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    Epilepsy is a group of neurological conditions consisting of recurrent, usually unprovoked epileptic seizures. Epileptic seizures have recently been defined as "a transient occurrence of signs and/or symptoms due to abnormal, excessive or synchronous neuronal activity in the brain". Epilepsy is one of the most common disorders of the brain, with one in 10 people suffering at least one seizure in their lifetime. There are over 40 different types of epilepsy, each of which presents with its own unique combination of seizure type, typical age of onset, EEG findings, treatment, and prognosis.


    Epileptogenesis and Seizures

    Epileptogenesis is the mechanism by which an epileptic condition is acquired, the critical step of which is neuronal damage. An initial brain-damaging insult triggers a cascade of molecular and cellular changes that ultimately leads to the occurrence of spontaneous and recurrent seizures. The initial insult does not begin the process, but sets into motion a cascade of changes in gene expression that alters the molecular and cellular constituents of neuronal and glial networks. There is often a long latency period, sometimes decades, between initial insult and the first seizure, and such insults include birth trauma, febrile seizures and encephalitis.

    Once epileptogenesis has occurred, there are multiple complex mechanisms that trigger recurrent seizures. Simplistically, seizures arise when there is a disruption in the systems that normally control the balance of glutamatergic excitation and GABAergic inhibition. Disturbances can occur through a vast array of mechanisms. Control of the resting potential of neurons is critical to prevent the excessive discharge that is often associated with seizures. The sodium-potassium ATPase is vital in maintaining the resting potential and blockade or mutation of this ion pump can lead to seizures. In order for a seizure to occur, the activity of a network of neurons, not just a single cell, must be altered. Cell synchronization can be achieved through glutamatergic interconnections, gap channels and GABAergic connections. Many of the changes during epileptogenesis promote cell synchronization, and this represents a mechanism by which seizures become recurrent. Environmental changes can trigger seizures, including circadian changes in hormones, peptides and other neuromodulators, stressful life events and visual stimuli. Normally, changes in the above would not trigger seizures, however, in a brain that has already been altered by epileptogenesis, there is an underlying state of increased excitability and these everyday stimuli can have a proconvulsant effect.


    Epilepsy can be controlled pharmacologically with anticonvulsant drugs. The main targets of current anticonvulsants include voltage-gated sodium channels, the GABA inhibitory system (including benzodiazepines) and voltage-gated calcium channels. Due to the diverse mechanisms by which seizures occur, epilepsy is refractory to treatment in a number of causes. There is therefore intense research into the development of novel antiepileptic agents.

Cat. No. Product Name CAS No. Information


PF-04895162 (ICA-105665, PF 4895162) is an orally available agonist of neuronal Kv7 potassium channel, opens Kv7.2/7.3 and Kv7.3/7.5 potassium channels, also known as KCNQ2/3 and KCNQ3/5 channels; ICA-105665 has demonstrated broad spectrum antiseizure activity in multiple animal models including maximal electroshock, 6 Hz seizures, pentylenetetrazole, and electrical kindling at doses from <1 to 5 mg/kg.


CI-966 hydrochloride


CI-966 (PD 126141) is a potent, selective inhibitor of the GABA transporter GAT-1 with IC50 of 0.26 and 1.2 uM for human and rat GAT-1, respectively; displays >200-fold selectivity over GAT-2 and GAT-3; shows anticonvulsive and neuroprotective activity in vivo.




CI-966 (PD 126141) is a potent, selective inhibitor of the GABA transporter GAT-1 with IC50 of 0.26 and 1.2 uM for human and rat GAT-1, respectively; displays >200-fold selectivity over GAT-2 and GAT-3; shows anticonvulsive and neuroprotective activity in vivo.




An allosteric, non-competitive antagonist of the AMPA receptor with IC50 of 2.8 uM; acts allosterically at the same regulatory site as GYKI 52466 and 53655 and other benzodiazepines but does not bind to the central diazepine binding site; shows selectivity for AMPA relative to kainate receptor sub-types.


ACT 709478


ACT 709478 is a potent, selective, orally-bioavailable, brain penetrant T-type calcium channel blocker with IC50 of 6.4, 18, and 7.5 nM for Cav3.1, Cav3.2, and Cav3.3 channels respectively; displays >100-fold selectivity over Cav1.2 channels; shows a significant decrease of the seizure severity in vivo (100 mg/kg, p.o.).




Becampanel (AMP 397) potent, competitive antagonist of the AMPA receptor (AMPAR) with IC50 of 11 nM; has anticonvulsant activity for the treatment of epilepsy, neuropathic pain and cerebral ischemia.




JNJ-26489112 (JNJ26489112) is a broad-spectrum anticonvulsant that displays activity in rodents against audiogenic, electrically-induced, and chemically-induced seizures; exhibits very weak inhibition of human CA-II (IC50=35 μM); inhibits Na+, kainate, and KCNQ2 channels to varying degrees, while moderately potentiating GABA current and inhibiting N-methyl-D-aspartic acid current, its action at several targets appears to be responsible for the observed neurostabilizing effects; shows limited seizure spread and elevated seizure threshold in preclinical animal models.




Cenobamate (YKP-3089, YKP3089) is a potential anti-seizure agent with currently unknown mechanisms of action.




TP003 is a potent, functional selectivity for α3 subunit-containing GABAA receptor agonist with Ki of <1 nM for α1β3γ2, α2β3γ2, α3β3γ2 and α5β3γ2, has no affinity for α4β3γ2 and α6β3γ2 (Ki>1 uM); produces a robust anxiolytic-like effect in both rodent and non-human primate behavioral models of anxiety, also retains efficacy in a stress-induced hyperthermia model.




CPP-115 is an orally available, small molecule, next-generation GABA aminotransferase (GABA-AT) inhibitor with Ki of 31 uM, without other GABAergic or off-target activities; displays superior enzyme inactivation properties compared to vigabatrin, decreases spasms in the multiple-hit rat model of infantile spasms, deonstrates high therapeutic potential for the treatment of cocaine addiction and for a variety of epilepsies.

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