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ADH-1 {[allProObj[0].p_purity_real_show]}

货号:A324415 同义名: N-Ac-CHAVC-NH2

ADH-1是一种血管靶向剂,具有潜在的抗肿瘤和抗血管生成活性,通过选择性竞争性结合并阻断 N-钙粘蛋白发挥作用。

ADH-1 化学结构 CAS号:229971-81-7
ADH-1 化学结构
CAS号:229971-81-7
ADH-1 3D分子结构
CAS号:229971-81-7
ADH-1 化学结构 CAS号:229971-81-7
ADH-1 3D分子结构 CAS号:229971-81-7
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ADH-1 纯度/质量文件 产品仅供科研

货号:A324415 标准纯度: {[allProObj[0].p_purity_real_show]}
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产品名称 Dehydrogenase 其他靶点 纯度
Trilostane 99+%
AGI-6780 +++

IDH2 R140Q mutant, IC50: 23 nM

99%+
Gimeracil 98%
AGI-5198 ++

R132H-IDH1, IC50: 70 nM

R132C-IDH1, IC50: 0.16 μM

99%+
SW033291 ++++

15-PGDH, IC50: 1.5 nM

15-PGDH, Ki: 0.1 nM

99%+
Mycophenolic acid 99+%
Fomepizole 98%
Leflunomide 98%
3-Nitropropanoic acid 99%+
Isovaleramide 99%
Mycophenolate Mofetil +++

Inosine monophosphate dehydrogenase I, IC50: 39 nM

Inosine monophosphate dehydrogenase II, IC50: 27 nM

98%
MK-8245 ++++

SCD1 (mouse), IC50: 1 nM

SCD1 (rat), IC50: 3 nM

99%+
Vidofludimus ++

Human DHODH, IC50: 134 nM

99%+
Emodin 98%
Ivosidenib 98%
NCT-501 ++

ALDH1A1, IC50: 40 nM

98%
Gossypol 99%+
Devimistat 98%
Disulfiram 98%+
Enasidenib ++++

IDH2, IC50: 12 nM

98%
PluriSIn 1 99%+
ML390 +

DHODH, IC50: 0.56 μM

99%+
Teriflunomide 99%+
Daidzin +++

ALDH-Ⅰ, Ki: 20 nM

98+%
18β-Glycyrrhetinic acid 99%
RRx-001 95%
NCT-503 +

PHGDH, IC50: 2.5 μM

99%+
Vorasidenib 99%+
Ammonium Glycyrrhizinate(x:1) 98+%
1. 鼠标悬停在“+”上可以显示相关IC50的具体数值。"+"越多,抑制作用越强。2. "✔"表示该化合物对相应的亚型有抑制作用,但抑制强度暂时没有相关数据。

ADH-1 生物活性

描述 ADH-1 (0.2 mg/mL) inhibits collagen I-induced alterations in pancreatic cancer cells and significantly suppresses cell motility induced by N-cadherin expression. ADH-1 (0, 0.1, 0.2, 0.5 and 1.0 mg/mL) induces apoptosis in a dose-dependent and N-cadherin-dependent manner [1].
体内研究

ADH-1 (50 mg/kg) markedly inhibits tumor growth and metastasis in a murine model of pancreatic cancer. Additionally, ADH-1 prevents tumor cell invasion and metastasis in an orthotopic model of pancreatic cancer using N-cadherin-overexpressing BxPC-3 cells [1].

ADH-1, at the doses tested, does not exhibit antiangiogenic activity in a rat aortic ring assay or demonstrate antitumor efficacy in a PC3 subcutaneous xenograft tumor model [2].

In A375 xenografts, but not in DM443 xenografts, ADH-1 treatment leads to an increase in phosphorylation of AKT at serine 473. Additionally, ADH-1 slightly reduces N-cadherin expression in both xenografts [3].

体外研究

ADH-1 (0.2 mg/mL) inhibits collagen I-induced alterations in pancreatic cancer cells and significantly suppresses cell motility induced by N-cadherin expression. ADH-1 (0, 0.1, 0.2, 0.5 and 1.0 mg/mL) induces apoptosis in a dose-dependent and N-cadherin-dependent manner [1].

ADH-1 细胞实验

Cell Line
Concentration Treated Time Description References
Fibroblasts (HCA2-hTERT) 1 mg/ml 12, 24 or 48 h ADH-1 had no effect on the survival of fibroblasts PLoS One. 2012;7(2):e31206
Human airway smooth muscle cells (HASM) 250 μg/ml 10 min To evaluate the effect of ADH-1 on F-actin remodeling in HASM cells, results showed that ADH-1 significantly reduced histamine-induced F-actin formation. Sci Adv. 2024 Nov 29;10(48):eadp8872
Human airway smooth muscle cells (HASM) 500 μg/ml 24 h To evaluate the effect of ADH-1 on HASM cell contractility, results showed that ADH-1 significantly inhibited histamine-induced cell contraction. Sci Adv. 2024 Nov 29;10(48):eadp8872
Human umbilical vein endothelial cells (HUVEC) 1mg/mL 1 hour To evaluate the effect of ADH-1 on HUVEC cell permeability. Results showed that ADH-1 treatment approximately doubled the permeability of HUVEC cells to 40kDa FITC-dextran. Ann Surg. 2015 Feb;261(2):368-77
MDA-MB-468 cells 40 µM 48 h To evaluate the effect of ADH-1 on the proliferation and attachment of MDA-MB-468 cells. Results showed that ADH-1 significantly inhibited the attachment of MDA-MB-468 cells. J Cell Mol Med. 2022 Apr;26(8):2392-2403
DU145 cells 40 µM 48 h To evaluate the effect of ADH-1 on the proliferation and attachment of DU145 cells. Results showed that ADH-1 had a weaker inhibitory effect on the attachment of DU145 cells. J Cell Mol Med. 2022 Apr;26(8):2392-2403
PC3 cells 40 µM 48 h To evaluate the effect of ADH-1 on the proliferation and attachment of PC3 cells. Results showed that ADH-1 significantly inhibited the proliferation and attachment of PC3 cells. J Cell Mol Med. 2022 Apr;26(8):2392-2403
SH-SY5Y cells 0.5 mg/ml 24 h Treatment with ADH-1 resulted in significant decrease of N-cadherin immunoreactivity at cell-cell contact sites J Biol Chem. 2011 Mar 4;286(9):7619-28
Epithelial cells (MCF-7) 1 mg/ml 12, 24 or 48 h ADH-1 had no effect on the survival of N-cadherin negative epithelial cells PLoS One. 2012;7(2):e31206
Neuroblastoma cell lines (CLB-GA, IMR32, SK-N-SH) 0.25; 0.50 or 1 mg/ml 12, 24 or 48 h ADH-1 strongly inhibited neuroblastoma cell proliferation in vitro by inducing apoptosis PLoS One. 2012;7(2):e31206

ADH-1 动物实验

Species
Animal Model
Administration Dosage Frequency Description References
Mice (Balb/c) Allergic airway inflammation model Intraperitoneal injection 200 mg/kg Single dose To evaluate the effect of ADH-1 on airway hyperresponsiveness in an allergic airway inflammation model, results showed that ADH-1 significantly reduced MCh-induced airway resistance. Sci Adv. 2024 Nov 29;10(48):eadp8872
NOD SCID gamma (NSG) mice PC3 tumor model Intraperitoneal injection 200 mg/kg 5 days a week To evaluate the adjuvant effect of ADH-1 on TIL-related therapy J Immunother Cancer. 2021 Mar;9(3):e002138.
Nude rats DM443 and A375 melanoma xenograft models Intraperitoneal injection 100 mg/kg Single injection To evaluate the effect of ADH-1 on melanoma xenograft models. Results showed that ADH-1 increased vascular permeability but did not significantly alter tumor interstitial fluid pressure. Additionally, ADH-1 increased LPAM delivery but had no significant effect on TMZ delivery. Ann Surg. 2015 Feb;261(2):368-77

ADH-1 参考文献

[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

ADH-1 实验方案

计算器
存储液制备 1mg 5mg 10mg

1 mM

5 mM

10 mM

1.75mL

0.35mL

0.18mL

8.76mL

1.75mL

0.88mL

17.52mL

3.50mL

1.75mL

ADH-1 技术信息

CAS号229971-81-7
分子式C22H34N8O6S2
分子量 570.69
SMILES Code O=C([C@@H](NC([C@H](C(C)C)NC([C@H](C)NC([C@H](CC1=CN=CN1)N2)=O)=O)=O)CSSC[C@H](NC(C)=O)C2=O)N
MDL No. MFCD18251730
别名 N-Ac-CHAVC-NH2
运输蓝冰
InChI Key FQVLRGLGWNWPSS-BXBUPLCLSA-N
Pubchem ID 9916058
存储条件

In solvent -20°C: 3-6个月 -80°C: 12个月

Pure form Keep in dark place, sealed in dry, store in freezer, under -20°C

溶解方案

DMSO: 250 mg/mL(438.07 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

请根据您的动物给药指南选择适当的溶解方案。
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
方案 一
方案 二
方案 三
配制的工作液建议现用现配,短期内尽快用完。 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
方案 一
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