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
- Cannabidiol (CBD) use continues to increase, particularly among older adults. However, knowledge of CBD disposition in this ever-growing and understudied population, along with the relative contributions of cytochrome P450 (CYP) and uridine 5'-diphospho-glucuronosyltransferase (UGT) enzymes to CBD metabolism, remain limited. Inclusion of UGT activators (e.g., alamethicin, MgCl) may alter in vitro estimates of enzyme contributions. CBD has also been reported to produce time-dependent inhibition (TDI) of certain CYPs, potentially affecting its own disposition. We combined in vitro data with physiologically based pharmacokinetic (PBPK) modeling to further characterize TDI and reversible CYP inhibition by CBD, quantify the contributions of CYPs and UGTs to CBD metabolism, and determine in vitro assay conditions that best reflect in vivo CBD metabolism. PBPK modeling was next used to extrapolate CBD exposure from young (18-64 years) to older (65-98 years) adults. CBD exhibited TDI only toward CYP1A2, which had a negligible effect on CBD metabolism. Inclusion of alamethicin + MgCl increased the apparent contribution by UGTs to CBD metabolism, leading to an overestimate of UGT-mediated metabolism. PBPK model validation using drug-drug interaction studies supported contributions of 86% and 14% for CYPs and UGTs, respectively, as best capturing observed CBD exposure. Simulations in older adults generally showed increased CBD exposure relative to young adults, with the magnitude depending on age and administration route. Overall, these results improve our understanding of CBD pharmacokinetics, support more informed risk assessment in older adults, and provide a more robust foundation for future studies. - Source: PubMed
Publication date: 2026/09/08
Qian LixuanNguyen Aiden-Hung PPaine Mary FZhou Zhu - Deoxynivalenol (DON) is among the most prevalent mycotoxins and exerts adverse effects on the liver. However, a systematic evaluation of its effects on hepatic cytochrome P450 enzymes (Cyp450) and carboxylesterases (Ces) in mice is lacking. - Source: PubMed
Publication date: 2026/09/08
Qin LinaLiu ChenCheng BolunZhao YichenZhao TongMao TingtingDa WeixuanLiu LiLiu HuanWen YanJia YumengZhang Feng - Humans are simultaneously exposed to multiple substances through diet and environmental sources, yet rigorously assessing the health risks of these combined exposures is challenging. New Approach Methodologies (NAMs) provide supporting tools, such as transcriptional analysis of cell models. Among relevant contaminants, pesticides and natural toxins, such as microcystins (MCs), may be of concern due to their potential co-occurrence in food. We investigated binary mixtures of two MCs (MC-LA, MC-LR) with the hepatotoxic pesticide propyzamide (PRO) using gene expression analysis in differentiated HepaRG cells. Marker genes for activity of the nuclear receptors AhR, CAR, PXR and NRF2 were analysed to model mixture effects. RT2 Profiler PCR Arrays and Ingenuity Pathway Analysis (IPA) were used to evaluate gene expression profiles and liver toxicity-related pathways. Individual MCs down-regulated the marker genes (i.e., CYP1A2, CYP2B6, CYP3A4, GPX2). IPA linked transcriptional patterns of MC-LR to cholestasis and hepatocarcinogenesis. In contrast, PRO induced the same nuclear receptors and affected liver-enriched pathways linked to inflammation, cholestasis, carcinogenesis, and oxidative stress. Based on marker genes, mixtures of MC congeners showed dose addition, whereas mixtures of MCs with PRO exhibited a functional antagonism, likely reflecting opposing effects on nuclear receptor signaling. Despite the antagonism on nuclear receptor level, pathway analysis indicated consistent or enhanced associations with liver toxicity endpoints including cholestasis, inflammation and hepatocellular carcinoma. Our findings indicate that co-exposure to pesticides and MCs may cause complex interactions including antagonism and helps to gain mechanistic knowledge on mixture toxicity. - Source: PubMed
Publication date: 2026/09/08
Kiessig SahraSilva Enzo Zini MoreiraSuciu IlincaLeme Daniela MoraisMarx-Stoelting Philip - Cytochrome P450 1B1 (CYP1B1) is selectively overexpressed in various tumor cells and plays a critical role in the metabolic inactivation of chemotherapeutic agents, leading to drug resistance. Therefore, the development of selective CYP1B1 inhibitors represents a promising strategy to overcome chemoresistance. In this study, we designed and synthesized 19 novel trans-stilbene derivatives by introducing fluorine atoms or fluorinated side chains, aiming to potentially enhance drug metabolic stability and binding affinity. Among them, compounds 4h and 4i exhibited the most potent inhibitory activity against CYP1B1, with ICvalues of 6.5 ± 0.9 nM and 5.4 ± 0.5 nM, respectively, and demonstrated high selectivity within the CYP1 family over CYP1A1 and CYP1A2. In A549 cell models, both compounds significantly reversed DMBA-induced PTX resistance in a concentration-dependent manner. Furthermore, fluorescence staining revealed that compound 4i preferentially bound to CYP1B1-overexpressing tumor cells, including A549, HeLa, MCF-7, and HCT-15 cells, but not to non-cancerous 293T cells. These findings highlight the potential of fluorinated trans-stilbene derivatives as promising CYP1B1-targeted therapeutics for combating drug-resistant cancers. - Source: PubMed
Publication date: 2026/09/02
Yang MeixianLiu XinWei XinQiu DachuanChen WeijuanCai Jiajing - Kashin-Beck disease (KBD) is a multifactorial endemic osteoarthropathy that has been associated with nutritional and environmental factors, including selenium deficiency and T-2 toxin exposure. However, whether combined selenium deficiency and T-2 toxin exposure affects hepatic xenobiotic metabolism has not been systematically investigated. Male C57BL/6 mice were fed a selenium-adequate or selenium-deficient diet for 4 weeks, followed by another 4 weeks with or without daily oral T-2 toxin (0.2 mg/kg). Plasma selenium and glutathione peroxidase (GPx) activity were measured. Hepatic histology, activities of major mouse cytochrome P450 (Cyp450) isoforms, and corresponding mRNA and protein expression were assessed. RNA sequencing was performed using liver samples from four biological replicates per group to identify differentially expressed genes (DEGs) and enriched pathways. Selenium deficiency was confirmed by significantly reduced plasma selenium levels and GPx activity. Histological examination revealed marked hepatic steatosis. Transmission electron microscopy further showed prominent ultrastructural alterations including endoplasmic reticulum dilation. The activities of five hepatic Cyp450 isoforms, Cyp1a2, Cyp2b10, Cyp2c29, Cyp2c50, and Cyp3a11, were significantly increased to 1.64-2.51 times the control levels, consistent with increased mRNA and protein expression. Combined selenium deficiency and T-2 toxin exposure was associated with increased hepatic Cyp450 enzyme activity and expression, identifying the liver as a responsive target of KBD-related exposures. These findings suggest the need to further evaluate hepatic xenobiotic metabolism in populations from KBD-endemic areas. - Source: PubMed
Publication date: 2026/09/04
Zhao TongZhao YichenMao TingtingDa WeixuanQin LinaLiu LiLiu HuanCheng BolunWen YanZhang FengJia Yumeng