Anethole trithione
(Synonyms: 茴三硫) 目录号 : GC33001
A dithiolthione with diverse biological activities
Cas No.:532-11-6
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
Anethole trithione is a dithiolthione with diverse biological activities.1,2,3,4 It selectively binds to α-adrenergic receptors (α-ARs) over β-ARs and muscarinic acetylcholine receptors (mAChRs) in isolated rat parotid acini (IC50s = 16.7, >100, and >100 ?M, respectively).1 Anethole trithione enhances saliva secretion induced by the mAChR agonist pilocarpine or electrical stimulation of the parasympathetic nerve in rats.2 It reduces tumor incidence and multiplicity in a rat model of azoxymethane-induced colon adenocarcinoma when administered in the diet at 100 and 200 ppm.3 Anethole trithione (500 mg/kg) prevents decreases in hepatic glutathione (GSH) levels and decreases mortality in mouse models of hepatotoxicity induced by acetaminophen or carbon tetrachloride.4 Formulations containing anethole trithione have been used in the treatment of dry mouth.
1.Glenert, U.Acute effects of a possible sialogogue, anethole trithione, in rat parotid glandsEur. J. Pharmacol.209(4)287-295(1991) 2.Ukai, Y., Taniguchi, N., Takeshita, K., et al.Chronic anethole trithione treatment enhances the salivary secretion and increases the muscarinic acetylcholine receptors in the rat submaxillary glandArch. Int. Pharmacodyn. Ther.271(2)206-212(1984) 3.Reddy, B.S., Rao, C.V., Rivenson, A., et al.Chemoprevention of colon carcinogenesis by organosulfur compoundsCancer Res.53(15)3493-3498(1993) 4.Ansher, S.S., Dolan, P., and Bueding, E.Chemoprotective effects of two dithiolthiones and of butylhydroxyanisole against carbon tetrachloride and acetaminophen toxicityHepatology3(6)932-935(1983)
| Cas No. | 532-11-6 | SDF | |
| 别名 | 茴三硫 | ||
| Canonical SMILES | S=C1SSC(C2=CC=C(OC)C=C2)=C1 | ||
| 分子式 | C10H8OS3 | 分子量 | 240.36 |
| 溶解度 | DMSO : ≥ 43 mg/mL (178.90 mM) | 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 | 4.1604 mL | 20.8021 mL | 41.6043 mL |
| 5 mM | 0.8321 mL | 4.1604 mL | 8.3209 mL |
| 10 mM | 0.416 mL | 2.0802 mL | 4.1604 mL |
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| 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 |
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| % DMSO % % Tween 80 % saline | ||||||||||
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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。
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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。
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Activation of UCP2 by Anethole trithione suppresses neuroinflammation after intracerebral hemorrhage
Acta Pharmacol Sin 2022 Apr;43(4):811-828.PMID:34183754DOI:10.1038/s41401-021-00698-1.
Intracerebral hemorrhage (ICH) is a devastating disease, in which neuroinflammation substantially contributes to brain injury. Uncoupling protein 2 (UCP2) is a member of the mitochondrial anion carrier family, which uncouples oxidative phosphorylation from ATP synthesis by facilitating proton leak across the mitochondrial inner membrane. UCP2 has been reported to modulate inflammation. In this study we investigated whether and how UCP2 modulated neuroinflammation through microglia/macrophages following ICH in vitro and in vivo. We used an in vitro neuroinflammation model in murine BV2 microglia to mimic microglial activation following ICH. ICH in vivo model was established in mice through collagenase infusion into the left striatum. ICH mice were treated with anetholetrithione (ADT, 50 mg· kg-1 ·d-1, ip) or the classical protonophoric uncoupler FCCP (injected into hemorrhagic striatum). We showed that the expression and mitochondrial location of microglial UCP2 were not changed in both in vitro and in vivo ICH models. Knockdown of UCP2 exacerbated neuroinflammation in BV2 microglia and mouse ICH models, suggesting that endogenous UCP2 inhibited neuroinflammation and therefore played a protective role following ICH. ADT enhanced mitochondrial ROS production thus inducing mitochondrial uncoupling and activating UCP2 in microglia. ADT robustly suppressed neuroinflammation, attenuated brain edema and improved neurological deficits following ICH, and these effects were countered by striatal knockdown of UCP2. ADT enhanced AMP-activated protein kinase (AMPK) activation in the hemorrhagic brain, which was abrogated by striatal knockdown of UCP2. Moreover, striatal knockdown of AMPK abolished the suppression of neuroinflammation by ADT following ICH. On the other hand, FCCP-induced mitochondrial uncoupling was independent of UCP2 in microglia; and striatal knockdown of UCP2 did not abrogate the suppression of neuroinflammation by FCCP in ICH mice. In conclusion, the uncoupling activity is essential for suppression of neuroinflammation by UCP2. We prove for the first time the concept that activators of endogenous UCP2 such as anetholetrithione are a new class of uncouplers with translational significance.
Chronic Anethole trithione treatment enhances the salivary secretion and increases the muscarinic acetylcholine receptors in the rat submaxillary gland
Arch Int Pharmacodyn Ther 1984 Oct;271(2):206-12.PMID:6508432doi
Chronic treatment with trithio-p-methoxyphenylpropene (Anethole trithione; ANTT) increased the salivary secretion from the rat submaxillary gland induced by electrical stimulation of the parasympathetic nerve and by injection of pilocarpine. In parallel with the enhancement of the salivary secretion, the number of the muscarinic acetylcholine receptors was significantly increased. The increased number of receptors may be involved in the enhancement of the salivary secretion by ANTT treatment.
Design, synthesis, and pharmacological evaluation of the aqueous prodrugs of desmethyl Anethole trithione with hepatoprotective activity
Eur J Med Chem 2010 Jul;45(7):3005-10.PMID:20392547DOI:10.1016/j.ejmech.2010.03.029.
A metabolite-based prodrug strategy to increase the solubility of Anethole trithione was reported to facilitate the clinical application of this hepatoprotective agent. Water-soluble analogs of Anethole trithione were synthesized via substituting the methyl group of Anethole trithione with the simple hydrophilic alkylamino group, and subjected to physiochemical, pharmacological and metabolic studies. The prodrugs displayed increased solubility as well as other physiochemical properties favorable for parenteral use. Among the analogs synthesized, the compound 5a exhibited best hepatoprotective activity at the dose of 2.0 mg/kg in mice equal to that of Anethole trithione. The in vivo metabolic investigation demonstrated that the straight-side chain prodrug 5a could convert to desmethyl Anethole trithione in vivo, while the ring-side chain prodrug 5d could not. The hepatoprotective activity of the prodrugs might result from the active metabolite desmethyl Anethole trithione.
HPLC determination of Anethole trithione and its application to pharmacokinetics in rabbits
J Pharm Biomed Anal 2006 Nov 16;42(5):613-7.PMID:16824723DOI:10.1016/j.jpba.2006.05.013.
To evaluate the relative bioavailability of Anethole trithione (ATT) from self-microemulsifying drug delivery system (SMEDDS) and tablet, a sensitive, accurate and reliable liquid chromatography method was developed and validated to determine ATT in rabbit plasma. Chromatographic separation was performed on a Diamonsil C18 column by using a mixture of methanol-water (90:10, v/v) delivered at a flow rate of 1.0 ml/min. The wavelength was set at 348 nm and mifepristone was used as the internal standard. A linear relationship for ATT was found in the range of 0.5-32 ng/ml. The mean extraction recoveries of ATT determined over three concentrations were 84.7+/-5.8, 92.3+/-3.4 and 89.9+/-5.1%. After administration of SMEDDS and tablets to rabbits, significant differences were found in main pharmacokinetic parameters of Tmax, Cmax and AUC(0-infinity) between these two formulations, and a 2.5-fold enhancement of relative bioavailability of ATT was observed from the SMEDDS compared with tablets.
Chemopreventive efficacy of Anethole trithione, N-acetyl-L-cysteine, miconazole and phenethylisothiocyanate in the DMBA-induced rat mammary cancer model
Int J Cancer 1997 Jul 3;72(1):95-101.PMID:9212229DOI:10.1002/(sici)1097-0215(19970703)72:1<95::aid-ijc14>3.0.co;2-9.
The chemopreventive efficacy of N-acetyl-L-cysteine (NAC), Anethole trithione, miconazole and phenethylisothiocyanate (PEITC), each of which would be expected to alter carcinogen metabolism, was examined in the dimethylbenzanthracene (DMBA) mammary carcinogenesis model. In this protocol, animals were exposed to non-toxic doses of the chemopreventives in the diet beginning 7 days prior to DMBA administration and then continuously throughout the duration of the assay (100 days post carcinogen). Miconazole, an antifungal agent with relatively broad inhibitory activity toward a variety of cytochromes P450, increased mammary tumor latency, decreased tumor incidence at the highest dose and decreased tumor multiplicity up to 60%. Anethole trithione, a substituted dithiolthione and an analog of the relatively broad-spectrum chemopreventive oltipraz, was administered in the diet and significantly inhibited mammary cancer multiplicity but not cancer incidence. NAC, an antimucolytic agent, failed to inhibit DMBA-induced mammary tumorigenesis. Surprisingly, treatment with DMBA plus PEITC, a potent inhibitor of cytochrome P450 2E1, actually increased the multiplicity of tumors relative to that observed with DMBA alone.