ischemic neurons

TRC051384 is a heat shock protein 70 (HSP70) inducer that reduces stroke-associated neuronal damage and increases survival in a rat model of transient ischemic stroke, activates heat shock factor-1 and leads to elevated molecular chaperone and anti-inflammatory activity, and enhances Hsp72 expression in neurons and glial cells.

Tat-NR2B9c (NA-1) is a postsynaptic density-95 (PSD-95) inhibitor with neuroprotective and antiepileptic effects.Tat-NR2B9c inhibits PSD-95d2, PSD-95d1, and PSD-95, which prevents the activation of NMDA-induced NADPH oxidase in neurons, thereby blocking the production of superoxide, which reduces ischemic injury in the acute phase after stroke.

HZS60 is a brain-penetrant NMDAR TRPM4 inhibitor that shows promise in ameliorating cerebral ischemia. It provides significant neuroprotection against ischemic injury in primary neurons caused by NMDA and oxygen-glucose deprivation reoxygenation. HZS60 demonstrates favorable pharmacokinetic properties and can inhibit cerebral ischemia-reperfusion injury, positioning it as a potential inhibitor for ischemic stroke.

KUS121 is a valosin-containing protein (VCP) modulator that inhibits VCP ATPase activity (IC50= 330 nM).1It inhibits cell death, ATP depletion, and upregulation of C/EBP-homologous protein (CHOP) induced by tunicamycin, an inducer of ER stress, in HeLa cells when used at concentrations of 20, 50, and 50 μM, respectively. KUS121 (100 μM) inhibits ATP depletion and cell death induced by oxygen-glucose deprivation (OGD) in rat primary cortical neurons in anin vitromodel of cerebral ischemia.2It reduces infarction volume and increases the latency to fall in an accelerating rotarod test in a mouse model of focal cerebral ischemia induced by transient distal middle cerebral artery occlusion (MCAO) when administered at a dose of 100 mg/kg immediately following occlusion and again at 50 mg/kg following reperfusion. KUS121 (50 mg/kg) inhibits thinning of the retinal outer nuclear layer and preserves visual function in an rd10 mouse model of retinitis pigmentosa.1 1.Ikeda, H.O., Sasaoka, N., Koike, M., et al.Novel VCP modulators mitigate major pathologies of rd10, a mouse model of retinitis pigmentosaSci. Rep.45970(2014) 2.Kinoshita, H., Maki, T., Yasuda, K., et al.KUS121, a valosin-containing protein modulator, attenuates ischemic stroke via preventing ATP depletionSci. Rep.9(1)11519(2019)

1. Rhynchophylline (Mitrinermine) can protect against ischemic damage, probably via regulating the Akt mTOR pathway. 2. Rhynchophylline can protect against glutamate-induced neuronal death, can inhibit MA impairment in cultured neurons in vitro. 3. Rhynchophylline and isorhynchophylline have a non-competitive antagonistic effect on the NMDA-type ionotropic glutamate receptors, suggest that these alkaloids exert their protective action against ischemia-induced neuronal damage by preventing NMDA, muscarinic M1, and 5-HT2 receptors-mediated neurotoxicity during ischemia.

LY836 is an orally active, neuroprotective compound that effectively inhibits the PSD95-nNOS association in cortical neurons. It has potential applications in the study of ischemic stroke [1].

B355252 protects against cell death caused by glutamate-evoked oxidative stress. B355252 shows neuroprotective effect, potentiating nerve growth factor (NGF)-induced neurite outgrowth.

Hinokiresinol is a novel inhibitor of LTB4 binding to the human neutrophils, it has antiallergic effect, it inhibits IgE-induced mouse passive cutaneous anaphylaxis reaction. Hinokiresinol (trans-hinokiresinol) and nyasol (cis-hinokiresinol) are estrogen