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Last update 08 May 2025

CDC25B

Last update 08 May 2025

Basic Info

Synonyms

CDC25B, CDC25HU2, cell division cycle 25B

+ [2]

Introduction

Tyrosine protein phosphatase which functions as a dosage-dependent inducer of mitotic progression (PubMed:1836978, PubMed:20360007). Directly dephosphorylates CDK1 and stimulates its kinase activity (PubMed:20360007). Required for G2/M phases of the cell cycle progression and abscission during cytokinesis in a ECT2-dependent manner (PubMed:17332740). The three isoforms seem to have a different level of activity (PubMed:1836978).

Drugs associated with CDC25B

NSC 663284

Target

CDC25A x CDC25B x CDC25C

Mechanism

CDC25A inhibitors [+2]

Active Org.

Shanghai Institute of Materia Medica Chinese Academy of Sci

Originator Org.

University of Pittsburgh

Active Indication

Neoplasms

Inactive Indication-

Drug Highest PhasePreclinical

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

LGH00031

Target

CDC25B

Mechanism

CDC25B inhibitors

Active Org.-

Originator Org.

Shanghai Institute of Materia Medica Chinese Academy of Sci

Active Indication-

Inactive Indication

Neoplasms

Drug Highest PhasePending

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with CDC25B

100 Translational Medicine associated with CDC25B

0 Patents (Medical) associated with CDC25B

659

Literatures (Medical) associated with CDC25B

01 Aug 2025·Computational Biology and Chemistry

Phytoflavonoids as alternative therapeutic effect for melanoma: Integrative Network pharmacology, molecular dynamics and drug-likeness profiling for lead discovery

Article

Author: Panda, Pritipadma ; Prajapati, Manoj Kumar ; Mittal, Abhilasha

Melanoma, an aggressive skin cancer, poses significant therapeutic challenges due to its resistance to conventional therapies and high metastatic potential. From this perspective, phytoflavonoids from different medicinal and aromatic plants gained attention due to their diverse multimodal anticancer effects with higher antioxidant and anti-inflammatory properties. This study explores phytoflavonoid potency against melanoma via a computer-aided drug design (CADD) platform. Using the core moiety of flavonoids (flavan), four most putative targets, such as cyclin-dependent kinases 1 and 5 (CDK1, CDK5), cell division cycles 25B and 225 C (CDC25B, and CDC225C), have been identified through a network pharmacology approach using TNMplot datasets (GenChip and RNA sequence). Further, 44 phytoflavonoids were selected from extensive literature, and molecular docking studies were carried out against four targets along with standard drugs using AutoDock 4.2 software. Subsequently, physicochemical, toxicity, pharmacokinetics, and drug-ability profiles of phytoflavonoids were predicted. Based on potency and drug-ability, we have selected 'CDK1-naringenin' with the standard drug complex, 'CDK1-dinaciclib,' for molecular dynamic simulation at 100 nanoseconds using GROMACS 2020 software. Based on potency (average docking score: 8.35 kcal/mol.), physicochemical properties (obeyed Lipinski rule of five), toxicity (class-IV), fifty percent lethal dose (2000 mg/kg), bioavailability (0.55), drug-likeness score (0.82), along with ideal pharmacokinetics profiles and higher protein-ligand stability, naringenin is considered as a potential and non-toxic anticancer candidate to be used for melanoma as alternative or complementary agent. The integrative and systematic analyses not only highlight the potential of phytoflavonoids but also select the potential lead from the library within limited resources to accelerate the current anticancer drug discovery process.

01 Apr 2025·Theriogenology

Editing the growth differentiation factor 9 gene affects porcine oocytes in vitro maturation by inactivating the maturation promoting factor

Article

Author: Bei, Chang ; Jiao, Yafei ; He, Zuyong ; Liu, Xiaohong ; Guo, Jinming ; Cong, Peiqing ; Liao, Alian ; Jiang, Tiantuan ; Mi, Bingqian ; Jiang, Xintong ; Chen, Yaosheng ; Li, Xinran

Growth differentiation factor 9 (GDF9), an oocyte-secreted factor, plays a vital role in porcine oocyte development. However, its function during oocyte in vitro maturation (IVM) remains unclear. In this study, we achieved GDF9 editing in approximately 59 % of cultured oocytes by cytoplasmic injection of a pre-assembled crRNA-tracrRNA-Cas9 ribonucleoprotein complex into porcine oocytes at the germinal vesicle (GV) stage. GDF9 editing caused significant damage to porcine oocytes during IVM. Additionally, GDF9 editing impaired mitochondrial function, increased reactive oxygen species (ROS) accumulation, and decreased glutathione (GSH) levels. The impaired IVM of GDF9-edited porcine oocytes was primarily driven by active cAMP-PKA signaling, which inhibited MOS expression, leading to the activation of the WEE1B/MYT1 kinase and inactivation of CDC25B phosphatase. This cascade resulted in the inactivation of CDK1, thereby preventing the activation of maturation-promoting factor (MPF) and inhibiting first polar body (PB1) extrusion. Our findings enhance the understanding of GDF9's regulatory role in porcine oocyte IVM and provide a theoretical foundation for improving porcine reproductive performance.

01 Feb 2025·European Journal of Pharmacology

A novel peptide CP29L, selected from the phage displayed cyclic random heptapeptide library, demonstrates its potent inhibitory effects to liver cancer HCCLM3 cells by targeting FOXM1

Article

Author: Xiang, Kun ; Hua, Xinyi ; Shang, Zhixian ; Liang, Anping ; Liu, Xinrong ; Jia, Shijie ; Jiang, Yuhong ; Mao, Canquan ; Chang, Miao

FOXM1 is the "Achilles' heel" of cancers and hence the potential therapeutic target for anticancer drug discovery. In this work, we selected high affinity peptides against the protein of human DNA binding domain of FOXM1 (FOXM1-DBD) from the disulfide-constrained, phage displayed random cyclic heptapeptide library Ph.D.-C7C. We obtained a novel peptide, 9 R-CP29L, which was identified to be a potent anticancer peptide with IC₅₀ values of 9.0 and 11.1 μM at 24 h for HCCLM3 and MD-MBA-231 cells respectively. Molecular docking, CETSA, ITC and immunoblot assays demonstrated that 9 R-CP29L can potentially specifically bind to FOXM1-DBD with a K_d value of 1.25 μM and reduced the expression of FOXM1. In addition, Annexin V/PI flow cytometry, AO/EB staining, PI flow cytometry, clone formation and Transwell assays revealed that 9 R-CP29L also induced cell apoptosis and cell cycle arrest while inhibited the proliferation and migration of HCCLM3 cells. The findings were further supported by the results of qRT-PCR and immunoblot assays for the associated gene (CMYC, CDC25B, BAX, CASPASE3 and MMP2, etc) expression in HCCLM3 cells. Finally, in vivo experiment showed that 9 R-CP29 significantly reduced the tumor growth and downregulated the expression of FOXM1 in HCCLM3 xenograft nude mouse models. Taking together, our work provides a novel FOXM1 targeted peptide which has potential in both anticancer drug development and scientific researches.

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CDC25B

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