Guanidinoethyl sulfonate (GES) is a taurine analogue that competitively inhibits taurine uptake, causes taurine depletion by acting as a competitive inhibitor of TauT, PAT1 and GAT2 as well as interfering with taurine biosynthesis[1][2]. Guanidinoethyl sulfonate is commonly used to study neurodegenerative diseases and epilepsy [1][3][4].
Guanidinoethyl sulfonate (50, 40, 30, 20, 10, 5, and 2.5mM; 1h) decreased the cellular uptake of VGB, GABA, and taurine in ARPE-19 cells[4]. Guanidinoethyl sulfonate (10, 100, 1000, 10,000 and 30,000μM; 120ms) activated inward currents in a dose-dependent fashion on cerebellar granule cells[5].
Guanidinoethyl sulfonate (1mg/kg/day, 10 days, i.v.) decreased the VGB retinal levels in rats by 1.5-folds (P< 0.001, n = 6) compared with rats administered with similar dose of VGB alone[4].
References:
[1] Sergeeva OA, Chepkova AN, Haas HL. Guanidinoethyl sulphonate is a glycine receptor antagonist in striatum. British journal of pharmacology. 2002 Nov;137(6):855-60.
[2] Richter M, Moroniak SJ, Michel H. Identification of competitive inhibitors of the human taurine transporter TauT in a human kidney cell line. Pharmacological Reports. 2019 Feb 1;71(1):121-9.
[3] Suárez LM, Muñoz MD, González JC, Bustamante J, Del Río RM, Solís JM. The taurine transporter substrate guanidinoethyl sulfonate mimics the action of taurine on long-term synaptic potentiation. Amino acids. 2016 Nov;48:2647-56.
[4] Police A, Shankar VK, Murthy SN. Role of taurine transporter in the retinal uptake of vigabatrin. AAPS PharmSciTech. 2020 Jul;21:1-9.
[5] Mellor JR, Gunthorpe MJ, Randall AD. The taurine uptake inhibitor guanidinoethyl sulphonate is an agonist at γ-aminobutyric acidA receptors in cultured murine cerebellar granule cells. Neuroscience letters. 2000 May 26;286(1):25-8.
Guanidinoethyl sulfonate（GES）是一种牛磺酸类似物，可竞争性抑制牛磺酸的摄取，通过作为TauT、PAT1和GAT2的竞争性抑制剂导致牛磺酸耗竭，并干扰牛磺酸的生物合成[1][2]。Guanidinoethyl sulfonate常用来研究神经退行性疾病和癫痫[1][3][4]。
Guanidinoethyl sulfonate（50、40、30、20、10、5和2.5mM；1h）降低了ARPE-19细胞对VGB、GABA和牛磺酸的细胞摄取[4]。Guanidinoethyl sulfonate（10、100、1000、10,000和30,000μM；120ms）以剂量依赖性方式激活小脑颗粒细胞的内向电流[5]。
与单独使用相似剂量VGB的大鼠相比，Guanidinoethyl sulfonate（1mg/kg/天，10天，静脉注射）使大鼠的VGB视网膜水平降低了1.5倍（P< 0.001，n = 6）[4]。