, Elahi Minhas M, Anas Muhammad M, Tahir Nimra N et al.

Cadmium (Cd) contamination limits plant growth and productivity. This study evaluated whether cold plasma (CP) seed treatment mitigates Cd stress in two wheat cultivars, Borlaug-16 (B-16) and Zincol-16 (Z-16). Seeds were exposed to CP for 1-4 min and grown under 50 ppm Cd. CP improved germination, with B-16 showing a 40% increase in germination percentage under CP1 and Z-16 a 90.47% increase in germination index under CdCP1 compared to the control. Growth and yield traits also improved; in B-16, grain yield increased by 45.19% (CdCP1) and biomass by 32.29% (CP1), while Z-16 showed an 83.07% increase in biomass (CP4) and a 66.94% increase in total chlorophyll (CdCP4). Oxidative damage declined, with malondialdehyde reduced by 7.79% (B-16, CP4) and 9.09% (Z-16, CP2), accompanied by increased activities of superoxide dismutase, catalase, peroxidase, and ascorbate peroxidase. Leaf Cd concentrations decreased by 38.73% in B-16 and 71.79% in Z-16 under CdCP1 relative to Cd-stressed plants. Overall, CP treatment was associated with reduced oxidative stress and improved physiological performance. These results indicate that CP is a practical approach to improve wheat performance under Cd-contaminated conditions.

PMID 42287008

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PubMedJournal of environmental science and health. Part. B, Pesticides, food contaminants, and agricultural wastes2026-06-13

Female reproductive toxicity induced by nitrate in drinking water and the comparative ameliorative effects of ascorbic acid, curcumin and their combination.

Sharma Mona M, Kaur Navdeep N

The reproductive toxicity of nitrate in juvenile and adult female rats, and its amelioration with ascorbic acid, curcumin or their combination, was studied. Rats were classified into five groups: control, nitrate, nitrate + ascorbic acid, nitrate + curcumin, and nitrate + ascorbic acid + curcumin. Nitrate at 250 mg/L drinking water and ascorbic acid and curcumin at 100 mg/kg body weight were provided to rats via oral gavage for 42 days. Results showed a significant increase in malondialdehyde (MDA) level and decreases in activity of superoxide dismutase (SOD) and catalase (CAT); level of estrogen, progesterone, luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in all treated groups of juvenile and adult rats, except for the group given a combination of both antioxidants. Glutathione peroxidase (GPx) activity decreased in the nitrate group of these rats. The number of atretic follicles increased and follicular diameter decreased in the nitrate group of juvenile and adult rats. A similar trend was also observed in juvenile rats given nitrate with ascorbic acid individually. In conclusion, nitrate caused higher toxicity in the ovaries of juveniles compared to adults. However, negative effects were reversed by amelioration with ascorbic acid and curcumin together, followed by curcumin and ascorbic acid separately.

PMID 42285372

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Effect of glycometabolism disorder mediated by TIGAR/PFKFB3 on liver damage in mice exposed to Cr(VI).

Zhu Yiran Y, Liu Wenhui W, Chen Peng P, Wang Wenchen W et al.

Various studies have shown that the harm of hexavalent chromium (Cr(VI)) to animals covers all aspects of the body, while glucose metabolism disorder is one of its hazard factors. In this study, the possible mechanism underlying Cr(VI) exposure on liver glycometabolism and damage was investigated. A mouse model was established by intragastrical administration of Cr(VI) for 5 days; liver tissues were collected and used to detect liver glycometabolism and balance between autophagy and apoptosis. Expose liver cells to a high dose of Cr(VI) significantly increased the levels of alanine aminotransferase, aspartate aminotransferase, malondialdehyde and reactive oxygen species production, suppressed glutathione peroxidase and superoxide dismutase release, upregulated 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase (PFKFB3) expression, inhibited tp53-induced glycolysis and apoptosis regulator (TIGAR) expression and promoted liver glycometabolism disorder. Moreover, the pathway network of glycometabolism has been analysised, showing that 21 differential metabolites levels were decreased and 6 increased. Carbohydrate metabolism pathways closely related to glycometabolism disorder were significantly enriched after Cr(VI) exposure. TIGAR/PFKFB3 inhibited the interactions between Beclin1/BAX and Bcl-2 via Bcl-2 regulated the balance between autophagy and apoptosis. Overall, Cr(VI) can lead to glycometabolism disorder through TIGAR/PFKFB3 imbalance and result in liver injuries in mice.

PMID 42285245

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Wheeler Alison A, Mehta Kush K, Sanders Danica D, Chin Cathy C et al.

Tofersen is a gene-targeted therapy for individuals with superoxide dismutase 1 (SOD1) (+) amyotrophic lateral sclerosis (ALS). Prior to U.S. Food and Drug Administration (FDA) approval, tofersen was made available through expanded access protocol. This study describes the clinical and operational experience of administering tofersen through expanded access protocols at a single academic medical center in the U.S. Individuals with symptomatic SOD1(+) ALS (≥ 18 years), who were ineligible for traditional ALS clinical trials, received tofersen via bedside lumbar punctures at Massachusetts General Hospital. Treatment was provided through single-patient and intermediate-sized expanded access protocols prior to FDA approval. Demographic and clinical characteristics, referral-to-treatment timelines, safety outcomes, and operational costs were collected. Eleven individuals with SOD1(+) ALS received monthly intrathecal tofersen over a two-year period (July 2021 to July 2023). Most participants were female, and 81.8% had leg-onset ALS. The mean (SD) referral-to-first dose duration was 36 (22.4) days. A total of 120 doses were administered over a two-year period. Tofersen was safe and well tolerated, with no treatment-related serious adverse events. Operational costs totaled $336,620, supported by philanthropy and insurance. The company provided the drug for free. This experience demonstrates the feasibility of implementing a resource-intensive expanded access protocol within an academic medical center using a mixed funding model to facilitate early access to emerging ALS therapies.

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Decoding the neuroprotective secrets of Tinospora sinensis: navigating the rotenone induced storm of behavioral and biochemical challenges in Parkinson's disease rat models.

Bhong Prabha P, Ingale Suvarna S, Jadhav Pallavi P

Parkinson's disease (PD) is a chronic neurodegenerative disorder that leads to motor and non-motor challenges, significantly impacting the quality of life. Research highlights body's antioxidant systems role in mitigating PD. This study investigated neuroprotective capabilities of Tinospora sinensis stem extract (TSSE) in a rat model of PD induced by rotenone. PD was induced in rats by subcutaneous rotenone injections (2 mg/kg/day) for 35 days. TSSE was administered orally at 100, 200, and 400 mg/kg doses, with levodopa-carbidopa as the standard reference. Motor impairments were assessed through catalepsy, locomotor activity, and rotarod tests. Biochemical evaluations included oxidative stress markers, antioxidant enzymes (glutathione, superoxide dismutase, and catalase), and dopamine levels, and monoamino oxidase-B (MAO-B). Histopathological examination of brain assessed neuronal integrity. Rotenone administration led to significant motor impairments, increased oxidative stress, reduced dopamine levels, and neuronal damage. Treatment with TSSE resulted in notable, dose-dependent enhancements in motor abilities and restored antioxidant enzyme activities, while also reducing lipid peroxidation, as indicated by decreased malondialdehyde levels. Additionally, TSSE decreased MAO-B level and increased brain dopamine level and maintained neuronal structure. The TSSE 400 mg/kg exhibited neuroprotective effects comparable to those of standard. TSSE shows significant neuroprotective effects, likely by enhancing endogenous antioxidant defenses and restoring dopaminergic neurotransmission. These findings suggest, TSSE could serve as a complementary therapeutic approach that targets oxidative and neurodegenerative mechanisms in PD.

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superoxide dismutase (bSOD, OXIS / Orgotase / Peroxinorm)

什么是 superoxide dismutase？

药物档案

治疗适应症

相关研究文献

Magnolol nanoparticles combat MRSA by disrupting TCA cycle and arginine metabolism to induce oxidative stress.

Cold plasma treatment alleviates cadmium stress by optimizing growth, yield, and antioxidant defense mechanisms in wheat (Triticum aestivum L.).

Female reproductive toxicity induced by nitrate in drinking water and the comparative ameliorative effects of ascorbic acid, curcumin and their combination.

Effect of glycometabolism disorder mediated by TIGAR/PFKFB3 on liver damage in mice exposed to Cr(VI).

Optimizing Research Operations and Resource Utilization in ALS Care: Insights From the Tofersen Antisense Oligonucleotide Expanded Access Protocol.

Decoding the neuroprotective secrets of Tinospora sinensis: navigating the rotenone induced storm of behavioral and biochemical challenges in Parkinson's disease rat models.

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