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Cuprizone is a copper chelating agent that forms a deep blue copper ketone complex with copper (II). The copper ketone reaction can be used in colorimetric tests for the presence of trace copper. Cuprizone can be used to induce some schizophrenia-like behavior in mice. Cuprizone acts on copper enzymes, including SOD1, cytochrome oxidase, and DβH, thereby causing oxidative stress and increasing DA levels in certain brain regions such as the medial prefrontal cortex (PFC) [1].
Tofersen (BIIB067) is an antisense oligonucleotide and SOD1 mRNA inhibitor with an IC50 of 320 pM. Tofersen mediates RNase H-dependent degradation of SOD1 mRNA to reduce SOD1 protein levels in cerebrospinal fluid and serum. Tofersen downregulates cerebrospinal fluid neurofilament light chain, neurofilament heavy chain, amyloid-beta 1-40, amyloid-beta 1-42, neuropeptide Y, ubiquitin C-terminal hydrolase L1, neuropentraxins 1, 2, R, corticotropin-releasing hormone, IL-15, and serum neurofilament light chain, neurofilament heavy chain. Tofersen can be used for the research of superoxide dismutase 1-associated amyotrophic lateral sclerosis [1] .
ATN-224 is an orally active Cu 2+/Zn 2+-superoxide dismutase 1(SOD1) inhibitor. ATN-224 inhibits SOD1 activity in endothelial cells, an effect that is dose dependent with an IC50 of 17.5 nM.
Tofersen (BIIB067) sodium is an antisense oligonucleotide and SOD1 mRNA inhibitor with an IC50 of 320 pM. Tofersen sodium mediates RNase H-dependent degradation of SOD1 mRNA to reduce SOD1 protein levels in cerebrospinal fluid and serum. Tofersen sodium downregulates cerebrospinal fluid neurofilament light chain, neurofilament heavy chain, amyloid-beta 1-40, amyloid-beta 1-42, neuropeptide Y, ubiquitin C-terminal hydrolase L1, neuropentraxins 1, 2, R, corticotropin-releasing hormone, IL-15, and serum neurofilament light chain, neurofilament heavy chain. Tofersen sodium can be used for the research of superoxide dismutase 1-associated amyotrophic lateral sclerosis [1] .
LCS-1 is a superoxide dismutase 1(SOD1) inhibitor. LCS-1 inhibits SOD1 activity with an IC50 value of 1.07 μM. LCS-1 induces the early- and late-stage apoptosis of multiple myeloma (MM.1S) cells [1] .
Perfluorotetradecanoic acid (PFTeDA) is an orally active perfluoroalkyl substance. Perfluorotetradecanoic acid directly binds to the ligand-binding domain of purified hPPARγ, with a Kd value of 157.8 μM. Perfluorotetradecanoic acid significantly reduces the activity of the SIRT1/PGC1α and AMPK signaling pathways while stimulating the activity of the AKT1/mTOR signaling pathway. Perfluorotetradecanoic acid significantly upregulates the expression of corticosterone biosynthesis genes. Perfluorotetradecanoic acid increases ROS levels and promotes Apoptosis. Perfluorotetradecanoic acid impairs Leydig cell function and male reproductive endocrine function in adult male rats [1] .
SOD1 Human Pre-designed siRNA Set A contains three designed siRNAs for SOD1 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
SOD1-Derlin-1 inhibitor-2 (compound 56-59) is an inhibitor of SOD1-Derlin-1 interaction. SOD1-Derlin-1 inhibitor-2 attenuates the interactions between Derlin-1 and SOD1mut. SOD1-Derlin-1 inhibitor-2 can be used for the research of amyotrophic lateral sclerosis (ALS) [1].
SOD1-Derlin-1inhibitor-1 (compound 56-20) is an inhibitor of SOD1-Derlin-1 interaction. SOD1-Derlin-1inhibitor-1 inhibits SOD1G93A-Derlin-1 complex with an IC50 value of 7.11 μM. SOD1-Derlin-1inhibitor-1 can be used for the research of amyotrophic lateral sclerosis [1].
NUCC-0000323 is a potent superoxide dismutase 1(SOD1) inhibitor. NUCC-0000323 inhibits SOD1 expression. NUCC-0000323 can be used in research of amyotrophic lateral sclerosis (ALS) [1].
Nurr1 agonist 12 (Compound 37) is the agonist for nuclear receptor-associated protein 1(Nurr1) that activates the transcriptional activity of Nurr1 with an EC50 of 0.06 μM. Nurr1 agonist 12 activates the human response elements NBRE, NurRE, and DR5 with EC50 of 0.07 μM, 0.027 μM, and 0.014 μM, respectively. Nurr1 agonist 12 induces the expression of Nurr1-regulated neurotrophic genes, such as tyrosine hydroxylase (TH), SOD1/2, BDNF, Sestrin 3, and BIRC5 (Survivin). Nurr1 agonist 12 exhibits neuroprotective efficacy against Paraquat-induced neurotoxicity [1].
Cu/Zn Superoxide dismutase (Cu/Zn SOD; SOD1) is a cytosolic copper-zinc dimer form of superoxide dismutase enzyme. Cu/Zn Superoxide dismutase has oxygen radical enzymatic dismutation [1].
SOD1 (147-153) human is a peptide fragment of Cu/Zn superoxide dismutase (SOD1) with a high propensity to form amyloid fibrils. SOD1 (147-153) human may trigger the aggregation of full-length SOD1 and is a common molecular determinant of familial amyotrophic lateral sclerosis (fALS) and sporadic amyotrophic lateral sclerosis (sALS) [1].
Sod1 Mouse Pre-designed siRNA Set A contains three designed siRNAs for Sod1 gene (Mouse), as well as a negative control, a positive control, and a FAM-labeled negative control.
Mycosporine 2 glycine is an anti-inflammatory agent and TYRP1 inhibitor. Mycosporine 2 glycine inhibits the expression of inflammatory genes and reduces nitric oxide production. Mycosporine 2 glycine binds tightly to the active pocket of TYRP1 and inhibits the activity of melanogenesis-related enzymes. Mycosporine 2 glycine can be used in the research of hyperpigmentation and inflammation-related diseases [1] .
Sod1 Rat Pre-designed siRNA Set A contains three designed siRNAs for Sod1 gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.
SOD1-aggregation-IN-1 (compound 20) is a potent SOD aggregation inhibitor. SOD1-aggregation-IN-1 inhibits MG132 (HY-13259)-induced mutant SOD1 intracellular aggregation in PC12-SOD1G85R YFP cells with an EC50 of 2.63 μM. SOD1-aggregation-IN-1 can be used for amyotrophic lateral sclerosis (ALS) research [1].
CMB-087229 is a mutant superoxide dismutase 1(SOD1) protein aggregation inhibitor with IC50 of 67 nM, which can be used in the research of amyotrophic lateral sclerosis [1].
Cuprizone is a copper chelating agent that forms a deep blue copper ketone complex with copper (II). The copper ketone reaction can be used in colorimetric tests for the presence of trace copper. Cuprizone can be used to induce some schizophrenia-like behavior in mice. Cuprizone acts on copper enzymes, including SOD1, cytochrome oxidase, and DβH, thereby causing oxidative stress and increasing DA levels in certain brain regions such as the medial prefrontal cortex (PFC) [1].
Tofersen-d27 (BIIB067-d27) is the deuterium labeled Tofersen (HY-132580). Tofersen (BIIB067) is an antisense oligonucleotide and SOD1 mRNA inhibitor with an IC50 of 320 pM. Tofersen mediates RNase H-dependent degradation of SOD1 mRNA to reduce SOD1 protein levels in cerebrospinal fluid and serum. Tofersen downregulates cerebrospinal fluid neurofilament light chain, neurofilament heavy chain, amyloid-beta 1-40, amyloid-beta 1-42, neuropeptide Y, ubiquitin C-terminal hydrolase L1, neuropentraxins 1, 2, R, corticotropin-releasing hormone, IL-15, and serum neurofilament light chain, neurofilament heavy chain. Tofersen can be used for the research of superoxide dismutase 1-associated amyotrophic lateral sclerosis.
MP-010 is a FKBP12 ligand that regulates cytosolic calcium by stabilizing RyR channel activity. MP-010 promotes functional improvement in SOD1G93A amyotrophic lateral sclerosis (ALS) mice, as evidenced by improved motor coordination, increased integrity of neuromuscular junctions, and significantly enhanced survival of spinal motor neurons. MP-010 can be used for research in the field of neurological diseases [1].
ROCK2-IN-5 (compound 1d) is a hybrid compound containing structural fragments of the Rho kinase inhibitor fasudil and the NRF2 inducers caffeic and ferulic acids. ROCK2-IN-5 has good multitarget profile and good tolerability. ROCK2-IN-5 has the potential for thr research of Amyotrophic lateral sclerosis (ALS) with a SOD1 mutation [1].
Fraxinellone analog 1 (compound 2) is a potent and rapid activator of the Nrf2 mediated antioxidant defense system, which protects against glutamate-mediated excitotoxicity and induces the expression of antioxidant genes Gpx4, Sod1, and Nqo1. Fraxinellone analog 1 has neuroprotective effects and regulatory effects against oxidative stress and inflammation, and can be used in the study of neurodegenerative diseases [1].
K811 is an orally active ASK1 inhibitor with an IC50 of 6 nM. K811 inhibits glial cell activation in the lumbar spinal cord of SOD1G93A transgenic mice. K811 extends the survival of SOD1G93A transgenic mice, a mouse model of amyotrophic lateral sclerosis. K811 can be used in studies related to amyotrophic lateral sclerosis [1].
CLR01 sodium is a blood-brain barrier-permeable anti-aggregation agent. CLR01 sodium inhibits the de novo aggregation of Amyloid-β 40/42, α-synuclein, IAPP, tau protein and SOD1. CLR01 sodium reduces amyloid plaque burden in the cortex of triple-transgenic mice and improves the memory and motor abilities of these mice. CLR01 sodium can be used in research related to Alzheimer's disease, Parkinson's disease, and amyotrophic lateral sclerosis (ALS) [1].
SRI-22818 is a NF-κB activator with an EC50 of 0.5 μM. SRI-22818 upregulates the expression of NF-κB and promotes its activation. SRI-22818 increases the level of SOD2. SRI-22818 exhibits activity in the SOD1G93A model of amyotrophic lateral sclerosis (ALS). SRI-22818 can be used for research related to amyotrophic lateral sclerosis [1].
SOD1 (147-153) human is a peptide fragment of Cu/Zn superoxide dismutase (SOD1) with a high propensity to form amyloid fibrils. SOD1 (147-153) human may trigger the aggregation of full-length SOD1 and is a common molecular determinant of familial amyotrophic lateral sclerosis (fALS) and sporadic amyotrophic lateral sclerosis (sALS) [1].
SOD1 Protein, an enzyme crucial for cellular defense, operates as a superoxide dismutase, neutralizing radicals to safeguard cells from oxidative stress. Its enzymatic activity underscores the importance of SOD1 in maintaining cellular homeostasis and protecting biological systems from the harmful effects of reactive oxygen species accumulation. SOD1 Protein, Human (His) is the recombinant human-derived SOD1 protein, expressed by E. coli , with N-6*His labeled tag.
SOD1 Protein, an enzyme crucial for cellular defense, operates as a superoxide dismutase, neutralizing radicals to safeguard cells from oxidative stress.Its enzymatic activity underscores the importance of SOD1 in maintaining cellular homeostasis and protecting biological systems from the harmful effects of reactive oxygen species accumulation.SOD1 Protein, Human (N-His) is the recombinant human-derived SOD1 protein, expressed by E.coli , with N-6*His labeled tag.
Tofersen-d27 (BIIB067-d27) is the deuterium labeled Tofersen (HY-132580). Tofersen (BIIB067) is an antisense oligonucleotide and SOD1 mRNA inhibitor with an IC50 of 320 pM. Tofersen mediates RNase H-dependent degradation of SOD1 mRNA to reduce SOD1 protein levels in cerebrospinal fluid and serum. Tofersen downregulates cerebrospinal fluid neurofilament light chain, neurofilament heavy chain, amyloid-beta 1-40, amyloid-beta 1-42, neuropeptide Y, ubiquitin C-terminal hydrolase L1, neuropentraxins 1, 2, R, corticotropin-releasing hormone, IL-15, and serum neurofilament light chain, neurofilament heavy chain. Tofersen can be used for the research of superoxide dismutase 1-associated amyotrophic lateral sclerosis.
Tofersen (BIIB067) is an antisense oligonucleotide and SOD1 mRNA inhibitor with an IC50 of 320 pM. Tofersen mediates RNase H-dependent degradation of SOD1 mRNA to reduce SOD1 protein levels in cerebrospinal fluid and serum. Tofersen downregulates cerebrospinal fluid neurofilament light chain, neurofilament heavy chain, amyloid-beta 1-40, amyloid-beta 1-42, neuropeptide Y, ubiquitin C-terminal hydrolase L1, neuropentraxins 1, 2, R, corticotropin-releasing hormone, IL-15, and serum neurofilament light chain, neurofilament heavy chain. Tofersen can be used for the research of superoxide dismutase 1-associated amyotrophic lateral sclerosis [1] .
Tofersen (BIIB067) sodium is an antisense oligonucleotide and SOD1 mRNA inhibitor with an IC50 of 320 pM. Tofersen sodium mediates RNase H-dependent degradation of SOD1 mRNA to reduce SOD1 protein levels in cerebrospinal fluid and serum. Tofersen sodium downregulates cerebrospinal fluid neurofilament light chain, neurofilament heavy chain, amyloid-beta 1-40, amyloid-beta 1-42, neuropeptide Y, ubiquitin C-terminal hydrolase L1, neuropentraxins 1, 2, R, corticotropin-releasing hormone, IL-15, and serum neurofilament light chain, neurofilament heavy chain. Tofersen sodium can be used for the research of superoxide dismutase 1-associated amyotrophic lateral sclerosis [1] .
SOD1 Human Pre-designed siRNA Set A contains three designed siRNAs for SOD1 gene (Human), as well as a negative control, a positive control, and a FAM-labeled negative control.
Sod1 Mouse Pre-designed siRNA Set A contains three designed siRNAs for Sod1 gene (Mouse), as well as a negative control, a positive control, and a FAM-labeled negative control.
Sod1 Rat Pre-designed siRNA Set A contains three designed siRNAs for Sod1 gene (Rat), as well as a negative control, a positive control, and a FAM-labeled negative control.
Tofersen-d27 (BIIB067-d27) is the deuterium labeled Tofersen (HY-132580). Tofersen (BIIB067) is an antisense oligonucleotide and SOD1 mRNA inhibitor with an IC50 of 320 pM. Tofersen mediates RNase H-dependent degradation of SOD1 mRNA to reduce SOD1 protein levels in cerebrospinal fluid and serum. Tofersen downregulates cerebrospinal fluid neurofilament light chain, neurofilament heavy chain, amyloid-beta 1-40, amyloid-beta 1-42, neuropeptide Y, ubiquitin C-terminal hydrolase L1, neuropentraxins 1, 2, R, corticotropin-releasing hormone, IL-15, and serum neurofilament light chain, neurofilament heavy chain. Tofersen can be used for the research of superoxide dismutase 1-associated amyotrophic lateral sclerosis.
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Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
MedchemExpress Validation 03
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
MedchemExpress Validation 04
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
MedchemExpress Validation
Western blot analysis of extracts from THP-1(lane 2(20μg), Jurkat (lane 3(20μg) and NIH3T3(lane 4(20μg) using FOXO1A (HY-P80132) Rabbit mAb. Proteins were transferred
to a PVDF membrane and blocked with 5% non-fat milk in TBST for 2 hour at room temperature. The primary antibody (1/1000) and Loading control antibody (Beta Actin, HY-P80438, 1/10000) was
used in 5% non-fat milk in TBST at 4°C overnight. Goat Anti-Mouse/Rabbit IgG-HRP Secondary Antibody (1/10000) was used for 1 hour at room temperature.
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