2-Bromo-LSD D-tartrate is both a potent partial agonist (EC50 of Gq dissociation = 0.81 nM, Eₘₐₓ = 59.8%) and a potent partial antagonist (KB of Gq dissociation = 0.18 nM) on the 5-HT2A receptor [2]. 2-Bromo-LSD D-tartrate has a weak blocking effect on hERG channels (IC50 = 31.6 μM) [2]. 2-Bromo-LSD D-tartrate (1-10 μM; 3 h) can promote dendrite formation and dendritic spine density in primary rat cortical neurons [2].

2-Bromo-LSD D-tartrate (0.125-4 mg/kg; intraperitoneal injection) dose-dependently increases striatal dopa accumulation in rats, reaching a maximum effect at a dose of 2-4 mg/kg, exceeding the effect of equimolar LSD. It antagonizes apomorphine-induced reduction in dopa accumulation and blocks the inhibitory effect of LSD on GBL-stimulated dopa accumulation [1]. Compared with the same dose of 2-bromo-LSD D-tartrate, co-administration of 2-bromo-LSD D-tartrate (0.125-2.0 mg/kg; intraperitoneal injection) with LSD did not cause statistically significant changes in striatal dopa accumulation [1]. 2-Bromo-LSD D-tartrate (0.1–10 mg/kg; intraperitoneal injection; single dose) did not induce hallucinogen-related head twitching in male C57BL/6J mice, but it dose-dependently blocked DOI-induced head twitching with a 76% inhibition rate at a dose of 3 mg/kg [2].

Animal/Disease Models:Sprague-Dawley (male, 188-298 g) [1]
Doses: 0.125 mg/kg; 0.250 mg/kg; 0.5 mg/kg; 2 mg/kg; 4 mg/kg
Route of Administration: Intraperitoneal injection; single dose; 30 minutes before sacrifice
Experimental Results: At a dose of 0.125 mg/kg, striatal DOPA accumulation increased to 1386 ± 106 ng/g (n=6), significantly higher than the saline control group (1042 ± 77 ng/g, p<0.001). At a dose of 0.250 mg/kg, striatal DOPA accumulation increased to 1951 ± 380 ng/g (n=6), significantly higher than the saline control group (p<0.001). At a dose of 0.5 mg/kg, striatal DOPA accumulation increased to 1924 ± 131 ng/g (n=9), significantly higher than the saline control group (p<0.001). Apomorphine (0.5 mg/kg) reduced DOPA accumulation from 472 ± 51 ng/g to 781 ± 28 ng/g, and apomorphine (5 mg/kg) reduced DOPA accumulation from 249 ± 31 ng/g to 594 ± 42 ng/g. It had no effect on reserpine-induced DOPA accumulation (2465 ± 243 ng/g vs. 2618 ± 136 ng/g, p=NS) and did not inhibit GBL-induced DOPA accumulation. At a dose of 2 mg/kg, striatal DOPA accumulation increased to 2630 ± 169 ng/g (n=6), significantly higher than that in the saline control group (p<0.001); the maximum increase was greater than the equimolar LSD; the DOPA accumulation reduced by apomorphine (0.5 mg/kg) from 472 ± 51 ng/g was restored to 2888 ± 111 ng/g (not significantly different from the level reduced by BOL 2 mg/kg alone), and the level reduced by apomorphine (5 mg/kg) from 249 ± 31 ng/g was restored to 828 ± 190 ng/g. It had no effect on the increase in dopamine accumulation induced by haloperidol or reserpine, and did not inhibit the increase in dopamine accumulation in the cut surface induced by brain hemisection (1915 ± 215 ng/g vs. 2647 ± 400 ng/g, p=NS), but increased the dopamine level in the uncut surface from 901 ± 232 ng/g to 2058 ± 158 ng/g (p<0.02); it blocked the inhibition of dopamine accumulation induced by LSD-induced GBL stimulation. Compared with the saline control group, striatal dopamine accumulation was significantly increased, and the maximum increase was greater than that of equimolar concentrations of LSD (4 mg/kg).

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Animal/Disease Models:C57BL/6J (male and female, 7-8 weeks old) [2]
Doses: 0.3 mg/kg; 1.0 mg/kg; 3.0 mg/kg
Route of Administration: Three doses
Experimental Results: The time spent in the open field test center increased by 88.18 ± 18.89 seconds (female, 1.0 mg/kg), but showed no significant trend (female, 3.0 mg/kg). In the forced swimming test (FST), the immobility time of female mice decreased by 35.18 ± 10.03 seconds (1.0 mg/kg), 20.89 ± 8.249 seconds (0.3 mg/kg), 27.27 ± 8.226 seconds (1.0 mg/kg), and 31.36 ± 8.226 seconds (3.0 mg/kg), respectively. In the open field test (OFT), the center dwell time of male mice tended to increase, but the difference was not significant (all dose groups). Compared with the solvent control group, the mean prefrontal cortex (PFC) ridge density was increased in both male and female mice (1.0 mg/kg).

[1]. The effect of LSD and 2-bromo LSD on the striatal DOPA accumulation after decarboxylase inhibition in rats. Eur J Pharmacol. 1977;43(1):73-83.

[2]. A non-hallucinogenic LSD analog with therapeutic potential for mood disorders. Cell Rep. 2023;42(3):112203.

C20H24BRN3O.1/2C4H6O6

477.39

2855123-30-5

2-Bromo-LSD

Light yellow to brown solid

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]

BOL-148 D-Tartrate; Bromolysergide D-Tartrate

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: 请将本产品存放在密封且受保护的环境中（例如氮气下），避免暴露在潮湿环境中。

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

May dissolve in DMSO (in most cases), if not, try other solvents such as H2O, Ethanol, or DMF with a minute amount of products to avoid loss of samples

Note: Listed below are some common formulations that may be used to formulate products with low water solubility (e.g. < 1 mg/mL), you may test these formulations using a minute amount of products to avoid loss of samples.

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Injection Formulation 1: DMSO : Tween 80： Saline = 10 : 5 : 85 (i.e. 100 μL DMSO stock solution → 50 μL Tween 80 → 850 μL Saline)
*Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH ₂ O to obtain a clear solution.
Injection Formulation 2: DMSO : PEG300 ：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL DMSO → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)
Injection Formulation 3: DMSO : Corn oil = 10 : 90 (i.e. 100 μL DMSO → 900 μL Corn oil)
Example: Take the Injection Formulation 3 (DMSO : Corn oil = 10 : 90) as an example, if 1 mL of 2.5 mg/mL working solution is to be prepared, you can take 100 μL 25 mg/mL DMSO stock solution and add to 900 μL corn oil, mix well to obtain a clear or suspension solution (2.5 mg/mL, ready for use in animals).

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Injection Formulation 4: DMSO : 20% SBE-β-CD in saline = 10 : 90 [i.e. 100 μL DMSO → 900 μL (20% SBE-β-CD in saline)]
*Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution.
Injection Formulation 5: 2-Hydroxypropyl-β-cyclodextrin : Saline = 50 : 50 (i.e. 500 μL 2-Hydroxypropyl-β-cyclodextrin → 500 μL Saline)
Injection Formulation 6: DMSO : PEG300 : castor oil : Saline = 5 : 10 : 20 : 65 (i.e. 50 μL DMSO → 100 μLPEG300 → 200 μL castor oil → 650 μL Saline)
Injection Formulation 7: Ethanol : Cremophor : Saline = 10： 10 : 80 (i.e. 100 μL Ethanol → 100 μL Cremophor → 800 μL Saline)
Injection Formulation 8: Dissolve in Cremophor/Ethanol (50 : 50), then diluted by Saline
Injection Formulation 9: EtOH : Corn oil = 10 : 90 (i.e. 100 μL EtOH → 900 μL Corn oil)
Injection Formulation 10: EtOH : PEG300：Tween 80 : Saline = 10 : 40 : 5 : 45 (i.e. 100 μL EtOH → 400 μLPEG300 → 50 μL Tween 80 → 450 μL Saline)

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Oral Formulation 1: Suspend in 0.5% CMC Na (carboxymethylcellulose sodium)
Oral Formulation 2: Suspend in 0.5% Carboxymethyl cellulose
Example: Take the Oral Formulation 1 (Suspend in 0.5% CMC Na) as an example, if 100 mL of 2.5 mg/mL working solution is to be prepared, you can first prepare 0.5% CMC Na solution by measuring 0.5 g CMC Na and dissolve it in 100 mL ddH2O to obtain a clear solution; then add 250 mg of the product to 100 mL 0.5% CMC Na solution, to make the suspension solution (2.5 mg/mL, ready for use in animals).

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Oral Formulation 3: Dissolved in PEG400
Oral Formulation 4: Suspend in 0.2% Carboxymethyl cellulose
Oral Formulation 5: Dissolve in 0.25% Tween 80 and 0.5% Carboxymethyl cellulose
Oral Formulation 6: Mixing with food powders

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Note: Please be aware that the above formulations are for reference only. InvivoChem strongly recommends customers to read literature methods/protocols carefully before determining which formulation you should use for in vivo studies, as different compounds have different solubility properties and have to be formulated differently.

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 (Please use freshly prepared in vivo formulations for optimal results.)