Alniditan is a receptors agonist of 5-HT1B/1D in HEK 293 cells (IC50: 1.7 and 1.3 nM). For 5-HT1B/1D receptors, the pKi values are 8.96 and 9.40, respectively.

5-HT1D receptor:1.3 nM (in HEK 293 cell), 5-HT1B receptor:1.7 nM (in HEK 293 cell)

Alniditan is 10 times more potent than sumatriptan at the h5-HT1B receptor, and twice as potent at the h5-HT1D receptor[3]. In vitro, alniditan exhibits little vasoconstrictive effects on the rat basilar artery, although at a very high concentration 1 mM, alniditan causes intensive constriction, most likely through a mechanism independent from 5-HT receptor activation[1].

Alniditan (3, 10, 30 and 100 μg/kg) produces a dose-dependent increase in the arteriovenous oxygen saturation difference, which seems to be attenuated in animals treated with GR127935. Alniditan also produces significant increases in vascular conductance to the skin, ear, bone, salivary gland, fat, tongue, brain and dura mater; no changes are observed in the muscles and eyes[2]. Alniditan dose-dependently decreases total carotid and arteriovenous anastomotic blood flow and concomitant conductance values; nutrient blood flow and conductance increase. The intraperitoneal administration of alniditan ED50=9 μg/kg and sumatriptan ED50=70 μg kg dose dependly reduces [125I]-BSA extravasation in the rat meninges when done 30 min before stimulation. The estimated ED values for alniditan are 9 μg/kg in the absence and 190 μg/kg in the presence of GR 127935[1].