BRL-15572 is a hydrochloride salt form of BRL-15572 which is a selective  serotonin receptor subtype 5-HT1D antagonist with an IC50 of 260 μM.  BRL-15572 indicates 60-fold selectivity over h5-HT1B, and displays little or no affinity for a range of other receptor types. In the presence of the 5-HT1D antagonist BRL15572 at a dose of 10 μM triggered a significant reduction in evoked IPSC (inhibitory postsynaptic currents) amplitude. Additionally, the antianti-migraine agent sumatriptan (1 μM) produced a striking reduction in evoked IPSC amplitude in the presence of BRL15572 (10 μM) which was not significantly different to that produced in its JPence. For a comparison, sumatriptan (1 μM) did not produce a marked reduction in evoked IPSC amplitude in the presence of both NAS181 (10 μM) and BRL15572 (10 μM). In addition, it was observed that the prevention of GABAergic synaptic transmission produced by 5-HT was abolished by the 5-HT1B antagonist NAS181, but not by the 5-HT1A and 5-HT1D antagonists WAY100135 and BRL15572, while that produced by sumatriptan was only abolished in the combined presence of NAS181 and BRL15572.

>98%

Store at -20℃ for one year（Powder）；Store at 2-4℃ for two weeks；Store at -20℃ for six months after dissolution.

BRL-15572

DMSO ：96 mg/mL (200.05 mM)

Ethanol ：40 mg/mL (83.35 mM)

5-HT1D,5-HT1A,5-HT2B,5-HT2A,5-HT7,,

BRL-15572 displays high affinity and selectivity for h5-HT1D receptors. BRL-15572 has 60-fold higher affinity for h5-HT1D than 5-HT1B receptors. BRL-15572 binds to h5-HT1B and h5-HT1D receptors with pKB of less than 6 and 7.1, respectively. BRL-15572 stimulates GTP γ S binding in both cell lines, with potencies that correlated with their receptor binding affinities in both h5-HT1B and h5-HT1D receptor expressing cell lines. BRL-15572 reveals receptor binding affinities for 5-HT1A, 5-HT1B, 5-HT1E, 5-HT1F, 5-HT2A, 5-HT2B, 5-HT2C, 5-HT6 and 5-HT7 with pKi of 7.7, 6.1, 5.2, 6.0, 6.6, 7.4, 6.2, 5.9 and 6.3, respectively. In the h5-HT1D cell line, both BRL-15572 (1 µM) shifts the 5-HT concentration response curve with pKB of 7.1, respectively. BRL-15572 does have moderately high affinity at human 5-HT1A and 5-HT2B receptors. In human atrial appendages, the electrically evoked tritium overflow is inhibited by 5-HT in a manner susceptible to antagonism by BRL-15572 (300 nM; 23 times Ki at h5-HT1D receptors). The inhibitory effect of 5-HT on the K+-evoked overflow of glutamate is antagonized by the h5-HT1D receptor ligand BRL-15572. BRL-15572 (1 μM) is unable to modify the effect of 5-HT at the autoreceptor regulating 5-HT release. The selective 5-HT1D/1B receptor antagonist BRL 15572 inhibits the effect of the agonist L-694 247.

In diabetic pithed rats, administration of the selective 5-HT1D receptor antagonist BRL-15572 (2 mg/kg) does not modify the decreased HR induced by vagal electrical stimulation. The effects of L-694,247 (50 μg/kg), a selective agonist for non-rodent 5-HT1B and 5-HT1D receptors, on the vagally induced bradycardia are not apparent after pretreatment with BRL-15572.