Background and purpose: The thiazolidine carboxylic acid, BML-241, has been proposed as a lead compound in development of selective antagonists at the sphingosine-1-phosphate receptor (S1P 3 ), based on its inhibition of the rise in intracellular calcium concentrations ([Ca 2 þ ] i ) in HeLa cells overexpressing S1P receptors. We have studied the antagonistic properties of BML-241 for the S1P 3 receptor in more detail. Experimental approach: Chinese hamster ovary (CHO) cells stably transfected with the S1P 3 , S1P 2 or a 1A -adrenoceptors were used to investigate the effect of BML-241 on increases in [Ca 2 þ ] i mediated via different receptors. CHO-K1 cells were used to study ATP-induced [Ca 2 þ ] i elevations. Effects on S1P 3 -mediated inhibition of forskolin-induced cAMP accumulation and on binding to a 1A -adrenoceptors were also investigated. In addition, the effect of BML-241 on contractions of rat mesenteric artery induced by phenylephrine was studied in an organ bath. Key results: High concentrations of BML-241 (10 mM) inhibited the rise in [Ca 2 þ ] i induced by S1P 3 and S1P 2 receptor stimulation; lower concentrations were ineffective. This high concentration of BML-241 also inhibited [Ca 2 þ ] i increases via P2 (nucleotide) receptor or a 1A -adrenoceptor stimulation. Moreover, BML-241 (10 mM) inhibited a 1 -adrenoceptor-mediated contraction of rat mesenteric artery but did not displace [3 H]-prazosin from a 1A -adrenoceptors in concentrations up to 100 mM. BML-241 (10 mM) did not affect the S1P 3 -mediated decrease of forskolin-induced cAMP accumulation. Conclusions and Implications: We conclude that BML-241 is a low potency, non-selective inhibitor of increases in [Ca 2 þ ] i , rather than a specific antagonist at the S1P 3 receptor.