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  3. Epilepsy

Epilepsy

Epilepsy is a neurological disorder characterized by recurrent, unprovoked seizures due to abnormal electrical activity in the brain, with symptoms ranging from brief lapses in awareness to convulsions. It is typically diagnosed after two or more seizures occurring more than 24 hours apart, or after a single seizure with high recurrence risk. Causes include genetic factors, brain injury, infections, tumors, stroke, developmental disorders, and metabolic or structural abnormalities. The SCN1A gene is notably associated with epilepsy, particularly in syndromes like Dravet syndrome and juvenile myoclonic epilepsy, with related pathways involving neuroscience and neuropathic pain signaling. Treatment includes anti-seizure medications, lifestyle modifications, and surgical options, though about 30% of patients continue to experience seizures despite therapy. Epilepsy can affect individuals of any age, with involvement of brain regions such as the temporal lobe and phenotypes related to nervous system dysfunction and growth abnormalities. Associated conditions include post-traumatic epilepsy, childhood absence epilepsy, and myoclonic epilepsy, with triggers including trauma, CNS infections, and degenerative brain disorders. Zinc cation and selenium have been explored in the context of management.

References:

Epilepsy (81):

Cat. No. Product Name CAS No. Purity Chemical Structure
  • HY-B1302
    Quinidine hydrochloride monohydrate 6151-40-2 99.97%
    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 IK(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.
    Quinidine hydrochloride monohydrate
  • HY-113413
    Imidazoleacetic acid 645-65-8 99.80%
    Imidazoleacetic acid (Imidazolyl-4-acetic acid) is a blood-brain barrier-permeable full agonist of the GABAA 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.
    Imidazoleacetic acid
  • HY-103504
    (S)-SNAP5114 157604-55-2 98.09%
    (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, pKi=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.
    (S)-SNAP5114
  • HY-106950
    Fosfructose 488-69-7 98.0%
    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.
    Fosfructose
  • HY-12783A
    SCH 50911 733717-87-8 99.62%
    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.
    SCH 50911
  • HY-Y0282
    Sodium bromide 7647-15-6
    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.
    Sodium bromide
  • HY-W702001
    Avizafone dihydrobromide 60067-15-4
    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.
    Avizafone dihydrobromide
  • HY-D2968
    DCM–ONOO 2759816-87-8 98.29%
    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.
    DCM–ONOO
  • HY-172431
    Opakalim 2376397-93-0 99.88%
    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.
    Opakalim
  • HY-107661
    Arundic Acid 185517-21-9 98.0%
    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.
    Arundic Acid
  • HY-103185
    CCPA 37739-05-2 99.77%
    CCPA (2-Chloro-N6-cyclopentyladenosine) a highly selective A1 adenosine receptors agonist with a Ki 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.
    CCPA
  • HY-B0696
    Tiagabine 115103-54-3 98.49%
    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.
    Tiagabine
  • HY-157786
    XPC-5462 2230145-14-7 99.65%
    XPC-5462 is a selective NaV1.6/1.2 inhibitor, with an IC50 of 0.0103 μM against hNaV1.6, 0.0137 μM against mNaV1.6, and 0.0109 μM against hNaV1.2. XPC-5462 significantly reduces epileptiform discharges. XPC-5462 is applicable for epilepsy-related research.
    XPC-5462
  • HY-B0188
    Mianserin 24219-97-4 99.42%
    Mianserin (Mianserine) is an orally active H1 receptor antagonist. Mianserin can activate κ-opioid receptor and octopamine receptor. Mianserin increases ERK1/2 and CREB phosphorylation, and antagonizes full κ-opioid agonist and Dynorphin A (HY-P1333)-induced MAPK phosphorylation. Mianserin modulates social and exploratory behaviour, raises electroconvulsive thresholds. Mianserin can be used for the research of neurological disease, such as depression and epilepsy.
    Mianserin
  • HY-118424
    JNJ-55511118 2036081-86-2 99.85%
    JNJ-55511118 is a selective TARP γ-8 binding AMPA receptor modulator with oral bioavailability and blood-brain barrier permeability, with a Ki of 26 nM. JNJ-55511118 reduces voluntary intake of sweetened alcohol in male mice. In rodent models, JNJ-55511118 inhibits hippocampal neurotransmission, reduces specific electroencephalogram frequency bands, induces transient hyperlocomotion, impairs learning and memory abilities, and exerts anticonvulsant effects. JNJ-55511118 is applicable to research related to alcohol use disorder and seizures.
    JNJ-55511118
  • HY-136661
    (-)-N6-Phenylisopropyl adenosine 38594-96-6 99.45%
    (-)-N6-phenylisopropyl adenosine (L-Phenylisopropyladenosine) is a selective A1 adenosine receptor agonist. (-)-N6-phenylisopropyl adenosine inhibits K+-induced Ca2+ uptake with an IC50 value of 0.5 µM. (-)-N6-phenylisopropyl adenosine protects against ischemia-induced ventricular arrhythmias and atrial fibrillation, and exacerbates ethanol withdrawal symptoms. (-)-N6-phenylisopropyl adenosine also has analgesic effects.
    (-)-N6-Phenylisopropyl adenosine
  • HY-153068
    CZL55 667408-87-9 98.92%
    CZL55 is a caspase-1 inhibitor. CZL55 can be used for the research of febrile seizures (FS).
    CZL55
  • HY-138668
    JW-65 2763378-71-6 99.05%
    JW-65 is a selective TRPC3 channel inhibitor with favorable blood-brain barrier penetration. JW-65 directly binds to human TRPC3 protein and modulates calcium signaling to reduce seizure susceptibility. JW-65 reduces seizure incidence, severity, and duration while prolonging seizure latency in multiple seizure models. JW-65 alleviates Aβ‑induced neuronal damage. JW-65 serves as a valuable tool for research on epilepsy, seizure disorders, and Alzheimer’s disease.
    JW-65
  • HY-111751
    JNJ-61432059 2035814-50-5 99.18%
    JNJ-61432059 is a blood-brain barrier-permeable, orally active TARP γ-8-associated AMPAR modulator with anticonvulsant activity. JNJ-61432059 negatively regulates GluA1 and positively modulates GluA2-containing AMPARs. JNJ-61432059 exerts potent protective effects in rodent epilepsy models. JNJ-61432059 is applicable for epilepsy-related research.
    JNJ-61432059
  • HY-B0265A
    (R)-Nimodipine 77940-92-2 99.87%
    (R)-Nimodipine ((R)-BAY-e 9736) is an orally active, blood-brain barrier-permeable L-type calcium channel blocker with an IC50 of 5 nM. (R)-Nimodipine inhibits corticosterone release by blocking calcium channels on the hypothalamic-pituitary-adrenal axis, thereby reversing immobilization stress-induced memory impairment and behavioral abnormalities. (R)-Nimodipine is widely used in studies related to aneurysmal subarachnoid hemorrhage, cerebral ischemia, epilepsy, age-related degenerative neurological diseases, and alcohol intoxication.
    (R)-Nimodipine