Phenytoin


CAS No. : 57-41-0

(Synonyms: 5,5-Diphenylhydantoin)

57-41-0
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Cat. No. : HY-B0448
M.Wt: 252.27
Formula: C15H12N2O2
Purity: >98 %
Solubility:
Introduction of 57-41-0 :

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]. In Vitro: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:Note:
Please do not refer to only one article to determine the experimental conditions. It is recommended to determine the optimal experimental conditions (animal strain, age, dosage, frequency and cycle, detection time and indicators, etc.) through preliminary experiments before the formal experiment
.

Phenytoin (60 mg/kg; once daily for 28 days) sodium reduces MDA-MB-231 cells in six-week-old female Rag2-/- Il2rg-/- mice[1].
Phenytoin can induce a model of gingival hyperplasia in mice[6].

Induction of Gingival Hyperplasia in Mice[5]
Background
Phenytoin induced gingival overgrowth, a side effect with multifactorial aetiology, is characterized by an increase in the volume of extracellular tissues, particularly collagenous components, with varying degrees of inflammation.
Specific Modeling Methods
Mice: BALB/cByJ • male • 8 week old
Administration: 30 mg/kg • miniosmotic pumps • 0.5-μL/h • 2 weeks
Note
(1) Mice are housed for 1 week before any procedure for acclimation.
(2) Pumps are replaced every 2 weeks throughout the 12-week experimental period.
(3) Mice are then euthanized and heads are immediately placed in freshly made 4% paraformaldehyde for 24 hours for fixation.
Modeling Indicators
Morphology: Gingival overgrowth was apparent in the maxillary anterior gingival tissue of mice; Increased the papillary height and area.
Histomorphometry: Increased epithelial thickness and area in the maxillary anterior zone.
Molecular changes: Ccn2 is overexpressed in all regions of the epithelium; TGF-β1 and LOXL2 is overexpressed in both epithelial and connective tissues.
Correlated Product(s): Cyclosporine A (HY-B0579)
Opposite Product(s): Lovastatin (HY-N0504)

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