Cat. No.: HY-184446

CDC25A/NF-κB-IN-1

CDC25A/NF-κB-IN-1 is an effective dual-target inhibitor of CDC25A and NF-κB, and is a prodrug of Pt(IV). CDC25A/NF-κB-IN-1 has anticancer activity and low cytotoxicity to normal cells. CDC25A/NF-κB-IN-1 can trigger a variety of anticancer mechanisms, including S phase cell cycle arrest, mitochondrial endogenous apoptosis, endoplasmic reticulum stress, autophagy-dependent ferroptosis. CDC25A/NF-κB-IN-1 has good safety and can be used for ovarian cancer research.

For research use only. We do not sell to patients.

Formula: C₁₈H₂₃Cl₄N₃O₆Pt
Molecular Weight:714.29

Storage:

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

CDC25A/NF-κB-IN-1 Chemical Structure

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Fluorescent Dye

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

Biological Activity
- Description
- IC₅₀ & Target
- Cellular Effect
- In Vitro
- Parmacokinetics
- In Vivo
Chemical Information
Purity & Documentation
References
Calculators
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Classifications
Bioz

Biological Activity

Description

IC₅₀ & Target^[1]

Caspase-9

Bcl-2

Bax

eIF2-α

Cdc25A

All CDK Isoforms :

All NF-κB Isoforms :

All Caspase Isoforms :

All Bcl-2 Family Isoforms :

Cellular Effect

Cell Line	Type	Value	Description	References
A2780	IC50	2.3 μM	Exhibits potent antiproliferative activity against A2780 for 48h. Exhibits potent antiproliferative activity against A2780 for 48h.	42275647
HeLa	IC50	9.1 μM	Exhibits potent antiproliferative activity against HeLa for 48h. Exhibits potent antiproliferative activity against HeLa for 48h.	42275647
HepG2	IC50	11.0 μM	Exhibits potent antiproliferative activity against HepG2 for 48h. Exhibits potent antiproliferative activity against HepG2 for 48h.	42275647
A549	IC50	13.4 μM	Exhibits potent antiproliferative activity against A549 for 48h. Exhibits potent antiproliferative activity against A549 for 48h.	42275647
HCT-116	IC50	23.3 μM	Exhibits potent antiproliferative activity against HCT116 for 48h. Exhibits potent antiproliferative activity against HCT116 for 48h.	42275647

In Vitro

CDC25A/NF-κB-IN-1 (complexe Pt6; 48 h) exhibits potent antiproliferative activity against A2780, HeLa, HepG2, A549 and HCT116 cells, with IC₅₀ values of 2.3, 9.1, 11.0, 13.4 and 23.3 μM, respectively, while showing low cytotoxicity against normal WI-38 fibroblasts (IC₅₀ = 38.4 μM)^[1].
CDC25A/NF-κB-IN-1 (10 μM; 24 h) shows higher cellular uptake in A2780 cells than Cisplatin (HY-17394), with Pt accumulation in the cytoplasm, mitochondria, and nucleus at 71.8, 88.9, and 98.3 ng, respectively^[1].
CDC25A/NF-κB-IN-1 (1-4 μM; 24 h) decreases intracellular GSH levels in A2780 cells in a concentration-dependent manner, with GSH relative contents reduced to approximately 78%, 56%, and 44% at 1, 2, and 4 μM, respectively, compared to the control group (100%)^[1]. CDC25A/NF-κB-IN-1 (4 μM; 24 h) significantly reduces CDC25A protein levels and increases γ-H2AX levels in A2780 cells^[1].
CDC25A/NF-κB-IN-1 (1-4 μM; 24 h) induces S-phase cell cycle arrest in A2780 cells (the proportion of S-phase cells increases from 23.8% to 67.5%) and downregulates CDK2 and Cyclin A levels^[1].
CDC25A/NF-κB-IN-1 (0.5-4 μM; 24 h) induces concentration-dependent apoptosis in A2780 cells (the apoptosis rate increases from 9.8% to 78.5%) and upregulates p53 expression; it also increases γ-H2AX levels in a concentration-dependent manner^[1].
CDC25A/NF-κB-IN-1 (1-4 μM; 24 h) induces a concentration-dependent decrease in mitochondrial membrane potential (the proportion of cells with decreased MMP increases from 1.6% to 33.4%) and ROS accumulation in A2780 cells, and upregulates the expression of Bax, Cyt c, and caspase-9, while downregulating Bcl-2 expression^[1].
CDC25A/NF-κB-IN-1 (2-4 μM; 24 h) upregulates the expression of endoplasmic reticulum stress-related proteins CHOP, p-PERK, and p-eIF2α in A2780 cells^[1].
CDC25A/NF-κB-IN-1 (0.1-0.4 μM; 10 d) inhibits colony formation in A2780 cells in a concentration-dependent manner^[1].
CDC25A/NF-κB-IN-1 (1-4 μM; 24 h) inhibits cell migration in A2780 cells, decreasing the migration rate from 58.2% to 19.7%^[1].
CDC25A/NF-κB-IN-1 (1-4 μM; 24 h) inhibits cell invasion in A2780 cells in a concentration-dependent manner^[1].
CDC25A/NF-κB-IN-1 shows a docking affinity of -9.4 kcal/mol to NF-κB (P65) protein, with an equilibrium dissociation constant (K_D) of 30.8 nM^[1].
CDC25A/NF-κB-IN-1 (4 μM; 24 h) downregulates the expression of p-P65, p-IκBα, and p-IKKβ in TNF-α-stimulated A2780 cells, inhibiting the NF-κB signaling pathway^[1].
CDC25A/NF-κB-IN-1 (1-4 μM; 24 h) induces concentration-dependent lipid peroxidation and autophagosome formation in A2780 cells, downregulates GPX4 and SLC7A11 expression, upregulates LC3-I/II expression, and induces p62 degradation; these effects can be reversed by Ferrostatin-1 (Fer 1) (HY-100579) and Chloroquine (CQ) (HY-17589A)^[1].
CDC25A/NF-κB-IN-1 (4 μM; 24 h) induces autophagy-dependent ferroptosis in A2780 cells, and combined treatment with CQ attenuates lipid peroxidation and restores GPX4 and SLC7A11 expression^[1].

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

Western Blot Analysis^[1]

Cell Line:

A2780 cells
Concentration:

4 μM (Pt6), 10 μM (c2), 10 μM + 10 μM (c2 + CDDP), 10 μM (CDDP)
Incubation Time:

24 h
Result:

Markedly depleted CDC25A protein levels and significantly increased γ-H2AX levels (DNA damage marker). The CDC25A fluorescent signal was attenuated following treatment, ranked as c2 > c2 + CDDP > Pt6 > control.

Western Blot Analysis^[1]

Cell Line:

A2780 cells
Concentration:

1, 2, and 4 μM
Incubation Time:

24 h
Result:

Induced dose-dependent S-phase arrest, with S-phase population increasing from 23.8% (control) to 41.9%, 53.0%, and 67.5% at 1, 2, and 4 μM, respectively, accompanied by decreases in G₀/G₁ fraction.

Western Blot Analysis^[1]

Cell Line:

A2780 cells
Concentration:

2 and 4 μM
Incubation Time:

24 h
Result:

Significantly upregulated pro-apoptotic proteins Bax, Cytm-c, and caspase-9 while downregulating the anti-apoptotic protein Bcl-2, indicating activation of the intrinsic mitochondrial apoptotic pathway.

Western Blot Analysis^[1]

Cell Line:

A2780 cells
Concentration:

2 and 4 μM
Incubation Time:

24 h
Result:

Remarkably upregulated the expression of ER stress-related proteins CHOP, p-PERK, and p-eIF2α, demonstrating effective induction of ER stress.

Cell Proliferation Assay^[1]

Cell Line:

A2780 cells
Concentration:

0.1, 0.2, and 0.4 μM
Incubation Time:

10 days
Result:

Significantly reduced colony formation in a concentration-dependent manner at low concentrations.

Cell Migration Assay ^[1]

Cell Line:

A2780 cells
Concentration:

1, 2, and 4 μM
Incubation Time:

24 h
Result:

Effectively inhibited cell migration, resulting in decreased migration rates of 38.9%, 27.6%, and 19.7%, compared to the control group (58.2%).

Western Blot Analysis^[1]

Cell Line:

A2780 cells
Concentration:

4 μM (Pt6), 10 μM (c2), 10 μM + 10 μM (c2 + CDDP), 10 μM (CDDP)
Incubation Time:

24h (pretreated with 50 ng/mL TNF-α for 6 h)
Result:

Effectively suppressed p65 protein expression. Significantly downregulated phosphorylated NF-κB pathway proteins including p-P65 (p-NF-κB), p-IκBα, and p-IKKβ.

Western Blot Analysis^[1]

Cell Line:

A2780 cells
Concentration:

2 and 4 μM
Incubation Time:

24 h
Result:

Significantly downregulated GPX4 and SLC7A11 levels (ferroptosis markers), upregulated LC3-I/II expression, and induced obvious p62 degradation (autophagy markers). These effects were reversed by Fer-1 (ferroptosis inhibitor) and CQ (autophagy inhibitor).

Cell Viability Assay^[1]

Cell Line:

A2780 cells
Concentration:

4 μM alone or in combination with Fer-1 (2 μM) or CQ (2 μM)
Incubation Time:

24 h
Result:

Cell viability was obviously increased by both Fer-1 and CQ in cells treated with the compound, confirming that cancer cell death is induced at least in part through the promotion of ferroptosis and autophagy.

Cell Invasion Assay^[1]

Cell Line:

A2780 cells
Concentration:

1, 2, and 4 μM
Incubation Time:

24 h
Result:

Showed a dose-dependent inhibitory effect on cell invasion at all tested concentrations.

Apoptosis Analysis^[1]

Cell Line:

A2780 cells
Concentration:

0.5, 1, 2, 3, and 4 μM
Incubation Time:

24 h
Result:

Induced concentration-dependent apoptosis, with total apoptosis rates ranging from 9.8 ± 1.5% to 78.5 ± 5.7%. Viable cells decreased from 96.1% to 21.5%, while early and late apoptotic populations increased dose-dependently.

Parmacokinetics

Species	Dose	Route	T_1/2	CL	AUC_0-∞	AUC_0-12
Mice^[1]	9.5 mg/kg	i.v.	5.2 h	0.26 L/h/kg	8699 μg/L·h	7616.7 μg/L·h

In Vivo

CDC25A/NF-κB-IN-1 (compound Pt6; female BALB/c nude mice; 8-16 mg/kg; intraperitoneal injection; every 2 days for 14 days) significantly inhibits tumor growth in the A2780 xenograft mouse model, with a dose-dependent tumor growth inhibition rate^[1].
CDC25A/NF-κB-IN-1 (compound Pt6; healthy Kunming mice; 8-24 mg/kg; intraperitoneal injection; every 2 days for 14 days) shows good safety, with stable body weight and no major organ damage; doses of 20 and 24 mg/kg cause mortality, while 16 mg/kg induces sharp body weight loss without mortality^[1].

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

Animal Model:

Female BALB/c nude mice bearing A2780 xenograft tumors^[1]^[1]
Dosage:

8 mg/kg, 16 mg/kg (MTD)
Administration:

Intraperitoneal injection (i.p.); seven times over 14 days
Result:

Tumor growth was significantly inhibited in a dose-dependent manner, with tumor volumes suppressed to 237.6 mm³ (8 mg/kg) and 160.1 mm³ (16 mg/kg), corresponding to TGI rates of 77.8% and 85.6%, respectively^[1]. Superior antitumor efficacy was demonstrated ^[1]. Mice in the 8 mg/kg group exhibited stable body weight gain, with less body weight gain suppression^[1]. No significant reduction in organ weights was observed in the experimental groups compared to the control group^[1]. H&E staining of tumor tissues revealed nuclear pyknosis, disordered growth, and abundant apoptotic cells in the experimental groups compared to the cisplatin and c2 + cisplatin groups^[1]. No obvious damage was observed in major organs (heart, liver, spleen, lungs, and kidneys) in the experimental groups^[1]. Higher Pt levels were accumulated in tumors of the experimental groups (8 mg/kg and 16 mg/kg) compared to the cisplatin and c2 + cisplatin groups^[1]. Pt was predominantly distributed in the kidney and liver, similar to the cisplatin group^[1].

Animal Model:

Healthy Kunming (KM) mice^[1]
Dosage:

8 mg/kg, 12 mg/kg, 16 mg/kg (MTD), 20 mg/kg, 24 mg/kg
Administration:

Intraperitoneal injection (i.p.); every 2 days for 14 days
Result:

Mice receiving 8 mg/kg exhibited more stable body weight gain than those in the Cisplatin (HY-17394) and c2 + Cisplatin positive control groups^[1]. Mice treated with 12 mg/kg showed comparable weight changes to the Cisplatin and c2 + Cisplatin groups^[1]. Administration at 20 and 24 mg/kg caused death in some mice within the 14-day period^[1]. At 16 mg/kg, no mortality was observed; however, it induced a sharp decline in body weight, establishing the maximum tolerated dose (MTD) at approximately 16 mg/kg^[1]. H&E staining of organs (heart, liver, spleen, lungs, and kidneys) from mice treated with Pt6 (8 mg/kg and 16 mg/kg) showed no organ damage compared to the control, Cisplatin, and c2 + Cisplatin groups^[1].

Chemical Information

Molecular Weight 714.29
Formula C₁₈H₂₃Cl₄N₃O₆Pt
SMILES

O=C1C(NCCCOC(CCCC(O[Pt](Cl)(Cl)([NH3])([NH3])Cl)=O)=O)=C(Cl)C(C2=CC=CC=C21)=O
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

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

Purity & Documentation

Handling Instructions (2659 KB)

References

[1]. Huang YH, et al. Pt(IV) Complexes Incorporating CDC25A/NF-κB Dual Inhibitory 1,4-Naphthoquinone Derivatives Trigger Multimodal Cell Death in A2780 Ovarian Cancer Cells. J Med Chem. 2026 Jun 25;69(12):14902-14920. [Content Brief]

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Help & FAQs

How should lyophilized recombinant proteins be reconstituted and stored?

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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CDC25A/NF-κB-IN-1

All CDK Isoforms

All NF-κB Isoforms

All Caspase Isoforms

All Bcl-2 Family Isoforms

Biological Activity

Chemical Information

Purity & Documentation

References

Calculators

Help & FAQs

CDC25A/NF-κB-IN-1 Related Classifications

HY-184446 Related Classifications