Thiophanate-Methyl
(Synonyms: 甲基硫菌灵) 目录号 : GC34839
Thiophanate-Methyl是一种内吸性杀菌剂。
Cas No.:23564-05-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
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Cell experiment [1]: |
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Cell lines |
A549 human lung cancer cells |
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Preparation method |
A549 human lung cancer cells were treated with various concentrations (10−8, 10−7, 10−6, 10−5 and 10−4 M) of 17β-estradiol and G-1 in 96-well plates and incubated for 48 or 72 h. Following incubation, MTT solution (Sigma-Aldrich) was added to each well at a concentration of 0.5 mg/ml, and incubated for 4 h at 37°C. |
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Reaction Conditions |
0.01-100 μM for 48 and 72 h |
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Applications |
Treatment with G-1 (10−5 and 10−4 M) for 48 and 72 h significantly decreased cell proliferation. |
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Animal experiment [2]: |
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Animal models |
SJL mice (5–7 weeks old) |
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Preparation method |
SJL mice were immunized s.c. with 50 µg PLP139-151 and CFA (400 µg Mycobacterium tuberculosis). Mice were treated with 50 mg/kg/day G-1 daily for 21 days beginning at the day of disease induction. Control mice were similarly treated with vehicle (5% Dimethyl sulfoxide (DMSO), 95% Polyethylene glycol (PEG)-300. |
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50 mg/kg/day for 21 days |
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Applications |
G-1 administration significantly reduced the severity of actively induced experimental allergic encephalomyelitis (EAE) but not the incidence of disease. |
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[1]: Kurt A H, Çelik A, Kelleci B M. Oxidative/antioxidative enzyme-mediated antiproliferative and proapoptotic effects of the GPER1 agonist G-1 on lung cancer cells[J]. Oncology Letters, 2015, 10(5): 3177-3182. [2]: Blasko E, Haskell C A, Leung S, et al. Beneficial role of the GPR30 agonist G-1 in an animal model of multiple sclerosis[J]. Journal of neuroimmunology, 2009, 214(1-2): 67-77. |
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G-1 is a selective and potent agonist of GPR30 with EC50 value about 2 nM [1].
G-1 treatment (10−5 and 10−4 M) for 48 and 72 h significantly decreased A549 cell proliferation, at 72 h, the IC50 value for G-1 was calculated to be 2×10−5 M [2]. G-1 treatment at a concentration of 2×10−5 M had no significant effect on CAT activity but led to a significant increase in SOD activity, GPx activity and NO level [2]. G-1 inhibited TNF-α and IL-6 release on primary human macrophages derived from monocytes treated with GM-CSF over 6 days. The agonist inhibited the induction of both cytokines with IC50 values of 209 nM and 317 nM, respectively [3]. G-1 was also able to inhibit LPS induction of TNF-α in a mouse macrophage cell line, RAW 264.7 [3].
G-1 (50 mg/kg/day, 21 days) administration significantly reduced the severity of actively induced experimental allergic encephalomyelitis (EAE). G-1 treatment reduced the qualitative degree of inflammation in the lumbar spinal cord. G-1 treatment reduced the fraction of CNS-infiltrating macrophages (CD45hiCD11b+) in three individually analyzed mice [3]. G-1 could exert protective effects on motoneurons. The intraperitoneal injection of the GPR30 agonist G-1 for 14 days induces neuroprotective effects similar with the same dose of E2 [4].
References:
[1]. Bologa C G, Revankar C M, Young S M, et al. Virtual and biomolecular screening converge on a selective agonist for GPR30[J]. Nature chemical biology, 2006, 2(4): 207-212.
[2]. Kurt A H, Çelik A, Kelleci B M. Oxidative/antioxidative enzyme-mediated antiproliferative and proapoptotic effects of the GPER1 agonist G-1 on lung cancer cells[J]. Oncology Letters, 2015, 10(5): 3177-3182.
[3]. Blasko E, Haskell C A, Leung S, et al. Beneficial role of the GPR30 agonist G-1 in an animal model of multiple sclerosis[J]. Journal of neuroimmunology, 2009, 214(1-2): 67-77.
[4]. Cheng Q, Meng J, Wang X, et al. G-1 exerts neuroprotective effects through G protein-coupled estrogen receptor 1 following spinal cord injury in mice[J]. Bioscience Reports, 2016, 36(4).
| Cas No. | 23564-05-8 | SDF | |
| 别名 | 甲基硫菌灵 | ||
| Canonical SMILES | COC(NC(NC1=C(NC(NC(OC)=O)=S)C=CC=C1)=S)=O | ||
| 分子式 | C12H14N4O4S2 | 分子量 | 342.39 |
| 溶解度 | DMSO : 300 mg/mL (876.19 mM);Water : < 0.1 mg/mL (insoluble) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 2.9206 mL | 14.6032 mL | 29.2065 mL |
| 5 mM | 0.5841 mL | 2.9206 mL | 5.8413 mL |
| 10 mM | 0.2921 mL | 1.4603 mL | 2.9206 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Thiophanate-Methyl induces severe hepatotoxicity in zebrafish
Chemosphere 2020 Jun;248:125941.PMID:32004883DOI:10.1016/j.chemosphere.2020.125941.
Thiophanate-Methyl (TM) is widely used all over the world and is a typical example of pesticide residues, which can be detected in the soil, and even in vegetables and fruits. However, the molecular mechanisms underlying the hepatotoxicity of TM are not well understood. In this study, we utilized zebrafish to comprehensively evaluate the hepatotoxicity of TM and explore how the molecular mechanisms of hepatotoxicity are induced. The zebrafish larvae were exposed in 6.25, 12.5 and 25 mg/L TM from 72 to 144 hpf, while the adults were exposed in 2, 4 and 6 mg/L TM for 28 days. Here, we found that 12.5 and 25 mg/L TM induces specifically serious hepatotoxicity but not the toxicity of other organs in zebrafish larvae and adults. Moreover, it might triggered hepatotoxicity by activating the caspase-3 through apoptotic pathways and oxidative stress in zebrafish. Subsequently, this resulted in a metabolic imbalance in the zebrafish's liver. In conclusion, our results disclosed the fact that TM may induce severe hepatotoxicity by mediating activation of caspase-3 and oxidative stress in zebrafish.
Molecular Diagnosis of Thiophanate-Methyl-Resistant Strains of Fusarium fujikuroi in Japan
Plant Dis 2022 Feb;106(2):634-640.PMID:34494869DOI:10.1094/PDIS-07-21-1501-RE.
Fusarium fujikuroi is the pathogen of rice bakanae disease and is subclassified into gibberellin and fumonisin groups (G and F groups). Thiophanate-Methyl (TM), a benzimidazole fungicide, has been used extensively to control F. fujikuroi. Previous investigation showed that F-group strains are TM sensitive (TMS), whereas most G-group strains are TM resistant (TMR) in Japan. The minimum inhibitory concentration in TMS strains was 1 to 10 μg ml-1, whereas that in TMR strains was >100 μg ml-1. E198K and F200Y mutations in β2-tubulin were detected in TMR strains. A loop-mediated isothermal amplification-fluorescent loop primer method was developed for diagnosis of these mutations and applied to 37 TMR strains and 56 TMS strains. The results indicated that 100% of TMR strains were identified as having either the E198K mutation (41%) or the F200Y mutation (59%), whereas none of the TMS strains tested showed either mutation. We found one remarkable TMR strain in the F group that had an F200Y mutation. These results suggest that E198K and F200Y mutations in β2-tubulin contribute to TM resistance in F. fujikuroi.
Peer review of the pesticide risk assessment of the active substance Thiophanate-Methyl
EFSA J 2018 Jan 17;16(1):e05133.PMID:32625680DOI:10.2903/j.efsa.2018.5133.
The conclusions of the EFSA following the peer review of the initial risk assessments carried out by the competent authorities of the rapporteur Member State, Sweden, and co-rapporteur Member State, Finland, for the pesticide active substance Thiophanate-Methyl are reported. The context of the peer review was that required by Commission Implementing Regulation (EU) No 844/2012. The conclusions were reached on the basis of the evaluation of the representative uses of Thiophanate-Methyl as a fungicide on wine grapes, tomato, aubergine, leek, fresh beans with pods and wheat (winter and durum). The reliable endpoints, appropriate for use in regulatory risk assessment, are presented. Missing information identified as being required by the regulatory framework is listed. Concerns are identified.
Substrate sterilization with Thiophanate-Methyl and its biodegradation to carbendazim in oyster mushroom (Pleurotus ostreatus var. florida)
Environ Sci Pollut Res Int 2020 Jan;27(1):899-906.PMID:31820249DOI:10.1007/s11356-019-07050-5.
Residue analysis to detect Thiophanate-Methyl and its primary metabolite (carbendazim) during oyster mushroom (Pleurotus ostreatus var. florida) cultivation was done for two consecutive years 2017 and 2018. Wheat straw substrate was chemically treated with different treatments of thiophate-methyl, viz, Thiophanate-Methyl 30 ppm + formalin 500 ppm (T1), Thiophanate-Methyl 40 ppm + formalin 500 ppm (T2), Thiophanate-Methyl 50 ppm + formalin 500 ppm (T3), Thiophanate-Methyl 60 ppm + formalin 500 ppm (T4), and formalin 500 ppm (T5 as control and recommended concentration), and utilized for cultivation of oyster mushroom. Treatments T3 and T4 exhibited significant difference in pH levels during both the trials. Minimum spawn run, pinhead formation, and fruit body formation time were recorded in treatments T3 and T4. Significantly higher biological efficiency (%) was recorded in treatments T3 and T4 as compared with all other treatments. No incidence of competitor molds was recorded in T3 and T4. Pesticide residue analysis for detection of Thiophanate-Methyl and its metabolite (carbendazim) was done in the fruit body produced in T3 and T4 treatments using liquid chromatography with tandem mass spectrometry method. No residue of Thiophanate-Methyl and carbendazim was detected at 50 ppm concentration of Thiophanate-Methyl during both the trials. However, in trial II, residue of carbendazim (5.39 μg/kg) was detected at 60 ppm. Based on the findings of the trials I and II, T3 (Thiophanate-Methyl 50 ppm + formalin 500 ppm) may be utilized for substrate sterilization for oyster mushroom cultivation and Pleurotus ostreatus var. florida could be recognized as microorganism which could play a role in degradation of Thiophanate-Methyl.
Hormetic Effects of Thiophanate-Methyl in Multiple Isolates of Sclerotinia homoeocarpa
Plant Dis 2019 Jan;103(1):89-94.PMID:30398944DOI:10.1094/PDIS-05-18-0872-RE.
Twenty-eight isolates of Sclerotinia homoeocarpa, causal agent of dollar spot disease in turf, were assessed for fungicide hormesis at sublethal concentrations of Thiophanate-Methyl (T-methyl). Each isolate was grown in corn meal agar amended with 11 concentrations of T-methyl (30,500 to 0.047 µg/liter), and the area of mycelial growth was determined relative to the control. Three replicates were used per concentration, and the experiment was repeated three to five times for each isolate. Reference isolates (EC50 > 20 µg/liter), with no prior history of T-methyl exposure, were highly sensitive and not stimulated by low doses. Likewise, no stimulation was observed in two highly sensitive isolates (EC50 > 30 µg/liter) that had been preconditioned by exposure to T-methyl, or in four T-methyl-tolerant isolates. Seventeen (81%) preconditioned T-methyl-tolerant isolates (EC50 = 294 to1,550 µg/liter) had statistically significant growth stimulation, in the range of 2.8 to 19.7% relative to the control. These results support that hormesis (low-dose stimulation, high-dose inhibition) is a common dose response in preconditioned S. homoeocarpa, particularly in response to subtoxic doses of T-methyl.