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Lactisole Sale

(Synonyms: 2-(4-甲氧基苯氧基)丙酸,na-PMP) 目录号 : GC44024

A sweet taste receptor antagonist

Lactisole Chemical Structure

Cas No.:150436-68-3

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产品描述

Lactisole is an antagonist of sweet taste receptors, reducing both sweetness intensity and persistence. [1][2] It blocks the activation of the sweet taste receptor T1R3 by natural and synthetic sweeteners and increases the inhibition of T1R2 by umami compounds. [3][4] Lactisole can be used to explore the roles of these receptors in diverse pathways, including glucose-induced insulin secretion in pancreatic β-cells and the secretion of glucagon-like peptides by enteroendocrine L-cells. [3][5][6]

Reference:
[1]. Johnson, C., Birch, G.G., and MacDougall, D.B. The effect of the sweetness inhibitor 2(-4-methoxyphenoxy)propanoic acid (sodium salt) (Na-PMP) on the taste of bitter-sweet stimuli. Chem.Senses 19(4), 348-358 (1994).
[2]. Schiffman, S.S., Booth, B.J., Sattely-Miller, E.A., et al. Selective inhibition of sweetness by the sodium salt of ±2-(4-methoxyphenoxy)propanoic acid. Chem.Senses 24(4), 439-447 (1999).
[3]. Hamano, K., Nakagawa, Y., Ohtsu, Y., et al. Lactisole inhibits the glucose-sensing receptor T1R3 expressed in mouse pancreatic β-cells. Journal of Endocrinology 226(1), 57-66 (2015).
[4]. Shim, J., Son, H.J., Kim, Y., et al. Modulation of sweet taste by umami compounds via sweet taste receptor subunit hT1R2. PLoS One 10(4), (2015).
[5]. Ohtsu, Y., Nakagawa, Y., Nagasawa, M., et al. Diverse signaling systems activated by the sweet taste receptor in human GLP-1-secreting cells. Molecular and Cellular Endocrinology 394(1-2), 70-79 (2014).
[6]. Sato, S., Hokari, R., Kurihara, C., et al. Dietary lipids and sweeteners regulate glucagon-like peptide-2 secretion. Am. J. Physiol Gastrointest. Liver Physiol. 304(8), 304-308 (2013).

Chemical Properties

Cas No. 150436-68-3 SDF
别名 2-(4-甲氧基苯氧基)丙酸,na-PMP
化学名 2-(4-methoxyphenoxy)-propanoic acid, monosodium salt
Canonical SMILES COC1=CC=C(OC(C)C([O-])=O)C=C1.[Na+]
分子式 C10H11O4•Na 分子量 218.2
溶解度 10mg/mL in DMSO,20mg/mL in DMF, 1mg/mL in Ethanol 储存条件 Store at -20°C
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1 mM 4.583 mL 22.9148 mL 45.8295 mL
5 mM 0.9166 mL 4.583 mL 9.1659 mL
10 mM 0.4583 mL 2.2915 mL 4.583 mL
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Research Update

Impact of Lactisole on the time-intensity profile of selected sweeteners in dependence of the binding site

Food Chem X 2022 Sep 16;15:100446.PMID:36211761DOI:10.1016/j.fochx.2022.100446.

Currently, there is limited insight into the influence of the different binding sites of agonists and antagonists of the sweet taste receptor TAS1R2/TAS1R3 on temporal sensory properties of sweet tasting compounds. We investigated whether the binding site and a competitive or allosteric inhibition of TAS1R2/TAS1R3 influence the time-dependent sensory perception and in vitro TAS1R2/TAS1R3-activation profiles. We compared time-intensity ratings of cyclamate, NHDC, acesulfame K, and aspartame with and without Lactisole with the corresponding TAS1R2/TAS1R3-activation in transfected HEK293 cells. In combination with Lactisole, cyclamate and NHDC demonstrated a shift of the dose-response curve corresponding to a competitive inhibition by Lactisole in the sensory and the cell experiments. Allosteric inhibition by Lactisole for aspartame and acesulfame K was seen in the cell experiments, but not the sensory ratings. In conclusion, the data do not support a major impact of the binding site on the time-intensity profile of the tested sweeteners.

Lactisole inhibits the glucose-sensing receptor T1R3 expressed in mouse pancreatic β-cells

J Endocrinol 2015 Jul;226(1):57-66.PMID:25994004DOI:10.1530/JOE-15-0102.

Glucose activates the glucose-sensing receptor T1R3 and facilitates its own metabolism in pancreatic β-cells. An inhibitor of this receptor would be helpful in elucidating the physiological function of the glucose-sensing receptor. The present study was conducted to examine whether or not Lactisole can be used as an inhibitor of the glucose-sensing receptor. In MIN6 cells, in a dose-dependent manner, Lactisole inhibited insulin secretion induced by sweeteners, acesulfame-K, sucralose and glycyrrhizin. The IC50 was ∼4 mmol/l. Lactisole attenuated the elevation of cytoplasmic Ca2+ concentration ([Ca2+]c) evoked by sucralose and acesulfame-K but did not affect the elevation of intracellular cAMP concentration ([cAMP]c) induced by these sweeteners. Lactisole also inhibited the action of glucose in MIN6 cells. Thus, Lactisole significantly reduced elevations of intracellular [NADH] and intracellular [ATP] induced by glucose, and also inhibited glucose-induced insulin secretion. To further examine the effect of Lactisole on T1R3, we prepared HEK293 cells stably expressing mouse T1R3. In these cells, sucralose elevated both [Ca2+]c and [cAMP]c. Lactisole attenuated the sucralose-induced increase in [Ca2+]c but did not affect the elevation of [cAMP]c. Finally, Lactisole inhibited insulin secretion induced by a high concentration of glucose in mouse islets. These results indicate that the mouse glucose-sensing receptor was inhibited by Lactisole. Lactisole may be useful in assessing the role of the glucose-sensing receptor in mouse pancreatic β-cells.

Differential modulation of the Lactisole 'Sweet Water Taste' by sweeteners

PLoS One 2017 Jul 10;12(7):e0180787.PMID:28700634DOI:10.1371/journal.pone.0180787.

Pre-exposure to taste stimuli and certain chemicals can cause water to have a taste. Here we studied further the 'sweet water taste' (SWT) perceived after exposure to the sweet taste inhibitor Lactisole. Experiment 1 investigated an incidental observation that presenting Lactisole in mixture with sucrose reduced the intensity of the SWT. The results confirmed this observation and also showed that rinsing with sucrose after Lactisole could completely eliminate the SWT. The generalizability of these findings was investigated in experiment 2 by presenting 5 additional sweeteners before, during, or after exposure to Lactisole. The results found with sucrose were replicated with fructose and cyclamate, but the 3 other sweeteners were less effective suppressors of the SWT, and the 2 sweeteners having the highest potency initially enhanced it. A third experiment investigated these interactions on the tongue tip and found that the Lactisole SWT was perceived only when water was actively flowed across the tongue. The same experiment yielded evidence against the possibility that suppression of the SWT following exposure to sweeteners is an aftereffect of receptor activation while providing additional support for a role of sweetener potency. Collectively these results provide new evidence that complex inhibitory and excitatory interactions occur between Lactisole and agonists of the sweet taste receptor TAS1R2-TAS1R3. Receptor mechanisms that may be responsible for these interactions are discussed in the context of the current model of the SWT and the possible contribution of allosteric modulation.

Lactisole interacts with the transmembrane domains of human T1R3 to inhibit sweet taste

J Biol Chem 2005 Apr 15;280(15):15238-46.PMID:15668251DOI:10.1074/jbc.M414287200.

The detection of sweet-tasting compounds is mediated in large part by a heterodimeric receptor comprised of T1R2+T1R3. Lactisole, a broad-acting sweet antagonist, suppresses the sweet taste of sugars, protein sweeteners, and artificial sweeteners. Lactisole's inhibitory effect is specific to humans and other primates; Lactisole does not affect responses to sweet compounds in rodents. By heterologously expressing interspecies combinations of T1R2+T1R3, we have determined that the target for Lactisole's action is human T1R3. From studies with mouse/human chimeras of T1R3, we determined that the molecular basis for sensitivity to Lactisole depends on only a few residues within the transmembrane region of human T1R3. Alanine substitution of residues in the transmembrane region of human T1R3 revealed 4 key residues required for sensitivity to Lactisole. In our model of T1R3's seven transmembrane helices, Lactisole is predicted to dock to a binding pocket within the transmembrane region that includes these 4 key residues.

Asymmetric Synthesis of Photophore-Containing Lactisole Derivatives to Elucidate Sweet Taste Receptors

Molecules 2020 Jun 17;25(12):2790.PMID:32560345DOI:10.3390/molecules25122790.

Lactisole, which has a 2-phenoxy propionic acid skeleton, is well-known as an inhibitor of sweet taste receptors. We recently revealed some of the structure-activity relationships of the aromatic ring and chiral center of Lactisole. Photoaffinity labeling is one of the common chemical biology methods to elucidate the interaction between bioactive compounds and biomolecules. In this paper, the novel asymmetric synthesis of Lactisole derivatives with common photophores (benzophenone, azide and trifluoromethyldiazirine) for photoaffinity labeling is described. The synthetic compounds are subjected to cell-based sweet taste receptors, and the substitution with trifluoromethyldiazirinyl photophore shows the highest affinity to the receptor of the synthesized compounds.