Jujuboside A


CAS No. : 55466-04-1

55466-04-1
Price and Availability of CAS No. : 55466-04-1
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5mg $50 In-stock
10mg $85 In-stock
25mg $180 In-stock
50mg $310 In-stock
100mg $520 In-stock
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Cat. No. : HY-N0659
M.Wt: 1207.35
Formula: C58H94O26
Purity: >98 %
Solubility: DMSO : 100 mg/mL (82.83 mM; Need ultrasonic); H2O : 50 mg/mL (41.41 mM; Need ultrasonic)
Introduction of 55466-04-1 :

Jujuboside A is a glycoside extracted from Semen Ziziphi Spinosae, a Chinese herbal medicine used to treat insomnia and anxiety. IC50 & Target:GABA Receptor, mTOR, PI3K, Akt[1][2] In Vitro: Jujuboside A at the low dose of 41 μM (about 0.05 g/L) induces significant increase of GABA(A) receptor α1, α5, β2 subunit mRNAs in both 24 and 72h treatments. Jujuboside A at the high dose of 82 μM (about 0.1 g/L) significantly increases GABA(A) receptor α1, α5 subunit mRNA levels and decreases β2 subunit mRNA level at 24h treatment, and decreases GABA(A) receptor subunit α1, β2 mRNAs expression at 72h treatment[1]. Jujuboside A pretreatment could reverse the reduction of cell viability and better the injury of H9C2 cells induced by ISO. Jujuboside A could accelerate the phosphorylation of PI3K, Akt, and mTOR. Jujuboside A could significantly decrease the ratio of microtubule-associated protein LC3-II/I in H9C2 cells[2]. In Vivo: During daytime (9:00-15:00), jujubosides significantly increases the total sleep and rapid eye movement (REM) sleep without significant influence on non-REM (NREM) sleep. During nighttime (21:00-3:00), jujubosides significantly increases the total sleep and NREM sleep especially the light sleep while shows no significant effect on REM sleep and slow wave sleep (SWS)[3]. Intracerebroventricular treatment with Jujuboside A significantly mitigates learning and memory impairment in mice induced by Aβ1–42 as measured by the Y-maze, active avoidance and Morris water maze. Intracerebroventricular treatment with Jujuboside A reduces the level of Aβ1–42 in hippocampus, significantly inhibits the activities of acetylcholinesterase (AChE) and NO, and decreases the amount of the increased malondialdehyde (MDA) in the hippocampus and cerebral cortex of mice treated with intracerebroventricular injection of Aβ1–42[4].

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