ogd/r

Safinamide mesylate (EMD 1195686 mesylate) , a mesylate salt of Safinamide, can reversibly and specifically inhibit MAO-B (IC50: 98 nM), has 5918-fold selectivity against MAO-A.

GGTI 2147 decreased Rac1 activity, down-regulated p65 expression, and ameliorated OGD/R-induced neuronal apoptosis.

ATN-161 acetate, a pentapeptide compound derived from the synergistic region of fibronectin, is a non-competitive integrin-alpha5 antagonist with antitumor activity that attenuates the pathology of caerulein-induced acute pancreatitis.

Terlipressin Acetate, a highly selective vasopressin V1 receptor agonist, on oxygen and glucose deprivation/re-oxygenation (OGD/R)-induced damage in intestinal epithelial cells (IEC-6).Terlipressin acetate exerts anti-inflammatory and anti-oxidative effects. Terlipressin acetate has the potential for hepatorenal syndrome and norepinephrine-resistant septic shock research.

Neuroprotective agent 6 (Compound Y12) functions as an antioxidant and displays prominent neuroprotective effects in both oxygen-glucose deprivation/reperfusion (OGD/R) induced cell models and transient middle cerebral artery occlusion (tMCAO) induced animal models. Additionally, this compound shows significant metal chelating activity towards Cu2+.

TREK inhibitor-3 (Cpd8l) is a selective inhibitor of TREK-1 that can cross the blood-brain barrier, with an IC50 of 0.81 μM. It offers neuroprotective effects by significantly reducing cortical neuron death induced by oxygen-glucose deprivation/reoxygenation (OGD/R) and alleviating brain injury in middle cerebral artery occlusion/reperfusion (MCAO/R) model mice. TREK inhibitor-3 is utilized in ischemic stroke research.

GSNOR-IN-1 is a prodrug of GSNOR-IN-2 and functions as an S-nitrosoglutathione reductase (GSNOR) inhibitor capable of crossing the blood-brain barrier. GSNOR-IN-1 offers significant protective effects against damage induced by oxygen-glucose deprivation/reoxygenation (OGD/R). It regulates calcium signaling and synaptic function through Clstn1 S-nitrosylation and inhibits neuronal apoptosis. Additionally, GSNOR-IN-1 markedly reduces infarct volume in rat models of ischemic stroke while enhancing neurological function. With its neuroprotective properties, GSNOR-IN-1 holds potential for ischemic stroke research.

Troponin-IN-1 is a troponin inhibitor that protects H9c2 cardiomyocytes from OGD/R injury by reducing LDH leakage, pyroptosis, and reactive oxygen species (ROS) accumulation. In LPS-induced RAW264.7 cells, it suppresses NO production and the release of IL-1β, TNF-α, and IL-18. Troponin-IN-1 functions through the caspase-1/GSDMD/IL-18 signaling pathway and reduces myocardial infarction size in a LAD-induced myocardial ischemia/reperfusion (MI/R) male rat model. It is a valuable compound for studying myocardial ischemia/reperfusion injury.

TRPM2-IN-2 is a potent and selective TRPM2 inhibitor (IC50= 0.66 μM) with minimal activity against TRPM8 and TRPV1 (IC50> 10 μM). It demonstrates significant neuroprotective effects in both an in vitro oxygen-glucose deprivation/reperfusion (OGD/R) model and an in vivo transient middle cerebral artery occlusion (tMCAO) mouse model. TRPM2-IN-2 can be used for research related to ischemic stroke.

iNOs-IN-8 (Compound 13h) is a potent and highly selective inhibitor of inducible nitric oxide synthase (iNOS), with an IC50 of 238 nM. It demonstrates significant neuroprotective effects against neuronal and endothelial cell damage induced by oxygen-glucose deprivation/reoxygenation (OGD/R) and hydrogen peroxide. In rat models, iNOs-IN-8 significantly reduces infarct volume and improves neurological function. It is used in ischemic stroke research.

PDPOB (phenyl carboxylic acid derivative) shows potential for cerebral ischemia studies by protecting SH-SY5Y cells against OGD/R-evoked neuronal deterioration, reducing mitochondrial dysfunction, oxidative stress, and apoptosis [1].

Ferroptosis-IN-10 (compound D1) is an inhibitor of ferroptosis, demonstrating a potent IC50 value of 22 nM. It exhibits neuroprotective activity in the oxygen-glucose deprivation/reoxygenation (OGD/R) model.