BETP is an agonist of GLP-1 receptor (EC50s: 0.66 and 0.755 μM for human and rat GLP-1 receptor).

GLP1:0.755 μM(Rat), GLP1:0.66 μM(Human)

BETP（化合物B）在表达GLP-2、GIP、PTH或胰高血糖素受体的细胞中无活性。BETP（1-10 μM）能增强正常和糖尿病患者胰岛的胰岛素分泌。此外，BETP与GLP-1联用时，对GLP-1受体信号的增强作用呈现加成效应[1]。BETP将羟硝苏肽的效力提高了10倍（EC50：80 pM）。GLP-1不会改变羟硝苏肽和胰高血糖素在胰高血糖素受体上的效力和效能。BETP（0-30 μM）提高了羟硝苏肽与GLP-1受体的结合亲和力[2]。

BETP（10 mg/kg，颈静脉导管）在静脉葡萄糖耐量试验（IVGTT）模型中显示出促进胰岛素分泌的活性。在SD大鼠高血糖夹持模型中，经BETP（10 mg/kg，静脉注射）处理的大鼠需要更高20%的葡萄糖输注率，并展现出更高的血浆胰岛素水平 [1]。此外，BETP（5 mg/kg）增强了oxyntomodulin刺激下的胰岛素分泌 [2]。

IVGTT studies are performed. Male SD rats are group-housed three per cage in polycarbonate cages with filter tops. Rats are maintained on a 12:12 h light-dark cycle (lights on at 6:00 a.m.) at 21°C and receive diet and deionized water ad libitum. Rats were fasted overnight and anesthetized with 60 mg/kg pentobarbital for the duration of the experiment. For glucose and compounds (BETP, etc.) administration, a catheter with a diameter of 0.84 mm is inserted into the jugular vein. For rapid blood collection, a larger catheter with 1.02-mm diameter is inserted into the carotid artery. Blood is collected for glucose and insulin levels at times 0, 2, 4, 6, 10, and 20 min after intravenous administration of the BETP which is immediately followed by an intravenous glucose bolus of 0.5 g/kg. Plasma levels of glucose and insulin are determined [1].