AGX51
目录号 : GC38590
AGX51是首个pan-Id(DNA结合/分化蛋白抑制剂)拮抗剂和降解剂,通过抑制Id1与E47蛋白的相互作用,诱导泛素介导的Ids蛋白降解,从而抑制细胞生长并降低细胞活力。
Cas No.:330834-54-3
Sample solution is provided at 25 µL, 10mM.
AGX51 is the first pan-Id (DNA binding/differentiation protein inhibitor) antagonist and degrader. It inhibits the interaction between Id1 and E47 protein, induces ubiquitin-mediated degradation of Ids protein, thereby inhibiting cell growth and reducing cell viability[1]. AGX51 can inhibit the formation of pathological ocular neovascularization and can also be used in cancer research[2, 3].
In vitro, AGX51 (0-60μM) treatment of breast cancer cell lines (4T1 and nine other cell lines) for 24-72h significantly inhibited cell growth and viability[4]. AGX51 (0-40μM) treatment of INA-6 BRE-luc cells reduced luciferase activity after BMP9 treatment, and this reduction was not dependent on cell death[5]. AGX51 (40μM) treatment of MDA-MB-231 cells for 72h significantly inhibited cell proliferation and significantly reduced Ki67 expression[6].
In vivo, AGX51 (15mg/kg) was intraperitoneally injected into mice bearing MDA-MB-231 cell xenografts for 12 days, significantly inhibiting tumor growth[6]. AGX51 (30mg/kg) was intraperitoneally injected into mice bearing low oscillatory shear stress (OSS)-mediated atherosclerosis for 4 weeks, significantly inhibiting the expression of ID1 protein, reducing foam cells, restoring intimal thickness, and inhibiting lipid and collagen fiber deposition caused by OSS[7].
References:
[1] Lighter D J. Characterization of the Inhibitor of Differentiation (ID) Family in Ovarian Cancer[D]. San Diego State University, 2023.
[2] Wojnarowicz P M, e Silva R L, Ohnaka M, et al. A small-molecule pan-id antagonist inhibits pathologic ocular neovascularization[J]. Cell reports, 2019, 29(1): 62-75. e7.
[3] Zhong G, Wang Y, Wang Q, et al. Discovery of novel ID2 antagonists from pharmacophore-based virtual screening as potential therapeutics for glioma[J]. Bioorganic & Medicinal Chemistry, 2021, 49: 116427.
[4] Wojnarowicz P M, Escolano M G, Huang Y H, et al. Anti-tumor effects of an ID antagonist with no observed acquired resistance[J]. NPJ Breast Cancer, 2021, 7(1): 58.
[5] Møen J. FKBP12 and regulation of ALK2-and ALK3-ligand activity in multiple myeloma cells[D]. NTNU, 2024.
[6] Toro C D, Real S M, Laurito S R, et al. Exploring ID4 as a Driver of Aggression and a Therapeutic Target in Triple-Negative Breast Cancer[J]. bioRxiv, 2025: 2025.02. 07.637072.
[7] Jun Q, Yang X, Wang B, et al. ID1 protein inhibitor depresses low-oscillating shear stress-mediated EndMT and atherosclerosis by Snail and Wnt/β-catenin signalling pathways[J]. 2024.
AGX51是首个pan-Id(DNA结合/分化蛋白抑制剂)拮抗剂和降解剂,通过抑制Id1与E47蛋白的相互作用,诱导泛素介导的Ids蛋白降解,从而抑制细胞生长并降低细胞活力[1]。AGX51能够抑制病理性眼部新生血管的形成,还能够用于癌症研究[2, 3]。
在体外,AGX51(0-60μM)处理乳腺癌细胞系(4T1和其他九种细胞)24-72h,显著抑制了细胞的生长和活力[4]。AGX51(0-40μM)处理INA-6 BRE-luc细胞,降低了BMP9处理后的荧光素酶活性,并且这种降低并不依赖于细胞死亡[5]。AGX51(40μM)处理MDA-MB-231细胞72h,显著抑制了细胞增殖,显著减少了Ki67的表达[6]。
在体内,AGX51(15mg/kg)通过腹腔注射治疗MDA-MB-231细胞异种移植小鼠12天,显著抑制了肿瘤生长[6]。AGX51(30mg/kg)通过腹腔注射治疗低振荡剪切应力(OSS)介导的动脉粥样硬化小鼠4周,显著抑制了ID1蛋白的表达,减少了泡沫细胞,恢复了内膜厚度,抑制了OSS引起的脂质沉积及胶原纤维沉积[7]。
Cell experiment [1]: | |
Cell lines | 4T1 cells and nine other breast cancer cell lines representing the major breast cancer subtypes (ER+, HER2+, and TNBC) |
Preparation Method | Cells were treated with AGX51 (0, 5, 10, 20, 40, 60μM) and incubated for 24, 48, and 72h, each condition was done in triplicate. At each time point, 40µL of MTT reagent (5mg/mL) was added per well and the cells were incubated for 4h. |
Reaction Conditions | 0, 5, 10, 20, 40, 60μM; 24, 48, 72h |
Applications | AGX51 treatment of cancer cell lines impairs cell growth and viability. |
Animal experiment [2]: | |
Animal models | ApoE-/- mice |
Preparation Method | 5 oscillating shear stress (OSS) ApoE-/- mice were intraperitoneally injected with the ID1 inhibitor AGX51 at a dose of 30mg/kg body weight for 4 weeks as the experimental group. The other 5 OSS ApoE-/- mice were intraperitoneally injected with the same amount of DMSO as the Ctrl group, and the mice were euthanized by excessive chloral hydrate. The samples were taken from the origin of the left common carotid artery at the aortic arch to the root of the bifurcation of the internal and external carotid arteries. After serial sectioning, oil red O, H&E Staining, Masson staining, immunohistochemistry, and immunofluorescence staining were performed. |
Dosage form | 30mg/kg; 4 weeks; i.p. |
Applications | AGX51 (30mg/kg) can effectively inhibit the expression of ID1 protein. After AGX51 treatment, foam cells were significantly reduced and the degree of intimal thickening was restored. AGX51 can inhibit OSS-induced lipid deposition and collagen fiber deposition. |
References: |
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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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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2.
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