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Company Name: Shenzhen Sendi Biotechnology Co.Ltd.
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Products Intro: CAS:298-46-4
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Products Intro: Product Name:Carbamazepine

Lastest Price from Carbamazepine manufacturers

  • carbamazepine
  • US $10.00 / KG
  • 2019-01-15
  • CAS:298-46-4
  • Min. Order: 10KG
  • Purity: 99%
  • Supply Ability: 10MT
  • Carbamazepine
  • US $15.00 / KG
  • 2018-08-01
  • CAS: 298-46-4
  • Min. Order: 1KG
  • Purity: 99%
  • Supply Ability: 1000kg
Carbamazepine Basic information
Overview Indication Dosage and administration Pharmacodynamics Mode of action Adverse reactions and precaution References
Product Name:Carbamazepine
Product Categories:Pharmaceutical;Acids and Derivatives;Heterocycles;Active Pharmaceutical Ingredients;APIs;Pharmaceutical raw material;TEGRETOL;Pharmaceutical Chemicals;Intermediates & Fine Chemicals;Pharmaceuticals;Aromatics;Isotope Labelled Compounds
Mol File:298-46-4.mol
Carbamazepine Structure
Carbamazepine Chemical Properties
Melting point 189-192 °C
Boiling point 378.73°C (rough estimate)
density 1.1099 (rough estimate)
refractive index 1.5906 (estimate)
Fp 9℃
storage temp. 2-8°C
solubility 45% (w/v) aq 2-hydroxypropyl-β-cyclodextrin: soluble29mg/mL
form Crystals
color Almost white
Water Solubility pract. insoluble
Merck 14,1781
CAS DataBase Reference298-46-4(CAS DataBase Reference)
NIST Chemistry ReferenceCarbamazepine(298-46-4)
Safety Information
Hazard Codes Xn,T,F
Risk Statements 42/43-22-20/21/22-39/23/24/25-23/24/25-11
Safety Statements 37-24-22-36/37/39-36-45-36/37-16
RTECS HN8225000
HS Code 29339900
Hazardous Substances Data298-46-4(Hazardous Substances Data)
ToxicityLD50 orally in mice, rats: 3750, 4025 mg/kg (Stenger, Roulet)
MSDS Information
Carbamazepine English
ACROS English
Carbamazepine Usage And Synthesis
OverviewCarbamazepine (CBZ) is an irninostilbene derivative, structurally similar to the tricyclic antidepressants. Chemically. CBZ is a neutral, liposoluble compound that can easily pass the bloodlbrain barrier and other membranes in the body. Developed and marketed for the treatment of epileptic seizures and trigeminal neuralgia, CBZ has been utilized more and more frequently in the last decade to treat psychiatric disorders.
Carbamazepine was first evaluated as a potential treatment in manic depressive psychosis by Takezaki and Hanaoka (1971)[1], and Okuma et al. (1973)[2]. In 1979, Okuma et al.[3] performed the first double-blind trial of carbamazepine in comparison with the antipsychotic chlorpromazine in mania and found that 70% and 60% of patients improved respectively. A further placebo-controlled double-blind study replicated the antimanic properties of carbamazepine under controlled circumstances (Ballenger and Post, 1980). There have since been many studies demonstrating the efficacy of carbamazepine in treating the acute manic and depressive symptoms of bipolar disorder, as well as in prophylaxis[4, 5].

Figure 1 the chemical structure of carbamazepine;
IndicationCarbamazepine has been used to treat many types of epilepsies since the early sixties[6]. The psychotropic properties of the drug were soon recognized and prompted studies in psychiatric disorders. Today, the main indications for CBZ in psychiatry are the treatment of acute manic states and the prophylaxis of recurrence in bipolar disorders[7]. The clinical studies reviewed consistently reported a CBZ success rate in acute manic states and recurrence prophylaxis in bipolar disorders ranging from 50 to 65%. More recent works confirmed the success rate in acute manic states[8], whereas data for the long-term prophylaxis of recurrence were more variable, and in general less positive[9]. Post et al. (1993) [10] suggested that poor long-term CBZ efficacy might be due to tolerance development and, on the basis of the CBZ action in experimental models. Speculated that periods of drug "holiday" may restore its efficacy. A similar warning has been reported for the long-term prophylactic efficacy of lithium[11].
Evidence of some positive action of CBZ in unipolar depression has also been reported[12]. More recently. Cullen et al. (1991) [13] retrospectively analyzed 16 melancholic patients who received CBZ alone or in combination with other psychotropic drugs. Seven patients had a moderate to marked improvement, but treatment had to be discontinued in five due to side effects. Stuppaeck et al. (1993) [14], in open observations in 15 patients with unipolar depression, concluded that CBZ had a positive effect in 11 patients.
Other psychiatric syndromes for which CBZ has been proved or suggested to be useful include aggressive agitation in demented patients[15]. Super-sensitivity psychosis[16], and alcohol[17] and benzodiazepine withdrawal syndromes[18]. In panic disorders, CBZ has been reported to attenuate panic attacks in subjects with underlying EEG abnormalities[19]. However, in the only controlled trial in 14 patients with panic disorders, CBZ was no better than placebo[20].
Dosage and administrationCarbamazepine dosages employed in the various pathologies are similar: in most cases therapeutic effects are obtained at doses of 10 to 20 mg/kg/day. Age has only a limited effect on CBZ disposition, but children may need a slightly higher dosage (in mg/kg). No dosage adjustments are required in relation to patient's sex or other genetic factors. Treatment should be started at low dosages (3 5 mg/kg/day) and increased progressively by a similar amount every 5-7 days, until the desired clinical effect is obtained or persistent side effects appear. This approach will determine the lowest effective (or the maximum tolerated) dose and reduce the incidence of dose-dependent side effects, which are more frequent and more troublesome for the patient at the beginning of therapy[15]. If tolerance is poor but the drug seems to be clinically effective, an even slower titration may prove useful. Treatment of acute manic states, however, may require a faster titration at the cost of an increased frequency of side effects[16]. A daily dose administered in conventional tablets or oral suspension should be divided into 3-4 intakes to avoid excessive fluctuations of plasma concentration; alternatively, slow-release preparations can be used. In some countries a chewable tablet formulation (100 mg) is available, which may be convenient in children[13].
PharmacodynamicsCarbamazepine given in conventional tablets shows a mean peak concentration time during chronic treatment of about 4 hours, with an estimated oral bioavailability of 80-90%[21]. Carbamazepine is readily distributed in the body with an apparent volume of distribution (estimated on the presumption of a 100% oral bioavailability) of 0.8 2.0 /kg. Brain concentrations are about 1.21.4 times those in plasma and the breast milk/ total plasma level ratio is about 0.4 [22]. In plasma, CBZ binds to circulating proteins, mostly albumin and a1-acid glycoprotein. The bound fraction is about 70-80% and is constant in the interval of plasma concentrations normally observed in therapy[23].
Carbamazepine is mainly eliminated through hepatic metabolism by microsomal enzymes of the cytochrome P450 family. The main metabolites are epoxy-CBZ and 10.11-dihydro, 10,lldihydroxy carbarnazepine (CBZ-DIOL). In man, the hydroxylated derivatives are conjugated with glucuronic acid and excreted by the kidneys. Small amounts of unmodified CBZ are found in feces and in urine[24]. Quantitatively, the main urinary metabolite is CBZ-DIOL, which is, however, inactive. Carbamazepine-l0, 11-epoxideh as anticonvulsant potency similar to the parent drug, and has comparable efficacy in trigerninal neuralgia in man. After repeated dose, CBZ induces its own metabolism and its half-life is reduced by about 50%. Changing, for example, from 36 hours at the beginning of therapy to 21 hours after 3 weeks of treatment. Patients treated with other enzyme-inducing drugs may have a CBZ half-life as short as 5 16 hours. Children present a slightly higher CBZ clearance[21].
Mode of actionThe many effects of CBZ on the central nervous system include: the ability to bind to neuron membrane sodium channels when they are in the inactivated state, slowing the speed of reactivation and thus reducing the neuron's capacity of high frequency firing[25]; selective interaction with adenosine receptors and modification of the activity of second messengers like CAMP and cGMP and modification of various neurotransmitter systems[26]. An interesting aspect of CBZ action on the brain is the apparent selectivity for the limbic system, a feature that may provide an anatomical basis for both the psychotropic action of the drug and its efficacy in psychomotor epilepsies.
Adverse reactions and precautionThe most common manifestations of acute CBZ toxicity at therapeutic dosages involve the central nervous and gastrointestinal systems (sedation. nystagmus, diplopia, ataxia, dizziness, nausea, vomiting, constipation, diarrhea) [27]. Dry mouth may occur as a consequence of some anticholinergic action of the drug. These symptoms respond to a dose reduction and, due to tolerance development, usually abate during treatment. Carbamazepine may induce involuntary movements such as myoclonic and choreoathetoid jerks, dystonia and asterixis[28]. Carbarnazepine has negative chmnotropic and dromotropic effects on cardiac conduction and may induce various types of bradyarrhythmia or even a complete atrioventricular block[28]. These dangerous complications are usually observed in elderly patients or patients with a preexisting impairment of cardiac conduction, are concentration-related, and require dose reduction or drug suspension.
During pregnancy, important modifications of CBZ kinetics may occur, requiring plasma concentration monitoring and, possibly, dosage adjustment[22]. CBZ enters breast milk (milk/plasma ratio of about 0.4)and a transfer of 1-4 mg/day of drug from mother to child takes place during nursing[22]. Concentrations in the breast-fed infant should not normally exceed 0.5 1.0 ug/ml, but somewhat higher concentrations, up to 4.7 ~ug /ml one case, have occasionally been reported[22]. These findings suggest that breast-feeding is not to be discouraged and that it should be discontinued only if the newborn shows signs of distress, such as blunted suck reflex.
  1. Takezaki H, Hanaoka M (1971). The use of carbamazepine (Tegretol) in the control of manic-depressive psychosis and other manic-depressive states. Clinical Psychiatry 13, 173–183.
  2. Okuma T, Kishimoto A, Inoue K, Matsumoto H, Ogura A, Matsushita T, Nakao T, Ogura C (1973). Anti-manic and prophylactic effects of carbamazepine (Tegretol) on manic-depressive psychosis: a preliminary report. Folia Psychiatrica et Neurologica 27, 283–297.
  3. Okuma T, Inanaga K, Otsuki S, Sarai K, Takahashi R, Hazama H, Mori A, Watanabe M (1979). Comparison of the antimanic efficacy of carbamazepine and chlorpromazine : a double-blind controlled study. Psychopharmacology 66, 211–217.
  4. Brambilla P, Barale F, Soares JC (2001). Perspectives on the use of anticonvulsants in the treatment of bipolar disorder. International Journal of Neuropsychopharmacology 4, 421–446.
  5. Post RM, Ketter TA, Denicoff K (1996a). The place of anticonvulsant therapy in bipolar illness. Psychopharmacology 128, 115–129.
  6. Loiseau. P, B. Duche: Carbamazepine. Clinical use. In: Levy, R H., E E. Dreifus. R H. Mattson, B. S. Me1drum.J. K. Penly (eds.): Antiepileptic drugs. Raven Press. New York 7989 p. 553-554
  7. Michels. R. P. M. Marzuk: Progress in psychiatry. N. Engl. J. Med. 329 (1993) 628 -638
  8. Okuma, 1, I. Yamashita, R Takahashi, H. Itoh, S. Otsuki. S. Watanabe. S. Sarai. H. Hazama. K. Inanaga: Comparison of the antimanic efficacy of carbamazepine and lithium carbonate by doubleblind controlled study. Pharmacopsychiatry 23 (1990) 143-150
  9. Small, J. G., M. H. Klapper, V. Milstein.].]. Kellmans, M.J. Miller.]. D. Marhenke, I. E Small: Carbamazepine compared with lithium in the treatment of mania. Arch. Gen. Psych. 48 (1991) 915-921
  10. Post, R M., 1 A. Ketter, P. J. Pauaglia. M. S. George, L. MamngelI, K. Denicoff: New developments in the use of anticonvulsants as mood stabilizers. Neuropsychobiology 27 (1993) 132-137
  11. Maj, M., R Pimzzi. D. Kemali: Long-term outcome of lithium prophylaxis in patients initially classified as complete responders. Psychopharmacology 98 (1989) 535-538
  12. Evans, R W., C. T. Gualtieri: Carbamazepine: a neurological and psychiatric profile. Clin. Neuropharrnacol. 8 (1985) 221 -241
  13. Cullen. M., P. Mitchell, H. Brodaty, I? Royce, G. Parker, I. Hickie. K Wilhelm: Carbamazepine for treatment-resistant melancholia. J. Clin. Psychiatry 52 (1991) 472-476
  14. Stuppaeck, C. H., C H. Barnas, K. Hackenberg, C. H. Miller. W. W. Neischhacker: Carbamazepine monotherapy in the treatment of alcohol withdrawal. Int. Clin. Psychopharmacol. 5 (1990)2 73 -278
  15. Gleason, R P, L, S. Schneider: Carbamazepine treatment of agitation in Alzheimer's outpatients refractory to neuroleptics. J. Clin. Psychiatry 51 (1990) 115118
  16. Chouinard G.. S. Sultan: Treatment of supersensitivity psychosis with antiepileptic drugs: report of a series of 43 cases. Psychopharmacol. Bull. 26 (1990) 337-341
  17. Stuppaeck, C. H., C H. Barnas, K. Hackenberg, C. H. Miller. W. W. Neischhacker: Carbamazepine monotherapy in the treatment of alcohol withdrawal. Int. Clin. Psychopharmacol. 5 (1990)2 73 -278
  18. Garcia. B.. E. Zaborras, V. Arease. G. Obeso, I. jimena, P. DeJuana, T. Bermejo: Interaction between isoniazid and carbamazepine potentiated by cimetidine. DlCP 26 (1992) 841
  19. Keck, F. E. jr, S. L McElroy. K. C. Tugrul. J. A. Bennett,. M. R. Smith: Antiepileptic drugs for the treatment of panic disorder. Neurobiology 27 (1993) 150-153
  20. Uhde, Z W.. M. B. Stein, R. M. Post: Lack of efficacy of carbamazepine in the treatment of panic disorder. Am. J. Psychiatry 145 (1988) 1104-1109
  21. Morselli, P. L: Carbamazepine. Absorption, distribution and excretion. In: Levy, R H., E E Dreifuss, R H. Mattson, B. S. Me1drum.J. K. Penry (eds.): Antiepileptic Drugs. Raven Press, New York 1989 p. 473-490
  22. Nau. H., W. Ku hnz, H. J. Egger. D. Rating, H. Helge: Anticonvulsants during pregnancy and lactation. Transplacental, maternal and neonatal pharmacokinetics. Clin. Pharmacokinet. 7 (1982) 508543
  23. Contin, M., R Riva, E Albani. E. Perucca. G. Lamonfanara, A. Banrui: a1-acid glycoprotein concentration and serum protein binding of carbamazepine and carbamazepine 10,ll-epoxide in children with epilepsy. Eur. J. Clin. Pharmacol. 29 (1985) 211 -214
  24. Faigle.J. W., K. E Feldmann: Carbamazepine Biotransformation In: Levy. R. H.. E E. Dreifuss, R H. Mattson, B. 5. Me1dnrm.j. K. Penry (eds.): Antiepileptic Drugs. Raven Press, New York 1989, p.491 – 504
  25. Macdonald, R. L: Carbamazepine. Mechanisms of action. In: Levy, R H.. E. Dreifiss, R H. Mattson. B. S. Meldrum,]. K. Penry (eds.): Antiepileptic drugs. Raven Press. New York 1989, p. 447-471
  26. Motohashi. N.: Gaba receptor alterations after chronic lithium administration. Comparison with carbamazepine and sodium valproate. Prog. Neuro-psychophannacol. Biol. Psychiatry 16 (1992) 571 – 579
  27. Askrnark, H.. B. E. Wiholm: Epidemiology of adverse reactions to carbamazepine as seen in a spontaneous reporting system. Acta Neurol. Scand. 81 (1990) 131 -140
  28. Gram L, P K. jensen: Carbarnazepine Toxicity. In: Levy. R. H., R. Mattson, B. Meldrum, J. K Pen% E E. Dreifuss (eds.): Antiepileptic Drugs. Raven Press. New York 1989, p. 555-565
Chemical PropertiesWhite Solid
Usesanalgesic, anticonvulsant
UsesUsed in treatment of pain associated with trigeminal neuralgia. Anticonvulsant
DefinitionChEBI: A dibenzoazepine that is 5H-dibenzo[b,f]azepine carrying a carbamoyl substituent at the azepine nitrogen, used as an anticonvulsant.
UsesCarbamazepine (CBZ) is a first generation anticonvulsant and mood stabilizing compound that has been used as a therapeutic in the context of neuropathic pain, epilepsy, and affective disorders. It exerts its effects by blocking voltage-gated sodium channels (IC50 = 640 μM), making fewer of these channels available to subsequently open, which leads to decreased high-frequency repetitive firing of action potentials. The estimated IC50 values for inhibition of Nav1.7-, Nav1.3-, and Nav1.8-type channels by CBZ following prolonged inactivation have been reported as 406, 900, and 138 μM, respectively. CBZ can also inhibit L-type Ca2+ channels (IC50 = 974 μM) and has been shown to potentiate GABAA receptors (IC50 >3 mM).
Brand nameCarbatrol (Shire); Epitol (Teva); Equetro (Shire); Tegretol (Novartis); Teril (Taro).
Carbamazepine Preparation Products And Raw materials
Raw materials2-Nitrotoluene-->Iminostilbene-->2,2'-ETHYLENEDIANILINE
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