Epilepsy

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.

Quinidine (15% dihydroquinidine) is an orally active antiarrhythmic agent. Quinidine (15% dihydroquinidine) reduces the expression level of P-gp, inhibits P-gp-mediated efflux, increases the intracellular accumulation of P-gp substrates, induces PARP cleavage and Caspase-3 activation, and elevates the proportion of Apoptotic cells at the sub-G1 phase. Quinidine (15% dihydroquinidine) exerts sustained block and open-channel block effects on I_K(f). Quinidine (15% dihydroquinidine) alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. Quinidine (15% dihydroquinidine) can be used in studies related to uterine sarcoma and seizures.

Losmapimod (GSK-AHAB; GW856553X) is an orally active p38α/β MAPK inhibitor, with pK_i values of 8.1 and 7.6 for p38α and p38β, respectively. Losmapimod reduces DUX4 expression, thus exerting efficacy in facioscapulohumeral muscular dystrophy. By inhibiting MAPK/NF-κB, Losmapimod reduces apoptosis of epileptiform hippocampal neurons, and exhibits anti-allodynia and anti-hyperalgesic activities. Losmapimod blocks the entry and fusion of Lassa fever virus (LASV). Losmapimod overcomes tyrosine kinase inhibitor resistance in non-small cell lung cancer (NSCLC). Losmapimod inhibits myocardial senescence and inflammation, and possesses cardioprotective activity against cardiotoxicity.

Quinidine hydrochloride monohydrate is an orally active antiarrhythmic agent. Quinidine hydrochloride monohydrate reduces the expression level of P-gp, inhibits P-gp-mediated efflux, increases the intracellular accumulation of P-gp substrates, induces PARP cleavage and Caspase-3 activation, and elevates the proportion of Apoptotic cells at the sub-G1 phase. Quinidine hydrochloride monohydrate exerts sustained block and open-channel block effects on I_K(f). Quinidine hydrochloride monohydrate alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. Quinidine hydrochloride monohydrate can be used in studies related to uterine sarcoma and seizures.

Imidazoleacetic acid (Imidazolyl-4-acetic acid) is a blood-brain barrier-permeable full agonist of the GABA_A receptor. Imidazoleacetic acid forms via histamine oxidation in the mouse brain. Imidazoleacetic acid exerts multiple neurochemical and behavioral effects. Imidazoleacetic acid induces a range of centrally mediated effects, including analgesia, sedation, hypnosis, as well as reductions in blood pressure, body temperature, isolation-induced aggression and motor activity.

Sodium bromide (NSC 77384; Sanibrom 40) is a GABA-ergic system modulator that crosses the blood-brain barrier, and it effectively reduces and blocks epileptiform discharges. Sodium bromide exerts significant anticonvulsant effects by enhancing GABA-ergic inhibitory functions, such as increasing the amplitude of inhibitory postsynaptic currents and paired-pulse inhibition. Sodium bromide specifically enhances stimulation-induced extracellular alkalosis without affecting baseline pH or subsequent acidosis processes. Sodium bromide exhibits species-specific pharmacokinetic characteristics, competes with chloride ions for renal tubular reabsorption sites, and serves as a marker for extracellular fluid volume. Sodium bromide can be used in the research of epilepsy and related neurological diseases.

Avizafone (Pro-diazepam) dihydrobromide, a pro-drug of Diazepam, is an anticonvulsant agent. Avizafone dihydrobromide can be used as an antidote of nerve agent poisoning. In vivo, Avizafone dihydrobromide is rapidly hydrolyzed by aminopeptidase to produce lysine and diazepam. Avizafone dihydrobromide has research areas including neurological disease, such as epilepsy.

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.

(S)-SNAP5114 is a non-covalent murine GABA transporter inhibitor with blood-brain barrier penetration ability, which exhibits significant subtype-selective inhibitory activity against mGAT4 (pIC₅₀=5.71, pK_i=4.56), much higher than its effects on mGAT1, mGAT2 and mGAT3. (S)-SNAP5114 elevates extracellular GABA concentrations by blocking the GABA reuptake mechanism, thereby enhancing thalamus-specific GABAergic signaling and exerting potential neuromodulatory effects. (S)-SNAP5114 is widely used in studies related to epilepsy, neuropathic pain, anxiety and depression, and various neurodegenerative diseases.

L-Aspartic acid-¹³C₄ 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.

Fosfructose is an orally active cyclooxygenase-2 inhibitor and Toll-like receptor 4 modulator. Fosfructose reduces the expression of cyclooxygenase-2, thereby decreasing prostaglandin production. By inhibiting the Toll-like receptor 4 signaling pathway, Fosfructose downregulates LPS-induced adhesion molecule expression. Fosfructose is applicable to research related to ischemic stroke, epilepsy, sepsis, myocardial injury, osteoporosis, and ultraviolet B-induced skin damage.

L-Aspartic acid-d₃ is the d₃-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 (Standard) is the analytical standard of L-Aspartic acid (HY-N0666). This product is intended for research and analytical applications. 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.

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.

CCPA (2-Chloro-N6-cyclopentyladenosine) a highly selective A1 adenosine receptors agonist with a K_i of 0.4 nM. CCPA inhibits adenylate cyclase with an IC₅₀ of 33 nM. CCPA exhibits anti-seizure and cardiacprotective activity. CCPA can be used for the research of seizure and myocardial infarction.

SCH 50911 is a selective, orally active, blood-brain barrier permeable GABA-B receptor (GABA-B Receptor) antagonist with an IC₅₀ of 1.1 μM in rats. SCH 50911 blocks baclofen-induced antitussive effects, regulates neuronal firing and GABA release. SCH 50911 promotes spontaneous seizures during withdrawal in ethanol-dependent rats, alters reward-related neurotransmission, and reduces or suppresses lever responding and self-administration behaviors of alcohol and sucrose in rats. SCH 50911 is applicable to research related to ethanol withdrawal syndrome, absence epilepsy and alcohol use disorder.

Arundic Acid is an orally effective astrocyte function modulator and neuroprotective agent. Arundic Acid increases the expression and function of the astrocytic glutamate transporter EAAT1 by activating the ERK, Akt and NF-κB pathways. Arundic Acid attenuates retinal ganglion cell death in a normal-tension glaucoma model. Arundic Acid exerts neuroprotective effects in a mouse model of Parkinson's disease. Arundic Acid is a S100β protein synthesis inhibitor that prevents neurological deficits and brain tissue damage after intracerebral hemorrhage in rats. Arundic Acid downregulates neuroinflammation and astrocytic dysfunction after status epilepticus in immature rats. Arundic Acid is applicable to research related to Parkinson's disease, cerebral ischemia, glaucoma, intracerebral hemorrhage and epilepsy.

Opakalim (BHV-7000) is a selective Kv7.2/7.3 potassium channels activator with an EC₅₀ of 0.6 μM. Opakalim shows minimal GABAA receptor activation and exhibits potent anti-seizure efficacy in the maximal electroshock seizure (MES) model. Opakalim can be used for the study of seizures.

Carveol is an orally active monoterpenoid alcohol with neuroprotective, antioxidant, anti-inflammatory, anticonvulsant, antidiabetic, hypolipidemic and hepatoprotective activities. Carveol upregulates the expression of Bcl2, downregulates the expression of caspase-3, TNF-α, IL1β and IL6, activates the Nrf2/HO-1 antioxidant signaling pathway, inhibits the RAGE/NF-κB signaling pathway, and suppresses neuroinflammation and neuronal apoptosis. Carveol inhibits α-synuclein aggregation, improves cognitive ability, and inhibits α-amylase activity. Carveol exerts neuroprotective effects in a rat model of Parkinson's disease. Carveol exhibits antidiabetic effects in alloxan-induced diabetic rats. Carveol alleviates PTZ-induced seizures in rats. Carveol can be used in research related to Parkinson's disease, epilepsy, diabetes and ischemic stroke.

Tiagabine (NO050328; NO328; TGB) is an orally active, highly selective, and reversible GAT-1 inhibitor and anticonvulsant that crosses the blood-brain barrier. By blocking the reuptake of GABA in neurons and glial cells, tiagabine increases extracellular GABA levels to enhance inhibitory signal transduction, thereby exerting multiple activities such as anticonvulsant, neuroprotective, and antioxidant effects. Tiagabine exhibits linear pharmacokinetic properties. Although it is metabolized by CYP3A and has a high protein binding rate, it carries a low risk of cognitive impairment. Tiagabine is widely used in research on related diseases including epilepsy (including refractory partial seizures), alcohol withdrawal symptoms, and Huntington's disease.