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Pathways Recommended: Cell Cycle/DNA Damage
Results for "

brain damage diseases

" in MedChemExpress (MCE) Product Catalog:

36

Inhibitors & Agonists

4

Peptides

11

Natural
Products

7

Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-121156A
    Anatibant hydrochloride

    LF 16-0687 hydrochloride; XY-2405 hydrochloride

    		 Bradykinin Receptor Neurological Disease
    Anatibant (LF 16-0687; XY-2405) hydrochloride is a selective non-peptide bradykinin B2 receptor antagonist. Anatibant hydrochloride binds to the human, rat and guinea-pig recombinant B2 receptor with Ki values of 0.67 nM, 1.74 nM and 1.37 nM, respectively. Anatibant hydrochloride crosses the blood-brain barrier (BBB). Anatibant hydrochloride can be used in research on brain damage diseases .
    Anatibant hydrochloride
  • HY-B1189
    Meglutol

    Dicrotalic acid; 3-Hydroxy-3-methylglutaric acid

    		 HMG-CoA Reductase (HMGCR) Autophagy Endogenous Metabolite Cardiovascular Disease Metabolic Disease
    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 .
    Meglutol
  • HY-139427
    3-Methylglutaconic acid

    β-Methylglutaconic acid

    		 GABA Receptor Cardiovascular Disease Neurological Disease Metabolic Disease
    3-Methylglutaconic acid is the major metabolites accumulating in 3-Methylglutaconic aciduria (MGTA). 3-Methylglutaconic acid can induce lipid oxidative damage and protein oxidative. 3-Methylglutaconic acid decreases the non-enzymatic antioxidant defenses in cerebral cortex supernatants to elicit oxidative stress in the cerebral cortex. 3-Methylglutaconic acid can be used for brain damage disease research .
    3-Methylglutaconic acid
  • HY-129056
    Melagatran

    		Thrombin NF-κB AP-1 Cardiovascular Disease Neurological Disease
    Melagatran is a reversible, selective, orally active direct inhibitor of thrombin with a Ki of 2 nM. Melagatran binds directly to the active site of thrombin, inhibiting thrombin-mediated conversion of fibrinogen to fibrin. Melagatran reduces the DNA binding activity of NF-κB and AP-1. Melagatran reduces fibrin deposition in organs, alleviates ischemic brain damage, and reduces the size of advanced atherosclerotic lesions. Melagatran can be used in the study of cardiovascular disease (coronary thrombosis, atherosclerosis) and ischemic brain damage .
    Melagatran
  • HY-113218
    Acetyl-L-carnitine
    2 Publications Verification

    O-Acetyl-L-carnitine; ALCAR

    		 Caspase Apoptosis Neurological Disease
    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 .
    Acetyl-L-carnitine
  • HY-B0762
    Acetyl-L-carnitine hydrochloride
    2 Publications Verification

    O-Acetyl-L-carnitine hydrochloride; ALCAR hydrochloride

    		 Caspase Apoptosis Neurological Disease
    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 .
    Acetyl-L-carnitine hydrochloride
  • HY-D0186
    2'-Deoxyuridine
    2 Publications Verification

    		 Endogenous Metabolite Thymidylate Synthase Infection
    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) .
    2'-Deoxyuridine
  • HY-176347S
    Alpha Feto Protein, Arg-13C6,15N4, Lys-13C6,15N2

    		Isotope-Labeled Compounds Cancer
    Alpha Feto Protein, Arg- 13C36, 15N4, Lys- 13C6, 15N2 is the 13C- and 15N-labeled Alpha Feto Protein.
    Alpha Feto Protein, Arg-13C6,15N4, Lys-13C6,15N2
  • HY-121156
    Anatibant

    LF 16-0687; XY-2405

    		 Bradykinin Receptor Neurological Disease
    Anatibant (LF 16-0687; XY-2405) is a selective non-peptide bradykinin B2 receptor antagonist. Anatibant binds to the human, rat and guinea-pig recombinant B2 receptor with Ki values of 0.67 nM, 1.74 nM and 1.37 nM, respectively. Anatibant crosses the blood-brain barrier (BBB). Anatibant can be used in research on brain damage diseases .
    Anatibant
  • HY-B1189R
    Meglutol (Standard)

    		HMG-CoA Reductase (HMGCR) Autophagy Endogenous Metabolite Cardiovascular Disease Metabolic Disease
    Meglutol (Standard) is the analytical standard of Meglutol. This product is intended for research and analytical applications. 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 .
    Meglutol (Standard)
  • HY-B0762S
    Acetyl-L-carnitine-d3 hydrochloride

    O-Acetyl-L-carnitine-d3 hydrochloride

    		 Isotope-Labeled Compounds Caspase Apoptosis Neurological Disease
    Acetyl-L-carnitine-d3 (O-Acetyl-L-carnitine-d3) hydrochloride is the deuterium labeled Acetyl-L-carnitine hydrochloride (HY-B0762). 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 .
    Acetyl-L-carnitine-d3 hydrochloride
  • HY-B0762S1
    Acetyl-L-carnitine-d3-1 hydrochloride

    O-Acetyl-L-carnitine-d3-1 hydrochloride

    		 Isotope-Labeled Compounds Caspase Apoptosis Neurological Disease
    Acetyl-L-carnitine-d3-1 (O-Acetyl-L-carnitine-d3-1) hydrochloride is the deuterium labeled Acetyl-L-carnitine hydrochloride (HY-B0762). 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 .
    Acetyl-L-carnitine-d3-1 hydrochloride
  • HY-W765177
    Acetyl-L-carnitine hydrochloride-13C3

    O-Acetyl-L-carnitine hydrochloride-13C3; ALCAR hydrochloride-13C3

    		 Isotope-Labeled Compounds Apoptosis Caspase Neurological Disease
    Acetyl-L-carnitine hydrochloride- 13C3 (O-Acetyl-L-carnitine hydrochloride- 13C3) is the 13C-labeled Acetyl-L-carnitine hydrochloride (HY-B0762). 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 .
    Acetyl-L-carnitine hydrochloride-13C3
  • HY-144874
    AZ3391

    		PARP Neurological Disease Cancer
    AZ3391 is a potent inhibitor of PARP. AZ3391 is a quinoxaline derivative. PARP family of enzymes play an important role in a number of cellular processes, such as replication, recombination, chromatin remodeling, and DNA damage repair. AZ3391 has the potential for the research of diseases and conditions occurring in tissues in the central nervous system, such as the brain and spinal cord (extracted from patent WO2021260092A1, compound 23) .
    AZ3391
  • HY-158696
    BChE/MAO-B-IN-1

    		Cholinesterase (ChE) Monoamine Oxidase Neurological Disease
    BChE/MAO-B-IN-1 (compound 7) is a dual BChE/MAO-B inhibitor with IC50 values ​​of 375 nM and 20 nM, respectively. BChE/MAO-B-IN-1 protects against oxidative damage induced by H2O2 and 6-OHDA in SH-SY5Y cells. BChE/MAO-B-IN-1 can penetrate the central nervous system in a cell model that mimics the blood-brain barrier. BChE/MAO-B-IN-1 can be used in the study of neurological diseases such as Alzheimer's disease (AD) .
    BChE/MAO-B-IN-1
  • HY-107661
    Arundic Acid
    2 Publications Verification

    ONO-2506; (R)-2-Propyloctanoic acid

    		 Others Neurological Disease
    Arundic acid (ONO-2506) is an astrocyte-modulating agent, which delays the expansion of cerebral infarcts by modulating the activation of astrocytes through inhibition of S-100β synthesis. Arundic acid also increases the expression level of EAAT1 by activating the Akt, ERK, and NF-κB signaling pathways, which has the potential to eliminate excess glutamate and inhibit excitotoxic brain damage or death. Arundic acid has the potential for stroke and Alzheimer’s disease research .
    Arundic Acid
  • HY-N7046
    Silybin B

    Silibinin B

    		 Amyloid-β Apoptosis JNK p38 MAPK Neurological Disease Cancer
    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 .
    Silybin B
  • HY-D0186R
    2'-Deoxyuridine (Standard)

    		Reference Standards Endogenous Metabolite Thymidylate Synthase Infection
    2'-Deoxyuridine (Standard) is the analytical standard of 2'-Deoxyuridine. This product is intended for research and analytical applications. 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) . In Vitro:The interaction between the 2-deoxyuridine and the column increases the duration of retention of 2-deoxyuridine .
    Gradient elution with sodium acetate buffer-ACN eluent on two ZIC-HILIC homemade columns separates 2-deoxyuridine in under 9 min .
    In Vivo:2'-Deoxyuridine (34.42 ng/mL, gavage, 15 min) passes the blood-brain barrier (BBB) to enter the hippocampus of mice brain .
    2'-Deoxyuridine (20 mg/kg, gavage, daily for 4 weeks) improves cognition and memory loss and attenuates the damage to the hippocampus in Aβ25-35-induced mice model .
    2'-Deoxyuridine (Standard)
  • HY-158695
    Dual AChE-MAO B-IN-4

    		Cholinesterase (ChE) Monoamine Oxidase Neurological Disease
    Dual AChE-MAO B-IN-4 (compound 7) is a dual AChE/MAO-B inhibitor, with IC50 values ​​of 261 nM and 15 nM, respectively. Dual AChE-MAO B-IN-4 protects against oxidative damage induced by H2O2 and 6-OHDA in SH-SY5Y cells. Dual AChE-MAO B-IN-4 can penetrate the central nervous system in a cell model that mimics the blood-brain barrier. Dual AChE-MAO B-IN-4 can be used in the study of neurological diseases such as Alzheimer's disease (AD) .
    Dual AChE-MAO B-IN-4
  • HY-W778990
    2-Deoxyuridine-1,2,3,4,5-13C5

    		Isotope-Labeled Compounds Thymidylate Synthase Endogenous Metabolite Infection
    2-Deoxyuridine-1,2,3,4,5- 13C5 is the 13C-labeled 2'-Deoxyuridine (HY-D0186). 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) .
    2-Deoxyuridine-1,2,3,4,5-13C5
  • HY-W424851
    DPQ hydrochloride

    6,7-Dimethoxy-2-(1-piperazinyl)-4-quinazolinamine hydrochloride

    		 PARP 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 .
    DPQ hydrochloride
  • HY-114869
    DPQ
    2 Publications Verification

    		 PARP Neurological Disease
    DPQ 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 inhibits NF-κB pathway activation, reduces the expression of pro-inflammatory factors (such as TNF-α, IL-6) and oxidative stress. DPQ can be used in inflammation-related studies of acute lung injury, myocardial infarction, and neurodegenerative diseases .
    DPQ
  • HY-N7046R
    Silybin B (Standard)

    Silibinin B (Standard)

    		 Reference Standards JNK Amyloid-β p38 MAPK Apoptosis Neurological Disease Cancer
    Silybin (Silibinin B) (Standard) is the analytical standard of Silybin B (HY-N7046). This product is intended for research and analytical applications. 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 .
    Silybin B (Standard)
  • HY-N7046S
    Silybin B-d3

    Silibinin B-d3

    		 Isotope-Labeled Compounds Amyloid-β Apoptosis JNK p38 MAPK Neurological Disease Cancer
    Silybin B-d3 (Silibinin B-d3) is a deuterated Silybin B (HY-N7046). 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 .
    Silybin B-d3
  • HY-161953
    O-GlcNAcase-IN-2

    		OGA Neurological Disease
    O-GlcNAcase-IN-2 (compound 81) is an orally effective, blood-brain barrier-permeable OGA inhibitor (IC50=4.93 nM). O-GlcNAcase-IN-2 can increase the O-GlcNAcylation level of proteins and phosphorylation of tau (p-Ser199, p-Thr205 and p-Ser396) in the OA-damaged SH-SY5Y cell model. O-GlcNAcase-IN-2 can also improve cognitive impairment in APP/PS1 mice and has potential anti-Alzheimer's disease (AD) effects .
    O-GlcNAcase-IN-2
  • HY-171936
    Ganglioside GM1 ammonium

    GM1 (d18:1/C18:0) ammonium; C18 Ganglioside GM1 (d18:1/18:0) ammonium

    		 Endogenous Metabolite Neurological Disease
    Ganglioside GM1 (ammonium) is a monosialylated ganglioside and the prototypic ganglioside for those containing one sialic acid residue. Ganglioside GM1 (ammonium) is one of the most abundant gangliosides in the brain which provides neuroprotection. Ganglioside GM1 (ammonium) exhibits anti-inflammatory property. Ganglioside GM1 (ammonium) has a well-balanced amphiphilic behavior. Ganglioside GM1 (ammonium) can reduce the fluidity of the plasma membrane that implies a retention and enrichment of the ganglioside in specific membrane domains that are called lipid rafts. Ganglioside GM1 (ammonium) can modify the process of differentiation, amplifies responses to neurotrophic factors, protects against excitatory amino acid-related neurotoxicity. Ganglioside GM1 (ammonium) can alleviate acute nerve cell damage through blocking cytotoxicity and potentiating neurotophic factors. Ganglioside GM1 (ammonium) can be studied in neurodegenerative diseases such as Alzheimer’s disease .
    Ganglioside GM1 ammonium
  • HY-169103
    Neuroprotective agent 5

    		NO Synthase COX Cholinesterase (ChE) Amyloid-β Neurological Disease Inflammation/Immunology
    Neuroprotective agent 5 (compound 28) is a brain permeabilizing agent with anti-neuritis, anti-oxidative damage and neuroprotective effects. Neuroprotective agent 5 exhibits a potent NO inhibitory effect (EC50=0.49 μM), inhibits the release of proinflammatory factors PGE2 and TNF-α, downregulates the expression of iNOS and COX-2 proteins, and promotes the polarization of BV-2 cells from the proinflammatory M1 phenotype to the anti-inflammatory M2 phenotype. In addition, Neuroprotective agent 5 can also inhibit acetylcholinesterase (AChE) activity and Aβ42 aggregation in a dose-dependent manner. Neuroprotective agent 5 can be used for the study of Alzheimer's disease .
    Neuroprotective agent 5
  • HY-128483
    Fusaric acid

    		TGF-beta/Smad PI3K NF-κB Akt Apoptosis Dopamine β-hydroxylase mTOR Adrenergic Receptor Cardiovascular Disease Endocrinology Cancer
    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 .
    Fusaric acid
  • HY-139192
    Brophenexin
    2 Publications Verification

    NMDAR/TRPM4-IN-2

    		 iGluR TRP Channel ERK 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 .
    Brophenexin
  • HY-139192A
    Brophenexin free base
    2 Publications Verification

    NMDAR/TRPM4-IN-2 free base

    		 iGluR TRP Channel ERK 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 .
    Brophenexin free base
  • HY-128483R
    Fusaric acid (Standard)

    		TGF-beta/Smad PI3K NF-κB Akt Apoptosis Dopamine β-hydroxylase mTOR Adrenergic Receptor Cardiovascular Disease Endocrinology Cancer
    Fusaric acid (Standard) is the analytical standard of Fusaric acid (HY-128483). This product is intended for research and analytical applications. 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 .
    Fusaric acid (Standard)
  • HY-N2255
    Crebanine
    3 Publications Verification

    		 Akt Apoptosis NF-κB Reactive Oxygen Species (ROS) p38 MAPK ERK Interleukin Related TNF Receptor NO Synthase nAChR Bacterial Infection Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    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. 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 .
    Crebanine
  • HY-P1363
    β-Amyloid (1-42), human TFA
    Maximum Cited Publications
    16 Publications Verification

    Amyloid β-peptide (1-42) (human) TFA

    		 Amyloid-β 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 ℃, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 ℃ 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 .
    β-Amyloid (1-42), human TFA
  • HY-P1363A
    β-Amyloid (1-42), human
    Maximum Cited Publications
    16 Publications Verification

    Amyloid β-peptide (1-42) (human)

    		 Amyloid-β 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 ℃, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 ℃ 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 .
    β-Amyloid (1-42), human
  • HY-P1363B
    β-Amyloid (1-42), human, HFIP-treated
    Maximum Cited Publications
    16 Publications Verification

    		 Amyloid-β 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 .
    β-Amyloid (1-42), human, HFIP-treated
  • HY-P1363S1
    β-Amyloid (1-42), human, Ala(13C3,15N) TFA

    		Isotope-Labeled Compounds Amyloid-β Neurological Disease
    β-Amyloid (1-42), human, Ala( 13C3, 15N) TFA is the 13C and 15N-labeled β-Amyloid (1-42), human (HY-P1363A). 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 ℃, which have synaptic toxicity and neurotoxicity; on the other hand, it can be incubated at 37 ℃ 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 .
    β-Amyloid (1-42), human, Ala(13C3,15N) TFA

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