c_Jun Antibody (Ab_243), pAb, Rabbit
- Known as:
- c_Jun Antibody (Ab_243), pAb, Rabbit
- Catalog number:
- A00238
- Product Quantity:
- 40ug
- Category:
- -
- Supplier:
- Genscript
- Gene target:
- c_Jun Antibody (Ab_243) pAb Rabbit
Related products to: c_Jun Antibody (Ab_243), pAb, Rabbit
Related articles to: c_Jun Antibody (Ab_243), pAb, Rabbit
- - Source: PubMed
- Sodium glucose cotransporter-2 (SGLT2) inhibitors are a class of antidiabetics with benefits including HbA1c-lowering, weight loss, cardiovascular and renal protection in addition to adverse effects including genitourinary tract infections, ketoacidosis, and bone loss. Here, we describe the rationale and design of the Genetics of Response to Canagliflozin (GRC) study and report on the pharmacodynamic findings. This study, for which enrollment has been completed, was conducted in healthy Amish individuals with a goal of identifying genetic predictors of variability in safety and efficacy of the SGLT2 inhibitor canagliflozin. Participants took canagliflozin 300 mg/day for 5 days, completed a 24-h urine collection, and had blood drawn at baseline, Day 3, and Day 6. The primary endpoint is glucosuria and the secondary endpoints assess additional biomarkers for safety and efficacy related to bone, cardiovascular disease, and ketosis. 402 participants completed the study. We identified significant variability in the degree of canagliflozin-induced glucosuria with a heritability of 34% (p = 8.69e-03). Canagliflozin induced significant increases in serum phosphorous (Day 3: +5.0%, p = 5.83e-21) and fibroblast growth factor-23 (Day 3: +20.2%, p = 1.58e-18), decrease in 1,25-dihydroxyvitamin D (Day 3: -25.0%, p = 5.71e-54), and increase in parathyroid hormone: (Day 3: +20.8%, p = 1.98e-33). Canagliflozin also significantly decreased serum uric acid (Day 6: -33.2%, p = 1.01e-65) and increased beta-hydroxybutyrate (Day 3: +71.9%, p = 8.11e-28). The most significant baseline characteristic associated with glucosuria was eGFR (p = 8.10e-10). This study will provide the opportunity to identify genetic and other 'omic predictors of safety and efficacy biomarkers for SGLT2 inhibitor response that could help guide diabetes treatment in the future. - Source: PubMed
Montasser May EBargal Salma AStreeten Elizabeth AWhitlatch Hilary BYazdi Zhinous ShahidzadehSirody JordinKiplagat RosannaBeshara MernaO'Connell Jeffrey RTaylor Simeon IBeitelshees Amber L - Colon cancer death toll due to metastasis is expected to rise. Extracellular vesicles are signalling molecules which can regulate communication between cells and either inhibit or promote cancer metastasis. - Source: PubMed
Al-Ozeir Fadia WalidMayasari Ni Luh Putu IkaMariya SilmiIndriawati IinDayana HepyDarusman Huda Shalahudin - Ecopipam is a dopamine-1 (D1) receptor antagonist in development for Tourette syndrome. In vitro data showed that ecopipam is metabolized to ecopipam glucuronide through uridine diphosphate-glucuronosyltransferase 1A9 and to EBS-101-40853 (previously called N-desmethylecopipam or SCH 40853) through cytochrome P450 3A4. This open-label, non-randomized, mass balance study investigated metabolism and elimination pathways of ecopipam. A single oral dose of ecopipam 179.2 mg containing 88.5 μCi (3.27 MBq) of [C]-labeled ecopipam was administered to 8 healthy males. Total radioactivity, ecopipam, and ecopipam metabolite concentrations were measured in blood, plasma, urine, and feces periodically until discharge (between Days 8 and 15 postdose). Pooled plasma was used to identify and quantify unknown metabolites. Overall, 83.3% of radioactivity was recovered in urine as metabolites (< 1% as ecopipam), and 8.27% was excreted in feces (6.43% as ecopipam). Ecopipam glucuronide accounted for 80.0% of radioactivity in plasma and 66.9% of radioactivity in urine. EBS-101-40853 accounted for 10.5% of the plasma AUC for ecopipam. Geometric mean half-lives of ecopipam, EBS-101-40853, and total radioactivity in plasma were 17.3, 25.6, and 94.1 h, respectively. Uncharacterized metabolites P3 and P5, 'corrected' for extraction efficiency, had plasma half-lives (97.4 and 122 h, respectively) similar to total radioactivity. Unknown P3, P4, and P5 metabolites accounted for 4.62%, 0.243%, and 6.03%, respectively, of plasma radioactivity. Ecopipam is primarily metabolized to ecopipam glucuronide, with only 10.5% metabolized to EBS-101-40853. The long half-life of plasma radioactivity was attributed to previously uncharacterized metabolites that each accounted for < 10% of radioactivity and were considered not clinically relevant. - Source: PubMed
Schmith Virginia DEnglish StephenDymond AngelaHoldsworth CatherineStow RuthHolbrook EmmaSchleyer JoyWanaski Stephen P - The Rare Diseases Clinical Research Network (RDCRN) was established to improve diagnosis, treatment, and research collaboration across rare diseases through collaborative, multi-site, translational, and clinical research. Its governance framework promotes efficient data sharing and collaboration among research consortia, NIH representatives, and patient advocacy groups (PAGs). This infrastructure facilitates coordinated efforts to advance rare disease research through shared resources and communication. Prompted by the COVID-19 pandemic's impact on rare disease patients, the RDCRN recognized cross-consortia collaboration as a priority. Its policies promote data sharing while protecting participant confidentiality. PAGs participate in governance, study design, and regulatory discussions, helping to identify patient-relevant priorities, improve recruitment and retention, and strengthen trust between researchers and patients. Cross-consortia efforts have addressed challenges like biomarker identification and harmonization of clinical measures, leading to new methods and standardized data collection that benefit multiple rare diseases. Studies by teams focusing on different diseases have led to improved diagnostic tools by addressing overlapping disease presentations. The RDCRN offers scholars cross-consortia opportunities for presentations, competitions, and NIH training collaborations, fostering growth and networking. Network meetings promote exchange and process standardization; pilot projects facilitate independent grant submissions, forming a pipeline of skilled investigators. The RDCRN fosters trust, shared vision, and open communication by cultivating a culture of mutual respect, shared learning, and collective problem solving. By engaging a wide range of stakeholders, it has aligned its research with patient needs, advancing innovation. Its high-impact publications, effective mentoring programs, and pioneering cross-consortia initiatives underscore the value of collaboration in rare disease research. - Source: PubMed
Chehade MirnaMeyers SheridanMcCright-Gill TalayaGifford RogerweneSahin MustafaShy Michael EManion MicheleCampbell DakotaRothenberg Marc EMacaluso Maurizio