1. GPCR/G Protein Neuronal Signaling
  2. 5-HT Receptor G protein-coupled Bile Acid Receptor 1
  3. 2-Bromo-LSD D-Tartrate

2-Bromo-LSD D-Tartrate  (Synonyms: BOL-148 D-Tartrate; Bromolysergide D-Tartrate)

Cat. No.: HY-121675A Purity: 99.91%
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2-Bromo-LSD D-Tartrate (BOL-148 D-Tartrate) is a blood-brain barrier-permeable 5-HT2A partial agonist and competitive partial antagonist. 2-Bromo-LSD D-Tartrate acts as both a potent partial agonist (with an EC50 of 0.81 nM for Gq dissociation) and a potent partial antagonist (with a KB of 0.18 nM for Gq dissociation) at the 5-HT2A receptor. 2-Bromo-LSD D-Tartrate exhibits partial agonist activity at multiple aminergic GPCRs, including 5-HT2A. 2-Bromo-LSD D-Tartrate lacks 5-HT2B agonist activity. 2-Bromo-LSD D-Tartrate induces dendritogenesis and spinogenesis. 2-Bromo-LSD D-Tartrate reverses the behavioral effects of chronic stress and increases active coping behaviors in mice.

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2-Bromo-LSD D-Tartrate

2-Bromo-LSD D-Tartrate Chemical Structure

CAS No. : 2855123-30-5

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Based on 1 publication(s) in Google Scholar

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Description

2-Bromo-LSD D-Tartrate (BOL-148 D-Tartrate) is a blood-brain barrier-permeable 5-HT2A partial agonist and competitive partial antagonist. 2-Bromo-LSD D-Tartrate acts as both a potent partial agonist (with an EC50 of 0.81 nM for Gq dissociation) and a potent partial antagonist (with a KB of 0.18 nM for Gq dissociation) at the 5-HT2A receptor. 2-Bromo-LSD D-Tartrate exhibits partial agonist activity at multiple aminergic GPCRs, including 5-HT2A. 2-Bromo-LSD D-Tartrate lacks 5-HT2B agonist activity. 2-Bromo-LSD D-Tartrate induces dendritogenesis and spinogenesis. 2-Bromo-LSD D-Tartrate reverses the behavioral effects of chronic stress and increases active coping behaviors in mice[1][2].

IC50 & Target[1]

5-HT2A Receptor

0.81 nM (EC50)

5-HT2A Receptor

0.18 nM (Kb)

In Vitro

2-Bromo-LSD D-Tartrate acts as both a potent partial agonist (EC50 = 0.81 nM, Eₘₐₓ = 59.8% for Gq dissociation) and a potent partial antagonist (KB = 0.18 nM for Gq dissociation) at the 5-HT2A receptor[2].
2-Bromo-LSD D-Tartrate exerts weak blocking effects on hERG channels (IC50 = 31.6 μM)[2].
2-Bromo-LSD D-Tartrate (1-10 μM; 3 h) promotes dendrogenesis and dendritic spine density in primary rat cortical neurons[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

In Vivo

2-Bromo-LSD D-Tartrate (0.125-4 mg/kg; i.p.) dose-dependently increases striatal DOPA accumulation in rats, with maximum effects at 2-4 mg/kg that exceed those of equimolar LSD, acts as an antagonist of Apomorphine (HY-12723)-induced DOPA accumulation reduction, and blocks LSD's inhibitory effect on GBL-stimulated DOPA accumulation[1].
2-Bromo-LSD D-Tartrate (0.125-2.0 mg/kg; i.p.) co-administered with LSD does not produce a statistically significant change in striatal DOPA accumulation compared to 2-Bromo-LSD D-Tartrate alone at matching doses[1].
2-Bromo-LSD D-Tartrate (0.1-10 mg/kg; i.p.; single dose) does not induce the hallucinogen-associated head-twitch response in male C57BL/6J mice, but dose-dependently blocks DOI-induced head-twitch responses, achieving 76% inhibition at the 3 mg/kg dose[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model: Sprague-Dawley (male, 188-298 g)[1]
Dosage: 0.125 mg/kg; 0.250 mg/kg; 0.5 mg/kg; 2 mg/kg; 4 mg/kg
Administration: i.p.; single dose; 30 minutes before sacrifice
Result: Increased striatal DOPA accumulation to 1386 ± 106 ng/g (n=6), significantly higher than saline control (1042 ± 77 ng/g, p<0.001) at 0.125 mg/kg.
Increased striatal DOPA accumulation to 1951 ± 380 ng/g (n=6), significantly higher than saline control (p<0.001) at 0.250 mg/kg.
Increased striatal DOPA accumulation to 1924 ± 131 ng/g (n=9), significantly higher than saline control (p<0.001) at 0.5 mg/kg; restored apomorphine (0.5 mg/kg)-reduced DOPA accumulation to 781 ± 28 ng/g from 472 ± 51 ng/g, and apomorphine (5 mg/kg)-reduced levels to 594 ± 42 ng/g from 249 ± 31 ng/g; showed no effect on reserpine-induced increased DOPA accumulation (2465 ± 243 ng/g vs.
2618 ± 136 ng/g, p=N.S.) and did not inhibit GBL-induced increased DOPA accumulation.
Increased striatal DOPA accumulation to 2630 ± 169 ng/g (n=6), significantly higher than saline control (p<0.001) at 2 mg/kg; produced larger maximum increase than equimolar LSD; restored apomorphine (0.5 mg/kg)-reduced DOPA accumulation to 2888 ± 111 ng/g from 472 ± 51 ng/g (levels not significantly different from BOL 2 mg/kg alone), and apomorphine (5 mg/kg)-reduced levels to 828 ± 190 ng/g from 249 ± 31 ng/g; showed no effect on haloperidol-induced or reserpine-induced increased DOPA accumulation, did not inhibit cerebral hemisection-induced increased DOPA accumulation on the sectioned side (1915 ± 215 ng/g vs.
2647 ± 400 ng/g, p=N.S.) but increased levels on the unsectioned side to 2058 ± 158 ng/g from 901 ± 232 ng/g (p<0.02); blocked LSD-induced inhibition of GBL-stimulated DOPA accumulation.
Significantly increased striatal DOPA accumulation compared to saline control and produced larger maximum increase than equimolar LSD at 4 mg/kg.
Animal Model: C57BL/6J (male and female, 7-8 weeks old)[2]
Dosage: 0.3 mg/kg; 1.0 mg/kg; 3.0 mg/kg
Administration: three dose
Result: Increased time spent in the center of the OFT by 88.18 ± 18.89 seconds (female, 1.0 mg/kg) and showed a non-significant trend (female, 3.0 mg/kg).
Reduced FST immobility time by 35.18 ± 10.03 seconds (female, 1.0 mg/kg), 20.89 ± 8.249 seconds (male, 0.3 mg/kg), 27.27 ± 8.226 seconds (male, 1.0 mg/kg), and 31.36 ± 8.226 seconds (male, 3.0 mg/kg).
Showed a non-significant trend toward increased center time in the OFT (male, all doses).
Increased average PFC spine density compared to vehicle controls (both sexes, 1.0 mg/kg).
Molecular Weight

477.39

Formula

C20H24BrN3O·1/2C4H6O6

CAS No.
Appearance

Solid

Color

Light yellow to brown

SMILES

OC([C@@H](O)[C@H](O)C(O)=O)=O.BrC1=C2C3=C(N1)C=CC=C3C4=C[C@@H](C(N(CC)CC)=O)CN(C)[C@]4([H])C2.[1/2]

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

4°C, stored under nitrogen

*In solvent : -80°C, 6 months; -20°C, 1 month (stored under nitrogen)

Purity & Documentation
References
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