brain damage

TRPM4 inhibitor 8 is an inhibitor of Transient receptor potential melastatin 4(TRPM4) which contributes to viability, migration, cell cycle shift, and adhesion.

10β,17β-dihydroxyestra-1,4-dien-3-one (DHED) is a brain-selective prodrug of 17β-estradiol, which has neuroprotective effects, improves cognitive dysfunction, and can be used to study brain damage.

Rocepafant (LAU8080) is a platelet-activating factor (PAF) antagonist that attenuates hypoxic-ischemic brain damage in neonatal rats.Rocepafant inhibits tumor necrosis factor-Afa-mediated cytotoxicity in mouse L929 tumor cells.

Vutiglabridin (HSG4112) is a novel and safe modulator of PON2, a racemic compound. vutiglabridin is an optimized structural analogue of Glabridin and is superior to Glabridin in terms of weight loss and chemical stability. vutiglabridin ameliorates mptp-induced neurodegeneration in Parkinson's disease mice by targeting mitochondrial paraoxonase-2. Vutiglabridin is a clinical phase 2 drug for the treatment of obesity and has therapeutic effects on p-mitochondrial PON2 in a PD model. vutiglabridin penetrates the brain, binds PON2, and restores 1-methyl-4-phenylpyridine (MPP*)-induced neuroblastoma in SH-SY5Y Vutiglabridin significantly attenuated 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced dyskinesia and dopaminergic neuronal damage in mice modeled with PD in mouse experiments.

CM-352 is a metalloproteinase inhibitor that reduces brain damage and improves functional recovery in rat models of cerebral hemorrhage.

isomer-CM 352 is a metalase inhibitor that can be used to slow brain damage.

L-Glutamic acid monosodium salt monohydrate (MSG monohydrate) is an important food additive with gastrointestinal protective effects. It plays a critical role in nutrient metabolism, energy demand, immune response, oxidative stress, signal transduction, and synaptic transmission. L-Glutamic acid monosodium salt monohydrate can induce oxidative stress, DNA damage, and apoptosis in mouse liver and brain tissues. It can protect against gastrointestinal damage caused by NSAIDs and Helicobacter pylori through multiple mechanisms.

3-Methyl-2-oxobutanoic acid (2-Oxoisovaleric acid) is an abnormal metabolite that arises from the incomplete breakdown of branched-chain amino acids. 3-Methyl-2-oxobutanoic acid is a neurotoxin, an acidogen, and a metabotoxin. A neurotoxin causes damage to nerve cells and nerve tissues. 3-Methyl-2-oxobutanoic acid is a keto-acid, which is a subclass of organic acids. Abnormally high levels of organic acids in the blood (organic acidemia), urine (organic aciduria), the brain, and other tissues lead to general metabolic acidosis.

Citric acid (Citro) is a weak organic tricarboxylic acid found in citrus fruits. Citric acid is a food additive and a natural preservative.

Dibutyl phthalate (1,2-Benzenedicarboxylic acid) is a plasticizer, commonly used in industrial manufacturing, that causes cardiac damage by disrupting Ca(2+) transfer from the endoplasmic reticulum to the mitochondria and triggering subsequent cellular death.Dibutyl phthalate induces oxidative damage in the brain of zebrafish.

Anatibant is a potent non-peptide bradykinin B2 receptor antagonist. Anatibant reduces intracranial hypertension and histopathological damage after experimental traumatic brain injury.

KL-50, a selective toxin, effectively targets tumors deficient in the DNA repair protein O6-methylguanine-DNA-methyltransferase (MGMT), which corrects O6-alkylguanine lesions. This compound induces both DNA damage response pathways and cell cycle arrest in MGMT-deficient cells, regardless of mismatch repair (MMR) status. KL-50 shows promise in the study of brain tumors lacking MGMT.

LDH-IN-3 (compound E38) is an inhibitor of lactate dehydrogenase (LDH) and a potential protective agent against ischemic neuronal damage in the eyes and brain. It functions through the HO-1/SIRT1 pathway.

NMDAR antagonist 2 (compound 3I) is a blood-brain barrier permeable antagonist of NMDA receptors, exhibiting IC50 values of 4.42 μM and 214.75 μM at membrane potentials of -60 mV and 40 mV, respectively, for hGluN1/hGluN2A. This compound has been shown to mitigate hippocampal damage.

AChE-IN-81 (compound 22) is a reversible, selective inhibitor of AChE with an 80.0% inhibition rate and an IC50 of 3.7 μM. It binds to AChE with an affinity (Kd) of 5.37 μM. AChE-IN-81 effectively reduces apoptosis in zebrafish brain cells and shows potential neuroprotective activity in an H2O2-induced SH-SY5Y cell damage model.

Nrf2 activator 19 is a compound capable of crossing the blood-brain barrier and acts as an NRF2/HO-1 activator, offering potent antioxidant and neuroprotective effects. It effectively reduces brain damage and minimizes the accumulation of Reactive Oxygen Species (ROS). Additionally, Nrf2 activator 19 inhibits neuronal apoptosis, aiding in the recovery of neural function and motor skills. It has demonstrated significant potential in ischemic stroke research.

Ferroptosis-IN-19 is a potent inhibitor of cellular ferroptosis, with an IC50 value of 0.097 μM. It demonstrates high metabolic stability and excellent predicted blood-brain barrier permeability. In mice, Ferroptosis-IN-19 has neuroprotective effects and can prevent ischemic brain damage.

Neuroprotective agent 10 (Compound 11c) is a brain-penetrant neuroprotective compound. It effectively scavenges ABTS radicals (IC50 for scavenging: 9.20 μM), DPPH radicals (IC50 for scavenging: 7.09 μM), and superoxide anion radicals (inhibition rate: 48.4%). Additionally, it mitigates oxidative damage induced by H2O2 and neuroinflammation induced by lipopolysaccharides, demonstrating antiepileptic properties. Neuroprotective agent 10 shows promise for research in epilepsy and neuroprotection.

Neuroprotective agent 9 (compound 7) is a neuroprotective compound with promising potential for use in research on neuronal damage, including conditions such as stroke, brain injury, and neuropathic pain.

BChE/MAO-B-IN-1 is a dual inhibitor of BChE and MAO-B, with IC50 values of 375 nM and 20 nM, respectively. It effectively counteracts oxidative damage induced by H2O2 and 6-OHDA in SH-SY5Y cells and can penetrate the central nervous system in cell models simulating the blood-brain barrier. BChE/MAO-B-IN-1 is applicable for research into neurological disorders such as Alzheimer's disease (AD).

Dual AChE-MAO B-IN-4 (compound 7) is a dual inhibitor of AChE and MAO-B, with IC50 values of 261 nM and 15 nM, respectively. It offers protection against oxidative damage induced by H2O2 and 6-OHDA in SH-SY5Y cells and can penetrate the central nervous system in a model simulating the blood-brain barrier. This compound is applicable in research on neurological disorders such as Alzheimer's disease (AD).

MT-125 is a specific and well-tolerated inhibitor of non-muscle myosin IIA [Ki, NMIIA = 2.7 μM] and IIB [EC50 = 1.7 μM]. It can cross the blood-brain barrier and induces ferroptosis and DNA damage by raising reactive oxygen species (ROS) levels within tumor cells. Additionally, MT-125 enhances the PDGFR signaling pathway and is utilized in glioblastoma 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.

β-Amyloid (1-42), human, Ala(13C3,15N) TFA is a β-Amyloid (1-42), human marked with 13C and 15N. This unprocessed HFIP peptide comprises 42 amino acids and is a brain-permeable amyloid fragment, useful for researching Alzheimer's and Down syndrome. In monomer form, β-Amyloid (1-42), human provides antioxidant and neuroprotective effects. Upon HFIP monomerization and DMSO solvent preparation, it forms soluble oligomers (AβOs) at 4°C, which exhibit synaptotoxicity and neurotoxicity, while at 37°C it forms insoluble fibrils with lower neurotoxicity, involved in oxidative damage. Aβ42 oligomers interact with neuronal surface receptors such as PrPc, mGluR5, and NMDA receptor, activating signaling pathways that induce oxidative stress, calcium imbalance, synaptotoxicity, leading to neuronal dysfunction and death.