330834-54-3
Chemical Structure
AGX51
- CAS No.: 330834-54-3
- Formula:C27H29NO4
- Molecular Weight:431.52
IUPAC Name: N-(3-(benzo[d][1,3]dioxol-5-yl)-3-(2-methoxyphenyl)propyl)-N-benzylpropionamide
InChIKey: SRADCMOCDMFMPS-UHFFFAOYSA-N
SMILES: CCC(N(CCC(C1=CC=C(OCO2)C2=C1)C3=CC=CC=C3OC)CC4=CC=CC=C4)=O
Biological Activity: AGX51 is a pan-Id (inhibitors of DNA-binding/differentiation proteins) antagonist that disrupts ID-E protein interactions, thereby triggering ubiquitin-mediated proteasomal degradation of ID1, ID2, ID3 and ID4. AGX51 induces ROS production, G0/G1 cell cycle arrest, non-apoptotic cell death, and regulates EMT-related proteins. AGX51 reduces the proliferation, migration and myofibroblast differentiation of lung fibroblasts, alleviates pulmonary fibrosis, inhibits cancer cell viability and tumor growth, impairs neovascularization, and shows no obvious toxicity in mice. AGX51 can be used in research related to idiopathic pulmonary fibrosis, triple-negative breast cancer, breast cancer, pancreatic ductal adenocarcinoma, colorectal tumors, wet age-related macular degeneration and retinopathy of prematurity[1][2][3][4].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
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AGX51 | 99.33% | AGX51 is a pan-Id (inhibitors of DNA-binding/differentiation proteins) antagonist that disrupts ID-E protein interactions, thereby triggering ubiquitin-mediated proteasomal degradation of ID1, ID2, ID3 and ID4. AGX51 induces ROS production, G0/G1 cell cycle arrest, non-apoptotic cell death, and regulates EMT-related proteins. AGX51 reduces the proliferation, migration and myofibroblast differentiation of lung fibroblasts, alleviates pulmonary fibrosis, inhibits cancer cell viability and tumor growth, impairs neovascularization, and shows no obvious toxicity in mice. AGX51 can be used in research related to idiopathic pulmonary fibrosis, triple-negative breast cancer, breast cancer, pancreatic ductal adenocarcinoma, colorectal tumors, wet age-related macular degeneration and retinopathy of prematurity. | ||||||||||||||||||||
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References
- [1]. Antar SA, et al. Simultaneous inhibition of ID1 and ID3 mitigates fibroblast activation via cell cycle and MEK/ERK pathways in pulmonary fibrosis. Theranostics. 2026;16(11):6081-6098.
- [2]. Toro C, et al. Exploring ID4 as a driver of aggression and a therapeutic target in triple-negative breast cancer. NPJ breast cancer. 2025 Jul 10;11(1):69.
- [3]. Wojnarowicz PM, et al. Anti-tumor effects of an ID antagonist with no observed acquired resistance. NPJ breast cancer. 2021 May 24;7(1):58. [Content Brief]
- [4]. Wojnarowicz PM, et al. A Small-Molecule Pan-Id Antagonist Inhibits Pathologic Ocular Neovascularization. Cell reports. 2019 Oct 01;29(1):62-75.e7.
