| Bioactivity | Phenytoin (5,5-Diphenylhydantoin) is a potent Voltage-gated Na+ channels (VGSCs) blocker. Phenytoin has antiepileptic activity and reduces breast tumour growth and metastasis in mice[1][2]. | ||||||||||||
| Invitro | Phenytoin is an antiepileptic drug. It is useful to partial seizures and generalized tonic-clonic seizures but not primary generalized seizures such as absence seizures or myoclonic seizures. Phenytoin is believed to protect against seizures by causing voltage-dependent block of voltage-gated sodium channels[2]. Phenytoin has low affinity for resting sodium channels at hyperpolarized membrane potentials[3]. When neurons are depolarized and the channels transition into the open and inactivated states, greater binding and block occur. The inhibitory potency is strongly use dependent, so that block accumulates with prolonged or repetitive activation, such as occurs during a seizure discharge. The blocking of sodium channels by phenytoin is of slow onset. The time course of fast sodium currents is therefore not altered in the presence of the drug and action potentials evoked by synaptic depolarizations of ordinary duration are not blocked. Thus phenytoin is able to selectively inhibit pathological hyperexcitability in epilepsy without unduly impairing ongoing activity. Phenytoin also blocks persistent sodium current and this may be of particular importance in seizure control. Phenytoin is a class 1b antiarrhythmic[4]. | ||||||||||||
| In Vivo | Phenytoin (5,5-Diphenylhydantoin; 60 mg/kg; daily; 28 days ) reduces tumour growth in six week-old female Rag2-/- Il2rg-/- mice with MDA-MB-231 cells[1]. | ||||||||||||
| Name | Phenytoin | ||||||||||||
| CAS | 57-41-0 | ||||||||||||
| Formula | C15H12N2O2 | ||||||||||||
| Molar Mass | 252.27 | ||||||||||||
| Appearance | Solid | ||||||||||||
| Transport | Room temperature in continental US; may vary elsewhere. | ||||||||||||
| Storage |
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| Reference | [1]. Michaela Nelson, et al. The sodium channel-blocking antiepileptic drug phenytoin inhibits breast tumour growth and metastasis. Mol Cancer. 2015 Jan 27;14(1):13. [2]. Rogawski, M.A. and W. Loscher, The neurobiology of antiepileptic drugs. Nat Rev Neurosci, 2004. 5(7): p. 553-64. [3]. Porter, R.J., et al., Mechanisms of action of antiseizure drugs. Handb Clin Neurol, 2012. 108: p. 663-81. [4]. Balaji, S., Medical therapy for sudden death. Pediatr Clin North Am, 2004. 51(5): p. 1379-87. |