2. GPCR/G Protein Neuronal Signaling
  3. 5-HT Receptor G protein-coupled Bile Acid Receptor 1
  4. 2-Bromo-LSD D-Tartrate

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

目录号: HY-121675A
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2-Bromo-LSD D-Tartrate 是一种能透过血脑屏障的 5-HT2A 部分激动剂和竞争性部分拮抗剂。2-Bromo-LSD D-Tartrate 在 5-HT2A 受体上同时发挥强效部分激动剂 (针对 Gq 解离的 EC50 = 0.81 nM) 和强效部分拮抗剂 (针对 Gq 解离的 KB = 0.18 nM) 的作用。2-Bromo-LSD D-Tartrate 对包括 5-HT2A 在内的多种胺能 GPCR 表现出部分激动作用。2-Bromo-LSD D-Tartrate 缺乏 5-HT2B 激动作用。2-Bromo-LSD D-Tartrate 可诱导树突生成和棘突生成。2-Bromo-LSD D-Tartrate 逆转慢性应激的行为影响，增加小鼠的主动应对行为。

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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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2-Bromo-LSD D-Tartrate 的其他形式现货产品:

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2-Bromo-LSD D-Tartrate 相关抗体

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  • 生物活性

  • 纯度 & 产品资料

  • 参考文献

生物活性

2-Bromo-LSD 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)

体外研究
(In Vitro)

2-Bromo-LSD D-Tartrate 在 5-HT2A 受体上同时发挥强效部分激动剂 (针对 Gq 解离的 EC50 = 0.81 nM，Eₘₐₓ = 59.8%) 和强效部分拮抗剂 (针对 Gq 解离的 KB = 0.18 nM) 的作用[2]。
2-Bromo-LSD D-Tartrate 对 hERG 通道产生微弱的阻断作用 (IC50 = 31.6 μM)[2]。
2-Bromo-LSD D-Tartrate (1-10 μM; 3 h) 可促进原代大鼠皮质神经元的树突发生、树突棘密度[2]。

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

2-Bromo-LSD D-Tartrate 相关抗体:
体内研究
(In Vivo)

2-Bromo-LSD D-Tartrate (0.125-4 mg/kg；腹腔注射) 可剂量依赖性地增加大鼠纹状体中 DOPA 的蓄积，在 2-4 mg/kg 剂量下达到最大效应，且该效应强于等摩尔浓度的 LSD；同时它可作为拮抗剂逆转 Apomorphine (HY-12723) 诱导的 DOPA 蓄积减少，并阻断 LSD 对 GBL 刺激的 DOPA 蓄积的抑制作用[1]。
2-Bromo-LSD D-Tartrate (0.125-2.0 mg/kg；腹腔注射) 与 LSD 联合时，相较于相同剂量的单独使用 2-Bromo-LSD D-Tartrate，并未引起纹状体 DOPA 累积量的统计学显著变化[1]。
2-Bromo-LSD D-Tartrate (0.1-10 mg/kg；腹腔注射) 不会在雄性 C57BL/6J 小鼠中诱导致幻剂相关的甩头反应，但会呈剂量依赖性地阻断 DOI 诱导的甩头反应，在 3 mg/kg 剂量下抑制率达 76%[2]。

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).
分子量

477.39

Formula

C20H24BrN3O·1/2C4H6O6
CAS 号
运输条件

Room temperature in continental US; may vary elsewhere.
储存方式

Please store the product under the recommended conditions in the Certificate of Analysis.
纯度 & 产品资料
参考文献

2-Bromo-LSD D-Tartrate 相关分类

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  • Do most proteins show cross-species activity?

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Keywords:

2-Bromo-LSD2855123-30-5BOL-148BromolysergideBOL148BOL 1485-HT ReceptorG protein-coupled Bile Acid Receptor 1Serotonin Receptor5-hydroxytryptamine ReceptorG-protein coupled receptor 19GPCR19TGR5GPBAR1primary rat cortical neuronshuman 5-HT7a receptorshuman Nav1.5 sodium channelsmale C57BL/6J micehuman hERG channelshuman 5-HT2A receptorshuman α2C adrenergic receptorshuman 5-HT6 receptorshuman D4 receptorshuman D2 receptorsInhibitorinhibitorinhibit

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