1415030-17-9
Chemical Structure
APX2014
- CAS No.: 1415030-17-9
- Formula:C18H19NO5
- Molecular Weight:329.35
IUPAC Name: (E)-N-methoxy-2-((3-methoxy-1,4-dioxo-1,4-dihydronaphthalen-2-yl)methylene)pentanamide
InChIKey: HVWUGMMHPTXECQ-ZHACJKMWSA-N
SMILES: O=C(/C(CCC)=C/C(C(C1=C2C=CC=C1)=O)=C(OC)C2=O)NOC
Biological Activity: APX2014 is a Ref-1/APE1 inhibitor that inhibits Ref-1-induced transcription factor-DNA binding, thereby reducing the activation level of NF-κB and the expression of downstream pro-angiogenic targets. APX2014 blocks endothelial cell proliferation, lumen formation, migration and choroidal sprouting to exert anti-angiogenic activity. APX2014 activates the ISR pathway, promotes the death of pancreatic cancer cells and cancer-associated fibroblasts, and induces apoptosis in the absence of PRDX1. APX2014 inhibits the growth of pancreatic cancer spheroids, reduces the volume/weight of xenograft tumors, and decreases Ki-67 levels by targeting PRDX1. APX2014 can be used in research related to macular degeneration, retinopathy and pancreatic ductal adenocarcinoma[1][2][3].
| Cat. No. | Product Name | Purity | Description | Pricing | |||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
|
|
APX2014 | APX2014 is a Ref-1/APE1 inhibitor that inhibits Ref-1-induced transcription factor-DNA binding, thereby reducing the activation level of NF-κB and the expression of downstream pro-angiogenic targets. APX2014 blocks endothelial cell proliferation, lumen formation, migration and choroidal sprouting to exert anti-angiogenic activity. APX2014 activates the ISR pathway, promotes the death of pancreatic cancer cells and cancer-associated fibroblasts, and induces apoptosis in the absence of PRDX1. APX2014 inhibits the growth of pancreatic cancer spheroids, reduces the volume/weight of xenograft tumors, and decreases Ki-67 levels by targeting PRDX1. APX2014 can be used in research related to macular degeneration, retinopathy and pancreatic ductal adenocarcinoma. | |||||||||||||||||||||
|
loading...
/
|
|||||||||||||||||||||||
References
- [1]. Sardar Pasha SPB, et al. Ref-1/APE1 Inhibition with Novel Small Molecules Blocks Ocular Neovascularization. The Journal of pharmacology and experimental therapeutics. 2018 Oct;367(1):108-118.
- [2]. Kiran S, et al. The absence of Peroxiredoxin-1 in human pancreatic ductal adenocarcinoma (PDAC) markedly reduces cell survival and tumor growth when coupled with the inhibition of Ref-1 redox signaling. Redox biology. 2025 Oct;86:103848.
- [3]. Mijit M, et al. Activation of the integrated stress response (ISR) pathways in response to Ref-1 inhibition in human pancreatic cancer and its tumor microenvironment. Frontiers in medicine. 2023;10:1146115.
