| 包装 | 价格(元) |
| 10mg | 电议 |
| 50mg | 电议 |
Cell lines | Xenopus oocytes |
Preparation method | The solubility of this compound in DMSO is >10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 ℃ for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below - 20 ℃ for several months. |
Reacting condition | 300nM or 1 μM |
Applications | At the concentration of 1 μM, Dihydro-β-erythroidine Hydrobromide almost completely blocked the α4β4 subunit but showed little effect on the α3β4 subunit. However, the blockade effect of Dihydro-β-erythroidine Hydrobromide on the α4β4 subunit could be reversed by increasing the agonist concentration. In the presence of 300 nM Dihydro-β-erythroidine Hydrobromide, the current response of α4β4-expressing oocytes to 5 μM and 500 μM ACh were 36.0 ± 9.0 % and 97.1 ± 9.6 % of the response to ACh alone, respectively. |
Animal models | A nicotine-induced hypothermia mouse model |
Dosage form | 0, 1.8, 3.6, 7.2 or 10.8 μmol/kg; s.c. |
Applications | In a nicotine-induced hypothermia mouse model, Dihydro-β-erythroidine Hydrobromide dose-dependently attenuated hypothermia, with the AD50 value of 6.2 μmol/kg. But it did not have a significant effect on the non-nicotine-induced increase in body temperature at the inducated doses. |
Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
| 产品描述 | IC50: 1.3 μM for α2β2, 2.3 μM for α2β4, 0.41 μM for α3β2, 23.1 μM for α3β4, 0.37 μM for α4β2, and 0.19 μM for α4β4 [1] Dihydro-β-erythroidine hydrobromide (DHβE), the hydrogenated derivative of erythroidine, is a competitive antagonist of neuronal nicotinic acetyicholine receptors (or nAChRs). Nicotinic acetyicholine receptors are neuron receptor proteins which respond to the neurotransmitter acetylcholine. In vitro: DHβE has been shown to be a purely competitive antagonist of the neuronal nicotinic receptor [1]. In vivo: DHβE is able to block some of the central actions of nicotine after systemic and intrathecal administration. The mechanism of blockade is different from that of mecamylamine, a classical ganglionic antagonist, and may involve a direct action of DHβE on nicotine receptor [2]. Clinical trial: DHβE can be given orally and may cross the blood-brain barriers. At 200 mg/kg, the effects were bradycardia and visual difficulty most often described as blurring of vision or double vision; at 6 mg/kg, produced aforementioned effects plus hypotension and reduction in grip strength with accompanying feelings of sedation [3]. References: |
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