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- 详细信息
- 文献和实验
- 技术资料
- 保存条件：
Powder:-20℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year
- 保质期：
Powder:-20℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year
- 英文名：
ADH-1
- 库存：
现询
- 供应商：
北京索莱宝科技有限公司
- CAS号：
229971-81-7
- 规格：
50mg/25mg/10mg/5mg
| 规格： | 50mg | 产品价格： | ￥5190.0 |
|---|---|---|---|
| 规格： | 25mg | 产品价格： | ￥3090.0 |
| 规格： | 10mg | 产品价格： | ￥1690.0 |
| 规格： | 5mg | 产品价格： | ￥990.0 |
| 基本信息 | |
| CAS | No.229971-81-7 |
| 英文名称 | ADH-1 |
| 分子式 | C22H34N8O6S2 |
| 分子量 | 570.69 |
| 溶解性 | Soluble in DMSO(Need ultrasonic) |
| 纯度 | ≥98% |
| 外观(性状) | White to off-white Solid |
| 储存条件 | Powder:-20℃，2 years;Insolvent(母液):-20℃，6 months;-80℃，1 year |
| MDL | MFCD18251730 |
| SMILES | CC1C(=O)NC(C(=O)NC(CSSCC(C(=O)NC(C(=O)N1)CC2=CN=CN2)NC(=O)C)C(=O)N)C(C)C |
| InChIKey | FQVLRGLGWNWPSS-BXBUPLCLSA-N |
| InChI | InChI=1S/C22H34N8O6S2/c1-10(2)17-22(36)29-15(18(23)32)7-37-38-8-16(27-12(4)31)21(35)28-14(5-13-6-24-9-25-13)20(34)26-11(3)19(33)30-17/h6，9-11，14-17H，5，7-8H2，1-4H3，(H2，23，32)(H，24，25)(H，26，34)(H，27，31)(H，28，35)(H，29，36)(H，30，33)/t11-，14-，15-，16-，17-/m0/s1 |
| PubChem CID | 9916058 |
| 靶点 | N-cadherin |
| 通路 | Others |
| 背景说明 | 是选择性和竞争性的N-钙粘蛋白（N-cadherin ）拮抗剂。 |
| 生物活性 | ADH-1 是一种 N-粘连蛋白拮抗剂，可抑制 N-粘连蛋白介导的细胞粘附。[1-3] |
| In Vitro | ADH-1 induced apoptosis in a concentration dependent and N-cadherin dependent manner in pancreatic cancer cells.[1] Cytotoxic activity in human umbilical vein endothelial cells，PC3，and Tsu-Pr1 cells，when ADH1 exposure was evaluated at 500 micromol/l or above.[2] |
| 细胞实验 | ADH-1 treatment resulted in significant reductions in tumor growth and lung metastasis in a mouse model for pancreatic cancer.[1] ADH-1 increased vascular permeability without effecting tumor interstitial fluid pressure，leading to increased delivery of LPAM but not TMZ.[3] |
| 数据来源文献 | [1]. Shintani Y，et al. ADH-1 suppresses N-cadherin-dependent pancreatic cancer progression. Int J Cancer. 2008 Jan 1;122(1):71-7. [2]. Li H，et al. ADH1，an N-cadherin inhibitor，evaluated in preclinical models of angiogenesis and androgen-independent prostate cancer. Anticancer Drugs. 2007 Jun;18(5):563-8. [3]. Turley RS，et al. Targeting N-cadherin increases vascular permeability and differentially activates AKT in melanoma. Ann Surg. 2015 Feb;261(2):368-77. |
| 单位 | 瓶 |
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