Ask about this productRelated genes to: CYP1A2 antibody
- Gene:
- CYP1A2 NIH gene
- Name:
- cytochrome P450 family 1 subfamily A member 2
- Previous symbol:
- -
- Synonyms:
- P3-450, CP12
- Chromosome:
- 15q24.1
- Locus Type:
- gene with protein product
- Date approved:
- 1990-04-25
- Date modifiied:
- 2019-04-23
Related products to: CYP1A2 antibody
Related articles to: CYP1A2 antibody
- Gastrointestinal stromal tumors (GIST) can become malignant upon recurrence and metastasis, yet no drugs specifically target these processes. This study explores the effectiveness and mechanism of paeoniflorin in treating GIST. Initially, the impact of paeoniflorin on the viability, proliferation, and migration of GIST cell lines (GIST-T1 and GIST-882) was assessed using CCK-8, transwell, and wound healing assays at low (5 μM) and high (20 μM) concentrations. Subsequently, datasets GSE136755 and GSE21315 were analyzed to identify potential therapeutic targets for inhibiting GIST transfer. Key genes and pathways related to Paeoniflorin's anti-GIST effects were identified through molecular docking and Western blotting. Paeoniflorin influenced cell viability, proliferation, and migration in GIST-T1 and GIST-882 cell lines at low (5 μM) and high (20 μM) concentrations. We identified 761 differentially expressed genes (DEGs) and selected 50 hub genes using a PPI network. By screening paeoniflorin's potential targets, we identified eight key genes (CYP1A2, CYP2C9, CYP3A4, F2, ICAM1, NR1H4, PLG, and SERPINE1) that were significantly elevated in metastatic GIST samples. CYP3A4 was confirmed as a target of Paeoniflorin in GIST treatment through molecular docking and Western blotting. Pan-cancer analysis showed CYP3A4's enrichment in the tight junction pathway and a significant negative correlation with AKT2 protein. Paeoniflorin treatment led to high AKT2 expression in the tight junction pathway in GIST cell lines. Paeoniflorin acts on the CYP3A4 protein to affect the tight junction pathway, inhibiting the malignant metastasis of GIST. - Source: PubMed
Publication date: 2026/04/23
Cui DapengCui ZeyinLi YansenFan ShuangLi LeiYang ChengYu RuixiaCui JiaxinFu RunjiaFei Jiandong - The application of human hepatic cell lines to early drug discovery and development instead of human primary hepatocytes (HPHs) has been limited because of the low level of drug-metabolizing enzymes (DMEs). - Source: PubMed
Yu HanaLee Song HeeKim Ji HyeonKim Seung JinKang Hee Eun - Olorofim is a novel oral antifungal agent which selectively inhibits the fungal enzyme dihydroorotate dehydrogenase found in molds including , , , and and in dimorphic fungi such as . Based on studies, clinical pharmacology, and pharmacokinetic (PK) data from the Phase 2b FORMULA study (F901318/0032) as well as physiologically based PK (PBPK) modeling of drug interactions, the drug's CYP-mediated interactions are now well understood. Olorofim is mainly metabolized by cytochrome P450 (CYP) CYP3A4, with minor contributions from CYP2C8 and CYP2C9. studies found that it inhibits CYP3A4, weakly inhibits CYP2D6 and CYP2C8, and weakly induces CYP1A2 and CYP2B6. Phase I studies confirm it is predominantly cleared by CYP3A4 and weakly inhibits CYP3A4. In the Phase 2b FORMULA study, co-administered sensitive CYP3A4 substrates required limited dose reductions when using olorofim. When used with strong CYP3A4 inhibitors, dual moderate inhibitors like fluconazole, or CYP3A4 inducers, dose adjustments were needed for olorofim. Physiologically based PK (PBPK) modeling predicted moderate effects with CYP3A4 inhibitors or inducers and negligible effects with weak CYP3A4 inhibitors or strong inhibitors of CYP2D6, CYP2C8, and CYP2C9. Overall, the drug's interaction profile is predictable and manageable, making it a suitable candidate drug to use in treating patients with invasive fungal disease (IFD), who often require polypharmacy.CLINICAL TRIALSThis study is registered with ClinicalTrials.gov as NCT02680808, NCT02730442, NCT02737371, NCT04171739, NCT03340597, and NCT03583164. - Source: PubMed
Publication date: 2026/04/20
Cornelissen KarenRex John HZinzi DanielaLaw DerekUpcott Gill RachelJones Hannah MMaertens JohanChen Sharon C-ABrüggemann Roger - Chronic kidney disease (CKD) and chronic obstructive pulmonary disease (COPD) frequently present as comorbid conditions, while the underlying mechanisms remain largely unknown. Therefore, we aimed to explore the genetic correlations, shared genetic variants, and potential causal relationships between five kidney function traits (serum creatinine-based estimated glomerular filtration rate (eGFRcrea), cystatin C-based estimated glomerular filtration rate (eGFRcys), blood urea nitrogen (BUN), urinary albumin-to-creatinine ratio (UACR), urate) and four lung function traits (forced vital capacity (FVC), forced expiratory volume in the first second (FEV1), FEV1/FVC ratio (RATIO), and peak expiratory flow (PEF)), using data from UK Biobank and CKDGen Consortium with a total of about 1 004 040 participants. Our genome-wide cross-trait study found a strong genetic correlation between eGFRcys, urate, and FVC, and causal analysis using summary effect estimates further confirmed a negative causal effect of FVC on urate while identifying a positive causal effect of eGFRcrea on the RATIO. Cross-trait analysis uncovered 6 overlapped genes significantly shared across 20 trait pairs. Another 7 key genes were further found via transcriptome-wide association, colocalization, and fine-mapping analyses. These 13 key genes converged on four major biological functions, including immune response, endogenous compounds, developmental regulation, and olfactory receptors. Notably, six genes: RF00017, ZNF391, CYP1A1, CYP1A2, OR2J2, and OR14J1, showed novel links to both kidney and lung function traits. These findings uncover the genetic basis of kidney-lung interorgan communication and identify potential therapeutic strategies for reducing multi-system comorbidity. - Source: PubMed
Su ShiqiXiang NanyanYao PeijiYang YongSu ShuFu TingtingWang LeLiao ShuyuanLi WeiminLin YifeiHuang Jin - Exploring the metabolic kinetics mediated by cytochrome P450 (CYP) enzymes is essential for understanding pharmacokinetic and toxicological mechanisms. However, real-time monitoring of CYP-mediated enzymatic reactions remains challenging for conventional techniques. Here, we report the first attempt to develop a surface-enhanced Raman scattering (SERS)-based analytical platform for the direct, real-time tracking of enzymatic metabolism and extraction of critical kinetic parameters. An in vitro CYP enzyme system was constructed to emulate hepatic microsomal activity, using pyrene (Pyr) as a model and polycyclic aromatic hydrocarbon (PAH) as the model substrate. Cetyltrimethylammonium bromide (CTAB)-induced Ag aggregates enabled simultaneous detection of Pyr (408 cm) and its metabolite 1-hydroxypyrene (1-OHPyr; 426/617 cm) directly within the reaction medium. The hydrophobic CTAB self-assembled monolayer enhanced analyte enrichment and suppressed protein interference, while the intrinsic Raman band of CTAB at 760 cm served as a reliable internal standard for quantitative kinetic assessment. This platform allowed real-time monitoring of CYP-catalyzed oxidation of Pyr, yielding pseudo-first-order kinetics ( = 0.00501 min) and the Michaelis constant of 13 μM. Furthermore, inhibition studies identified CYP1A2 as the principal isoform responsible for Pyr metabolism, corroborated by the potent inhibitory activity of α-naphthoflavone (with calculated IC). To our knowledge, this work represents the first instance of SERS for time-resolved monitoring of CYP-mediated metabolism, expanding its capability from static detection to dynamic biochemical analysis. The proposed strategy provides a simple, label-free, and time-resolved approach for enzyme kinetic studies, inhibitor screening, and metabolic analysis. - Source: PubMed
Publication date: 2026/04/19
Li YifanLi JunboYang YangWei ChunyiSong YutingJiang BoXie YunfeiJi Wei