SLC47A2 Antibody
- Known as:
- SLC47A2 Antibody
- Catalog number:
- 42-923
- Product Quantity:
- 0.1 mg
- Category:
- -
- Supplier:
- Prosci
- Gene target:
- SLC47A2 Antibody
Related genes to: SLC47A2 Antibody
- Gene:
- SLC47A2 NIH gene
- Name:
- solute carrier family 47 member 2
- Previous symbol:
- -
- Synonyms:
- FLJ31196, MATE2, MATE2-K
- Chromosome:
- 17p11.2
- Locus Type:
- gene with protein product
- Date approved:
- 2007-05-18
- Date modifiied:
- 2016-02-17
Related products to: SLC47A2 Antibody
Related articles to: SLC47A2 Antibody
- Metformin is a widely used drug with a relatively good efficacy in diabetes treatment, a good safety profile, and the potential for use in other indications. The variability in the individual responses to metformin therapy is partially determined by genetic factors. This narrative review aimed to summarize information on single nucleotide variant (SNVs) in genes for transporter proteins associated with metformin pharmacokinetics and pharmacodynamics and/or the occurrence of adverse effects. The Pharmacogenomics Knowledge Base (PharmGKB) and Web of Science databases were searched for metformin-associated gene variants that could affect its action. Seven transporter genes with twelve SNVs common in the European population were identified in the PharmGKB database, namely SNVs in genes (OCT1), (OCT2), (OCT3), (OCTN1), (MATE1), (MATE2-K) and (GLUT2); it is worth noting that GLUT2 is not metformin transported but a glucose transporter and as such, it can also influence metformin action. Based on 63 retrieved studies, the association of individual SNVs with metformin effectiveness and adverse effects is discussed. In view of the high variability of study designs, populations, and reporting patterns, we also propose a framework for the design and reporting of metformin-associated pharmacogenetic studies, suggesting also that determining a complete set of these SNVs could help in comprehensive understanding of genetically conditioned individual responsiveness to metformin therapy, thus opening the path to maximizing the utilization of its positive effects while minimizing the risk of adverse effects. In addition, given the large variability in designs among studies, we also propose a framework for future studies on SNVs in metformin action-associated transporters that could improve comparability of future studies. - Source: PubMed
Publication date: 2026/06/19
Mlcuchova NatalieLipovy BretislavZendulka OndrejJanosek JaroslavBorilova Linhartova Petra - Doravirine (DOR), a potent nonnucleoside reverse transcriptase inhibitor for HIV-1 treatment, is primarily metabolized by cytochrome P450 3A enzymes to form doravirine carboxylic acid metabolite (M9), the major plasma metabolite excreted in urine. To investigate the estimated glomerular filtration rate decrease observed in phase 3 DOR studies, we investigated DOR and M9 interactions with renal transporters organic cation transporter 2 (OCT2), organic anion transporter 2 (OAT2), and multidrug and toxin extrusion proteins 1 and 2K (MATE1 and MATE2K). In vitro assays were conducted in OCT2- and OAT2-transfected human embryonic kidney 293 (HEK293) cells and MATE1- and MATE2K-transfected Madin-Darby canine kidney II cells. The inhibitory potency (half-maximal inhibitory concentration [IC]) of DOR and M9 on OCT2-, OAT2-, MATE1-, and MATE2K-mediated uptake of creatinine or metformin were measured, whereas substrate-dependent inhibition was assessed for OCT2 and MATE1. DOR inhibited OCT2-mediated creatinine uptake with an IC of 6.9 ± 0.8 μM, approximately 6.2-fold lower than that observed using metformin as probe. DOR also inhibited OAT2 at concentrations higher than clinically relevant (IC of 28.7 ± 4.9 μM). DOR did not inhibit MATE1-mediated creatinine uptake (IC >100 μM). M9, at concentrations higher than clinically relevant, inhibited OAT2-mediated creatinine uptake (IC of 18.0 ± 2.1) but did not inhibit creatinine or metformin uptake by OCT2, MATE1, or MATE2K (IC >30 μM for all). In conclusion, at clinically relevant exposures, DOR exhibited substrate-dependent inhibition of creatinine transport via OCT2, which could explain the slight decrease in calculated estimated glomerular filtration rate observed with DOR treatments, without reduction in renal function. SIGNIFICANCE STATEMENT: At clinically relevant concentrations, doravirine inhibits the renal transporter organic cation transporter 2 in a substrate-dependent manner, but not organic anion transporter 2, multidrug and toxin extrusion proteins 1 and 2K, indicating that doravirine-associated estimated glomerular filtration rate reductions are caused by inhibition of renal creatinine transport and do not reflect a reduction in renal function. - Source: PubMed
Publication date: 2026/05/05
Li YangSaran ChitraChu XiaoyanSanchez Rosa IThomas Alana FCarstens Russ PPisculli Mary LKlopfer Stephanie OXu Zhi JinLahoulou RimaPlank Rebeca M - Platinum-based chemotherapeutics remain clinically indispensable for treating various malignancies despite causing severe side effects, with ototoxicity being particularly limiting. This study reports the synthesis and evaluation of platinum(IV) prodrugs incorporating the hearing-protective ligand RG108. Among the synthesized mono- and di-substituted cisplatin and oxaliplatin derivatives, compound 4 exhibited exceptional antitumor activity with an IC value of 0.07 ± 0.08 µM in FaDu cells. Mechanistic investigations revealed that the enhanced anti-tumor effect was primarily mediated via the EZH2/SLC47A2 regulatory axis. These prodrugs significantly mitigated ototoxicity, preserving cochlear hair cell viability, stabilizing auditory brainstem response thresholds, and maintaining cochlear basement membrane morphology. Our findings establish a framework for designing dual-functional platinum agents that synergize antitumor efficacy with organoprotective properties, addressing critical hearing loss limitations of conventional platinum chemotherapy while maintaining robust therapeutic outcomes. - Source: PubMed
Publication date: 2026/03/12
Wu JiyongNie JingWu HuinaWang DongboLi YameiLiang MinyanQian HuimeiWang Yong - Diabetes type 2 (DT2) entails significant health, economic, and productivity repercussions around the world. Poor glycaemic control, defined as an HbA1c >7.0%, has been associated with a number of complications. In spite of the large share of healthcare resources allocated to DT2 treatment, the proportion of controlled Mexican patients is among the lowest in the world (34.4%). Certain protein-encoding genetic polymorphisms involved in metformin transport may affect glycaemic control. We focused on determining the frequency of rs2289669, rs2252281, rs12943590, and rs34834489 polymorphisms in Mexican-Mestizo patients from the Tertiary Care Regional Hospital of Ixtapaluca, State of Mexico, Mexico, as well as assessing their possible association with therapeutic efficacy, as estimated through glycated haemoglobin. The individual polymorphism analysis did not reveal an association with glycaemic control; however, when combined with rs72552763 and rs622342, we found a significant positive correlation between HbA1c levels and metformin dose, which prevailed among patients carrying allelic variants of rs2289669 or rs12943590 who were also simultaneously carrying allelic variants of rs72552763 or rs622342. Patients carrying the reference allele of rs34834489 reported a significant positive correlation between HbA1c levels and metformin dose as well, regardless of their rs72552763 or rs622342 genotype. Thus, we identified alleles and allelic combinations of , , and polymorphisms posing a potential glycaemic control risk in Mexican-Mestizo patients. - Source: PubMed
Publication date: 2025/09/05
Gómez-Hernández Milton AbrahamOrtega-Ayala AdielRodríguez-Lima OscarLanda AbrahamAcosta-Altamirano GustavoMolina-Guarneros Juan A - This study explores the relationship between gene polymorphisms and glycemic responses across ethnic populations and identifies optimal therapy combinations for glycemic control. However, the definition of glycemic response varied across included studies (e.g., HbA1c <7 %, or >0.5 % reduction), which may affect the comparability and interpretation of pooled data. - Source: PubMed
Publication date: 2025/06/24
Ahmad FikryAbubakar SuhailiSyed Alwi Sharifah SakinahChuan Ng Ooi