Ask about this productRelated genes to: ABCG2 antibody
- Gene:
- ABCG2 NIH gene
- Name:
- ATP binding cassette subfamily G member 2 (Junior blood group)
- Previous symbol:
- -
- Synonyms:
- EST157481, MXR, BCRP, ABCP, CD338
- Chromosome:
- 4q22.1
- Locus Type:
- gene with protein product
- Date approved:
- 1999-10-26
- Date modifiied:
- 2019-04-23
Related products to: ABCG2 antibody
Related articles to: ABCG2 antibody
- Osimertinib is a third-generation EGFR TKI with proven efficacy in EGFR-mutant NSCLC, including patients with CNS disease. However, pharmacokinetic studies demonstrate low CNS penetration (CSF:plasma 0.8-22%), largely due to ABCB1/ABCG2 efflux. OB-001, a KinetiSol® amorphous solid dispersion formulation of elacridar, was developed to overcome poor bioavailability of crystalline elacridar and evaluated as a strategy to enhance osimertinib brain delivery. In CD-1 mice, we compared the oral bioavailability of OB-001 (10, 30, 100 mg/kg) with crystalline elacridar (100 mg/kg) and assessed osimertinib (50 mg/kg PO) brain distribution after pretreatment with OB-001 (10 or 50 mg/kg) or crystalline elacridar (100 mg/kg). Plasma and perfused brain pharmacokinetic parameters derived by noncompartmental analysis. AUClast values were compared using Bailer's randomization test. OB-001 achieved greater systemic elacridar exposure than the crystalline methylcellulose suspension (p<0.001). In vehicle-pretreated mice, osimertinib produced a brain:plasma AUC ratio of 7.1. OB-001 pretreatment increased brain AUClast 4.0-fold (10 mg/kg; p<0.001) and 9.3-fold (50 mg/kg; p<0.001) with minimal plasma change (1.1-1.4-fold). Crystalline elacridar at 100 mg/kg increased brain AUClast 5.0-fold (p<0.001). Thus, OB-001 at 10 mg/kg achieved comparable brain enhancement to 10-fold higher dose of crystalline elacridar, while OB-001 at 50 mg/kg exceeded it. Translational benchmarking against in-vitro potency suggested that raising estimated Kp,uu from ~0.15 to ~0.60 could improve efficacy. OB-001 selectively boosts osimertinib brain exposure while sparing systemic PK. These preclinical data support further evaluation of OB-001 as a strategy to enhance CNS efficacy of osimertinib in EGFR-mutant NSCLC. - Source: PubMed
Publication date: 2026/05/07
Mistry Hitesh BMillen JimFleet JoshBrimble Mark - Here we describe the different TOP1 poisons used a "payload" for tumor-targeted anticancer therapies in comparison with the widely used first generation TOP1 poisons: Topotecan, Irinotecan and Belotecan. We review the determinants of response to tumor-targeted TOP1 poison inhibitors (TTTis) as candidate companion diagnostic (Dx) biomarkers for precision medicine and patient selection, such as high expression of surface epitopes for ADCs (Antibody Drug Conjugates), high tumor proliferation (Ki67), Schlafen 11 (SLFN11) expression, homologous recombination deficiencies (HRD/BRCAness) and expression of drug efflux transporters such as (BCRP (MXR) encoded by ABCG2. We also summarize the mechanistic rationale for combining TTTis with small molecule inhibitors of poly(ADPribose) polymerase (PARP), ATR (Ataxia Telangiectasia and Rad3-related), CHK1 (Checkpoint Kinase 1) and ATM (Ataxia Telangiectasia Mutated). - Source: PubMed
Publication date: 2026/05/04
Pommier Yves - Epidermal growth factor receptor-tyrosine kinase inhibitors (EGFR-TKIs) have transformed non-small cell lung cancer (NSCLC) treatment, offering substantial survival benefits. However, acquired resistance remains a significant obstacle, undermining long-term efficacy. While specific mechanisms of EGFR-TKI resistance have been reported, potential shared mechanisms across EGFR-TKI generations have remained unclear. - Source: PubMed
Publication date: 2026/05/06
Zhang YuGültekin OkanKupčík RudolfBudagaga YoussifVagiannis DimitriosSabet ZibaLehti KaisaHofman Jakub - Hyperuricemia (HUA), a metabolic disorder characterized by elevated serum uric acid (UA) levels, is closely linked to various chronic diseases. Galangin (GAL), a natural polyphenol abundant in and propolis, has been reported to alleviate HUA by inhibiting hepatic UA production and promoting renal UA excretion. However, its impact on intestinal UA elimination is poorly understood. This study investigated GAL's protective role in HUA mice, focusing on intestinal UA transport, inflammatory response, and barrier integrity. Our findings demonstrate that GAL suppressed xanthine oxidase activity in the serum, jejunum, and ileum, attenuated intestinal morphological damage and oxidative stress, and enhanced expression of ABCG2 and GLUT9 in the small intestine. GAL also upregulated the tight junction proteins Occludin and ZO-1 while inhibiting MAPK/NF-κB pathway in the intestine. Collectively, GAL ameliorates HUA by modulating intestinal UA metabolism and repairing intestinal injury, highlighting its potential as a nutraceutical for UA-lowering therapy. - Source: PubMed
Publication date: 2026/05/05
Zhao YananWang RuiCao RanChen LeyaoJu SitingTeng HuiChen Lei - - Source: PubMed
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