2. Disease Areas
  3. Neurological, Eye or Ear Disease

Neurological, Eye or Ear Disease

Neurological disorders are conditions that target how your nervous system (brain, spinal cord and nerves) functions. There are hundreds of neurological disorders like Alzheimer’s disease, multiple sclerosis and meningitis, for example. They cause symptoms that affect how you move, think and feel.

 

Neurological, Eye or Ear Disease (10):

Cat. No. Product Name CAS No. Purity Chemical Structure
  • HY-15608
    MPTP hydrochloride 23007-85-4 99.82%
    MPTP hydrochloride is a brain penetrant dopaminergic neurotoxin. MPTP hydrochloride can be used to induce Parkinson’s Disease model. MPTP hydrochloride, a precusor of MPP+, induces apoptosis. MPTP hydrochloride has been verified by MCE with professional biological experiments.
    MPTP hydrochloride
  • HY-P0128
    β-Amyloid (25-35) 131602-53-4 99.84%
    β-Amyloid (25-35) (Amyloid beta-peptide (25-35)) is the fragment Aβ(25-35) of the Alzheimer's amyloid β-peptide, has shown neurotoxic activities in cultured cells.
    β-Amyloid (25-35)
  • HY-P1363
    β-Amyloid (1-42), human TFA 99.66%
    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-W015229
    3-Indolepropionic acid 830-96-6 99.89%
    3-Indolepropionic acid is shown to be a powerful antioxidant and has potential in the treatment for Alzheimer’s disease.
    3-Indolepropionic acid
  • HY-P1363B
    β-Amyloid (1-42), human, HFIP-treated 107761-42-2 99.89%
    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-P0198
    Neuropeptide Y (human,rat,mouse) 90880-35-6 99.94%
    Neuropeptide Y (human,rat,mouse) is involved in Alzheimer's disease (AD) and protects rat cortical neurons against β-Amyloid toxicity.
    Neuropeptide Y (human,rat,mouse)
  • HY-P0128A
    β-Amyloid (25-35), HFIP-treated 131602-53-4 99.71%
    β-Amyloid (25-35) (Amyloid beta-peptide (25-35)), HFIP-treated is a β-Amyloid (25-35) (HY-P0128) treated with HFIP. β-Amyloid (25-35) (Amyloid beta-peptide (25-35)) is the fragment Aβ(25-35) of the Alzheimer's amyloid β-peptide, has shown neurotoxic activities in cultured cells.
    β-Amyloid (25-35), HFIP-treated
  • HY-N0385
    Gomisin J 66280-25-9 99.97%
    Gomisin J is a Schisandra chinensis-derived lignan that can inhibit multiple targets such as eNOS, AMPK (LKB1, CaMKIIβ), fetuin-A, NF-κB, Nrf2/HO-1, and can pass through the blood-brain barrier. Gomisin J increases NO bioavailability by activating eNOS, regulates lipid metabolism by activating the AMPK pathway, inhibits fetuin-A and NF-κB to exert anti-inflammatory effects, and activates Nrf2/HO-1 to enhance antioxidant capacity. Gomisin J has the activities of anti-hypertension, regulating liver lipid metabolism, and reducing cerebral ischemia-reperfusion injury, and can be used for research on hypertension, non-alcoholic fatty liver disease, cerebral ischemia-reperfusion injury, etc.
    Gomisin J
  • HY-106262
    Delcasertib 949100-39-4 98.21%
    Delcasertib (KAI-9803) is a potent and selective δ-protein kinase C (δPKC) inhibitor. Delcasertib (KAI-9803) could ameliorate injury associated with ischemia and reperfusion in animal models of acute myocardial infarction (MI).
    Delcasertib
  • HY-P99886
    Pexelizumab 219685-93-5
    Pexelizumab (h5G1. 1-SC) is a humanized scFv monoclonal antibody directed against the C5 complement component. Pexelizumab inhibits apoptosis and leukocyte infiltration. Pexelizumab can be used for the research of cerebral IR injury and myocardial infarction.
    Pexelizumab