9-cis-视黄酸 (ALRT1057) 是维生素 A 的一种衍生物，是有效的 RAR/RXR 激动剂。它诱导细胞凋亡、调节细胞周期，并表现出抗癌、抗炎和神经保护活性。
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There will be a HazMat fee per item when shipping a dangerous goods. The HazMat fee will be charged to your UPS/DHL/FedEx collect account or added to the invoice unless the package is shipped via Ground service. Ship by air in Excepted Quantity (each bottle), which is up to 1g/1mL for class 6.1 packing group I or II, and up to 25g/25ml for all other HazMat items.
Type
HazMat fee for 500 gram (Estimated)
Excepted Quantity
USD 0.00
Limited Quantity
USD 15-60
Inaccessible (Haz class 6.1), Domestic
USD 80+
Inaccessible (Haz class 6.1), International
USD 150+
Accessible (Haz class 3, 4, 5 or 8), Domestic
USD 100+
Accessible (Haz class 3, 4, 5 or 8), International
9-cis-Retinoic acid (ALRT1057), a derivative of vitamin A, acts as a potent agonist for RAR/RXR. It induces apoptosis, regulates the cell cycle, and exhibits anticancer, anti-inflammatory, and neuroprotective properties[1][2][3][4][5].
体内研究
9-cis-Retinoic acid (1 mg/kg; via intravenous injection; daily for 10 days; in male C57BL/6J mice) notably lowers the levels of serum ALT and AST, and mitigates liver necrosis in mice subjected to bile duct ligation (BDL)[3].
体外研究
9-cis-Retinoic acid at concentrations ranging from 1 to 10 μM for 0 to 5 days significantly reduces proliferation in a dose-dependent manner in CA 9-22 and NA cells[1].
After 24 hours of treatment with 9-cis-Retinoic acid at a concentration of 1 μM, PPARγ functional activity increases by over 200% in CA 9-22 and NA aerodigestive cells[1].
9-cis-Retinoic acid treatment leads to the creation of a PPARγ-RXRα heterodimer supershift complex in the nucleus of CA 9-22 cells[1].
9-cis-Retinoic acid hampers the growth and triggers cell death in cutaneous T-cell lymphoma (CTCL) in both dose-dependent and time-dependent manners. Furthermore, this compound prompts cell cycle arrest at the G0/G1 phase by reducing cyclin D1 levels. It markedly diminishes the phosphorylation of JAK1, STAT3, and STAT5, and reduces the expression of Bcl-xL and cyclin D1[2].
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