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AGX51 Sale

目录号 : GC38590

AGX51, a first-in-class pan-Id (inhibitors of DNA-binding/differentiation proteins) antagonist and degrader, inhibits the Id1-E47 interaction, leading to ubiquitin-mediated degradation of Ids, cell growth arrest, and reduces viability, also inhibits pathologic ocular neovascularization.

AGX51 Chemical Structure

Cas No.:330834-54-3

规格 价格 库存 购买数量
1mg
¥864.00
现货
5mg
¥2,520.00
现货
10mg
¥3,960.00
现货
25mg
¥7,128.00
现货
50mg
¥11,880.00
现货
100mg
¥16,200.00
现货

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Sample solution is provided at 25 µL, 10mM.

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产品描述

AGX51, a first-in-class pan-Id (inhibitors of DNA-binding/differentiation proteins) antagonist and degrader, inhibits the Id1-E47 interaction, leading to ubiquitin-mediated degradation of Ids, cell growth arrest, and reduces viability, also inhibits pathologic ocular neovascularization.

[1] Wojnarowicz PM, et al. Cell Rep. 2019 Oct 1;29(1):62-75.e7.

Chemical Properties

Cas No. 330834-54-3 SDF
Canonical SMILES CCC(N(CCC(C1=CC=C(OCO2)C2=C1)C3=CC=CC=C3OC)CC4=CC=CC=C4)=O
分子式 C27H29NO4 分子量 431.52
溶解度 DMSO: 250 mg/mL (579.35 mM); Ethanol: 100 mg/mL (231.74 mM); Water: < 0.1 mg/mL (insoluble) 储存条件 Store at -20°C
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储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.3174 mL 11.5869 mL 23.1739 mL
5 mM 0.4635 mL 2.3174 mL 4.6348 mL
10 mM 0.2317 mL 1.1587 mL 2.3174 mL
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Research Update

Anti-tumor effects of an ID antagonist with no observed acquired resistance

NPJ Breast Cancer 2021 May 24;7(1):58.PMID:34031428DOI:10.1038/s41523-021-00266-0.

ID proteins are helix-loop-helix (HLH) transcriptional regulators frequently overexpressed in cancer. ID proteins inhibit basic-HLH transcription factors often blocking differentiation and sustaining proliferation. A small-molecule, AGX51, targets ID proteins for degradation and impairs ocular neovascularization in mouse models. Here we show that AGX51 treatment of cancer cell lines impairs cell growth and viability that results from an increase in reactive oxygen species (ROS) production upon ID degradation. In mouse models, AGX51 treatment suppresses breast cancer colonization in the lung, regresses the growth of paclitaxel-resistant breast tumors when combined with paclitaxel and reduces tumor burden in sporadic colorectal neoplasia. Furthermore, in cells and mice, we fail to observe acquired resistance to AGX51 likely the result of the inability to mutate the binding pocket without loss of ID function and efficient degradation of the ID proteins. Thus, AGX51 is a first-in-class compound that antagonizes ID proteins, shows strong anti-tumor effects and may be further developed for the management of multiple cancers.

A Small-Molecule Pan-Id Antagonist Inhibits Pathologic Ocular Neovascularization

Cell Rep 2019 Oct 1;29(1):62-75.e7.PMID:31577956DOI:10.1016/j.celrep.2019.08.073.

Id helix-loop-helix (HLH) proteins (Id1-4) bind E protein bHLH transcription factors, preventing them from forming active transcription complexes that drive changes in cell states. Id proteins are primarily expressed during development to inhibit differentiation, but they become re-expressed in adult tissues in diseases of the vasculature and cancer. We show that the genetic loss of Id1/Id3 reduces ocular neovascularization in mouse models of wet age-related macular degeneration (AMD) and retinopathy of prematurity (ROP). An in silico screen identifies AGX51, a small-molecule Id antagonist. AGX51 inhibits the Id1-E47 interaction, leading to ubiquitin-mediated degradation of Ids, cell growth arrest, and reduced viability. AGX51 is well-tolerated in mice and phenocopies the genetic loss of Id expression in AMD and ROP models by inhibiting retinal neovascularization. Thus, AGX51 is a first-in-class compound that antagonizes an interaction formerly considered undruggable and that may have utility in the management of multiple diseases.

Discovery of novel ID2 antagonists from pharmacophore-based virtual screening as potential therapeutics for glioma

Bioorg Med Chem 2021 Nov 1;49:116427.PMID:34600240DOI:10.1016/j.bmc.2021.116427.

Glioma, especially the most aggressive type glioblastoma multiforme, is a malignant cancer of the central nervous system with a poor prognosis. Traditional treatments are mainly surgery combined with radiotherapy and chemotherapy, which is still far from satisfactory. Therefore, it is of great clinical significance to find new therapeutic agents. Serving as an inhibitor of differentiation, protein ID2 (inhibitor of DNA binding 2) plays an important role in neurogenesis, neovascularization and malignant development of gliomas. It has been shown that ID2 affects the malignant progression of gliomas through different mechanisms. In this study, a pharmacophore-based virtual screening was carried out and 16 hit compounds were purchased for pharmacological evaluations on their ID2 inhibitory activities. Based on the cytotoxicity of these small-molecule compounds, two compounds were shown to effectively inhibit the viability of glioma cells in the micromolar range. Among them, AK-778-XXMU was chosen for further study due to its better solubility in water. A SPR (Surface Plasma Resonance) assay proved the high affinity between AK-778-XXMU and ID2 protein with the KD value as 129 nM. The plausible binding mode of ID2 was studied by molecular docking and it was found to match AGX51 very well in the same binding site. Subsequently, the cancer-suppressing potency of the compound was characterized both in vitro and in vivo. The data demonstrated that compound AK-778-XXMU is a potent ID2 antagonist which has the potential to be developed as a therapeutic agent against glioma.