3,4,5-Trimethoxybenzoic acid (Eudesmic acid)
(Synonyms: 3,4,5-三甲氧基苯甲酸,Eudesmic acid; Trimethylgallic Acid) 目录号 : GC33623
An active metabolite of trimebutine
Cas No.:118-41-2
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
3,4,5-Trimethoxybenzoic acid (TMBA) is an active metabolite of the opioid receptor agonist and prokinetic agent trimebutine .1 It is active against S. aureus (MIC = 0.97 ?g/ml).2
1.Wang, H., Zhou, H., Horimoto, S., et al.Quantitative determination of trimebutine maleate and its three metabolites in human plasma by liquid chromatography-tandem mass spectrometryJ. Chromatogr. B Analyt. Technol. Biomed. Life Sci.779(2)173-187(2002) 2.Bisignano, G., Sanogo, R., Marino, A., et al.Antimicrobial activity of Mitracarpus scaber extract and isolated constituentsLett. Appl. Microbiol.30(2)105-108(2000)
| Cas No. | 118-41-2 | SDF | |
| 别名 | 3,4,5-三甲氧基苯甲酸,Eudesmic acid; Trimethylgallic Acid | ||
| Canonical SMILES | O=C(O)C1=CC(OC)=C(OC)C(OC)=C1 | ||
| 分子式 | C10H12O5 | 分子量 | 212.2 |
| 溶解度 | DMSO: 100 mg/mL (471.25 mM); Water: 1 mg/mL (4.71 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 | 4.7125 mL | 23.5627 mL | 47.1254 mL |
| 5 mM | 0.9425 mL | 4.7125 mL | 9.4251 mL |
| 10 mM | 0.4713 mL | 2.3563 mL | 4.7125 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。
3,4,5-Trimethoxybenzoic acid, a new mescaline metabolite in humans
Drug Metab Dispos 1978 Sep-Oct;6(5):507-9.PMID:30599doi
After ingestion of 400 mg of mescaline sulfate by human volunteers, 3,4,5-Trimethoxybenzoic acid was isolated from urine and identified by gas chromatography-mass spectrometry. The amount of this anionic mescaline metabolite was found to be very low as compared with that of the well-konwn 3,4,5-trimethoxyphenylacetic acid. The significance of this finding is discussed.
A role for the Val291 residue within the transmembrane domain 2 in diltiazem- and TMB-8 [3,4,5-Trimethoxybenzoic acid 8-(diethylamino)octyl ester]-mediated 5-hydroxytryptamine type 3A receptor regulations
Biol Pharm Bull 2009 May;32(5):861-7.PMID:19420755DOI:10.1248/bpb.32.861.
Previous reports have shown that diltiazem and TMB, calcium channel antagonists, inhibit 5-hydroxytryptamine type 3A (5-HT(3A)) receptor-mediated currents (I(5-HT)) in cell lines and in heterologously expressed Xenopus oocytes. In the present study, we sought to elucidate the molecular mechanisms underlying diltiazem- and TMB-induced 5-HT(3A) receptor regulations. We used the two-microelectrode voltage clamp technique to investigate the effect of diltiazem and TMB on 5-HT-mediated ion currents in Xenopus oocytes expressing wild-type or 5-HT(3A) receptors harboring mutations in the gating pore region of transmembrane domain 2 (TM2). In oocytes expressing wild-type 5-HT(3A) receptors, diltiazem and TMB dose-dependently inhibited peak I(5-HT) with an IC(50) of 71.4+/-4.9 and 4.5+/-0.3 microM, respectively. Among various mutants of TM2, mutation V291A greatly attenuated and abolished the TMB- and diltiazem-induced inhibition of peak I(5-HT), respectively. Mutation V291A also induced constitutively active ion currents in the absence of 5-HT. Diltiazem and TMB inhibited constitutively active ion currents in a dose-dependent manner. The IC(50) values of constitutively active ion currents in V291A receptors were 165.3+/-11.1 and 6.6+/-0.5 microM for diltiazem and 3,4,5-Trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8), respectively. Results of site-directed mutagenesis experiments suggest that the Val291 residue could be a candidate for common interaction site for diltiazem- and TMB-8-mediated 5-HT(3A) receptor regulations.
Characterization of interaction of 3,4,5-Trimethoxybenzoic acid 8-(diethylamino)octyl ester with Torpedo californica nicotinic acetylcholine receptor and 5-hydroxytryptamine3 receptor
J Pharmacol Exp Ther 1999 Jul;290(1):129-35.PMID:10381768doi
The widely used calcium channel antagonist 3,4,5-Trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8) has been identified as a noncompetitive antagonist (NCA) and open-channel blocker of both muscle- and neuronal-type nicotinic acetylcholine receptors (AChRs). To further examine the interaction of TMB-8 with the AChR, the compound was tested as a competitor for the binding of two NCAs of the Torpedo californica AChR, phencyclidine and 3-trifluoromethyl-3-(m[125I]iodophenyl)diazirine, for which the binding to the AChR has been pharmacologically well characterized and a channel binding loci has been established. TMB-8 fully inhibited specific photoincorporation of 3-trifluoromethyl-3-(m[125I]iodophenyl)diazirine into the resting AChR channel (IC50 = 3.1 microM) and inhibited high-affinity [3H]phencyclidine binding to the desensitized AChR (IC50 = 2.4 microM). We conclude that TMB-8 is a potent NCA of the nicotinic AChR, interacting with the resting, open-channel, and desensitized channel conformations. TMB-8 was next tested as an inhibitor of the structurally homologous 5-hydroxytryptamine (5-HT)3 receptor (5-HT3R). Using 5-HT3R containing Sf21 cell membranes, TMB-8 completely inhibited specific binding of the radiolabeled 5-HT3R antagonist [3H]GR65630 (Ki = 2.5 microM). Furthermore, TMB-8 antagonized 5-HT-evoked currents of both mouse and human 5-HT3Rs expressed in Xenopus laevis oocytes, and additional analysis was consistent with a competitive antagonistic mechanism of action. These results, taken together, indicate that TMB-8 antagonizes the function of the AChR and 5-HT3R by different mechanisms. Given the sequence similarity and emerging evidence of structural homology in the channels of these two receptors, these results underscore the existence of subtle yet important structural differences in each channel.
The "calcium antagonist" TMB-8 [3,4,5-Trimethoxybenzoic acid 8-(diethylamino)octyl ester] is a potent, non-competitive, functional antagonist at diverse nicotinic acetylcholine receptor subtypes
J Pharmacol Exp Ther 1995 Dec;275(3):1418-26.PMID:8531111doi
[3,4,5-Trimethoxybenzoic acid 8-(diethylamino)octyl ester] (TMB-8) has seen wide use as an "intracellular Ca2+ antagonist." However, this study shows that TMB-8 acts as a noncompetitive, functional antagonist at diverse nicotinic acetylcholine receptor (nAChR) subtypes with potencies that exceed those for other reported effects of TMB-8, including inhibition of intracellular Ca2+ mobilization. TMB-8 is a potent inhibitor (IC50 approximately 400 nM) of agonist-stimulated ion flux mediated by functional human muscle nAChR or ganglionic alpha 3 beta 4-nAChR subtypes expressed by TE671/RD or SH-SY5Y cells. TMB-8 is also a potent inhibitor (IC50 approximately 500 nM) of a functional, central nervous system nAChR subtype that mediates nicotinic agonist-stimulated [3H]dopamine release from rat brain synaptosomes. TMB-8 is much less potent (IC50 approximately 30-200 microM) as an inhibitor of high-affinity 3H-labeled acetylcholine or 125I-labeled alpha-bungarotoxin binding to human muscle nAChR, ganglionic alpha 3 beta 4-nAChR, or ganglionic alpha 7-nAChR subtypes. Moreover, functional inhibition by TMB-8 of muscle-type nAChR is due to a reduction in agonist efficacy, but not potency, and is proportionately stronger with increasing agonist concentration, thereby suggesting that TMB-8 acts as a noncompetitive inhibitor. Similar effects are observed for local anesthetics such as tetracaine and procaine (functional IC50 values of approximately 5 and approximately 50 microM, respectively), although TMB-8 is the most potent of these agents. Studies with TMB-8 or BAPTA [1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid] analogues indicate that the amino group of TMB-8 is essential and that Ca2+ chelation is not required for inhibition of nAChR function.(ABSTRACT TRUNCATED AT 250 WORDS)
Spectroscopic studies on the interaction between 3,4,5-Trimethoxybenzoic acid and bovine serum albumin
Spectrochim Acta A Mol Biomol Spectrosc 2006 Nov;65(3-4):988-92.PMID:16679051DOI:10.1016/j.saa.2006.02.004.
The interaction between 3,4,5-Trimethoxybenzoic acid (TMBA) and bovine serum albumin (BSA) was studied by fluorescence and UV-vis absorption spectroscopy. In the mechanism discussion, it was proved that the fluorescence quenching of BSA by TMBA is a result of the formation of TMBA-BSA complex. Quenching constants were determined using the Stern-Volmer equation to provide a measure of the binding affinity between TMBA and BSA. The thermodynamic parameters DeltaH, DeltaG, DeltaS at different temperatures were calculated, and electrostatic interactions play an important role to stabilize the complex. The distance r between donor (BSA) and acceptor (TMBA) was obtained according to fluorescence resonance energy transfer (FRET).