| Size | Price | Stock | Qty |
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| 50mg |
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| 100mg |
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| 250mg | |||
| 500mg | |||
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| Other Sizes |
Purity: ≥98%
Fosphenytoin sodium, the sodium salt form of fosphenytoin, is a prodrug of phenytoin with similar anticonvulsant properties. It is intended for parenteral administration; As a prodrug, it is hydrolyzed to the phenytoin,which is the active metabolite. Phenytoin exerts its effect most likely through an enhancement of sodium efflux from neurons in the motor cortex. This leads to a suppression of excessive neuronal firing and spread of seizure activity. Other physiologic effects from actions of phenytoin include modulation of the voltage-dependent calcium channels of neurons, inhibition of calcium flux across neuronal membranes and enhancement of sodium-potassium ATPase activity of neurons and glial cells.
| Targets |
Voltage-dependent neuronal sodium (Na+) channel blocker (proposed primary mechanism for neuroprotection). [1]
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| ln Vivo |
A powerful neuroprotective medication against damage brought on by ischemia is fosphenytoin. Hippocampal CA1 pyramidal neurons in rats given fosphenytoin (30 mg/kg, im) five minutes after the commencement of the ischemic episode stayed close to control levels (13.90 +/- 0.92), although there were no appreciable alterations in GFAP staining[1]. Rats given 84 mg/kg of fosphenytoin had an 83% relative bioavailability of the drug. In completely kindled female Wistar rats, fosphenytoin dose-dependently raises the focal seizure (post-discharge) threshold. Only after administering the largest dose of fosphenytoin tested (84 mg/kg) did seizure intensity and threshold duration decrease [2].
In a rat model of transient global ischemia induced by 12-minute cardiac arrest, a single intramuscular dose of Fosphenytoin Sodium (30 mg/kg) administered 5 minutes after resuscitation significantly reduced neuronal damage in the hippocampal CA1 region. Seven days post-ischemia, the number of normal-appearing CA1 pyramidal neurons in the treated group (13.90 ± 0.92 per 100 μm²) was nearly identical to sham-operated controls (14.33 ± 1.73) and significantly higher than in the saline-treated ischemic group (2.19 ± 0.16). [1] Despite its potent neuroprotective effect, post-ischemic treatment with Fosphenytoin Sodium did not significantly alter the increased glial fibrillary acidic protein (GFAP) immunoreactivity (a marker of astrocyte activation) observed in the hippocampal CA1 region 7 days after the ischemic insult. The optical density of GFAP staining in the CA1 region of the treated group (93.5 ± 0.71) was not significantly different from the saline-treated ischemic group (89 ± 9.9), but was significantly lower than the sham group (112 ± 3.54). [1] |
| Animal Protocol |
Global Ischemia Model: Transient global ischemia was induced in male Long-Evans hooded rats (250-350 g) under ketamine anesthesia. A padded, weighted bar was lowered onto the chest for 12 minutes, causing cardiac arrest. Circulation was restored by cardiopulmonary resuscitation after the ischemic period. Brain temperature was monitored and maintained at 35 ± 0.4°C. [1]
Drug Treatment: Animals were randomly assigned to groups. The treatment group received a single intramuscular injection of Fosphenytoin Sodium (30 mg/kg) in the right hind limb, administered 5 minutes after resuscitation. The control ischemic group received an intramuscular injection of saline at the same time point. Sham-operated animals underwent the same procedures except for chest compression. [1] Tissue Analysis: All animals were sacrificed 7 days post-ischemia. Brains were fixed, and the dorsal hippocampus was sectioned. For neuronal quantification, 1 μm thick plastic-embedded sections of the mid-CA1 region were stained with toluidine blue. Normal-appearing pyramidal neurons were counted blind in defined 100 μm² fields. For astrocyte assessment, 40 μm vibratome sections from the same region were processed for GFAP immunohistochemistry using a standard avidin-biotin-peroxidase method, and immunoreactivity was quantified by optical density analysis. [1] |
| ADME/Pharmacokinetics |
Fosphenytoin sodium is a water-soluble prodrug of phenytoin. In tissues and blood, it is rapidly converted to the active ingredient phenytoin by phosphatases. [1] Fosphenytoin sodium is suitable for intramuscular injection and has been reported to be rapidly absorbed. [1]
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| Toxicity/Toxicokinetics |
In this study, intramuscular injection of fosphenytoin sodium (30 mg/kg) in rats did not cause significant local tissue irritation at the injection site. [1] The literature cited in the article indicates that fosphenytoin sodium has a higher safety profile compared to intravenous phenytoin, as intravenous phenytoin may cause severe tissue irritation and intravenous complications. [1]
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| References | |
| Additional Infomation |
Phosphotoxin sodium is the sodium salt form of phosphotoxin, a prodrug that is hydrolyzed into the antiepileptic drug phenytoin after parenteral administration. Phenytoin most likely works by enhancing sodium efflux from motor cortical neurons. This leads to suppression of excessive neuronal firing and the spread of seizures. Other physiological effects of phenytoin include modulating voltage-dependent calcium channels in neurons, inhibiting calcium ion flow across neuronal membranes, and enhancing sodium-potassium ATPase activity in neurons and glial cells. (NCI05) See also: Phosphotoxin (in its salt form). Phosphotoxin sodium (Cerebyx®) is the disodium phosphate prodrug of the antiepileptic drug phenytoin. This formulation was developed to overcome the solubility and tissue irritation problems of injectable phenytoin sodium formulations. [1] Its neuroprotective mechanism is primarily achieved by blocking voltage-dependent neuronal sodium channels through its active metabolite phenytoin. This may inhibit a series of events leading to neuronal death after ischemia (Na+ influx, Ca2+ overload, glutamate release). [1]
This study showed that there was a separation between neuroprotective effects and astrocyte GFAP responses after treatment with fosphenytoin sodium, suggesting that the enhanced GFAP immunoreactivity after ischemia may reflect metabolic activation of astrocytes, rather than just a marker of neuronal damage. [1] |
| Molecular Formula |
C16H15N2NAO6P
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|---|---|
| Molecular Weight |
385.263635873795
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| Exact Mass |
406.031
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| CAS # |
92134-98-0
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| Related CAS # |
Fosphenytoin;93390-81-9;Fosphenytoin-d10 disodium
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| PubChem CID |
56338
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| Appearance |
White to off-white solid powder
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| Melting Point |
220ºC
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| LogP |
2.691
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| Hydrogen Bond Donor Count |
1
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| Hydrogen Bond Acceptor Count |
6
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| Rotatable Bond Count |
4
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| Heavy Atom Count |
27
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| Complexity |
536
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| Defined Atom Stereocenter Count |
0
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| InChi Key |
GQPXYJNXTAFDLT-UHFFFAOYSA-L
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| InChi Code |
InChI=1S/C16H15N2O6P.2Na/c19-14-16(12-7-3-1-4-8-12,13-9-5-2-6-10-13)17-15(20)18(14)11-24-25(21,22)23;;/h1-10H,11H2,(H,17,20)(H2,21,22,23);;/q;2*+1/p-2
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| Chemical Name |
disodium;(2,5-dioxo-4,4-diphenylimidazolidin-1-yl)methyl phosphate
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| Synonyms |
Cerebyx; Pro-Epanutin; HMPDP; ACC-9653; ACC-9653; ACC9653; Fosphenytoin Sodium; Prodilantin
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| HS Tariff Code |
2934.99.9001
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| Storage |
Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture. |
| Shipping Condition |
Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)
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| Solubility (In Vitro) |
H2O : ≥ 100 mg/mL (~246.16 mM)
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| Solubility (In Vivo) |
Solubility in Formulation 1: 25 mg/mL (61.54 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.
(Please use freshly prepared in vivo formulations for optimal results.) |
| Preparing Stock Solutions | 1 mg | 5 mg | 10 mg | |
| 1 mM | 2.5956 mL | 12.9782 mL | 25.9565 mL | |
| 5 mM | 0.5191 mL | 2.5956 mL | 5.1913 mL | |
| 10 mM | 0.2596 mL | 1.2978 mL | 2.5956 mL |
*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.
Calculation results
Working concentration： mg/mL；
Method for preparing DMSO stock solution： mg drug pre-dissolved in μL DMSO (stock solution concentration mg/mL). Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug.
Method for preparing in vivo formulation:：Take μL DMSO stock solution, next add μL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL ddH2O，mix and clarify.
(1) Please be sure that the solution is clear before the addition of next solvent. Dissolution methods like vortex, ultrasound or warming and heat may be used to aid dissolving.
(2) Be sure to add the solvent(s) in order.
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