Epilepsy

Glutamate dehydrogenase (NADP) is the catalytic enzyme for glutamate production. Dysfunction of Glutamate dehydrogenase (NADP) may induce various neurodegenerative diseases, such as Parkinson's disease, epilepsy, Alzheimer's disease, schizophrenia, and frontotemporal dementia. Glutamate dehydrogenase (NADP) can be used in research on neurological diseases such as Parkinson's disease, epilepsy, and Alzheimer's disease.

Pirlindole is an orally active, selective and reversible MAO-A inhibitor with an IC₅₀ value of 250 nM. Pirlindole inhibits genomic replication of Enterovirus species B and D, and exhibits moderate activity against enterovirus species A. Pirlindole inhibits MAO-A-mediated monoamine metabolism, promotes adult hippocampal neurogenesis, rescues stress-induced dendritic atrophy of hippocampal granule neurons, reverses behavioral effects associated with chronic mild stress, and also possesses anticonvulsant, analgesic, local anesthetic, hypotensive, antiplatelet aggregation and antispasmodic activities. Pirlindole shows no detectable mutagenic, clastogenic or carcinogenic properties. Pirlindole can be used in research related to depression and enterovirus infections.

L-Aspartic acid-1,4-¹³C₂ is the ¹³C-labeled L-Aspartic acid (HY-N0666). L-Aspartic acid is a NMDA receptor agonist and acidic amino acid. L-Aspartic acid has no independent analgesic activity. L-Aspartic acid can antagonize the analgesic effects of D-Aspartic acid and Morphine. L-Aspartic acid regulates polymorph transformation, crystal growth/aggregation and nucleation processes of calcium carbonate, and can serve as a biomineralization template. L-Aspartic acid promotes burst firing of central neurons. L-Aspartic acid can be used in studies related to cerebral ischemia and epilepsy.

L-Aspartic acid-¹³C is the ¹³C-labeled L-Aspartic acid (HY-N0666). L-Aspartic acid is a NMDA receptor agonist and acidic amino acid. L-Aspartic acid has no independent analgesic activity. L-Aspartic acid can antagonize the analgesic effects of D-Aspartic acid and Morphine. L-Aspartic acid regulates polymorph transformation, crystal growth/aggregation and nucleation processes of calcium carbonate, and can serve as a biomineralization template. L-Aspartic acid promotes burst firing of central neurons. L-Aspartic acid can be used in studies related to cerebral ischemia and epilepsy.

UCB-J is a ligand for synaptic vesicle protein 2A (SV2A) with pIC₅₀ values for human and rat SV2A of 8.15 and 7.6 respectively. UCB-J can be used to display and quantify the total synaptic density throughout the brain.

Ricinine is a central nervous system stimulant found in Ricinus communis. Ricinine binds near the benzodiazepine site of the GABA_A receptor, reducing benzodiazepine binding affinity through an allosteric effect, and shows no interaction with AMPA, 5-HT_1A, muscarinic receptors, or α₁ adrenergic receptors. Ricinine improves memory consolidation in mice at low doses, while at high doses it induces seizures, an effect that is selectively inhibited by diazepam. Ricinine shortens the lifespan of Anopheles mosquitoes through sugar feeding and promotes the development of Plasmodium falciparum in mosquitoes. Ricinine is used in research related to epilepsy, amnesia, and malaria.

Fluorothyl (Bis (2,2,2-trifluoroethyl) ether; Flurothyl) is a GABAA receptor modulator and epileptogenic agent. Fluorothyl induces generalized epilepsy in mice. Fluorothyl is used for epilepsy research.

Metaldehyde is an orally active molluscicide. Metaldehyde acts as a feeding inhibitor. Metaldehyde disrupts the feeding cycle, impairs righting ability, delays fecal excretion, induces toxic symptoms in slugs, reduces the concentrations of neurotransmitters (Noradrenaline, 5-HT (HY-B1473A)) in the mouse brain, and induces lethal clonic-tonic convulsions in mice.

DCM-ONOO is a near-infrared two-photon fluorescence probe specifically designed for real-time monitoring of the dynamic fluctuations of peroxynitrite (ONOO⁻) in epilepsy models. DCM-ONOO exhibits excellent optical properties, with a single photon excitation (Ex) of 520 nm; a single photon emission (Em) of 685 nm; a two-photon excitation of 820 nm; and a Stokes shift of 165 nm. When DCM-ONOO is combined with ONOO⁻, it shifts from 460 nm to 512 nm, and only generates a significant fluorescence response to ONOO⁻. DCM-ONOO has been successfully applied to rat epilepsy models.

4-Methyloctanoic acid is an endogenous branched-chain medium-chain fatty acid and a negative regulator of the cAMP/PKA signaling pathway. 4-Methyloctanoic acid exerts antiepileptic effects by inhibiting epileptiform discharges and terminating behavioral and electroencephalographic seizures. 4-Methyloctanoic acid has neuroprotective effects; its polar metabolites can cross the blood-brain barrier, repair presynaptic release defects, improve motor function and alleviate neuromuscular degeneration in ALS models. 4-Methyloctanoic acid regulates phosphatidylinositol metabolism, reduces PIP/PIP₂ levels and increases inositol levels. 4-Methyloctanoic acid can be used in studies related to epilepsy and amyotrophic lateral sclerosis.

Cx43 HC-IN-1 (Compound D4) is a selective and orally active inhibitor of connexin hemichannels (Cx43 HC). Cx43 HC-IN-1 effectively inhibits the hemichannel activity mediated by Cx43/Cx45 in denervated skeletal muscle fibers, significantly increasing the reinnervation rate of muscle fibers by neurons. Cx43 HC-IN-1 reduces neuroinflammation and neuronal overexcitation by inhibiting hemichannels in glial cells in the brain, and alleviates epilepsy in mice. Cx43 HC-IN-1 can be used for research on epilepsy and muscle diseases.

L-Aspartic acid monocesium (monocesium L-aspartate) is a NMDA receptor agonist and acidic amino acid. L-Aspartic acid monocesium has no independent analgesic activity. L-Aspartic acid monocesium can antagonize the analgesic effects of D-Aspartic acid and Morphine. L-Aspartic acid monocesium regulates polymorph transformation, crystal growth/aggregation and nucleation processes of calcium carbonate, and can serve as a biomineralization template. L-Aspartic acid monocesium promotes burst firing of central neurons. L-Aspartic acid monocesium can be used in studies related to cerebral ischemia and epilepsy.

N-Methyl-DL-aspartic acid acts as an agonist for N-methyl-D-aspartic acid receptors and D-isomer-specific aspartate receptors. N-Methyl-DL-aspartic acid activates hypothalamic neurons that regulate gonadotropin-releasing hormone secretion, and stimulates prepubertal male rhesus monkeys to produce sustained intermittent gonadotropin-releasing hormone secretion and pulsatile luteinizing hormone secretion. N-Methyl-DL-aspartic acid activates excitatory effects mediated by N-methyl-D-aspartic acid receptors. N-Methyl-DL-aspartic acid exhibits convulsant effects, inducing clonic convulsions with loss of righting reflex, generalized tonic-clonic seizures or persistent clonic seizures. N-Methyl-DL-aspartic acid causes precocious puberty. N-Methyl-DL-aspartic acid can be used in studies related to convulsions and seizures.

Aspartic acid calcium (calcium L-aspartate) is a NMDA receptor agonist and acidic amino acid. Aspartic acid calcium has no independent analgesic activity. Aspartic acid calcium can antagonize the analgesic effects of D-Aspartic acid and Morphine. Aspartic acid calcium regulates polymorph transformation, crystal growth/aggregation and nucleation processes of calcium carbonate, and can serve as a biomineralization template. Aspartic acid calcium promotes burst firing of central neurons. Aspartic acid calcium can be used in studies related to cerebral ischemia and epilepsy.

QO-83, Retigabine analogue, is a voltage-gated potassium channel KCNQ2 (Kv7.2) activator with an EC₅₀ of 0.56 μM. QO-83 binds to a single hydrophobic pocket of KCNQ2-CaM complex in closed conformation. QO-83 induces a negative shift in the voltage-dependent activation curve of KCNQ2 channels, increasing the channel's voltage sensitivity. QO-83 can be used for the research of epilepsies.

UCB1244283 is a synaptic vesicle glycoprotein 2A (SV2A) allosteric modulator. UCB1244283 binds to a secondary ligand-binding site in SV2A and enhances orthosteric ligand engagement when the orthosteric site is occupied, by stabilizing the occluded state and slowing ligand dissociation. UCB1244283 shows a clear protective effect against both tonic and clonic convulsions in sound-sensitive mice. UCB1244283 can be used for epilepsy research.

Penicillinase is an enzyme capable of hydrolyzing penicillin. Penicillinase converts penicillin into penicilloic acid, which has no antigenicity, and destroys the antibacterial, antigenic and epileptogenic properties of penicillin. Penicillinase shortens the duration of penicillin-induced seizures and neutralizes the ability of penicillin to form epileptogenic foci. Penicillinase can be used in research related to penicillin hypersensitivity and penicillin-induced encephalopathy.

L-Aspartic acid-¹³C₄,¹⁵N,d₃ is the ¹⁵N, deuterated, ¹³C-labeled L-Aspartic acid (HY-N0666). L-Aspartic acid is a NMDA receptor agonist and acidic amino acid. L-Aspartic acid has no independent analgesic activity. L-Aspartic acid can antagonize the analgesic effects of D-Aspartic acid and Morphine. L-Aspartic acid regulates polymorph transformation, crystal growth/aggregation and nucleation processes of calcium carbonate, and can serve as a biomineralization template. L-Aspartic acid promotes burst firing of central neurons. L-Aspartic acid can be used in studies related to cerebral ischemia and epilepsy.

(RS)-(Tetrazol-5-yl)glycine (D,L-(tetrazol-5-yl)glycine) is a highly potent and selective N-methyl-D-aspartate (NMDA) receptor agonist. (RS)-(Tetrazol-5-yl)glycine has EC₅₀s of 99 nM, 1.7 μM for GluN1/GluN2D and GluN1/GluN2A, respectively. (RS)-(Tetrazol-5-yl)glycine induces seizure responses and Fos in mice.

Norfluoxetine-d5 hydrochloride is the d₅-labeled Norfluoxetine hydrochloride (HY-W011235). Norfluoxetine hydrochloride is the active metabolite of the antidepressant Fluoxetine (HY-B0102); it is also a TREK-2 K₂P potassium channel inhibitor. Norfluoxetine hydrochloride exhibits neuroimmunological activity, induces apoptosis in primary microglial cells, and inhibits the release of pro-inflammatory factors. Norfluoxetine hydrochloride inhibits high-threshold voltage-gated Ca²⁺ currents in neurons with an EC₅₀ of 20.4 μM. Norfluoxetine hydrochloride can be used in research related to depression, ischemic stroke, and epilepsy.