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    BRL-15572 dihydrochloride
    BRL-15572 dihydrochloride

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V0978
    CAS #: 193611-72-2Purity ≥98%

    Description: BRL-15572 (BRL-15,572; BRL-15572; BRL 15,572; BRL15,572) dihydrochloride salt is a potent and selective 5-HT1D receptor antagonist with important biological activity. It inhibits 5-HT1D with a pKi of 7.9.

    References: Naunyn Schmiedebergs Arch Pharmacol. 1997;356:312-20; Clin Exp Pharmacol Physiol. 2007;34:1199-206.

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    Molecular Weight (MW)479.87 
    CAS No.193611-72-2 
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 96 mg/mL (200.1 mM)
    Water: <1 mg/mL
    Ethanol: 40 mg/mL (83.4 mM)
    Solubility (In vivo)30% Propylene glycol, 5% Tween 80, 65% D5W: 20 mg/mL 
    SynonymsBRL15572; BRL 15572 HCl; BRL-15,572; BRL-15572; BRL 15,572; BRL15,572.
    SMILES CodeOC(CN1CCN(C2=CC(Cl)=CC=C2)CC1)C(C3=CC=CC=C3)C4=CC=CC=C4.[H]Cl.[H]Cl

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    In Vitro

    In vitro activity: 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 [35S]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 [3H]5-HT release. The selective 5-HT1D/1B receptor antagonist BRL 15572 inhibits the effect of the agonist L-694 247.

    Cell Assay: [35S]GTPγS binding studies. [35S]GTPγS binding studies in CHO cells expressing the h5-HT1B or h5-HT1D receptors are performed. In brief, membranes from 1 × 106 cells are preincubated at 30°C for 30 minutes, in HEPES buffer (HEPES [20 mM], MgCl2 [3 mM], NaCl [100 mM], ascorbate [0.2 mM]), containing GDP (10 µ M), with or without BRL-15572. The reaction is started by the addition of 10 µL of [35S]GTPγS (100 pM, assay concentration) followed by a further 30 minutes incubation at 30°C. Non-specific binding is determined by addition of unlabelled GTPγS (10 µM), prior to the addition of cells. The reaction is stopped by rapid filtration using Whatman GF/B grade filters followed by five washes with ice-cold HEPES buffer. Radioactivity is determined by liquid scintillation spectrometry.

    In VivoIn 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. 
    Animal modelMale Wistar rats with diabetes 
    Formulation & DosageDissolved in 20% propylene glycol; 1 mg/kg, 2 mg/kg; i.v. injection

    Naunyn Schmiedebergs Arch Pharmacol. 1997 Sep;356(3):312-20; Clin Exp Pharmacol Physiol. 2007 Nov;34(11):1199-206. 

    These protocols are for reference only. InvivoChem does not independently validate these methods.


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