EthionamideAnti-tuberculosis antibiotic CAS# 536-33-4 |
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Quality Control & MSDS
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Chemical structure
3D structure
| Cas No. | 536-33-4 | SDF | Download SDF |
| PubChem ID | 2761171 | Appearance | Powder |
| Formula | C8H10N2S | M.Wt | 166.24 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | 2-ethylthioisonicotinamide | ||
| Solubility | DMSO : ≥ 100 mg/mL (601.54 mM) H2O : < 0.1 mg/mL (insoluble) *"≥" means soluble, but saturation unknown. | ||
| Chemical Name | 2-ethylpyridine-4-carbothioamide | ||
| SMILES | CCC1=NC=CC(=C1)C(=S)N | ||
| Standard InChIKey | AEOCXXJPGCBFJA-UHFFFAOYSA-N | ||
| Standard InChI | InChI=1S/C8H10N2S/c1-2-7-5-6(8(9)11)3-4-10-7/h3-5H,2H2,1H3,(H2,9,11) | ||
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Ethionamide(2-ethylthioisonicotinamide) is an antibiotic used in the treatment of tuberculosis.
Target: Antibacterial
Ethionamide is a second-line antitubercular agent that inhibits mycolic acid synthesis. It also may be used for treatment of leprosy. Ethionamide is a prodrug. It is activated by the enzyme EthA, a mono-oxygenase in Mycobacterium tuberculosis, and binds NAD+ to form an adduct which inhibits InhA in the same way as isoniazid. Expression of the ethA gene is controlled by EthR, a transcriptional repressor. It is understood that improving ethA expression will increase the efficacy of ethionamide and so EthR inhibitors are of great interest to co-drug developers. The action may be through disruption of mycolic acid [1, 2]. References: | |||||
Ethionamide Dilution Calculator
Ethionamide Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 6.0154 mL | 30.077 mL | 60.154 mL | 120.308 mL | 150.385 mL |
| 5 mM | 1.2031 mL | 6.0154 mL | 12.0308 mL | 24.0616 mL | 30.077 mL |
| 10 mM | 0.6015 mL | 3.0077 mL | 6.0154 mL | 12.0308 mL | 15.0385 mL |
| 50 mM | 0.1203 mL | 0.6015 mL | 1.2031 mL | 2.4062 mL | 3.0077 mL |
| 100 mM | 0.0602 mL | 0.3008 mL | 0.6015 mL | 1.2031 mL | 1.5038 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Ethionamide is part of a group of drugs used in the treatment of drug resistant TB called thioamides. It is used as part of treatment regimens, generally involving 5 medicines, to treat MDR and XDR TB.
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Fragment-Sized EthR Inhibitors Exhibit Exceptionally Strong Ethionamide Boosting Effect in Whole-Cell Mycobacterium tuberculosis Assays.[Pubmed:28314097]
ACS Chem Biol. 2017 May 19;12(5):1390-1396.
Small-molecule inhibitors of the mycobacterial transcriptional repressor EthR have previously been shown to act as boosters of the second-line antituberculosis drug Ethionamide. Fragment-based drug discovery approaches have been used in the past to make highly potent EthR inhibitors with Ethionamide boosting activity both in vitro and ex vivo. Herein, we report the development of fragment-sized EthR ligands with nanomolar minimum effective concentration values for boosting the Ethionamide activity in Mycobacterium tuberculosis whole-cell assays.
Preparation and biological evaluation of ethionamide-mesoporous silicon nanoparticles against Mycobacterium tuberculosis.[Pubmed:28057421]
Bioorg Med Chem Lett. 2017 Feb 1;27(3):403-405.
Ethionamide (ETH) is an important second-line antituberculosis drug used for the treatment of patients infected with multidrug-resistant Mycobacterium tuberculosis. Recently, we reported that the loading of ETH into thermally carbonized-porous silicon (TCPSi) nanoparticles enhanced the solubility and permeability of ETH at different pH-values and also increased its metabolization process. Based on these results, we synthesized carboxylic acid functionalized thermally hydrocarbonized porous silicon nanoparticles (UnTHCPSi NPs) conjugated with ETH and its antimicrobial effect was evaluated against Mycobacterium tuberculosis strain H37Rv. The activity of the conjugate was increased when compared to free-ETH, which suggests that the nature of the synergy between the NPs and ETH is likely due to the weakening of the bacterial cell wall that improves conjugate-penetration. These ETH-conjugated NPs have great potential in reducing dosing frequency of ETH in the treatment of multidrug-resistant tuberculosis (MDR-TB).
Investigation of isoniazid and ethionamide cross-resistance by whole genome sequencing and association with poor treatment outcomes of multidrug-resistant tuberculosis patients in South Africa.[Pubmed:28043598]
Int J Mycobacteriol. 2016 Dec;5 Suppl 1:S36-S37.
OBJECTIVE/BACKGROUND: Ethionamide (ETH) and isoniazid (INH) are part of the backbone regimen used for the treatment of multidrug-resistant tuberculosis (MDR-TB). Both ETH and INH are structurally similar and are activated by ethA and katG gene products. Resistance to INH among MDR-TB patients may cause ETH to be ineffective, as both target nicotinamide adenine dinucleotide-dependent enoyl-acyl carrier protein reductase inhA protein and mutations within inhA gene may lead to their cross-resistance. Furthermore, ETH resistance is caused by mutations within ethA and ethR genes forming part of the ETH drug activation pathway. Nicotinamide adenine dinucleotide is coded by the ndh gene, and its overexpresion may lead cross-resistance between INH and ETH drugs. Phenotypic drug susceptibility testing of ETH is difficult and often unreliable. We used whole genome sequencing to compare inhA, inhA promoter, ethA, ethR ndh, and katG genetic regions in serial isolates (baseline and follow-up) with treatment outcomes. METHODS: MDR-TB strains were collected from 46 patients before and during second-line drug treatment in KwaZulu-Natal and Eastern Cape between 2005 and 2009. All patients had phenotypically determined MDR-TB at baseline and had treatment outcomes documented. Unfavorable treatment outcomes were defined as death, default, and failure, while favorable outcomes were cure and treatment completion. Each strain had baseline and at least one strain collected on follow-up. From each strain, DNA was extracted from colonies grown on Lowenstein-Jensen slants, and fragment and jumping paired-end Illumina DNA libraries were constructed and sequenced on the Illumina HiSeq 2000 (Broad Institute, Cambridge, MA, USA). Sequences were aligned to H37Rv genome and Pilon was run to generate a list of SNPs. In silico spoligotyping was performed to a database 43 unique spacer sequences. Cross-resistance was defined as the presence of both inhA and either ethA or ethR mutations in clinical isolates. RESULTS: A total of 92 sequences from 46 serial isolates of MDR-TB patients from KwaZulu-Natal (29 isolates) and Eastern Cape (17 isolates) were analyzed. Most patients (29/46; 63.0%) had unfavorable outcomes, 13 (28.3%) had favorable outcomes, while four (8.7%) had unknown outcomes. Phylogenetic reconstruction revealed that primary genotype differed by province. The Beijing genotype was predominant in Eastern Cape, while EuroAmerican lineage (S, T, LAM, X) was found in KwaZulu-Natal. Whole genome analysis revealed nonsynonymous insertions and deletions within katG, ethA, ethR, ndh, and inhA and its promoter region. Among patients with treatment outcome data, mutations were detected in 92.8% in katG, 50% in inhA, 53.6% in ethA, 2.4% in ethR, and 19% in ndh. The majority of mutations causing ETH (20/29; 68.9%) and INH (18/29; 62.1%) resistance occurred among patients with unfavorable outcomes. Both inhA and either ethA or ethR mutations were detected in 16/29 (55.2%) patients with unfavorable outcomes. Cross-resistance of both INH and ETH drugs was associated with unfavorable treatment outcomes (p=0.021) in 16/29 (55.2%) patients compared with favorable treatment outcomes in 2/13 (15.4%) patients. CONCLUSION: Baseline ETH molecular resistance before second-line treatment is a concern. Unfavorable treatment outcomes of patients with ethA, ethR, and inhA mutations highlight the importance of genotypic testing before initiation of treatment containing ETH. The clinical significance of whole genome analysis for early detection of mutations predictive of treatment failure needs further investigation.
