Overview Indications Pharmacokinetics Mode of action Safety & Tolerability Precautions Reference
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Tetrabenazine

Overview Indications Pharmacokinetics Mode of action Safety & Tolerability Precautions Reference
Product Name
Tetrabenazine
CAS No.
58-46-8
Chemical Name
Tetrabenazine
Synonyms
Xenazine;Nitoman;Rubigen;Ro 1-9569;TETRABENAZINE;(3R,11bR)-rel-;TBZ,racemic mixture;TetrabezineImpurity5;Tetrabenazine(Xenazine);Butyl benzene that lamictal
CBNumber
CB5339246
Molecular Formula
C19H27NO3
Formula Weight
317.42
MOL File
58-46-8.mol
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Tetrabenazine Property

Melting point:
128-130?C
Boiling point:
456.71°C (rough estimate)
Density 
1.12
refractive index 
1.5180 (estimate)
storage temp. 
2-8°C
solubility 
DMSO: >10mg/mL
form 
solid
pka
6.46±0.40(Predicted)
color 
White
Merck 
14,9182
BRN 
40090
Stability:
Stable for 1 year from date of purchase as supplied. Solutions in DMSO or ethanol may be stored at -20° for up to 1 week.
InChIKey
MKJIEFSOBYUXJB-UHFFFAOYSA-N
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Safety

Hazard Codes 
Xn
Risk Statements 
22
Safety Statements 
24/25
RIDADR 
3249
WGK Germany 
3
RTECS 
DK2275000
HazardClass 
6.1(b)
PackingGroup 
III
HS Code 
29339900
Hazardous Substances Data
58-46-8(Hazardous Substances Data)
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Hazard and Precautionary Statements (GHS)

Symbol(GHS)
Signal word
Warning
Hazard statements

H302Harmful if swallowed

Precautionary statements

P264Wash hands thoroughly after handling.

P264Wash skin thouroughly after handling.

P270Do not eat, drink or smoke when using this product.

P301+P312IF SWALLOWED: call a POISON CENTER or doctor/physician IF you feel unwell.

P501Dispose of contents/container to..…

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N-Bromosuccinimide Price

Sigma-Aldrich
Product number
T2952
Product name
Tetrabenazine
Purity
≥98% (HPLC), solid
Packaging
10mg
Price
$162
Updated
2024/03/01
Sigma-Aldrich
Product number
T2952
Product name
Tetrabenazine
Purity
≥98% (HPLC), solid
Packaging
50mg
Price
$748
Updated
2024/03/01
Sigma-Aldrich
Product number
5.09892
Product name
Tetrabenazine, TBZ - CAS 58-46-8 - Calbiochem
Packaging
10mg
Price
$167
Updated
2024/03/01
TCI Chemical
Product number
T2839
Product name
Tetrabenazine
Purity
>99.0%(HPLC)(T)
Packaging
200mg
Price
$223
Updated
2024/03/01
TCI Chemical
Product number
T2839
Product name
Tetrabenazine
Purity
>99.0%(HPLC)(T)
Packaging
1g
Price
$696
Updated
2024/03/01
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Tetrabenazine Chemical Properties,Usage,Production

Overview

Tetrabenazine(TBZ) is a drug formerly used as an antipsychotic but now used primarily in the symptomatic treatment of various hyperkinetic disorders. It is a monoamine depletor and used as symptomatic treatment of chorea associated with Huntington's disease. FDA approved on August 15, 2008. Tetrabenazine, a dopamine-depleting agent first synthesized half a century ago, was initially developed for the treatment of schizophrenia. Although psychotic disorders have since been treated more successfully with other neuroleptic medications, many studies have shown this drug to be effective in the treatment of hyperkinetic movement disorders (hyperkinesias). Hyperkinesias are neurologic disorders characterized by abnormal involuntary movements such as chorea associated with Huntington's disease, tics in Tourette's syndrome and stereotypies in tardive dyskinesia.
In the United States, only tetrabenazine(TBZ) is indicated by the US Food and Drug Administration(FDA) for chorea of HD, haloperidol and pimozide for TS, and botulinum toxin injectable for idiopathic focal dystonias[1-4]. TBZ is a benzoquinolizine pharmacophore that selectively depletes monoamines and improves hyperkinetic movement symptoms[5]. Although initially tested as a potential antiparasitic agent as well as a potential antihypertensive, TBZ was first marketed in Switzerland in 1959 as a tranquilizer. Clinicians soon observed that TBZ improved hyperkinetic movements and, in 1971, the United Kingdom and Ireland were the first countries to market TBZ for hyperkinetic movement disorders. Subsequently, TBZ become available in several countries for official use in various hyperkinetic movement disorders. In 2008, the United States approved TBZ for the management of chorea associated with HD. A literature search revealed that recent TBZ review articles primarily highlight its role in the management of HD chorea[6-10] and one review focused on the off-label use of TBZ for TDk[11]. Two recent reviews of TBZ summarized efficacy and tolerability for a broader range of hyperkinetic movement disorders[5, 12].
TBZ, also named Ro 1-9569 by Hoffmann-LaRoche, Inc., is a benzoquinolizine derivative with the chemical name, 2-oxo-3isobutyl-9, 10-dimethoxy-1, 2, 3, 4, 6, 7-hexahydrobenzo(a) quinolizine FIGURE 1. In contrast to an analogous drug, reserpine, TBZ lacks an indole group[13]. Based on the acid–basic transition, TBZ is characterized by a negative logarithm of the acid ionization constant (pKa) of 6.0[14]. Chromatographic analysis of TBZ reveals peak fluorescence at 282 nm[15].

Figure 1 the chemical structure of tetrabenazine

Indications

Tetrabenazine is used for the treatment of hyperkinetic movement disorders like chorea in Huntington's disease, hemiballismus, senile chorea, Tourette syndrome and other tic disorders, and tardive dyskinesia (TD).

Pharmacokinetics

A thorough review of the medical literature reveals a paucity of information regarding the pharmacodynamics of TBZ. After intravenous administration of radiolabeled 3H-TBZ, 54% was excreted in urine after 48h[16]. A 1987 study found no evidence of unchanged TBZ in the urine of four patients indicating extensive metabolism[17]. TBZ is excreted in human breast milk, thus breastfeeding while taking TBZ should be avoided. Although no case of teratogenicity has been reported, TBZ does cross the placenta[18].
After oral administration, TBZ is rapidly absorbed within 1 hour; however, the systemic bioavailability of the parent drug is low(5%) due to a high first-pass metabolism[19]. TBZ undergoes first-pass metabolism, by hepatic carbonyl reductase, to at least two isomers of dihydrotetrabenazine (DHTBZ): alpha-DHTBZ and beta-DHTBZ[20]. Both metabolites are pharmacologically active, with alpha-DHTBZ demonstrating activity similar to the parent drug[6]. Both metabolites reach Cmax within 1 to 2 hours and are primarily metabolized by cytochrome P450(CYP) 2D6(CYP2D6). The t1⁄2 of alphaand beta-DHTBZ ranges from 2 to 8 hours and 2 to 5 hours, respectively[6, 7].
In humans, the steady-state AUC values of the DHTBZ metabolites are 82.6 to 199 fold higher than that of TBZ[21]. In rats; the mean (SD) Vd of DHTBZ is 7.8 (4.08) L/kg. Protein binding of TBZ, alpha-DHTZ, and beta-DHTBZ ranges from 82% to 85%, 60% to 68%, and 59% to 63%, respectively[6].
Neither TBZ nor its metabolites induce or inhibit major CYP450 isozymes. Therefore, TBZ will not interfere with metabolism of other drugs that are CYP450 substrates. However, because some of the DHTBZ metabolites are substrates for CYP2D6, other drugs that induce or inhibit this isozyme may alter DHTBZ concentrations[6, 7].

Mode of action

In the CNS, neurons communicate with one another through the release of neurotransmitters. Neurotransmitters are synthesized in the neuronal cytoplasm and then packaged into vesicles; otherwise, they undergo rapid degradation by ubiquitous monoamine oxidases. TBZ acts as a reversible inhibitor of monoamine uptake into granular vesicles of presynaptic neurons[22,23] through its ability to bind to vesicular monoamine transporter (VMAT)-2[24] thereby potentiating monoamine degradation in the cytoplasm. Monoamine neurotransmitters that are depleted via VMAT2 inhibition by TBZ include serotonin, dopamine, and norepinephine[23, 25]. In one in vivo study of rats, TBZ decreased dopamine levels by 40%, serotonin by 44% and norepinephrine by 41% in the brain[26]. Levels of acetylcholine, aspartate and glutamate were decreased to a lesser degree. In an autopsy study of 18 patients with Huntington’s disease(HD), those who had received TBZ displayed an overall depletion of monoamines in the caudate, amygdala, hip-pocampus and temporal lobe when compared with patients not exposed to TBZ[27,28]. The most pronounced depletion involved dopamine in the caudate nucleus.
VMAT2, a large protein with 12 transmembrane helices encoded by the VMAT2 gene and localized to chromosome 10q25, is expressed mostly in the brain. In contrast, VMAT1, encoded by a gene on chromosome 8p21.3, is expressed in the periphery[29]. TBZ binds with high affinity to VMAT2, but not to VMAT1[30].
Although in vitro studies have shown that TBZ blocks dopamine D2 receptors, as suggested by its ability to inhibit(3H) spiperone binding to striatal membranes with a Ki of approximately 2.1 × 10-6M, this affinity is 1000-fold lower than its affinity for VMAT2[31,32]. Therefore, it is unlikely that the weak D2 receptor antagonism is responsible for TBZ clinical effects, although it may be possibly involved in acute dystonic reactions rarely reported with TBZ[33]. Although TBZ has also been found to block the pharmacologic action of apomorphine, a dopamine agonist[23], providing further evidence of dopamine receptor-blocking activity, this action of TBZ is relatively weak and most likely explains the low risk of TBZ-induced TD. The presynaptic depletion and weak postsynaptic dopamine receptor inhibition may be responsible for increased dopamine turnover as suggested by the increased levels of the major dopamine metabolite, homovanillic acid, in the cerebrospinal fluid of patients with HD taking TBZ[7].

Safety & Tolerability

TBZ has been used most commonly in the range of 25 200mg/day, although a typical therapeutic dose is 50 75 mg/day. In studies and in daily practice, TBZ is slowly titrated from approximately 25 mg/day in two or three divided doses up to 150mg/day in increments of 25 mg/week. Given the short half-life, dosing three-times per day is sometimes necessary. The dose escalation is stopped when the patient experiences intolerable side effects or a satisfactory effect. Nearly all drug-related side effects can be eradicated by lowering the dose. Therefore, most studies with TBZ are designed to increase the dose until intolerable side effects are noted and then the dose is slightly decreased to alleviate the side effects. Using this technique of dose escalation, it is not surprising that many patients develop side effects. The dose-dependent nature of side effects is an important point to consider when discussing the adverse event profile of TBZ[18,34,35]. Common side effects include sedation, parkinsonism, depression, insomnia, and akathisia, all of which are reversible[16]. Several investigators have observed that younger patients tolerate TBZ better than the elderly. These findings have been confirmed and reported that younger patients (<50 years) experienced more insomnia and depression, while older patients were more likely to develop parkinsonism[37]. Serious side effects of TBZ described in the literature include severe hyperthermia, neuroleptic malignant syndrome (NMS), acute dystonic reaction[33], pneumonia, severe dysphagia[1,10] and suicide[6]. NMS usually occurs within the first 4 weeks of treatment, but may be delayed several years[38,39]. Prescribing physicians should be aware that a number of publications mention fatalities occurring in those taking TBZ without an obvious etiology. It should be considered that the frequency of dysphagia, suicide and death would be expected to be increased in a study population of patients with HD. Most authors state that the deaths were not directly related to TBZ, but the frequency of unexplained death in certain clinical studies warrants caution and close monitoring of patients' physical and mental well-being throughout the course of treatment.

Precautions

When you take tetrabenazine, you should follow the following tips[40]:
Tell all of your health care providers that you take tetrabenazine including your doctors, nurses, pharmacists, and dentists.
You should avoid driving and doing other tasks or actions that call for you to be alert until you see how tetrabenazine affects you.
To lower the chance of feeling dizzy or passing out, you should rise slowly if you have been sitting or lying down. Be careful when you go up and down stairs.
You should often have your blood pressure checked and keep in touch with your doctor. Talk with your doctor before you drink alcohol or use other drugs and natural products that slow your actions. If you have Huntington's disease, your signs can still get worse while you use drugs like this one. Call your doctor right away if you have any signs that are new or worse. Tell your doctor if you are pregnant or plan on getting pregnant. You will need to talk about the benefits and risks of using tetrabenazine while you are pregnant. Tell your doctor if you are breast-feeding. You will need to talk about any risks to your baby.

Reference

  1. Mestre T, Ferreira J, Coelho MM, et al. Therapeutic interventions for symptomatic treatment in Huntington’s disease. Cochrane Database Systematic Rev. 2009; 3: CD006456.
  2. Soares-WeiserK,FernandezHH.Tardivedyskinesia.Semin Neurol. 2007;27:159 –169.
  3. Cloud LJ, Jinnah HA. Treatment strategies for dystonia. Expert Opin Pharmacother. 2010;11:5–15.
  4. HuysD,Hardenacke K,PoppeP,etal.Update on the role of antipsychotics in the treatment of Tourette syndrome. Neuropsychiatr Dis Treat. 2012;8:95–104.
  5. Fasano A, Bentivoglio AR. Tetrabenazine. Expert Opin Pharmacother. 2009;10:2883–2896.
  6. ScottLJ.Tetrabenazine:for chorea associated with Huntington’s disease. CNS Drugs. 2011;25:1073–1078.
  7. JankovicJ,Clarence-SmithK.Tetrabenazine for the treatment of chorea and other hyperkinetic movement disorders. Expert Rev Neurother. 2011;11:1509 –1523.
  8. de Tommaso M, Serpino C, Sciruicchio V. Management of Huntington’s disease: role of tetrabenazine. Ther Clin Risk Manag. 2011;7:123–129.
  9. Frank S. Tetrabenazine: the first approved drug for the treatment of chorea in US patients with Huntington disease. Neuropsychiatr Dis Treat. 2010;6:657– 665.
  10. Poon LH, Kang GA, Lee AJ. Role of tetrabenazine for Huntington’s disease-associated chorea. Ann Pharmacother. 2010;44:1080 –1089.
  11. Leung JG, Breden EL. Tetrabenazine for the treatment of tardive dyskinesia. Ann Pharmacother. 2011;45:525–531.
  12. Guay DR. Tetrabenazine, a monoamine-depleting drug used in the treatment of hyperkinetic movement disorders. Am J Geriatr Pharmacother. 2010;8:331–373.
  13. Quinn GP, Shore PA, Brodie BB. Biochemical and pharmacological studies of RO 19569 (tetrabenazine), a nonindole tranquilizing agent with reserpine-like effects. J. Pharmacol. Exp. Ther. 127, 103–109 (1959).
  14. Scherman D, Henry JP. Acido–basic properties of the catecholamine uptake inhibitors tetrabenazine and dihydrotetrabenazine. Biochimie 64, 915–921 (1982).
  15. Roberts MS, Watson HM, McLean S, Millingen KS. Determination of therapeutic plasma concentrations of tetrabenazine and an active metabolite by high-performance liquid chromatography. J. Chromatogr. 226, 175–182 (1981).
  16. Stumpf W. Untersuchungen uber ‘Nitoman’. Psychiatr. Neurol. 140, 63–68 (1960).
  17. Mehvar R, Jamali F, Watson MW, Skelton D. Pharmacokinetics of tetrabenazine and its major metabolite in man and rat. Bioavailability and dose dependency studies. Drug. Metab. Dispos. 15, 250–255 (1987).
  18. Roberts MS, McLean S, Millingen KS, Galloway HM. The pharmacokinetics of tetrabenazine and its hydroxy metabolite in patients treated for involuntary movement disorders. Eur. J. Clin. Pharmacol. 29, 703–708 (1986).
  19. RobertsMS,McLeanS,MillingenKS,GallowayHM.The pharmacokinetics of tetrabenazine and its hydroxy metabolite in patients treated for involuntary movement disorders. Eur J Clin Pharmacol. 1986;29:703–708.
  20. YaoZ,WeiX,WuX,etal.Preparationandevaluationof tetrabenazine enantiomers and all eight stereoisomers of dihydrotetrabenazine as VMAT2 inhibitors. Eur J Med Chem. 2011;46:1841–1848.
  21. Mehvar R, Jamali F, Watson MW, et al. Pharmacokinetics of tetrabenazine and its major metabolite in man and rat. Bioavailability and dose dependency studies. Drug Metab Dispos. 1987;15:250 –255.
  22. Caine ED, Shoulson I. Psychiatric syndromes in Huntington’s disease. Am J Psychiatry. 1983;140:728 –733.
  23. Lawrence AD, Sahakian BJ, Hodges JR, et al. Executive and mnemonic functions in early Huntington’s disease. Brain. 1996;119(Pt 5):1633– 1645.
  24. Kirkwood SC, Su JL, Conneally P, et al. Progression of symptoms in the early and middle stages of Huntington disease. Arch Neurol. 2001;58:273–278.
  25. Ho AK, Sahakian BJ, Brown RG, et al. Profile of cognitive progression in early Huntington’s disease. Neurology. 2003;61:1702–1706.
  26. Lanska DJ, Lanska MJ, Lavine L, et al. Conditions associated with Huntington’s disease at death. A casecontrol study. Arch Neurol. 1988;45: 878 – 880.
  27. Sorensen SA, Fenger K. Causes of death in patients with Huntington’s disease and in unaffected first degree relatives. J Med Genet. 1992;29: 911–914. Huntington’sDiseaseCollaborative Research
  28. Group. A novel gene containing a trinucleotide repeat that is expanded and unstable on Huntington’s disease chromosomes. Cell. 1993;72:971–983.
  29. RubinszteinDC,LeggoJ,ColesR,et al. Phenotypic characterization of individuals with 30-40 CAG repeats in the Huntington disease (HD) gene reveals HD cases with 36 repeats and apparently normal elderly individuals with 36-39 repeats. Am J Hum Genet. 1996;59:16 –22.
  30. Ranen NG, Stine OC, Abbott MH, et al. Anticipation and instability of IT-15 (CAG)n repeats in parentoffspring pairs with Huntington disease. Am J Hum Genet. 1995;57:593– 602.
  31. Laccone F, Engel U, Holinski-Feder E, et al. DNA analysis of Huntington’s disease: five years of experience in Germany, Austria, and Switzerland. Neurology. 1999; 53: 801–806.
  32. Kenney C, Powell S, Jankovic J. Autopsy-proven Huntington’s disease with 29 trinucleotide repeats. Mov Disord. 2007; 22: 127–130.
  33. FerranteRJ, KowallNW, BealMF,et al. Selective sparing of a class of striatal neurons in Huntington’s disease. Science. 1985; 230:561–563.
  34. Jankovic J, Ashizawa T. Tourettism associated with Huntington’s disease. Mov Disord. 1995;10:103–105.
  35. BonelliRM,HofmannP. A systematic review of the treatment studies in Huntington’s disease since 1990. Expert Opin Pharmacother. 2007;8:141–153.
  36. Watson MW, Skelton D, Jamali F. Treatment of tardive dyskinesia: preliminary report on use of tetrabenazine. Can J Psychiatry. 1988;33:11–13.
  37. Ondo WG, Hanna PA, Jankovic J. Tetrabenazine treatment for tardive dyskinesia: assessment by randomized videotape protocol. Am J Psychiatry. 1999;156:1279 –1281.
  38. Jankovic J, Rohaidy H. Motor, behavioral and pharmacologic findings in Tourette’s syndrome. Can J Neurol Sci. 1987;14(Suppl 3):541–546.
  39. Kenney CJ, Hunter CB, Mejia N, Jankovic J. Tetrabenazine in the treatment of Tourette’s syndrome. J Ped Neurol. 2007;5:9 –13.
  40. https://www.drugs.com/cdi/tetrabenazine.html

Description

Tetrabenazine (58-46-8) is a potent inhibitor of the vesicular monoamine transporter (VMAT), IC50=3.2 nM with selectivity for VMAT2 over VMAT1. Promotes late stage differentiation of Pdx1-positive pancreatic progenitor cells into Neurog3-positive endocrine precursors.

Chemical Properties

White to Off-White Solid

Originator

Nitoman,Roche,UK,1960

Uses

Dopamine depleting agent. An antidyskinetic; antipsychotic.

Uses

Tetrabenazine has been used for dopamine uptake assays in mouse brain cells1. Tetrabenazine has also been used for non-specific binding assays in postnuclear supernatants derived from PC-12 and CV-1 cells2.

Definition

ChEBI: A benzoquinolizine that is 1,2,3,4,4a,9,10,10a-octahydrophenanthrene in which the carbon at position 10a is replaced by a nitrogen and which is substituted by an isobutyl group at position 2, an oxo group at position 3, and methoxy groups at positions 6 an 7.

Manufacturing Process

280 grams of 1-carbethoxymethyl-6,7-dimethoxy-1,2,3,4- tetrahydroisoquinoline, 150 grams of mono-isobutylmalonic acid dimethyl ester and 35 grams of paraformaldehyde were refluxed for 24 hours in 1,000 ml of methanol. Upon cooling, 1-carbethoxymethyl-2-(2,2-dicarbomethoxy-4- methyl-n-pentyl)-6,7-dimethoxy-1,2,3,4-tetrahydroisoquinoline crystallized; MP after recrystallization from methanol, 94° to 96°C. The latter was subjected to Dieckmann cyclization, hydrolysis and decarboxylation in the following manner.
28 grams of sodium was dissolved in 650 ml of absolute ethanol, the solution was concentrated to dryness, and the residue was mixed with 3,600 ml of toluene and 451 grams of the intermediate prepared above. The mixture was heated, and the methanol formed by condensation was distilled off until the boiling point of toluene was reached. The mixture was thereupon refluxed for 2 hours, and then it was concentrated to dryness. The residue was dissolved in 5,200 ml of 3 N hydrochloric acid and heated for 14 hours at 120°C, thereby effecting hydrolysis and decarboxylation. The mixture was cooled, washed with diethyl ether, decolorized with carbon, made alkaline and taken up in diethyl ether. The process yields 2-oxo-3-isobutyl-9,10-dimethoxy- 1,2,3,4,6,7-hexahydro-11b-benzo[a]quinolizine; MP after recrystallization from diisopropyl ether, 126° to 128°C.

Therapeutic Function

Tranquilizer

General Description

A cell permeable benzoquinolizine based compound that acts as a monoamine-depleting agent by blocking the activity vesicular monoamine transporter 2. Promotes late-stage differentiation of Pdx1-positive pancreatic progenitor cells into Neurog3 (Ngn3)-positive endocrine precursors without increasing their proliferation. Increases the number of insulin expressing cells in a dose dependent manner (EC50 = 220 nM) and this effect is significantly enhanced when cells are simultaneously treated with dibutyryl cAMP. Embryonic stem cells treated with TBZ and/or dibutyryl cAMP and then grafted into kidney capsule of AKITA mice reduce hyperglycemia, improve fasting blood glucose levels, and show an increase in plasma C-peptide levels.

Biological Activity

Potent inhibitor of vesicular monoamine uptake; depletes stores of dopamine, serotonin and noradrenalin. Binds with high affinity (IC 50 = 3.2 nM) to vesicular monoamine transporter (VMAT) in chromaffin granule membranes and displays higher affinity for VMAT2 than VMAT1. Also reported to block dopamine receptors. Causes behavioral depression; inhibits locomotor activity and produces hypothermia upon systemic administration in rats and mice.

Biochem/physiol Actions

Primary TargetVMAT2

storage

+4°C

Purification Methods

Crystallise it from MeOH. The hydrochloride has m 208-210o, and the oxime has m 158o (from EtOH). [Beilstein 21 III/IV 6488.]

Tetrabenazine Preparation Products And Raw materials

Raw materials

Preparation Products

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View Lastest Price from Tetrabenazine manufacturers

Hebei Zhanyao Biotechnology Co. Ltd
Product
Tetrabenazine 58-46-8
Price
US $10.00/Kg/Bag
Min. Order
1Kg/Bag
Purity
99%
Supply Ability
20 Tons
Release date
2021-10-20
Shaanxi Dideu Medichem Co. Ltd
Product
Tetrabenazine 58-46-8
Price
US $0.00-0.00/Kg
Min. Order
1KG
Purity
99.0%+
Supply Ability
800 tons
Release date
2020-04-29
Zhenfei Industrial Co. Ltd.
Product
TETRABENAZINE 58-46-8
Price
US $1.00/KG
Min. Order
1KG
Purity
98%
Supply Ability
2000kg
Release date
2018-11-21

58-46-8, Tetrabenazine Related Search:

1-(3-METHOXY-PHENYL)-ETHYLAMINE 1-Phenethyl-4-piperidone 1-Methyl-4-piperidone N-Methylhomoveratrylamine 1-Ethyl-4-piperidone Salsoline Tetrabenazine 2-Methyl-4-piperidone 1-Propyl-4-piperidone Tetrabenazine metabolite A,Tetrabenazine metabolite B 2H-BENZO[A]QUINOLIZIN-2-ONE, 1,3,4,6,7,11B-HEXAHYDRO-9,10-DIMETHOXY-3-(2-METHYLPROPYL)-, (3S,11BS)- 6,7-DIMETHOXY-1,2,3,4-TETRAHYDROISOQUINOLINE 1-PHENYL-BUTYLAMINE AKOS BC-3154 1-(4-METHOXY-PHENYL)-PROPYLAMINE Isoquinoline, 1,2,3,4-tetrahydro-2-methyl- Benzenepentanamine CHEMBRDG-BB 6594188

  • 1,3,4,6,7,11b-Hexahydro-9,10-dimethoxy-3-(2-methylpropyl)-2H-benzo[a]quinolizin-2-one
  • Nitoman
  • Ro 1-9569
  • Rubigen
  • cis-9,10-Dimethoxy-1,3,4,6,7,11b-hexahydro-3-isobutyl-2H-benzo[a]quinolizin-2-one
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  • Tetrabenazine Related Impurity 5
  • 3-isobutyl-9,10-dimethoxy-1,3,4,6,7,11b-hexahydropyrido[2,1-a]isoquinolin-2-one
  • 9,10-dimethoxy-3-(2-methylpropyl)-1,3,4,6,7,11b-hexahydropyrido[2,1-a]isoquinolin-2-one
  • 3-Isobutyl-9,10-diMethoxy-3,4,6,7-tetrahydro-1H-pyrido[2,1-a]isoquinolin-2(11bH)
  • (3R,11bR)-rel-
  • 3-Isobutyl-9,10-dimethoxy-1,3,4,6,7,11b-hexahydro-2H-benzo[a]quinolizin-2-one
  • 9,10-dimethoxy-3-isobutyl-1,3,4,6,7,11b-hexahydro-2H-pyrido[2,1-a]isoquinolin-2-one
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  • TETRABENAZINE
  • 2H-Benzo[a]quinolizin-2-one, 1,3,4,6,7,11b-hexahydro-9,10-dimethoxy-3-(2-methylpropyl)-, (3R,11bR)-rel-
  • 9,10-Dimethoxy-1,3,4,6,7,11b-hexahydro-3-isobutyl-2H-benzo[a]quinolizin-2-one
  • Tetrabenazine, 99%, a VMAT-inhibitor
  • TBZ,racemic mixture
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  • TETRABENAZINE ISO 9001：2015 REACH
  • TetrabenazineQ: What is Tetrabenazine Q: What is the CAS Number of Tetrabenazine Q: What is the storage condition of Tetrabenazine Q: What are the applications of Tetrabenazine
  • Butyl benzene that lamictal
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  • 58-46-8
  • 164106-49-8
  • Serotonin receptor
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  • Intermediates & Fine Chemicals
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  • 58-46-8