SCH-900776 CHK1 inhibitor
- Known as:
- SCH-900776 CHK1 suppressor
- Catalog number:
- a-1202
- Product Quantity:
- USD
- Category:
- -
- Supplier:
- ActivBio Active Biochem
- Gene target:
- SCH-900776 CHK1 inhibitor
Related genes to: SCH-900776 CHK1 inhibitor
- Gene:
- CHEK1 NIH gene
- Name:
- checkpoint kinase 1
- Previous symbol:
- -
- Synonyms:
- CHK1
- Chromosome:
- 11q24.2
- Locus Type:
- gene with protein product
- Date approved:
- 1998-04-21
- Date modifiied:
- 2011-11-11
Related products to: SCH-900776 CHK1 inhibitor
Related articles to: SCH-900776 CHK1 inhibitor
- : Serous ovarian cancer (SOC) is the most aggressive subtype of epithelial ovarian cancer, frequently diagnosed at advanced stages with poor prognosis and chemotherapy resistance. Checkpoint kinase 1 (CHEK1), a key regulator of the DNA damage response, is overexpressed in ovarian cancer, making it a promising therapeutic target. No study has systematically evaluated natural compounds as CHEK1 inhibitors in SOC through an integrative transcriptomic and computational framework. : A meta-analysis of three GEO datasets (GSE27651, GSE36668, GSE54388; n = 83) was performed using ImaGEO. DEGs were identified at |logFC| ≥ 2 and FDR < 0.05. Pathway enrichment, PPI network analysis, virtual screening of 40 phytochemicals against CHEK1 (PDB: 9CE4), 100 ns MD simulations, and ADMET profiling were conducted using established bioinformatics and computational tools. : A total of 511 DEGs were identified, with significant dysregulation of apoptosis, DNA repair, and cell cycle pathways. CHEK1 emerged as the central hub gene. Baicalein exhibited the highest binding affinity (-9.334 kcal/mol), surpassing Prexasertib (-7.2 kcal/mol). MD simulations confirmed complex stability, and ADMET profiling demonstrated favorable drug-likeness with zero Lipinski violations. : CHEK1 is established as a validated therapeutic target in SOC, and Baicalein is identified as a computationally superior natural lead compound, warranting experimental validation in ovarian cancer models. - Source: PubMed
Publication date: 2026/08/05
Jayagopal PoojhashriPrabhakar SandhiyaPonneri Adithavarman AbhinandChaudhari Somdatta Yashwant - Metastatic castration-resistant prostate cancer (mCRPC) remains a leading cause of cancer-related mortality in men. Although poly(ADP-ribose) polymerase inhibitors (PARP inhibitor) are approved for mCRPC patients with homologous recombination repair (HRR) deficiencies, clinical trials combining Olaparib with PD-1/PD-L1 inhibitors have shown limited efficacy in unselected populations. To investigate the immunomodulatory effects of PARP inhibitor in an unbiased manner, we performed bulk RNA sequencing on HRR-proficient MycCaP cells treated with the PARP inhibitor (Olaparib) versus vehicle control. Transcriptomics analysis revealed robust upregulation of CD73 (NT5E), an ectoenzyme and emerging immune checkpoint that generates extracellular adenosine, suggesting an adaptive mechanism that undermines Olaparib efficacy and promotes immunosuppression. CD73 induction by Olaparib was validated in both human and mouse prostate cancer cell lines, with more pronounced effects in HRR-compromised PTEN knockout (KO) cells. Mechanistically, olaparib-driven CD73 expression was mediated through DNA damage-activated ATR-CHEK1-IRF1 and TGF-β1-AKT signaling pathways. In parallel, Olaparib enhanced tumor immunogenicity by activating type I interferon (IFN) signaling and antigen presentation machinery. In vivo, combining olaparib with CD73 blockade significantly delayed tumor growth, improved T-cell infiltration, and augmented CD8⁺ T-cell effector function across HRR-proficient and PTEN KO prostate cancer models. These findings identify Olaparib-induced CD73 upregulation as an adaptive resistance mechanism and support Olaparib plus CD73 blockade as a promising therapeutic strategy for advanced prostate cancer, irrespective of HRR status. - Source: PubMed
Publication date: 2026/08/18
Xie PingMa RenqiangZhang MinghuiFan JieTang HuiSong LongzhenWan YongKuzel Timothy MFang DeyuCui WeiguoWu Jennifer DAbdulkadir Sarki AZhang YiPatnaik AkashZhang Bin - Aflatoxin B1 (AFB1) is a potent group 1 carcinogen closely associated with hepatocellular carcinoma (HCC), particularly in regions with high dietary exposure and concurrent hepatitis B virus infection. However, the molecular mechanisms by which AFB1 promotes HCC progression remain incompletely understood, and there is a lack of prognostic models specifically tailored to AFB1-associated HCC. Integrating bioinformatics and network toxicology approaches may help identify key genes and construct reliable predictive tools for this unique subtype of liver cancer. This study aims to identify AFB1-liver cancer key genes and their functional pathways, to establish a prognosis prediction model for AFB1-liver cancer patient, and analyze its performance, and to reveal the binding characteristics between AFB1 and model proteins. - Source: PubMed
Publication date: 2026/06/24
Wang ChunmeiLi JingYuan YumanLiu LiliHe YanLei Bingxi - Non-small cell lung cancer (NSCLC) remains a leading cause of cancer-related mortality worldwide, with limited therapeutic efficacy due to tumor heterogeneity in conventional treatments. In the present study, an integrative, network pharmacology approach was employed to elucidate the multi-target mechanism of action of phytochemicals derived from Glossocardia bosvallia against NSCLC. Among 38 phytocompounds identified, 31 compounds that satisfied pharmacokinetic properties were selected for subsequent analysis. Ligand-based target prediction identified 429 potential protein targets, which are integrated with the top 250 differentially expressed genes obtained from the GSE33532 dataset. Intersection analysis identified eight therapeutic targets: PTGES, SRD5A1, CDK1, KIF11, TOP2A, CDC45, MB, and CHEK1. Protein-protein interaction and enrichment analyses demonstrated that these targets are predominantly involved in cell cycle regulation, mitotic cell cycle, and DNA replication pathways. Gene expression analysis demonstrated significant overexpression of the prioritized targets in NSCLC tissues, while survival analysis identified CHEK1 as the gene significantly associated with survival (p < 0.05). Molecular docking identified TOP2A_quinic acid as the most favorable complex, exhibiting a binding affinity of -12.27 kcal/mol, KIF11_linoleic acid as -12.10 kcal/mol and CHEK1_2,3-dihydro-3,5-dihydroxy-6-methyl-4h-pyran-4-one as -6.75 kcal/mol, which was further validated by dynamic simulations, principal component analysis based free energy landscape, and DSSP analysis, confirming the stability of the protein. This integrative framework provides a robust strategy for identifying biologically relevant and therapeutically actionable targets supporting the potential of G. bosvallia-derived phytochemicals as promising candidates for NSCLC. - Source: PubMed
Publication date: 2026/08/04
Kulandhaivel Soundar RajanStalin AntonyMuthuramalingam PandiyanSivaprakasam BalasubramanianJesudass Joseph Sahayarayan - This study aims to identify biologically relevant genes associated with DNA repair pathways in gastric cancer (GC) by integrating multi-omics analyses with causal inference approaches. - Source: PubMed
Publication date: 2026/07/30
Yang JianhuaQiu ZhengSong WenchaoLiu XingWang JinghuiYang Yinfeng