Referencia número: HY-120153

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.

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No. CAS: 1415030-17-9
Fòrmula: C₁₈H₁₉NO₅
Peso molecular:329.35

Almacenamiento:

Please store the product under the recommended conditions in the Certificate of Analysis.

APX2014 Chemical Structure

No. CAS: 1415030-17-9

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Use of MCE Products

Strong Fluorescence Signal / Multi-Disciplinary Applications / High Fluorescence Specificity

Actividad biológica
- Descripciòn
- Cellular Effect
- In Vitro
- In Vivo
Chemical Information
Pureza y Documentación
Referencias
Calculators
Help & FAQs
Classifications
Bioz

Actividad biológica

Descripciòn

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Cellular Effect

Cell Line	Type	Value	Description	References
RF/6A	GI50	5.0 μM	Antiproliferative activity against macaque choroidal endothelial cells (Rf/6a) assessed as reduction in cell viability incubated for 24-48 hrs by alamarBlue assay. Antiproliferative activity against macaque choroidal endothelial cells (Rf/6a) assessed as reduction in cell viability incubated for 24-48 hrs by alamarBlue assay.	30076264
Pa03C	IC50	8.8 μM	Reduction of cell viability in human Pa03C pancreatic ductal adenocarcinoma scrambled control cells assessed by alamarBlue fluorescence after 48 h incubation. Reduction of cell viability in human Pa03C pancreatic ductal adenocarcinoma scrambled control cells assessed by alamarBlue fluorescence after 48 h incubation.	40902319
Pa03C	IC50	3.1 μM	Reduction of cell viability in human Pa03C pancreatic ductal adenocarcinoma PRDX1 knockdown cells assessed by alamarBlue fluorescence after 48 h incubation. Reduction of cell viability in human Pa03C pancreatic ductal adenocarcinoma PRDX1 knockdown cells assessed by alamarBlue fluorescence after 48 h incubation.	40902319
PANC-1	IC50	8.4 μM	Reduction of cell viability in human Panc-1 pancreatic ductal adenocarcinoma scrambled control cells assessed by alamarBlue fluorescence after 48 h incubation. Reduction of cell viability in human Panc-1 pancreatic ductal adenocarcinoma scrambled control cells assessed by alamarBlue fluorescence after 48 h incubation.	40902319
PANC-1	IC50	2.0 μM	Reduction of cell viability in human Panc-1 pancreatic ductal adenocarcinoma PRDX1 knockdown cells assessed by alamarBlue fluorescence after 48 h incubation. Reduction of cell viability in human Panc-1 pancreatic ductal adenocarcinoma PRDX1 knockdown cells assessed by alamarBlue fluorescence after 48 h incubation.	40902319

In Vitro

APX2014 (0.3-4 μM; 30 min) potently inhibits Ref-1-induced AP-1 DNA binding in cell-free EMSA assays, with an IC₅₀ of 0.2 μM^[1].
APX2014 binds directly to a small surface pocket on purified Ref-1 and targets the redox regulatory function of Ref-1 without affecting its DNA repair activity^[2].
APX2014 (24-48 h) inhibits the proliferation of human retinal microvascular endothelial cells in vitro with a GI₅₀ of 110 nM; it also inhibits the proliferation of rhesus monkey choroidal endothelial cells (Rf/6a) in vitro with a GI₅₀ value of 5.0 μM^[1].
APX2014 (0.5-10 μM; 8-16 h) dose-dependently inhibits the migration of human retinal microvascular endothelial cells (HRECs) and rhesus monkey choroidal endothelial cells (Rf/6a) in vitro scratch assays^[1].
APX2014 (0.03-0.3 μM) dose-dependently inhibits tube formation by human retinal microvascular endothelial cells (HRECs) and rhesus monkey choroidal endothelial cells (Rf/6a) in in vitro Matrigel assays^[1].
APX2014 (0.03-0.3 μM; 17 h) dose-dependently blocks human retinal microvascular endothelial cells (HRECs) from entering the S phase and reduces their proliferative capacity^[1].
APX2014 (0.03-0.3 μM; 17 h) dose-dependently inhibits TNF-α-mediated nuclear translocation of NF-κB p65 and reduces the mRNA expression of pro-angiogenic genes (VEGFA, VCAM1, CCL20) in human retinal microvascular endothelial cells (HRECs)^[1].
APX2014 (0.63‑12.5 μM; 48 h) exhibited enhanced cellular sensitivity upon PRDX1 knockdown in Pa03C, Panc‑1 pancreatic ductal adenocarcinoma (PDAC) cells and CAF19 fibroblasts; knockdown of other peroxiredoxins did not alter cellular sensitivity to this agent^[2].
APX2014 (5-10 μM; 24 h) inhibits the transcriptional activities of HIF-1α and NF-κB in Pa03C pancreatic ductal adenocarcinoma (PDAC) cells, and enhanced inhibition is observed in PRDX1-knockdown or PRDX1-knockout cells^[2].
APX2014 (2.5-10 μM; administered on days 4-12 of spheroid culture) exerts stronger growth inhibitory effects on Pa03C PRDX1KO PDAC spheroids than on Cas9 control spheroids, both in monoculture and CAF co-culture systems; when co-cultured with PRDX1KD CAFs, it also induces significant CAF death at multiple concentrations^[2].
APX2014 (5-10 μM; 24-48 h) induces dose- and time-dependent late apoptosis/necrosis in Pa03C PRDX1KO 1A2 pancreatic ductal adenocarcinoma (PDAC) cells^[2].
APX2014 (5-20 μM; 6 h) activates the integrated stress response (ISR) pathway in Pa03C human pancreatic ductal adenocarcinoma (Pa02C, Panc10.05) cells via dose-dependent induction of p-PERK, p-eIF2α and ATF4^[3].
APX2014 (0.0001-100 μM; 6 h) potently activates the transcriptional activity of ATF4 in HEK293 cells, and its efficacy is superior to that of APX2009 (HY-120069) and APX3330 (HY-19357)^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Cell Cycle Analysis^[1]

Cell Line:

human retinal microvascular endothelial cells (HRECs)
Concentration:

0.0, 0.1, 0.3 μM
Incubation Time:

17 h
Result:

Dose-dependently reduced the percentage of HRECs incorporating EdU (HY-118411) (a marker of S-phase entry) and expressing Ki-67 (a marker of proliferating cells).

Cell Migration Assay ^[1]

Cell Line:

human retinal microvascular endothelial cells (HRECs)
Concentration:

0.5, 5, 10 μM
Incubation Time:

8 h (HRECs)
16 h (Rf/6a cells)
Result:

Dose-dependently reduced the percentage of migrated HRECs relative to DMSO control.
Dose-dependently reduced the percentage of migrated Rf/6a cells relative to DMSO control.

Cell Viability Assay^[2]

Cell Line:

Pa03C and Panc-1 pancreatic ductal adenocarcinoma cells, CAF19 cancer-associated fibroblasts (with siRNA-mediated PRDX1 knockdown or scrambled control)
Concentration:

0.63, 1.3, 2.5, 5, 10, 12.5 μM
Incubation Time:

48 h
Result:

Reduced cell viability in Pa03C cells with an IC₅₀ of 8.8 μM in scrambled control cells and 3.1 μM in PRDX1 knockdown cells.
Reduced cell viability in Panc-1 cells with an IC₅₀ of 8.4 μM in scrambled control cells and 2.0 μM in PRDX1 knockdown cells.
Reduced cell viability in CAF19 cells with an IC₅₀ of 4.7 μM in scrambled control cells and 2.5 μM in PRDX1 knockdown cells.
Enhanced cytotoxicity was significantly increased by PRDX1 knockdown across all cell lines.
Did not have altered cytotoxicity enhancement from knockdown of PRDX2-6 in Pa03C cells.

Apoptosis Analysis^[2]

Cell Line:

Pa03C Cas9 control and PRDX1-knockout 1A2 PDAC cells
Concentration:

5, 10 μM
Incubation Time:

24 h, 48 h
Result:

Induced late apoptosis in 11.2% of PRDX1KO 1A2 cells and 3.8% of Cas9 control cells after 24 h treatment with 10 μM.
Induced late apoptosis in 52.6% of PRDX1KO 1A2 cells and 12.4% of Cas9 control cells after 48 h treatment with 10 μM.
Induced late apoptosis in 14.0% of PRDX1KO 1A2 cells after 48 h treatment with 5 μM, showing dose-dependent apoptosis in these cells.

Cell Proliferation Assay^[2]

Cell Line:

Pa03C Cas9 control, PRDX1KO 1A2, and PRDX1KO 1C3 PDAC cells, CAF19 fibroblasts (with or without siRNA-mediated PRDX1 knockdown)
Concentration:

2.5, 5, 10 μM
Incubation Time:

administered on Days 4, 8, and 12 of spheroid culture
Result:

Reduced growth of PRDX1KO tumor spheroids (1A2 and 1C3) significantly more than Cas9 control spheroids.
Reduced tumor spheroid growth in co-cultures of PRDX1KO tumor cells and PRDX1-intact CAFs, with CAFs providing protection compared to monocultures, but did not reduce CAF viability.
Reduced tumor spheroid growth modestly at 2.5 μM and caused significant, dose-dependent reduction in CAF viability across 2.5-10 μM in co-cultures of PRDX1KO tumor cells and PRDX1KD CAFs.

Western Blot Analysis^[3]

Cell Line:

human pancreatic ductal adenocarcinoma (PDAC) Pa03C cells
Concentration:

5, 10, 20 μM
Incubation Time:

6 h
Result:

Induced dose-dependent activation of the ISR kinase p-PERK (with stronger induction than APX2009) and, to a lesser extent, p-GCN2.
Triggered dose-dependent increases in phosphorylated eIF2α (p-eIF2α) and its downstream target ATF4.
Left Ref-1 protein levels unchanged.

Western Blot Analysis^[3]

Cell Line:

human PDAC cell lines (Pa02C, Panc10.05)
Concentration:

5, 10, 20 μM
Incubation Time:

6 h
Result:

Induced dose-dependent activation of the ISR pathway, including increased levels of p-PERK, p-eIF2α, and ATF4, consistent with results in Pa03C cells.

In Vivo

APX2014 (50 mg/kg; i.t.; once daily; 5 days of treatment followed by 2 days of rest) significantly reduces tumor volume, tumor weight, and tumor cell proliferation, and improves survival in NSG mice bearing PRDX1-knockout pancreatic ductal adenocarcinoma xenografts^[2].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

Animal Model:

NSG (NOD.Cg-Prkdc scid Il2rg tm1Wjl/SzJ) (4-6-week-old, age-matched)^[2]
Dosage:

50 mg/kg
Administration:

i.t.; once daily; 5 days of treatment followed by 2 days of rest
Result:

Reduced tumor volumes significantly compared to vehicle controls in mice bearing PRDX1-knockout clones 1A2 and 1C3.
Reduced tumor weights significantly compared to vehicle controls in mice bearing PRDX1-knockout clones 1A2 and 1C3.
Extended survival in all treatment groups.
Reduced Ref-1 levels in PRDX1-knockout 1A2 tumors.
Reduced Ki-67 staining in PRDX1-knockout 1A2 tumors, indicating decreased tumor cell proliferation.

Chemical Information

No. CAS 1415030-17-9
Peso molecular 329.35
Fòrmula C₁₈H₁₉NO₅
SMILES

O=C(/C(CCC)=C/C(C(C1=C2C=CC=C1)=O)=C(OC)C2=O)NOC
Envío

Room temperature in continental US; may vary elsewhere.
Almacenamiento

Please store the product under the recommended conditions in the Certificate of Analysis.

Pureza y Documentación

Instrucciones de manejo (2659 KB)

Referencias

[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.

Calculators

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Help & FAQs

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1. Before opening the cap, centrifuge the vial at 13000 rpm for 20-30 seconds. This step will ensure that any lyophilized powder that may have adhered to the cap or walls is collected at the bottom of the vial, minimizing the risk of product loss.

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APX2014

Ver todos los productos específicos de isoformas NF-κB

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