Parbendazole - CAS 14255-87-9
Catalog number:
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Certificate of Analysis-Parbendazole 14255-87-9 B15W0630  
Parbendazole, a benzimidazole carbamat used as an antinematodal agent, is a potent inhibitor of microtubule assembly and functions.
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B0084-485433 500 mg $499 In stock
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White solid
methyl N-(6-butyl-1H-benzimidazol-2-yl)carbamate; N-(6-Butyl-1H-benzimidazol-2-yl)carbamic Acid Methyl Ester; 5-Butyl-2-(carbomethoxyamino)benzimidazole; Helatac; Helmatac; Methyl (5-butyl-1H-benzimidazol-2-yl)carbamate; Methyl 5(6)-butyl-2-benzimidazolecarbamate; Methyl 5-butylbenzimidazole-2-carbamate; PBZ; PBZ (fungicide); Parbendazole; SKF 29044
Soluble in DMSO
Store in a cool and dry place and at 0 - 4℃ for short term (days to weeks) or -42℃ for long term (months to years).
Boiling Point:
1.234±0.06 g/cm3 Temp: 20 °C Press: 760 Torr
Melting Point:
>220°C (dec.)
Canonical SMILES:
1.Microtubule disruption synergizes with oncolytic virotherapy by inhibiting interferon translation and potentiating bystander killing.
Arulanandam R1, Batenchuk C1, Varette O1, Zakaria C2, Garcia V1, Forbes NE1, Davis C1, Krishnan R1, Karmacharya R1, Cox J1, Sinha A1, Babawy A1, Waite K1, Weinstein E1, Falls T1, Chen A1, Hamill J1, De Silva N1, Conrad DP1, Atkins H1, Garson K1, Ilkow C1, Nat Commun. 2015 Mar 30;6:6410. doi: 10.1038/ncomms7410.
In this study, we show that several microtubule-destabilizing agents used for decades for treatment of cancer and other diseases also sensitize cancer cells to oncolytic rhabdoviruses and improve therapeutic outcomes in resistant murine cancer models. Drug-induced microtubule destabilization leads to superior viral spread in cancer cells by disrupting type I IFN mRNA translation, leading to decreased IFN protein expression and secretion. Furthermore, microtubule-destabilizing agents specifically promote cancer cell death following stimulation by a subset of infection-induced cytokines, thereby increasing viral bystander effects. This study reveals a previously unappreciated role for microtubule structures in the regulation of the innate cellular antiviral response and demonstrates that unexpected combinations of approved chemotherapeutics and biological agents can lead to improved therapeutic outcomes.
2.Oral pharmacological treatments for parasitic diseases of rainbow trout Oncorhynchus mykiss. I: Hexamita salmonis.
Tojo JL1, Santamarina MT. Dis Aquat Organ. 1998 May 14;33(1):51-6.
Various drugs were evaluated as regards efficacy for the treatment of Hexamita salmonis infection in rainbow trout. The results confirm the efficacy of nitroimidazoles: infection was completely eradicated not only by metronidazole (which has been recommended previously for the treatment of hexamitosis), but also by benznidazole, ronidazole and secnidazole, which have not been assayed previously. The non-nitroimidazoles albendazole, aminosidine, diethylcarbamazine and nitroscanate also completely eliminated infection. The remaining non-nitroimidazoles tested (amprolium, bithionol, febantel, flubendazole, levamisole, netobimin, niclosamide, nitroxynil, oxibendazole, parbendazole, piperazine, praziquentel, tetramisole, thiophanate, toltrazuril, trichlorfon and triclabendazole) were not effective.
3.Albendazole resistance in Giardia is correlated with cytoskeletal changes but not with a mutation at amino acid 200 in beta-tubulin.
Upcroft J1, Mitchell R, Chen N, Upcroft P. Microb Drug Resist. 1996 Fall;2(3):303-8.
Albendazole resistance was induced in three different Giardia cultures following growth in successively increasing amounts of drug. One of the lines was previously resistant to high levels of metronidazole and was able to grow in 2 microM albendazole. The other two survived exposure to 0.8 microM, while normally lethal levels of albendazole against Giardia in vitro were around 0.1-0.2 microM. Albendazole-resistant Giardia were cross-resistant to parbendazole. Major chromosome rearrangements were evident in the line resistant to 2 microM albendazole and IFA with antitubulin antibody indicated differences in the cytoskeleton, particularly the median body, between sensitive and resistant lines. This implicates the cytoskeleton in the mechanism of resistance. Substitution of Tyr for Phe is a consistent beta-tubulin amino acid change in the benzimidazole-resistant helminths and fungi so far analyzed. PCR primers were designed from the published Giardia beta-tubulin gene sequence and spanned the region encoding Phe at position 200.
4.A new in vitro assay of benzimidazole activity against adult Oesophagostomum dentatum.
Petersen MB1, Friis C, Bjørn H. Int J Parasitol. 1997 Nov;27(11):1333-9.
A new in vitro assay of benzimidazole activity against adult Oesophagostomum dentatum is described. The method is based on the ability of O. dentatum to migrate through polyamide nets after exposure to various concentrations of benzimidazole. To determine an appropriate mesh size, control worms and worms exposed to 10 microM oxfendazole for 24 h were allowed to migrate through nets with various mesh sizes (300-500 microns) for up to 1 h. A mesh size of 350 microns and migration periods of 10, 20 and 30 min were selected. Exposure to oxfendazole at 10 microM for 24, 48 and 72 h inhibited the migration in a time-dependent manner. After 72 h of exposure and with a 20-min migration period, the EC50 of oxfendazole for O. dentatum was 0.564 microM. In further studies the activities of albendazole sulphoxide, albendazole, cambendazole, fenbendazole, flubendazole, luxabendazole, mebendazole, oxfendazole, oxibendazole, parbendazole and thiabendazole were compared.
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CAS 14255-87-9 Parbendazole

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