Epilepsy

Scorpion toxin Tf2 is a selective human voltage-gated sodium channel Nav1.3 (hNav1.3) activator. Scorpion toxin Tf2 selectively shifts the channel's activation voltage to more negative values, enabling channel opening at resting membrane potentials. Scorpion toxin Tf2 can be used for the research of epilepsy, nociception (after spinal cord injury).

AmmTX3 is a peptide toxin identified from the venom of the scorpion Androctonus mauretanicus. AmmTX3 is a highly specific blocker of K_v4 channels, which selectively and almost completely blocks transient A-type K⁺ currents with a K_i of 131 nM. AmmTX3 induces epileptiform behaviors and causes death in mice receiving intracerebroventricular injection. AmmTX3 increases the excitability of dentate gyrus granule cells, reduces GABAergic inhibition, enhances and stabilizes the EPSP-spike component of long-term potentiation, and impairs reference memory. AmmTX3 can be used in research related to pain, epilepsy, and autism spectrum disorder.

L-Aspartic acid-¹³C-1 ([3-¹³C]Aspartic acid) 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.

Quinidine polygalacturonate is an orally active antiarrhythmic agent. Quinidine polygalacturonate 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 polygalacturonate exerts sustained block and open-channel block effects on I_K(f). Quinidine polygalacturonate alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. Quinidine polygalacturonate can be used in studies related to uterine sarcoma and seizures.

Quinidine gluconic acid is an orally active antiarrhythmic agent. Quinidine gluconic acid 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 gluconic acid exerts sustained block and open-channel block effects on I_K(f). Quinidine gluconic acid alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. Quinidine gluconic acid can be used in studies related to uterine sarcoma and seizures.

Quinidine sulfate is an orally active antiarrhythmic agent. Quinidine sulfate 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 sulfate exerts sustained block and open-channel block effects on I_K(f). Quinidine sulfate alters the urinary metabolic ratio of Amphetamine, modulates the Pentylenetetrazol-induced seizure threshold, and regulates the anticonvulsant effect of Dextromethorphan. Quinidine sulfate can be used in studies related to uterine sarcoma and seizures.

Pirlindole mesylate is an orally active, selective and reversible MAO-A inhibitor with an IC₅₀ value of 250 nM. Pirlindole mesylate inhibits genomic replication of Enterovirus species B and D, and exhibits moderate activity against enterovirus species A. Pirlindole mesylate 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 mesylate shows no detectable mutagenic, clastogenic or carcinogenic properties. Pirlindole mesylate can be used in research related to depression and enterovirus infections.

PPM-18 (NSC 73233) is a Vitamin K (HY-B2172) analog. PPM-18 prevents LPS-induced IκBα degradation, thereby inhibiting NF-κB activation and nuclear translocation of NF-κB. PPM-18 inhibits LPS-induced nitrite production and iNOS expression. PPM-18 inhibits HDAC6. PPM-18 induces ROS accumulation, activates AMPK, inhibits the mTORC1 and PI3K/AKT pathways, initiates Autophagy, and induces Apoptosis. PPM-18 suppresses seizures in zebrafish and mouse epilepsy models. PPM-18 prevents LPS-induced lethal toxicity and delayed hypotension. PPM-18 exhibits anticancer activity against leukemia and bladder cancer. PPM-18 can be used in research related to septic shock, bladder cancer and atherosclerosis.

L-Aspartic acid-¹⁵N,d₃ is the ¹⁵N, deuterated-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-1,4-¹³C₂,¹⁵N is the ¹⁵N, 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.

Quinidine-d₃ is the d₃-labeled Quinidine (15% dihydroquinidine) (HY-B1751). 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.

FGIN 1-27 (Standard) is the analytical standard of FGIN 1-27 (HY-101059). This product is intended for research and analytical applications. FGIN-1-27 is a blood-brain barrier-penetrant TSPO ligand with a K_i value of 5 nM. FGIN 1-27 inhibits PKC-β, PKA/CREB, p38/ERK MAPK, MITF, tyrosinase, TRP-1, and TRP-2, thereby inhibiting melanogenesis and pigmentation. FGIN-1-27 alleviates X-ray radiation-induced astrocyte mitochondrial hyperfunction, reduces ROS and superoxide production, inhibits excessive activation of A1-type astrocytes, downregulates GFAP and C3 protein expression, and restores astrocyte proliferative capacity. FGIN-1-27 produces anticonvulsant effects in normal mice; in diazepam-withdrawn mice, the brain MDR pathway becomes subsensitive, and the anticonvulsant activity disappears. FGIN-1-27 attenuates pigmentation in zebrafish embryos and ameliorates UVB-induced skin pigmentation in guinea pigs. FGIN-1-27 directly stimulates testicular Leydig cells while upregulating luteinizing hormone levels, causing an acute increase in serum testosterone in male rats. FGIN 1-27 can be used for research related to hyperpigmentation, epilepsy, brain injury, and other diseases.

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

GW438014A free base is a selective NPY-Y5 receptor competitive antagonist capable of crossing the blood-brain barrier, with IC₅₀ values of 197 nM and 211 nM against human receptors. GW438014A free base reverses PYY-mediated inhibition of Forskolin (HY-15371)-induced cAMP production, reduces NPY-induced food intake and nocturnal food intake in rodents, decreases body weight gain and fat mass in Zucker rats, and inhibits centrally mediated feeding behavior. GW438014A free base can be used in research related to obesity and epilepsy.

Dysiherbaine is an excitatory amino acid. Dysiherbaine is isolated from the marine sponge Lendenfeldia chondrodes. Dysiherbaine activates AMPA and kainate receptors. Dysiherbaine has minor NMDA receptor agonist activity, while it has no effect on L-type voltage-dependent calcium channels. Dysiherbaine induces convulsions and epileptogenic activity in mice. Dysiherbaine is used in epilepsy research.

BW284C51 is a highly selective Acetylcholinesterase inhibitor. BW284C51 exerts non-competitive, voltage-dependent blocking effects on the Torpedo nicotinic acetylcholine receptor channel. BW284C51 impairs acetylcholine clearance to increase acetylcholine exposure, and enhances the acetylcholine-mediated expression response of melanogenesis-related genes. BW284C51 can be used in research related to Alzheimer's disease, Parkinson's disease, congenital myasthenia, schizophrenia and familial epilepsy.

Quinidine (15% dihydroquinidine) (Standard) is the analytical standard of Quinidine (15% dihydroquinidine) (HY-B1751). This product is intended for research and analytical applications. 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.

L-Aspartic aicd sodium (Standard) (Sodium L-aspartate (Standard)) is the analytical standard of L-Aspartic aicd sodium (HY-N0666C). This product is intended for research and analytical applications. L-Aspartic acid sodium (Sodium L-aspartate) is a NMDA receptor agonist and acidic amino acid. L-Aspartic acid sodium has no independent analgesic activity. L-Aspartic acid sodium can antagonize the analgesic effects of D-Aspartic acid and Morphine. L-Aspartic acid sodium regulates polymorph transformation, crystal growth/aggregation and nucleation processes of calcium carbonate, and can serve as a biomineralization template. L-Aspartic acid sodium promotes burst firing of central neurons. L-Aspartic acid sodium can be used in studies related to cerebral ischemia and epilepsy.

Methsuximide (Standard) (Mesuximide (Standard); Celontin (Standard)) is the analytical standard of Methsuximide (HY-B1376). This product is intended for research and analytical applications. Methsuximide (Mesuximide) is an orally active succinimide-derived antiepileptic agent. Methsuximide interacts with cytochrome P-450, increases the level of hepatic microsomal cytochrome P-450, and inhibits or competes with the cytochrome P-450 CYP 2C9/10 subtype. Methsuximide can be used in epilepsy-related research.

Mepyramine maleate (Standard) (Pyrilamine maleate (Standard)) is the analytical standard of Mepyramine maleate (HY-B1281). This product is intended for research and analytical applications. Mepyramine maleate (Pyrilamine maleate) is a selective histamine H1 receptor antagonist and KCNQ channel inhibitor, with an IC₅₀ of 12.5 μM against KCNQ2/Q3. Mepyramine maleate shows no activity against allergic asthma in mice when used alone, but modulates the effect of JNJ 7777120 (HY-13508) on allergic asthma in mice; it inhibits the development of morphine physical dependence and increases histamine levels in mouse brains. Mepyramine maleate can be used in studies related to seizures, convulsions, allergic asthma and morphine physical dependence.