DL-TBOA ammonium is a potent, non-transportable inhibitor of excitatory amino acid transporters. Its inhibitory effects are demonstrated by IC50 values of 70 μM, 6 μM, and 6 μM for excitatory amino acid transporter-1 (EAAT1), EAAT2, and EAAT3, respectively. Additionally, DL-TBOA ammonium significantly hampers the uptake of [14C]glutamate in COS-1 cell lines expressing human EAAT1 and EAAT2, evident by Ki values of 42 μM and 5.7 μM, respectively. Furthermore, this compound competitively blocks EAAT4 and EAAT5, with Ki values of 4.4 μM and 3.2 μM, respectively.

EAAT2 (human):5.7 μM (IC50), EAAT1 (human):Ki: 42 μM, EAAT4:4.4 μM (IC50), EAAT1:70 μM (IC50), EAAT5:3.2 μM (IC50), EAAT3:6 μM (IC50), EAAT2:6 μM (IC50)

DL-TBOA ammonium (70-350 μM; 48 hours) treatment concentration-dependently enhances SN38-induced loss of viability. DL-TBOA reversed Oxaliplatin-induced loss of viability[4]. DL-TBOA ammonium (350 μM; 24 hours) decreases p53 induction by SN38 and oxaliplatin[4]. Cell Viability Assay[4]Cell Line: HCT116 cells, LoVo cells Concentration: 70 μM, 350 μM Incubation Time: 48 hours Result: Enhanced SN38-induced, and counteracted Oxaliplatin-induced, cell death. Cell Viability Assay[4]Cell Line: HCT116 cells, LoVo cells Concentration: 350 μM Incubation Time: 24 hours Result: Decreased p53 induction by SN38 and oxaliplatin.

DL-TBOA ammonium (10 nmol; i.c.v.) to morphine-dependent rats significantly facilitates the expression of naloxone-precipitated somatic signs and conditioned place aversion[5]. Animal Model: Male Sprague-Dawley rats (180-250 g)[5]Dosage: 1 nmol, 3 nmol, 10 nmol Administration: Intracerebroventricularly injection (i.c.v.) Result: Dose dependently facilitated various somatic signs induced by Naloxone (0.1 mg/kg)-precipitated morphine withdrawal.