post-stroke

The quinuclidine PHA 568487 free base is an agonist of the alpha 7 nicotinic acetylcholine receptor that was designed to mitigate the bioactivation associated with the core scaffold and subsequently remove associated liabilities with in vivo tolerability.

Tat-M2NX, a peptide antagonist of transient receptor potential melastatin 2 (TRPM2), blocks hydrogen peroxide-induced calcium influx in HEK293 cells expressing human TRPM2 at concentrations between 25 to 100 µM. In male mice models of stroke caused by middle cerebral artery occlusion (MCAO), Tat-M2NX (20 mg/kg) demonstrates efficacy in reducing brain infarct volume when applied before or 3 hours-post occlusion, yet it shows no such effect in female mice.

TAT-NEP1-40 acetate, a potential therapeutic for axonal regeneration and functional recovery post-stroke, safeguards PC12 cells from oxygen and glucose deprivation (OGD) and encourages neurite outgrowth. This compound also affords cerebral protection against ischemia/reperfusion injury by hindering neuronal apoptosis and can be effectively administered into rat brains [1] [2].

TAT-NEP1-40 TFA, a blood-brain barrier-permeable peptide, safeguards PC12 cells against oxygen and glucose deprivation (OGD) and fosters neurite outgrowth. Additionally, it enhances neurological outcomes post-ischemia by curtailing apoptosis in ischemic cerebral tissues. This compound has utility in investigating central nervous system (CNS) injuries, encompassing axonal regeneration and functional recuperation following a stroke [1].

N-Acetyl lysyltyrosylcysteine amide is a non-toxic, potent, reversible, and specific myeloperoxidase (MPO) tripeptide inhibitor that effectively inhibits MPO production in vivo, attenuates neuronal damage, preserves brain tissue and neurological function post-stroke, and inhibits MPO-dependent hypochlorite (HOCl) production, protein nitration, and LDL oxidation. It is also used in the study of bronchial dysplasia.

TAT-NEP1-40, a blood-brain barrier (BBB) permeable peptide, confers protection to PC12 cells against oxygen and glucose deprivation (OGD) while promoting neurite outgrowth. Furthermore, it enhances neurologic outcomes post-ischemia by mitigating apoptosis in affected cerebral regions. This compound holds potential for central nervous system (CNS) injury research, including studies on axonal regeneration and post-stroke functional recovery [1].