货号:A1396006
同义名:
Alitretinoin; NSC 659772
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。9-cis Retinoic Acid增加从大鼠神经干细胞培养物中衍生的神经元数量,促进少突胶质前体细胞的分化和在培养细胞及小鼠小脑切片中的髓鞘形成,诱导在胶原凝胶中培养的胚胎小鼠胰腺中胰腺导管的形成,但不包括腺泡。9-cis Retinoic Acid还增强 BMP9 诱导的间充质祖细胞成骨分化,诱导 C2C12 成肌祖细胞的肌生成分化。
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 | USD 200+ |
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描述 | 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]. |
Concentration | Treated Time | Description | References | |
human lymphatic endothelial cells (LECs) | 1 µM | 24 h | promotes LEC migration | Circulation. 2012 Feb 21;125(7):872-82 |
human lymphatic endothelial cells (LECs) | 1 µM | 48 h | promotes LEC proliferation | Circulation. 2012 Feb 21;125(7):872-82 |
Rat hepatic stellate cells | 0.01, 0.1, 1 µM | 48, 72, 96 h | To examine the influence of 9-cis retinoic acid on extracellular matrix production and proliferation of activated hepatic stellate cells. Results showed that 9RA increased procollagen I mRNA 1.9-fold but did not affect other matrix proteins. | Gut. 1999 Jul;45(1):134-42 |
Cultured human mesangial cells (CHMC) | 1 μM | 24 h | To study the inhibitory effect of 9-cRA on monocyte adhesion to FCS-stimulated CHMC. Results showed that 1 μM 9-cRA significantly inhibited monocyte adhesion. | Br J Pharmacol. 2000 Dec;131(8):1673-83 |
Cultured human mesangial cells (CHMC) | 10 nM | 24 h | To study the preventive effect of 9-cRA on H2O2-induced CHMC death. Results showed that 10 nM 9-cRA significantly prevented H2O2-induced cell death. | Br J Pharmacol. 2000 Dec;131(8):1673-83 |
Cultured human mesangial cells (CHMC) | 10 nM to 100 nM | 24 h | To study the inhibitory effect of 9-cRA on FCS-induced CHMC proliferation. Results showed that 9-cRA dose-dependently inhibited FCS-induced CHMC proliferation at concentrations ranging from 10 nM to 100 nM. | Br J Pharmacol. 2000 Dec;131(8):1673-83 |
A818-4 pancreatic adenocarcinoma cells | 500 nM | 6 days | Did not induce apoptosis | Br J Cancer. 2002 Aug 27;87(5):555-61 |
AsPc-1 pancreatic adenocarcinoma cells | 500 nM | 6 days | Induced apoptosis | Br J Cancer. 2002 Aug 27;87(5):555-61 |
T3M-4 pancreatic adenocarcinoma cells | 500 nM | 6 days | Induced apoptosis, decreased Bcl-2/Bax ratio | Br J Cancer. 2002 Aug 27;87(5):555-61 |
BxPc-3 pancreatic adenocarcinoma cells | 500 nM | 6 days | Induced apoptosis, decreased Bcl-2/Bax ratio | Br J Cancer. 2002 Aug 27;87(5):555-61 |
Administration | Dosage | Frequency | Description | References | ||
Nude rats | Human neuroblastoma xenograft model | Oral | 2 mg/day or 2.5 mg twice daily | Once or twice daily for 10-12 days | Evaluate the anti-tumor effects and toxicity of 9-cis-retinoic acid. Results showed that 2.5 mg twice daily significantly reduced tumor volume at day 10 but did not significantly reduce tumor weight. | Br J Cancer. 2001 Dec 14;85(12):2004-9 |
Mice | Mouse tail lymphedema model | Intraperitoneal injection | 0.8 mg/kg | Daily for 32 days | 9-cisRA significantly reduced tail lymphedema and promoted lymphatic vessel regeneration in mice | Circulation. 2012 Feb 21;125(7):872-82 |
计算器 | ||||
存储液制备 | ![]() |
1mg | 5mg | 10mg |
1 mM 5 mM 10 mM |
3.33mL 0.67mL 0.33mL |
16.64mL 3.33mL 1.66mL |
33.28mL 6.66mL 3.33mL |
CAS号 | 5300-03-8 |
分子式 | C20H28O2 |
分子量 | 300.44 |
SMILES Code | CC(/C=C/C=C(\C=C\C1=C(CCCC(C)1C)C)C)=C\C(O)=O |
MDL No. | MFCD00270072 |
别名 | Alitretinoin; NSC 659772; Panrexin; Panretin. Panretyn; 9-cis-retinoic acid. Alitretinoin; LGD1057; 9-CRA. 9-cis-RA. ALRT1057; 9-cis RA; Panretin |
运输 | 蓝冰 |
存储条件 |
In solvent -20°C: 3-6个月 -80°C: 12个月 Pure form Keep in dark place, inert atmosphere, store in freezer, under -20°C |
溶解方案 |
DMSO: 25 mg/mL(83.21 mM),配合低频超声助溶,注意:DMSO长时间开封后,会吸水并导致溶解能力下降,请避免使用长期开封的DMSO 以下溶解方案都请先按照体外实验的方式配制澄清的储备液,再依次添加助溶剂: ——为保证实验结果的可靠性,澄清的储备液可以根据储存条件,适当保存;体内实验的工作液,建议现用现配,当天使用; 以下溶剂前显示的百分比是指该溶剂在终溶液中的体积占比;如在配制过程中出现沉淀、析出现象,可以通过加热和/或超声的方式助溶
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