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brain death model

" in MedChemExpress (MCE) Product Catalog:

8

Inhibitors & Agonists

3

Peptides

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-151808

    Btk Cancer
    JS25 is a selective and covalent inhibitor of BTK that inactivates BTK with an IC50 value of 5.8 nM by chelating Tyr551. JS25 inhibits cancer cells proliferation, pronounces cell death, and promotes murine xenograft model of Burkitt’s lymphoma. JS25 effectively crosses the blood-brain barrier .
    JS25
  • HY-P1263A
    tcY-NH2 TFA
    1 Publications Verification

    (trans-Cinnamoyl)-YPGKF-NH2 TFA

    Protease Activated Receptor (PAR) Metabolic Disease Inflammation/Immunology
    tcY-NH2 ((trans-Cinnamoyl)-YPGKF-NH2) TFA is a potent selective PAR4 antagonist peptide. tcY-NH2 TFA inhibits thrombin- and AY-NH2-induced platelet aggregation and endostatin release, and can be used in the research of inflammation, immunology .
    tcY-NH2 TFA
  • HY-P10019

    NLY01

    GCGR Neurological Disease
    Pegsebrenatide (NLY01) is a long-acting GLP-1R agonist. Pegsebrenatide has an extended half-life and favorable blood-brain barrier penetration. Pegsebrenatide can block A1 astrocyte transformation, reducing dopaminergic cell death, and improving motor symptoms in mouse models of PD .
    Pegsebrenatide
  • HY-161117

    Others Cancer
    AD-8007 is an acetyl CoA synthase 2 (ACSS2) inhibitor that can cross the blood-brain barrier. AD-8007 can significantly reduce lipid storage and cell colony formation in vitro models, and increase tumor cell death. AD-8007 has anti-cancer activity and can be used in the research of breast cancer .
    AD-8007
  • HY-P1263

    (trans-Cinnamoyl)-YPGKF-NH2

    Protease Activated Receptor (PAR) Metabolic Disease Inflammation/Immunology
    tcY-NH2 ((trans-Cinnamoyl)-YPGKF-NH2) is a potent selective PAR4 antagonist peptide. tcY-NH2 inhibits thrombin- and AY-NH2-induced platelet aggregation and endostatin release, and can be used in the research of inflammation, immunology .
    tcY-NH2
  • HY-110155
    LM11A-31 dihydrochloride
    Maximum Cited Publications
    6 Publications Verification

    Neurotensin Receptor Neurological Disease
    LM11A-31 dihydrochloride, a non-peptide p75 NTR (neurotrophin receptor p75) modulator, is an orally active and potent proNGF (nerve growth factor) antagonist. LM11A-31 dihydrochloride is an amino acid derivative with high blood-brain barrier permeability and blocks p75-mediated cell death. M11A-31 dihydrochloride reverses cholinergic neurite dystrophy in Alzheimer's disease mouse models with mid- to late-stage disease progression .
    LM11A-31 dihydrochloride
  • HY-126049

    (S)-(-)-Oxiracetam; (S)-ISF2522

    Apoptosis Neurological Disease
    (S)-oxiracetam (S-ORC) is an inhibitor targeting apoptosis. S-ORC reduces brain infarct size and lessens neurological dysfunction in middle cerebral artery occlusion/reperfusion (MCAO/R) models. S-ORC prevents neuronal apoptosis via activating PI3K/Akt/GSK3β signaling pathway via α7 nAChR after ischemic stroke. S-ORC can prevent neuronal death after ischemic stroke .
    (S)-Oxiracetam
  • HY-138185

    SF 2738A

    Bacterial Infection
    Collismycin A is a bacterial metabolite originally isolated from Streptomyces that has diverse biological activities, including antibacterial, antiproliferative, and neuroprotective properties. It is active against a variety of bacteria (MICs=6.25 and 100 μg/mL) and fungi (MICs=12.5-100 μg/mL). It inhibits proliferation of A549 lung, HCT116 colon, and HeLa cervical cancer cells (IC50s=0.3, 0.6, and 0.3 μM, respectively) and NIH373 fibroblasts (IC50=56.6 μM) but not MDA-MD-231 breast cancer cells (IC50=>100 μM). Collismycin A forms a complex with Fe(II) and Fe(III) at a 2:1 ratio, and the addition of iron ions inhibits the antiproliferative effect of collismycin A on HeLa cells, an effect that does not occur with the addition of zinc, manganese, copper, or magnesium ions.3 Collismycin A (1 μM) prevents apoptosis in the brain region of zebrafish larvae by 44% in a model of neuronal cell death induced by all-trans retinoic acid.
    Collismycin A

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