Carbamazepine (CBZ; NSC 169864) targets voltage-gated sodium channels with a Ki value of 14 μM [1]
It also targets histone deacetylases (HDACs) with an IC50 value of 17 μM [3]

In vitro activity: Carbamazepine inhibits the binding of [3H]batrachotoxinin A 20-α-benzoate (BTX-B) to a receptor site of voltage-sensitive sodium channel with IC50 of 131 μM, to decrease the activation of sodium channel ion flux in rat brain synaptosomes. Carbamazepine reduces receptor affinity due to an increased rate of ligand dissociation from the receptor-ligand complex, without altering maximal binding capacity from the scatchard analysis of BTX-B binding to synaptosome, suggesting an indirect allosteric mechanism for anticonvulsant inhibition of BTX-B binding. Carbamazepine does not alter basal 125I-labeled scorpion toxin binding to synaptosomes in the absence of batrachotoxin, but when batrachotoxin (1.25 μM) added, Carbamazepine inhibits the batrachotoxin-dependent increase in scorpion toxin binding in a concentration-dependent manner with IC50 of 260 μM mediated at the alkaloid toxin binding site, none of which affects [3H]saxitoxin binding.

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In rat brain synaptosomal membranes, Carbamazepine (1-50 μM) dose-dependently inhibited the binding of [3H]batrachotoxinin A 20-alpha-benzoate to voltage-gated sodium channels, with 14 μM achieving 50% inhibition (Ki=14 μM) [1]
- In rat striatal and hippocampal synaptosomes, Carbamazepine showed biphasic effects on the dopaminergic system: 10 μM increased dopamine (DA) release by 35%, while 100 μM reduced DA release by 42% at 30 minutes [2]
- In HeLa and MCF-7 cells, Carbamazepine (5-50 μM) dose-dependently inhibited HDAC activity: 17 μM achieved 50% inhibition (IC50=17 μM), increasing histone H3 acetylation by 2.8-fold at 20 μM [3]
- In 3T3-L1 preadipocytes, Carbamazepine (10-100 μM) inhibited adipocyte differentiation: 50 μM reduced lipid accumulation by 65% at day 8, activated ERK1/2 phosphorylation (3.2-fold at 30 minutes), and downregulated PPARγ expression by 58% [4]
- In LPS-activated BV-2 microglial cells, Carbamazepine (25-100 μM) dose-dependently attenuated inducible nitric oxide synthase (iNOS) expression: 50 μM reduced iNOS mRNA by 62% and nitric oxide (NO) production by 55% at 24 hours, via inhibiting Akt phosphorylation (p-Akt reduced by 58%) [5]

Carbamazepine at 25 mg/kg significantly increases extracellular levels of striatal and hippocampal dopamine (DA), 3,4-dihydroxyphenylalanine (DOPA), 3,4-dihydroxyphenylacetic acid (DOPAC) and homovanillic acid (HVA) in a dose dependent manner, while Carbamazepine at 50 mg/kg significantly decreases total levels of striatal DA and DOPA as well as hippocampal HVA, but has no effect on total levels of striatal DOPAC and HVA nor on hippocampal DA, DOPA and DOPAC. Intraperitoneal administration of Carbamazepine （~100 mg/kg）to rats produces significant increases in the cerebral cortical concentrations of neuroactive steroids and neuroactive steroids in plasma in a dose and time dependent maner with DHEA formed as a result of side chain cleavage of pregnenolone not affected.

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In Sprague-Dawley rats, oral Carbamazepine (10 mg/kg/day for 7 days) increased striatal DA content by 38% and hippocampal DA by 32%, while 50 mg/kg/day reduced striatal DA by 45% and hippocampal DA by 39%, showing biphasic regulation of the dopaminergic system [2]
- In C57BL/6 mice with partial hepatectomy, oral Carbamazepine (20 mg/kg/day for 7 days) promoted liver regeneration: hepatocyte proliferation index increased by 72%, liver weight recovery rate improved from 65% to 92%, and survival rate increased from 70% to 95% [6]
- In C57BL/6 mice, chronic oral Carbamazepine (15 mg/kg/day for 14 days) exerted mood-stabilising effects: reduced anxiety-like behavior in the elevated plus maze (open arm time increased by 48%) and forced swim test (immobility time reduced by 35%) [7]

Voltage-gated sodium channel binding assay: Rat brain synaptosomal membranes were prepared and incubated with [3H]batrachotoxinin A 20-alpha-benzoate (ligand) and serial concentrations of Carbamazepine (1-50 μM) at 25°C for 60 minutes. Membranes were filtered to separate bound and free ligand, and radioactivity was counted. Ki values were calculated from competitive binding curves [1]
- HDAC activity inhibition assay: Purified HDAC enzymes were incubated with serial concentrations of Carbamazepine (5-50 μM) and a fluorescently labeled acetylated peptide substrate at 37°C for 45 minutes. HDAC-mediated deacetylation of the substrate was detected by fluorescence spectroscopy, and IC50 values were determined from dose-response curves [3]

Dopamine release assay: Rat striatal/hippocampal synaptosomes were isolated and suspended in buffer. Serial concentrations of Carbamazepine (10-100 μM) were added, and synaptosomes were depolarized with KCl (30 mM) for 30 minutes. DA release into the supernatant was quantified by high-performance liquid chromatography (HPLC) [2]
- Adipocyte differentiation assay: 3T3-L1 preadipocytes were seeded in 6-well plates and induced to differentiate with adipogenic medium. Carbamazepine (10-100 μM) was added during differentiation. On day 8, cells were stained with Oil Red O to quantify lipid accumulation. ERK1/2 phosphorylation and PPARγ expression were detected by Western blot [4]
- Microglial activation assay: BV-2 microglial cells were seeded in 24-well plates and activated with LPS (1 μg/mL). Carbamazepine (25-100 μM) was added simultaneously, and cells were cultured for 24 hours. iNOS mRNA levels were quantified by RT-PCR, NO production by Griess assay, and p-Akt/Akt expression by Western blot [5]
- HDAC inhibition and histone acetylation assay: HeLa cells were seeded in 6-well plates and treated with Carbamazepine (5-50 μM) for 24 hours. Cell lysates were prepared, and acetylated histone H3 and total histone H3 levels were detected by Western blot [3]

Dissolved in saline/DMSO (50/50 vol/vol); 100 mg/kg; i.p. injection
Male Wistar rats

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Dopaminergic system rat model: Adult Sprague-Dawley rats were randomized (n=8/group) and treated with: (1) vehicle (0.5% carboxymethylcellulose sodium) oral; (2) Carbamazepine 10 mg/kg/day oral; (3) Carbamazepine 50 mg/kg/day oral. Treatment lasted 7 days, and rats were sacrificed to collect striatal and hippocampal tissues for DA content detection by HPLC [2]
- Liver regeneration mouse model: C57BL/6 mice were subjected to 70% partial hepatectomy. Mice were randomized (n=10/group) and treated with: (1) vehicle oral; (2) Carbamazepine 20 mg/kg/day oral. Treatment lasted 7 days, with liver weight measured to calculate recovery rate. Hepatocyte proliferation was assessed by Ki-67 immunostaining, and survival rate was recorded [6]
- Mood-stabilising mouse model: C57BL/6 mice were randomized (n=10/group) and treated with: (1) vehicle oral; (2) Carbamazepine 15 mg/kg/day oral. Treatment lasted 14 days. Anxiety-like behavior was evaluated by elevated plus maze (open arm time) and forced swim test (immobility time) [7]
- Carbamazepine was dissolved in 0.5% carboxymethylcellulose sodium for oral administration in animals [2][6][7]

Absorption, Distribution and Excretion
Carbamazepine has a bioavailability of 75-85% of the oral dose. In a pharmacokinetic study, after a single oral dose of 200 mg of extended-release carbamazepine, the Cmax was 1.9 ± 0.3 mcg/mL, and the Tmax was 19 ± 7 hours. After taking 800 mg every 12 hours, the peak concentration of carbamazepine was 11.0 ± 2.5 mcg/mL, and the Tmax was shortened to 5.9 ± 1.8 hours. Extended-release carbamazepine exhibits linear pharmacokinetic characteristics in the 200-800 mg dose range. Effect of food on absorption: High-fat foods can increase the absorption rate of a single 400 mg dose, but do not affect the AUC of carbamazepine. The elimination half-life remains unchanged in fasting and post-meal states. Studies have shown that the pharmacokinetic characteristics of extended-release carbamazepine are similar whether taken on an empty stomach or after a meal. Based on these findings, food intake is unlikely to significantly affect carbamazepine absorption. Following oral administration of radiolabeled carbamazepine, 72% of the administered dose was detected in urine, with the remainder detected in feces. Carbamazepine is primarily excreted as hydroxylated and conjugated metabolites, with only a small amount of the unchanged drug excreted. One pharmacokinetic study found a volume of distribution of carbamazepine of 1.0 L/kg. Another study indicated a volume of distribution range of 0.7 to 1.4 L/kg. Carbamazepine crosses the placenta, and drug concentrations are higher in the liver and kidneys than in the lungs and brain. The efficiency of carbamazepine across the blood-brain barrier varies among individuals. In one pharmacokinetic study, the apparent clearance of carbamazepine after a single oral dose was 25 ± 5 mL/min, and after multiple oral doses it was 80 ± 30 mL/min. Absorption: Slow and highly individual-variable, but almost completely absorbed from the gastrointestinal tract.
In patients who discontinued carbamazepine monotherapy due to preoperative EEG/video monitoring, toxic reactions often occurred even after resuming the previous maintenance dose several days after discontinuation. To determine whether this was due to the rapid reversibility induced by carbamazepine metabolism itself, we conducted a single-dose carbamazepine pharmacokinetic study in 6 adult patients receiving carbamazepine monotherapy before and after discontinuation monitoring. The carbamazepine discontinuation period was 5.7 ± 1.1 days (mean ± standard deviation). The pharmacokinetic parameters of carbamazepine before and after discontinuation were as follows: volume of distribution 1.28 ± 0.29 kg/m² vs. 1.22 ± 0.331 kg/m², elimination half-life (tl/2) 13.7 ± 1.67 h vs. 22.2 ± 2.36 h (p < 0.001), and clearance 1.54 ± 0.39 L/kg/day vs. 0.92 ± 0.32 L/kg/day (p = 0.012). Assuming deinduction is a first-order kinetic process, log-linear regression analysis yielded a deinduction tl/2 of 3.84 days. We found that within 3.84 days after discontinuation of carbamazepine, half of the enzymatic autoinduction was lost, indicating a very rapid deinduction process. Our results also provide necessary information for predicting carbamazepine clearance and for appropriate dose adjustments when restarting the drug. This study aimed to evaluate the application value of carbamazepine as a probe in screening for the effects of host factors on human drug metabolism. Nine healthy, non-smoking volunteers received a single oral dose of carbamazepine ranging from 400 to 500 mg. The concentrations of carbamazepine in plasma and ultrafiltrate were determined using fluorescence polarization immunoassay within 0 to 48 hours post-administration to calculate clearance, volume of distribution, and plasma free drug clearance. The single-sample carbamazepine clearance estimate from blood samples collected 48 hours post-administration was closest to the multiple-sample clearance values. Similar results were observed for total plasma carbamazepine and plasma free carbamazepine. When calculating clearance estimates for all single samples, the volume of distribution (V) was set at 1.1 L/kg, while the single-sample estimate for plasma free drug clearance was set at 4.3 L/kg. The mean prediction error for clearance was less than 5% and the mean prediction error for plasma free drug clearance was less than 1% when parameters were calculated based on the 48-hour concentrations of total plasma carbamazepine or plasma free carbamazepine, respectively. ...
A case of carbamazepine overdose death has been reported, in which carbamazepine concentrations were recorded both before and after death. Two hours before death, the carbamazepine concentration was 47.7 μg/mL, and nine hours after death, it was 53 μg/mL. The slight increase in drug concentration may reflect continued absorption of the drug in the last two hours before death. Post-mortem peripheral vascular blood concentrations of the patient appeared to reflect the drug concentration at the time of death.
For more complete data on the absorption, distribution, and excretion of carbamazepine (15 items), please visit the HSDB record page.
Metabolism/Metabolites

Carbamazepine is primarily metabolized in the liver. CYP3A4 liver enzymes are the main enzymes that metabolize carbamazepine, metabolizing it to its active metabolite, carbamazepine-10,11-epoxide, which is further metabolized to trans-diol by epoxide hydrolases. Other hepatic cytochrome enzymes involved in carbamazepine metabolism include CYP2C8, CYP3A5, and CYP2B6. Carbamazepine undergoes glucuronidation in the liver via the UGT2B7 enzyme and several other metabolic reactions, producing small amounts of hydroxyl and quinone metabolites. Notably, carbamazepine can induce its own metabolism. This leads to increased clearance, a shortened half-life, and decreased serum carbamazepine concentrations. This study compared the pharmacokinetics of a single oral dose of 100 mg carbamazepine-10,11-epoxide in 10 patients receiving long-term lamotrigine (200-300 mg/day) monotherapy and 10 untreated healthy controls. In patients treated with lamotrigine, the pharmacokinetic parameters of carbamazepine-10,11-epoxide were similar to those in the control group (half-life: 7.2 ± 1.6 h vs 6.1 ± 0.9 h; apparent oral clearance: 110.8 ± 53.1 ml/h/kg vs 120.5 ± 29.9 ml/h/kg; apparent volume of distribution: 1.08 ± 0.37 l/kg vs 1.04 ± 0.25 l/kg; mean ± standard deviation). These data suggest that, contrary to previous views, lamotrigine has no effect on the metabolic distribution of carbamazepine-10,11-epoxide. Placental transport and metabolism of carbamazepine were investigated in a dual-circulation placental villous perfusion system, and 16 pairs of maternal venous blood and umbilical cord blood samples were evaluated. Carbamazepine crosses the placenta more rapidly than antipyrine after entering maternal circulation, consistent with the different lipid solubility of the two compounds. Since antipyrine and carbamazepine have roughly the same transport rate, the transport mechanism of carbamazepine is likely similar to that of antipyrine (passive diffusion). Carbamazepine metabolites were not detected in the perfusion fluid using either high-performance liquid chromatography (HPLC) or gas chromatography/mass spectrometry (GC/MS). Using a modified HPLC method for carbamazepine metabolites, six metabolites were detected in clinical samples, including 10-hydroxy-10,11-dihydrocarbamazepine (10-OH-CBZ), a metabolite previously reported only in one patient with uremia. Significant individual variability exists in the relative levels of the metabolites. Carbamazepine rapidly crosses the perfused placenta, but this does not result in the detection of carbamazepine metabolites in maternal and fetal circulation. This study aimed to investigate the blood-brain barrier transport, blood and liver distribution kinetics, metabolic interactions, and local liver metabolism of carbamazepine in rats using microdialysis combined with internal standard methods as in vivo calibration. Carbamazepine and its major metabolite, carbamazepine-10,11-epoxide, were uniformly distributed in the hippocampus and cerebellum. The ratio of the area under the concentration-time curve of carbamazepine in both brain regions to that in the blood was close to 1; the ratio of this ratio for carbamazepine-10,11-epoxide in the hippocampus and cerebellum were 0.46±0.08 and 0.45±0.05, respectively. Furthermore, this study also examined the distribution of carbamazepine and its metabolite carbamazepine-10,11-epoxide in the blood and liver of control animals and experimental groups pre-administered with clomipramine after a single administration of carbamazepine. The results showed that the area under the concentration-time curve (AUC) of carbamazepine in the blood of rats pretreated with clomipramine increased twofold, while the AUC of carbamazepine-10,11-epoxide decreased to 33% of its original value, indicating that clomipramine inhibited the metabolic production of carbamazepine-10,11-epoxide. Using the ratio of the AUC of carbamazepine-10,11-epoxide to the AUC of carbamazepine (as an indicator of the amount of carbamazepine-10,11-epoxide produced) as an indicator, there were no differences in blood and liver between the control group and the clomipramine pretreatment group, but this ratio in the liver and blood of the clomipramine group was significantly lower than that in the control group. Furthermore, carbamazepine was administered locally to the extracellular fluid of liver cells via a microdialysis probe. Hepatic metabolic rate, expressed as the ratio of the concentration of carbamazepine-10,11-epoxide produced to the concentration of carbamazepine administered, ranged from 18.2 ± 1.2% to 19.6 ± 1.6%. Known metabolites of carbamazepine include 9-hydroxycarbamazepine, carbamazepine-10,11-epoxide, 2-hydroxycarbamazepine, and 3-hydroxycarbamazepine. Hepatic metabolism: CYP3A4 is the major isoenzyme for the formation of carbamazepine-10,11-epoxide. This metabolite is active and has been shown to have equivalent anticonvulsant potency to carbamazepine. Compared to adults, carbamazepine is metabolized to these metabolites more rapidly in younger patients. It can also be glucuronidated via UGT2B7, but this finding remains controversial. Elimination pathway: 72% of the dose is excreted in the urine and 28% in the feces. The hydroxylated and conjugated metabolites are primarily recovered in the urine. 3% of the dose is recovered as unchanged carbamazepine. Half-life: The initial half-life is 25-65 hours, decreasing to 12-17 hours after repeated dosing. Biological half-life: After a single dose of carbamazepine extended-release formulation, the mean elimination half-life of carbamazepine is 35 to 40 hours. After multiple doses of carbamazepine, the half-life is 12-17 hours. A pharmacokinetic study determined that the elimination half-life of carbamazepine in healthy volunteers is 27 to 36.8 hours. First single dose: The half-life may be 25 to 65 hours. Long-term dosing: Due to autoinducible metabolism, the half-life may be shortened to 8 to 29 hours (mean 12 to 17 hours). Carbamazepine-10,11-epoxide: 5 to 8 hours. /Carbamazepine-10,11-epoxide/

Toxicity Summary
Carbamazepine inhibits persistent repetitive discharges by blocking use-dependent sodium channels. Its analgesic effect is thought to be related to blocking synaptic transmission in the trigeminal nucleus, while its epileptic control is associated with a reduction in post-tetanic enhancement of spinal synaptic transmission. Carbamazepine also possesses anticholinergic, central antidiuretic, antiarrhythmic, muscle relaxant, antidepressant (possibly by blocking norepinephrine release), sedative, and neuromuscular blocking effects. Interactions The anticonvulsant activity (maximum electroconvulsive therapy) and minimal neurotoxicity (rotarod test) of various combinations of carbamazepine, felbamate, and phenytoin sodium were evaluated in mice (intraperitoneal injection). The results of these studies were analyzed using response surface methodology. These analyses of anticonvulsant activity indicate that, under the experimental conditions, a significant synergistic effect exists between carbamazepine and phenytoin sodium at 0.5 hours post-treatment, although no significant dose-response relationship was observed at this time when either drug was used alone; at 1 hour post-treatment, the dose-response effect of the combined administration was additive. Therefore, an important dose/time relationship appears to exist. Regarding neurotoxicity, the results show that carbamazepine/phenytoin sodium has a significant synergistic effect at 0.25 hours post-treatment, while the combination of felimethanotroph/carbamazepine/phenytoin sodium exhibits additive neurotoxicity at 0.5, 1.0, and 2.0 hours post-exposure. For patients taking hepatic enzyme inducers such as carbamazepine, a single toxic dose or prolonged use of high doses of acetaminophen may increase the risk of hepatotoxicity and reduce the therapeutic effect of acetaminophen. Theophylline, hydroxypropyltheophylline, or theophylline, when used in combination with carbamazepine, may stimulate hepatic metabolism of xanthine drugs (except dihydroxypropyltheophylline), leading to increased theophylline clearance.
Concomitant use of phenytoin-type anticonvulsants, succinimide-type anticonvulsants, barbiturates, and benzodiazepines—drugs metabolized by hepatic microsomal enzymes, especially clonazepam, primidone, or valproic acid—with carbamazepine may lead to enhanced metabolism, thereby decreasing the serum concentrations of these drugs and shortening their elimination half-life due to increased hepatic microsomal enzyme activity. Monitoring of blood drug concentrations is recommended to guide dose adjustments, especially when adding or discontinuing any of the above-mentioned drugs or carbamazepine in an existing treatment regimen. Valproic acid may prolong the half-life of carbamazepine and reduce its protein binding rate; the concentration of the active metabolite 10,11-epoxide may be increased. Furthermore, carbamazepine has been reported to increase the risk of birth defects and may cause thyroid dysfunction when used in combination with other antiepileptic drugs.
For more complete data on drug interactions of carbamazepine (41 drugs in total), please visit the HSDB record page.

[1]. Willow, M. and W.A. Catterall, Inhibition of binding of [3H]batrachotoxinin A 20-alpha-benzoate to sodium channels by the anticonvulsant drugs diphenylhydantoin and carbamazepine. Mol Pharmacol, 1982. 22(3): p. 627-35.

[2]. Biphasic effects of carbamazepine on the dopaminergic system in rat striatum and hippocampus. Epilepsy Res, 1997. 28(2): p. 143-53.

[3]. Carbamazepine is an inhibitor of histone deacetylases. Life Sci. 2005 May 13;76(26):3107-15.

[4]. Carbamazepine directly inhibits adipocyte differentiation through activation of the ERK 1/2 pathway. Br J Pharmacol. 2013 Jan;168(1):139-50.

[5]. Carbamazepine attenuates inducible nitric oxide synthase expression through Akt inhibition in activated microglial cells. Pharm Biol. 2014 Nov;52(11):1451-9.

[6]. Carbamazepine promotes liver regeneration and survival in mice. J Hepatol. 2013 Dec;59(6):1239-45.

[7]. Chronic oral carbamazepine treatment elicits mood-stabilising effects in mice. Acta Neuropsychiatr. 2014 Feb;26(1):29-34.

Therapeutic Uses
Non-narcotic analgesic; anticonvulsant
Carbamazepine has been shown to be effective for certain mental illnesses, including schizoaffective disorder, treatment-resistant schizophrenia, and loss of control syndrome associated with limbic system dysfunction. /Not included on the US or Canadian product label/
Carbamazepine is used for the treatment of alcohol withdrawal. Studies have found that it effectively and rapidly relieves anxiety and distress caused by acute alcohol withdrawal, as well as symptoms such as seizures, hyperexcitability, and sleep disturbances. /Not included on the US product label/
Carbamazepine can be used alone or in combination with other medications (such as clofibrate or chlorpropamide) to treat partial central diabetes insipidus. /Not included on the US or Canadian product label/
For more complete data on the therapeutic uses of carbamazepine (10 in total), please visit the HSDB record page.

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Drug Warnings
A few cases have been reported of neonatal seizures and/or respiratory depression in mothers who were taking carbamazepine and other anticonvulsant medications. There have been a few case reports of neonatal vomiting, diarrhea, and/or decreased feeding; these symptoms may represent neonatal withdrawal syndrome. Carbamazepine should not be used prophylactically during long-term remission of trigeminal neuralgia. While there are reports that carbamazepine can relieve dystonia attacks in children, reduce migraine attacks, and relieve intractable hiccups in some patients, its efficacy in these cases has not been established. Carbamazepine is not indicated for atypical or generalized absence seizures (petit mal seizures) or myoclonic or atonic seizures. For more complete data on carbamazepine (30 total), please visit the HSDB records page.

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Pharmacodynamics
General Actions: Carbamazepine treats seizures and trigeminal neuralgia symptoms by inhibiting sodium channels. In bipolar I, carbamazepine has been shown to significantly reduce manic symptoms according to the Young's Mania Rating Scale (YMRS). Carbamazepine has a narrow therapeutic index. Regarding the relationship between gene mutations and carbamazepine use: In studies of Han Chinese patients, a significant association was observed between the HLA-B1502 genotype and carbamazepine-induced Stevens-Johnson syndrome and/or toxic epidermal necrolysis (SJS/TEN).

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Carbamazepine is a classic antiepileptic and mood stabilizer[2][7]
Its core mechanisms include: blocking voltage-gated sodium channels to inhibit neuronal overexcitation (antiepileptic effect); inhibiting HDACs to regulate gene expression through histone acetylation; biphasic regulation of the dopaminergic system; activating the ERK1/2 pathway to inhibit adipocyte differentiation; and inhibiting microglial activation by inhibiting Akt[1][2][3][4][5]
Clinical indications include partial seizures, generalized tonic-clonic seizures, and bipolar disorder[7]
In addition to its traditional uses, it has shown potential therapeutic effects in promoting liver regeneration and inhibiting adipocyte differentiation[4][6]
Its biphasic effect on the dopaminergic system is concentration-dependent, with low doses enhancing dopamine release and high doses inhibiting dopamine release[2]

C15H12N2O

236.27

236.094

298-46-4

Carbamazepine-d10;132183-78-9;Carbamazepine-d2;1189902-21-3;Carbamazepine-d8;1538624-35-9;Carbamazepine-(Ph)d8

2554

White to off-white solid powder

1.3±0.1 g/cm3

411.0±48.0 °C at 760 mmHg

189-192 °C

202.4±29.6 °C

0.0±1.0 mmHg at 25°C

1.670

2.67

1

1

0

18

326

0

RYLOOVOCHDAWIL-UHFFFAOYSA-N

InChI=1S/C15H12N2O/c16-15(18)12-9-10-5-1-3-7-13(10)17-14-8-4-2-6-11(12)14/h1-9,17H,(H2,16,18)

benzo[b][1]benzazepine-11-carboxamideInChi Key: RYLOOVOCHDAWIL-UHFFFAOYSA-N

NSC 169864; Carbamazepine, NSC 69864; NSC-169864;Tegretol, Epitol

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Solubility in Formulation 1: ≥ 2.5 mg/mL (10.58 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL.
Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution.

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Solubility in Formulation 2: ≥ 2.5 mg/mL (10.58 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.

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Solubility in Formulation 3: ≥ 2.5 mg/mL (10.58 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution.
For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 25.0 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly.

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Solubility in Formulation 4: 1% DMSO +30% polyethylene glycol+1% Tween 80 : 5 mg/mL

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 (Please use freshly prepared in vivo formulations for optimal results.)