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Results for "

neurocognitive

" in MedChemExpress (MCE) Product Catalog:

7

Inhibitors & Agonists

2

Peptides

1

Natural
Products

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-P0299

    TGF-β Receptor Cancer
    LSKL, Inhibitor of Thrombospondin (TSP-1) is a latency-associated protein (LAP)-TGFβ derived tetrapeptide and a competitive TGF-β1 antagonist. LSKL, Inhibitor of Thrombospondin (TSP-1) inhibits the binding of TSP-1 to LAP and alleviates renal interstitial fibrosis and hepatic fibrosis. LSKL, Inhibitor of Thrombospondin (TSP-1) suppresses subarachnoid fibrosis via inhibition of TSP-1-mediated TGF-β1 activity, prevents the development of chronic hydrocephalus and improves long-term neurocognitive defects following subarachnoid hemorrhage (SAH). LSKL, Inhibitor of Thrombospondin (TSP-1) can readily crosse the blood-brain barrier .
    LSKL, Inhibitor of Thrombospondin (TSP-1)
  • HY-B2209
    Hydroxocobalamin
    3 Publications Verification

    Vitamin B12a

    Endogenous Metabolite Neurological Disease Metabolic Disease
    Hydroxocobalamin (Vitamin B12a) is a cyanide antidote. Hydroxocobalamin can decrease the cell and plasma cyanide concentrations and increase survival rate in acute cyanide poisoning. Hydroxocobalamin can improve newborn Cbl-C defect-induced metabolic profile and neurocognitive outcome. Hydroxocobalamin can normalize Vitamin B12 deficiency. Hydroxocobalamin can induce acute kidney injury. Hydroxocobalamin can be used for the researches of metabolic and neurological disease .
    Hydroxocobalamin
  • HY-P0299A

    TGF-β Receptor Cancer
    LSKL, Inhibitor of Thrombospondin (TSP-1) TFA is a latency-associated protein (LAP)-TGFβ derived tetrapeptide and a competitive TGF-β1 antagonist. LSKL, Inhibitor of Thrombospondin (TSP-1) TFA inhibits the binding of TSP-1 to LAP and alleviates renal interstitial fibrosis and hepatic fibrosis. LSKL, Inhibitor of Thrombospondin (TSP-1) TFA suppresses subarachnoid fibrosis via inhibition of TSP-1-mediated TGF-β1 activity, prevents the development of chronic hydrocephalus and improves long-term neurocognitive defects following subarachnoid hemorrhage (SAH). LSKL, Inhibitor of Thrombospondin (TSP-1) TFA can readily crosse the blood-brain barrier .
    LSKL, Inhibitor of Thrombospondin (TSP-1) TFA
  • HY-119386

    Sigma Receptor Calcium Channel Neurological Disease
    SAS-0132 is a selective Sigma 2 receptor (Sig2R) antagonist (Ki: 90 nM) that can cross the blood-brain barrier. SAS-0132 is capable of regulating intracellular Ca 2+ levels and modulating PGRMC1-related pathways. SAS-0132 exhibits neuroprotective activity and can improve cognitive impairment in Alzheimer's disease mice. SAS-0132 can be used in the research of neurocognitive disorders such as Alzheimer's disease .
    SAS-0132
  • HY-16505

    Endogenous Metabolite Neurological Disease
    Triclofos sodium is a drug used to suppress insomnia and for sedation and has sedative activity. Triclofos sodium is used in children for sedation during painless medical procedures, particularly in children with neurocognitive disorders. Triclofos sodium has similar physiological and pharmacological properties to chloral and therefore can be used as a substitute when necessary. The safety and efficacy of Triclofos sodium have been demonstrated in pediatric populations with high rates of neurocognitive disorders .
    Triclofos sodium
  • HY-175534

    Dopamine Receptor HIV Infection Neurological Disease
    SRI-45949 is an allosteric modulator of the HIV-DAT-Tat interaction. SRI-45949 has IC50 values of 9.56 μM and 9.34 μM for [ 3H]DA uptake and [ 3H]WIN35,428 binding, respectively. SRI-45949 can be used in research related to HIV-associated neurocognitive disorders .
    SRI-45949
  • HY-181888

    HIV HIV Protease Infection
    GRL-142 is a potent HIV-1 protease inhibitor capable of crossing the blood-brain barrier. GRL-142 exhibits extremely high inhibitory activity against both wild-type and multidrug-resistant strains (IC50=0.0094 nM). GRL-142 acts synergistically with the P2/P2' segments via a unique scaffold binding mechanism, utilizes fluorine-mediated stable interactions to maintain its bioactive conformation, adapts to p51 HIV-1 protease mutants, and maintains the flap-closed state by directly acting on the flap tip residues. GRL-142 disrupts the flap-water hydrogen bond network of wild-type protease, thereby effectively blocking viral replication. GRL-142 can be used to study HIV-1 infection and the associated neurocognitive disorder (HAND) .
    GRL-142

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