75 Results for "

brain damage diseases

" in MedChemExpress (MCE) Product Catalog:
Products (75)

75 Results for "brain damage diseases" in MCE Product Catalog:

27
β-Amyloid (1-42), human TFA
β-Amyloid (1-42), human TFA
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27 Publications Verification
Cat. No.: HY-P1363
Synonyms: Amyloid β-peptide (1-42) (human) TFA
Target:  

Amyloid-β

Research Areas:  

Neurological Disease

β-Amyloid (1-42) (Amyloid β-peptide (1-42), human TFA, a 42-amino acid peptide that has not been treated with HFIP, is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human TFA remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human TFA, after being monomericized by HFIP and dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4 °C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 °C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death .
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27
β-Amyloid (1-42), human
β-Amyloid (1-42), human
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27 Publications Verification
Cat. No.: HY-P1363A
CAS No.: 107761-42-2
Synonyms: Amyloid β-peptide (1-42) (human)
Target:  

Amyloid-β

Research Areas:  

Neurological Disease

β-Amyloid (1-42) (Amyloid β-peptide (1-42)), human, a 42-amino acid peptide that has not been treated with HFIP, is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human, after being monomericized by HFIP and dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4 °C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 °C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death .
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27
β-Amyloid (1-42), human, HFIP-treated
β-Amyloid (1-42), human, HFIP-treated
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27 Publications Verification
Cat. No.: HY-P1363B
CAS No.: 107761-42-2
Target:  

Amyloid-β

Research Areas:  

Neurological Disease

β-Amyloid (1-42), human, HFIP-treated, a 42-amino acid peptide that has been treated with HFIP from β-Amyloid (1-42), human (HY-P1363A), is a brain-penetrant amyloid protein fragment, which can be used in research on Alzheimer's disease and Down’s syndrome. β-Amyloid (1-42), human, HFIP-treated remaining as a monomer exhibits antioxidant and neuroprotective effects. β-Amyloid (1-42), human, HFIP-treated, after being dissolved in DMSO to form the stock solution, on the one hand, can form soluble oligomers (AβOs) when incubated at 4°C, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37°C to form insoluble fibrils, with lower neurotoxicity, and participating in the oxidative damage process. Aβ42 oligomers bind to various neuronal surface receptors (such as PrPc, mGluR5, NMDA receptors, etc.), triggering oxidative stress, calcium homeostasis imbalance, and synaptic toxicity via activating downstream signaling pathways, leading to neuronal dysfunction and death .
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6
Isobavachin
Isobavachin
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6 Cited Publications
Cat. No.: HY-N0762
CAS No.: 31524-62-6
Category:  

Flavonoids Neurological Disease Leguminosae Flavonones Phenols Polyphenols Psoralea corylifolia L. Plants Disease Research Fields

Target:  

Cytochrome P450 UGT p38 MAPK NF-κB NO Synthase COX Fc Receptor (FcR) RANKL/RANK Keap1-Nrf2 Reactive Oxygen Species (ROS) Apoptosis Autophagy

Isobavachin is an orally active, blood-brain barrier-penetrating prenylated flavonoid present in Psoralea corylifolia. Isobavachin inhibits human CYP2B6, CYP2C9, CYP2C19, UGT1A1, UGT1A9, and UGT2B7. Isobavachin suppresses MAPK activation, NF-κB nuclear translocation, overexpression of iNOS/COX-2, FcεRI-mediated signaling pathways, and RANKL-induced osteoclastogenesis. Isobavachin induces autophagy, cytotoxicity, neuronal differentiation, and NRF2 activation; it alleviates oxidative damage, inflammatory responses, apoptosis, iron accumulation, mitochondrial biogenesis, and mast cell degranulation. Isobavachin is applicable to research related to liver injury, inflammatory diseases, osteoporosis, liver cancer, prostate cancer, glioma, periodontitis-induced bone loss, and Alzheimer's disease .
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5
Coptisine Sulfate
Coptisine Sulfate
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5 Cited Publications
Cat. No.: HY-N0430A
CAS No.: 1198398-71-8
Category:  

Alkaloids Chelidonium majus Metabolic Disease Quinoline Alkaloids Plants Disease Research Fields Papaveraceae

Target:  

Indoleamine 2,3-Dioxygenase (IDO) NF-κB p38 MAPK PI3K Akt Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism DNA/RNA Synthesis ROCK LDLR

Coptisine Sulfate is an orally active and brain-penetrant alkaloid found in Coptis chinensis. Coptisine Sulfate is a reversible, uncompetitive IDO inhibitor with a Ki of 5.8 μM and an IC50 of 6.3 μM. Coptisine Sulfate suppresses neuroinflammation, reduces Aβ plaque burden and shows neuroprotective activity. Coptisine Sulfate shows anti-inflammation activity by blocking NF-κB, MAPK, and PI3K/Akt activation. Coptisine Sulfate inhibits cancer cells proliferation, induces DNA damage, G2/M phase cell cycle arrest, apoptosis, ROS production and mitochondrial dysfunction. Coptisine Sulfate inhibits Rho/ROCK pathway activation, reduces arrhythmia, limits cardiac injury marker release, reduces infarct size, and preserves cardiac function in rat myocardial ischemia/reperfusion models. Coptisine Sulfate downregulates HMGCR and upregulates LDLR and CYP7A1 to modulate cholesterol metabolism, reduces abnormal serum lipid levels, and promotes fecal bile acid excretion. Coptisine Sulfate be used for the research of cancer, hypercholesterolemia, Alzheimer’s disease, inflammatory disorders and cardiovascular disease .
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5
Crebanine
Crebanine
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5 Cited Publications
Cat. No.: HY-N2255
CAS No.: 25127-29-1
Category:  

Cardiovascular Disease Alkaloids Stephania venosa Other Alkaloids Plants Disease Research Fields Inflammation/Immunology Menispermaceae

Target:  

Akt Apoptosis NF-κB Reactive Oxygen Species (ROS) p38 MAPK ERK Interleukin Related TNF Receptor NO Synthase nAChR Bacterial

Crebanine is an isoquinoline-like alkaloid that can be derived from Stephania. Crebanine is an antagonist of the α7-nAChR with an IC50 of 19.1 μM. Crebanine suppresses the proliferation, migration, and invasion of cancer cells, triggers reactive oxygen species (ROS) burst, and promotes apoptosis. Crebanine inhibits the AKT/FoxO3a, NF-κB and MAPK signaling pathways. Crebanine attenuates NOX2 hyperactivation, exhibits antioxidant properties by reducing reactive oxygen species and peroxidation in microglia cells. Crebanine inhibits voltage-dependent Na + current in guinea-pig ventricular myocytes. Crebanine has high inhibitory activity against gram-positive animal pathogenic bacteria. Crebanine ameliorates ischemia-reperfusion brain damage in middle cerebral artery occlusion and reperfusion (MCAO/R) rats. Crebanine significantly improves Scopolamine (HY-N0296)-induced cognitive deficits in ICR mice. Crebanine can be used for the study of hepatocellular carcinoma (HCC), cerebral ischemia and Alzheimer's disease .
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4
DPQ hydrochloride
DPQ hydrochloride
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4 Cited Publications
Cat. No.: HY-W424851
CAS No.: 84050-22-6
Synonyms: 6,7-Dimethoxy-2-(1-piperazinyl)-4-quinazolinamine hydrochloride
Target:  

PARP

Research Areas:  

Infection Inflammation/Immunology

DPQ hydrochloride is a blood-brain barrier permeable and selective PARP-1 inhibitor that blocks PARP-1-mediated DNA damage repair and NAD +/ATP consumption, thereby inhibiting excessive inflammatory responses. DPQ hydrochloride inhibits NF-κB pathway activation, reduces the expression of pro-inflammatory factors (such as TNF-α, IL-6) and oxidative stress. DPQ hydrochloride can be used in inflammation-related studies of acute lung injury, myocardial infarction, and neurodegenerative diseases .
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3
2'-Deoxyuridine
2'-Deoxyuridine
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3 Cited Publications
Cat. No.: HY-D0186
CAS No.: 951-78-0
Category:  

Infection Natural Products Microorganisms Immune System Disorder Disease markers Endogenous metabolite Disease Research Fields

Target:  

Endogenous Metabolite Thymidylate Synthase

2’-deoxyuridine is a brain-penetrant pyrimidines nucleotide that is associated with nervous system diseases. 2'-Deoxyuridine could increase chromosome breakage and results in a decreased thymidylate synthetase activity. 2'-Deoxyuridine is a precursor in the synthesis of Edoxudine (HY-B1011) and also an analogue of 5-ethynyl-2'-deoxyuridine, EdU (HY-118411). 2’-deoxyuridine reduces microglial activation and improve oxidative stress damage by modulating glycolytic metabolism on the Aβ25-35-induced brain injury, which is promising for research of Alzheimer’s disease (AD) .
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3
Vinburnine
Vinburnine
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3 Cited Publications
Cat. No.: HY-B1180
CAS No.: 4880-88-0
Synonyms: (-)-Eburnamonine; (-)-Vincamone
Category:  

Cardiovascular Disease Apocynaceae Alkaloids Hunteria zeylanica Plants Disease Research Fields Indole Alkaloids

Target:  

Apoptosis p38 MAPK

Vinburnine ((-)-Eburnamonine; (-)-Vincamone) is an orally active, blood-brain barrier permeable immunomodulator and apoptosis inducer. Vinburnine drives the secretion of IL-24 by activating the P38/MAPK/ATF3 signaling axis. Vinburnine induces reactive oxygen species production and DNA damage in cancer cells, thereby inhibiting cancer cell proliferation, activating the apoptotic cascade, and enhancing CD8+ T cell function to remodel the tumor immune microenvironment. Vinburnine can be used in the research of diseases such as melanoma .
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3
Brophenexin
Brophenexin
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3 Cited Publications
Cat. No.: HY-139192
CAS No.: 2243506-33-2
Purity:  99.59%
Synonyms: NMDAR/TRPM4-IN-2
Target:  

iGluR TRP Channel ERK

Research Areas:  

Neurological Disease

Brophenexin (compound 8) is a potent NMDAR/TRPM4 interaction interface inhibitor. Brophenexin shows neuroprotective activity. Brophenexin prevents NMDA-induced cell death and mitochondrial dysfunction in hippocampal neurons, with an IC50 of 2.1 μM. Brophenexin protects mice from MCAO-induced brain damage and NMDA-induced retinal ganglion cell loss .
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3
Brophenexin free base
Brophenexin free base
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3 Cited Publications
Cat. No.: HY-139192A
CAS No.: 1353979-43-7
Purity:  99.24%
Synonyms: NMDAR/TRPM4-IN-2 free base
Target:  

iGluR TRP Channel ERK

Research Areas:  

Neurological Disease

Brophenexin free base (compound 8) is a potent NMDAR/TRPM4 interaction interface inhibitor. Brophenexin free base shows neuroprotective activity. Brophenexin free base prevents NMDA-induced cell death and mitochondrial dysfunction in hippocampal neurons, with an IC50 of 2.1 μM. Brophenexin free base protects mice from MCAO-induced brain damage and NMDA-induced retinal ganglion cell loss .
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2
Acetyl-L-carnitine hydrochloride
Acetyl-L-carnitine hydrochloride
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2 Cited Publications
Cat. No.: HY-B0762
CAS No.: 5080-50-2
Synonyms: O-Acetyl-L-carnitine hydrochloride; ALCAR hydrochloride
Category:  

Alkaloids Other Alkaloids Endogenous metabolite

Target:  

Caspase Apoptosis

Acetyl-L-carnitine (O-Acetyl-L-carnitine; ALCAR) hydrochloride is an orally active mitochondrial energy metabolism regulator and neuroprotectant that can penetrate the blood-brain barrier. Acetyl-L-carnitine hydrochloride selectively enters cells and the brain through the organic cation transporter OCTN2. Acetyl-L-carnitine hydrochloride can participate in fatty acid β-oxidation, promote acetylcholine synthesis, regulate mitochondrial function and inhibit oxidative stress as an acetyl donor. Acetyl-L-carnitine hydrochloride exerts its activity by enhancing energy metabolism, protecting neurons and improving synaptic plasticity. Acetyl-L-carnitine hydrochloride is mainly used in the study of neurodegenerative diseases and metabolic disorder-related diseases such as neonatal hypoxic-ischemic brain damage, Alzheimer's disease, and depression .
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2
Acetyl-L-carnitine
Acetyl-L-carnitine
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2 Cited Publications
Cat. No.: HY-113218
CAS No.: 3040-38-8
Purity:  ≥98.0%
Synonyms: O-Acetyl-L-carnitine; ALCAR
Category:  

Natural Products Animals

Target:  

Caspase Apoptosis

Acetyl-L-carnitine (O-Acetyl-L-carnitine; ALCAR) is an orally active mitochondrial energy metabolism regulator and neuroprotectant that can penetrate the blood-brain barrier. Acetyl-L-carnitine selectively enters cells and the brain through the organic cation transporter OCTN2. Acetyl-L-carnitine can participate in fatty acid β-oxidation, promote acetylcholine synthesis, regulate mitochondrial function and inhibit oxidative stress as an acetyl donor. Acetyl-L-carnitine exerts its activity by enhancing energy metabolism, protecting neurons and improving synaptic plasticity. Acetyl-L-carnitine is mainly used in the study of neurodegenerative diseases and metabolic disorder-related diseases such as neonatal hypoxic-ischemic brain damage, Alzheimer's disease, and depression .
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2
Arundic Acid
Arundic Acid
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2 Cited Publications
Cat. No.: HY-107661
CAS No.: 185517-21-9
Purity:  ≥98.0%
Synonyms: ONO-2506; (R)-2-Propyloctanoic acid
Target:  

ERK Akt NF-κB EAAT

Research Areas:  

Cardiovascular Disease Neurological Disease

Arundic Acid is an orally effective astrocyte function modulator and neuroprotective agent. Arundic Acid increases the expression and function of the astrocytic glutamate transporter EAAT1 by activating the ERK, Akt and NF-κB pathways. Arundic Acid attenuates retinal ganglion cell death in a normal-tension glaucoma model. Arundic Acid exerts neuroprotective effects in a mouse model of Parkinson's disease. Arundic Acid is a S100β protein synthesis inhibitor that prevents neurological deficits and brain tissue damage after intracerebral hemorrhage in rats. Arundic Acid downregulates neuroinflammation and astrocytic dysfunction after status epilepticus in immature rats. Arundic Acid is applicable to research related to Parkinson's disease, cerebral ischemia, glaucoma, intracerebral hemorrhage and epilepsy .
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1
Homogentisic acid
Homogentisic acid
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1 Cited Publications
Cat. No.: HY-113283
CAS No.: 451-13-8
Purity:  99.46%
Category:  

Other disease Ketones, Aldehydes, Acids Disease markers Metabolic Disease Phenols Polyphenols Endogenous metabolite Disease Research Fields

Target:  

Amyloid-β Natriuretic Peptide Receptor (NPR) α-synuclein Transthyretin (TTR) Claudin

Homogentisic acid is an orally active, blood-brain barrier-permeable amyloidogenic compound that functions as both an amyloid component and a pigment precursor. Accumulation of homogentisic acid downregulates tight junction proteins (such as claudin-5, occludin, ZO-1) and impairs blood-brain barrier integrity. Homogentisic acid and its oxidation product benzoquinone acetic acid not only induce the aggregation and fibrosis of multiple proteins (such as Aβ1-42, α-synuclein, SAA, Transthyretin (TTR), atrial natriuretic peptide), but also trigger oxidative stress, damage to the Wnt/β-catenin pathway, and neurotoxicity, leading to ochronosis pigment deposition and synaptic dysfunction. At specific concentrations, homogentisic acid exerts no cytotoxicity or genotoxicity on human peripheral blood lymphocytes, and even counteracts the genotoxicity induced by Irinotecan (HY-16562). Homogentisic acid serves as an important tool molecule for investigating the mechanisms of diseases including ochronosis, secondary amyloidosis, Alzheimer's disease, and colorectal cancer .
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N-Propargylglycine
N-Propargylglycine
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1 Cited Publications
Cat. No.: HY-142035
CAS No.: 58160-95-5
Purity:  99.70%
Target:  

Mitochondrial Metabolism

Research Areas:  

Neurological Disease Metabolic Disease Inflammation/Immunology Cancer

N-Propargylglycine is a brain-penetrant and orally active PRODH inhibitor. N-Propargylglycine covalently modifies enzyme-bound FAD and active site lysine, causing enzyme structural distortion, protein decay, and irreversible inhibition of proline and 4-hydroxyproline catabolism. N-Propargylglycine induces UPRmt, upregulates mitochondrial chaperones and YME1L1, enhances mitochondrial proteostasis, blocks astrocytic L-proline consumption, and abolishes L-proline’s ATP-maintaining and viability-protective effects. N-Propargylglycine stimulates neural processes, increases brain proline, hydroxyproline, and sarcosine levels, partially normalizes Huntington’s disease whole brain transcriptomes. N-Propargylglycine reduces hyperoxaluria, prevents calcium oxalate stone formation, reduces kidney tubular damage, and restores weight and survival in Grhpr knockout mice. N-Propargylglycine can be used for the research of breast cancer, neurodegenerative disorders, Huntington’s disease, and primary hyperoxaluria type 2 .
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Fusaric acid
Fusaric acid
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Cat. No.: HY-128483
CAS No.: 536-69-6
Purity:  99.94%
Category:  

Infection Microorganisms Ketones, Aldehydes, Acids Disease Research Fields

Target:  

TGF-beta/Smad PI3K NF-κB Akt Apoptosis Dopamine β-hydroxylase mTOR Adrenergic Receptor

Fusaric acid is an orally active multi-pathway inhibitor with the activity of inducing oxidative stress and apoptosis. Fusaric acid can chelate divalent metal cations, damage mitochondrial membrane structure, and activate apoptosis-related proteases such as Caspase-3/7, -8, and -9. Fusaric acid also regulates Bax/Bcl-2 protein, inhibits fibrosis-related signaling pathways such as NF-κB, TGF-β1/SMADs, and PI3K/AKT/mTOR, and reduces collagen deposition. Fusaric acid is also a dopamine β-hydroxylase inhibitor, which reduces endogenous levels of norepinephrine and epinephrine in the brain, heart, spleen, and adrenal glands. Fusaric acid can play a role in myocardial fibrosis and improve cardiac hypertrophy in heart disease, and can also be used in the study of esophageal cancer and liver cancer .
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Silybin B
Silybin B
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Cat. No.: HY-N7046
CAS No.: 142797-34-0
Synonyms: Silibinin B
Category:  

Flavanonols Glycine soya Flavonoids Phenols Polyphenols Cyamopsis tetragonoloba (L.) Taub. Plants Compositae

Target:  

Amyloid-β Apoptosis JNK p38 MAPK

Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .
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Ginkgo biloba extract
Ginkgo biloba extract
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Cat. No.: HY-N12060
CAS No.: 90045-36-6
Category:  

Natural Products Ginkgoaceae Ginkgo biloba L. Plants

Target:  

Bcl-2 Family Caspase Apoptosis Autophagy Reactive Oxygen Species (ROS) Akt JNK ERK

Ginkgo biloba extract is a natural product that can be isolated from Ginkgo biloba leaves . Ginkgo biloba extract alleviates oxidative stress-induced neuronal apoptosis (Apoptosis) by stabilizing mitochondrial function, regulating Bcl-2 family proteins and inhibiting caspase activation. Ginkgo biloba extract alleviates testicular injury by upregulating SKP2 and inhibiting Beclin1-independent autophagy (Autophagy) . Ginkgo biloba extract alleviates various types of neuronal damage in animal models. Ginkgo biloba extract reduces behavioral sensitization in rats. Ginkgo biloba extract counteracts Aβ-induced neurotoxicity by blocking a series of Aβ-triggered events, including glucose uptake, ROS accumulation, AKT activation, mitochondrial dysfunction, JNK and ERK 1/2 pathways, and apoptosis, and also interferes with the formation of Aβ oligomers. Ginkgo biloba extract is applicable to research related to cerebral hypoperfusion, testicular injury, Alzheimer's disease, Parkinson's disease, multi-infarct dementia, stroke, traumatic brain injury and amyotrophic lateral sclerosis .
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Meglutol
Meglutol
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Cat. No.: HY-B1189
CAS No.: 503-49-1
Synonyms: Dicrotalic acid; 3-Hydroxy-3-methylglutaric acid
Category:  

Cardiovascular Disease Ketones, Aldehydes, Acids Endogenous metabolite Disease Research Fields

Target:  

HMG-CoA Reductase (HMGCR) Autophagy Endogenous Metabolite

Meglutol is a lipid-lowering agent. Meglutol can reduces cholesterol, triglycerides, serum β-lipoprotein, and phospholipids, and inhibits the activity of HMG-CoA reductase (a rate-limiting enzyme in cholesterol biosynthesis). Meglutol can induce significant lipid oxidative damage in brain tissue. It is promising for research in the field of cardiovascular diseases and metabolic diseases .
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