UCE 6

UCE 6

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UCE 6
Category Enzyme inhibitors
Catalog number BBF-01582
CAS 150829-94-0
Molecular Weight 436.4
Molecular Formula C24H20O8

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Description

UCE 6 is an antitumor metabolite with topoisomerase I mediated DNA cleavage activity.

Specification

Synonyms UCE-6; UCE6
IUPAC Name 1,3,8,11-tetrahydroxy-10-(4-hydroxy-2-oxopentyl)-2-methyltetracene-5,12-dione
Canonical SMILES CC1=C(C=C2C(=C1O)C(=O)C3=C(C4=C(C=C(C=C4C=C3C2=O)O)CC(=O)CC(C)O)O)O
InChI InChI=1S/C24H20O8/c1-9(25)3-13(26)4-11-5-14(27)6-12-7-15-20(23(31)18(11)12)24(32)19-16(22(15)30)8-17(28)10(2)21(19)29/h5-9,25,27-29,31H,3-4H2,1-2H3
InChI Key YNAKLZFMOFNLRE-UHFFFAOYSA-N

Properties

Appearance Orange-red Solid
Antibiotic Activity Spectrum neoplastics (Tumor)
Boiling Point 330.6ºC at 760 mmHg
Density 1.23 g/cm3

Reference Reading

1. Parkinson's disease and COVID-19: a systematic review and meta-analysis
Reza Jalili Khoshnood, Alireza Zali, Arash Tafreshinejad, Mahsa Ghajarzadeh, Narges Ebrahimi, Saeid Safari, Omid Mirmosayyeb Neurol Sci. 2022 Feb;43(2):775-783. doi: 10.1007/s10072-021-05756-4. Epub 2021 Nov 17.
Background: Patients with Parkinson's disease (PD) are at higher risk of COVID-19 infection as most of them are at older age. The goal of this study is to update the pooled prevalence of COVID-19 infection in patients with PD. Methods: Two researchers systematically searched PubMed, Scopus, EMBASE, Web of Science, Google Scholar, and also gray literature including references of the included studies which were published before September 2021. We extracted data regarding the total number of participants, first author, publication year, the country of origin, mean age, number with COVID-19, symptoms, hospitalization, and death. Results: We found 1693 articles by literature search; after deleting duplicates, 798 remained. Thirty articles remained for meta-analysis. The pooled prevalence of COVID-19 infection in PD cases was 5% (95%CI: 4-6%) (I2 = 98.1%, P < 0.001). The pooled prevalence of fever in cases with PD was 4% (95%CI: 2-6%) (I2 = 96%, P < 0.001). The pooled prevalence of cough in cases with PD was 3% (95%CI: 2-4%) (I2 = 95.9%, P < 0.001). The pooled prevalence of hospitalization in cases with COVID-19 infection was 49% (95%CI: 29-52%) (I2: 93.5%, P < 0.001). The pooled prevalence of mortality in COVID-19 cases was 12% (95%CI: 10-14%) (I2 = 97.6%, P < 0.001). Conclusion: The results of this systematic review and meta-analysis show that the pooled prevalence of COVID-19 infection in PD cases is 5% besides hospitalization and mortality rates which are 49% and 12%.
2. Long-Term Urinary Copper Excretion on Chelation Therapy in Children with Wilson Disease
Atchariya Chanpong, Anil Dhawan J Pediatr Gastroenterol Nutr. 2021 Feb 1;72(2):210-215. doi: 10.1097/MPG.0000000000002982.
Objectives: In Wilson disease (WD), 24-hour urinary copper excretion (UCE) is recommended to be used for diagnosis. It may be a useful tool to assess the efficacy of treatment during follow-up; however, there are limited data regarding the cutoff value of 24-hour UCE during follow-up in children. Therefore, we aim to evaluate the clinical use of 24-hour UCE during follow-up in children with WD. Patients and methods: Medical records of children diagnosed with WD at Kings' College Hospital from 2005 to 2018 were retrospectively reviewed. The UCE, serum copper, and ceruloplasmin levels, tested during follow-up, were statistically analyzed. Results: Over the median duration of 7 years (range 1.4-14.4), 28 patients (age ranged 3.8-17.3 years) had UCE tests during follow-up. Of those, 21 patients had at least one 24-hour UCE test and 7 children had only spot UCE tests. In comparison with the level of 24-hour UCE collected at the first visit after penicillamine challenge test, the median excretion rate was significantly reduced over the follow-up period (P < 0.001), from 26.2 to 8.9 μmol/day following 1-2 years of therapy (P = 0.15), then reduced significantly to 2.2 μmol/day after 3-4 years (P = 0.009), and 5.6 μmol/day at >5 years of follow-up (P = 0.003). Conclusions: Our study suggests that within 1 year of treatment, the level of nonceruloplasmin-bound copper concentration (NCC) drops to <0.8 μmol/L. In the absence of progressive liver disease or signs of copper deficiency, 24-hour UCE decreases to ≤8 μmol/day and <6 μmol/day after 1 and 5 years of treatment, respectively.
3. miRNA-185 regulates retained fetal membranes of cattle by targeting STIM1
C Y Zheng, X Zou, B C Zhao, M L Zhang, H J Lin, C H Luo, Z M Xu, L Y Shao, S X Fu Theriogenology. 2019 Mar 1;126:166-171. doi: 10.1016/j.theriogenology.2018.11.030. Epub 2018 Nov 27.
Retained fetal membranes (RFM) of cows is an important reproductive disturbance, and is related to miRNA-185. Stromal interaction molecule 1 (STIM1), a potential target gene of miRNA-185, could influence placenta release via regulating Ca2+ concentration intracellular. The aim of this study was to explore the mechanism of RFM by investigating the regulatory relationship between miRNA-185 and STIM1 in primary uterine caruncel epithelial (UCE) cells. Serum samples of healthy Holstein dairy cows (n = 20) and RFM cows (n = 12), with a similar age, parity, weight, and milk yield, were collected to detect Ca2+ concentration at prepartum 1-5 d and postpartum 6, 12 and 24 h. Caruncle tissues were collected from healthy (n = 6) and RFM cows (n = 6) at 12 h after calving. Quantitative polymerase chain reaction (Q-PCR) and western blotting (WB) were performed to detect the mRNA and protein levels of STIM1, respectively. UCE cells were cultured by the explant culture method, further purified, and subsequently treated with PmirGLO-STIM1-Mut + miRNA-185 mimics and mirGLO-STIM1-Mut + miRNA-185 NC. Q-PCR and WB were performed to detect mRNA and protein levels of STIM1 with treated miRNA-185 mimics. Serum levels of Ca2+ from RFM cows were abnormally decreased at prepartum 1 d and postpartum 6, 12 and 24 h. Expression level of STIM1 was down-regulated in the caruncle tissue of RFM cows. The luciferase activity was decresed about 30.9% by miRNA-185 mimics (p < 0.01), and the mRNA and protein levels of STIM1 were downregulated miRNA-185-mimics. It was suggesting that miRNA-185 might play an important role in RFM through regulating the expression of STIM1.

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