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Postion:Product Catalog >Biochemical Engineering>Inhibitors>Apoptosis>Mdm2 activator>XI-006
XI-006
  • XI-006

XI-006 NEW

Price $51 $74 $122
Package 1mg 2mg 5mg
Min. Order:
Supply Ability: 10g
Update Time: 2024-11-19

Product Details

Product Name: XI-006 CAS No.: 58131-57-0
Purity: 99.12% Supply Ability: 10g
Release date: 2024/11/19

Product Introduction

Bioactivity

NameXI-006
DescriptionXI-006 (XI-006) suppresses MDMX with IC50 of 2.5 μM, leading to enhanced p53 stabilization/activation and DNA damage, and also regulates MDM2, an E3 ligase.
Cell ResearchMCF-7 cells treated with dimethyl sulfoxide (DMSO), nutlin-3a, or NSC-207895 are permeabilized with cold 70% ethanol overnight, and stained with a solution containing 50 μg/mL propidium iodide and 20 μg/mL RNase A at 37°C for 20 minutes. The cells are then subjected to flow cytometry analysis. The FlowJo software is used to calculate percentages of cells in each cell cycle phase. For terminal deoxynucleotidyl transferase–mediated dUTP nick end labeling (TUNEL) staining, MCF-7 cells treated with the NSC-207895 for 2 days are fixed with 4% paraformadelhyde for 1 hour, and then subjected to dUTP labeling using In Situ Cell Death Detection Kit TMR Red according to the manufacturer's protocol. For quantitation, at least 300 cells are randomly chosen and the numbers of TUNEL-positive cells are counted. (Only for Reference)
In vitroXI-006 decreases both the MDMX mRNA and protein in MCF-7 cells. XI-006 induces expression of p53 as well as well-characterized p53-target gene, p21 and MDM2, in a dose-dependent manner in MCF-7 cells. XI-006 extends the half-life of p53 from 20 to 30 minutes to more than 3 hours as revealed by cycloheximide chase assays in MCF-7 cells. XI-006 also activates p53 and induces p21 and MDM2 expression in LNCaP prostate and A549 lung cancer cells. XI-006 increases the mRNA levels of proapoptotic genes including PUMA, BAX, and PIG3 in a dose-dependent manner in MCF-7 cells. XI-006 results in a significant increase in the numbers of sub-G0/G1 cells as well as G2 arrest. XI-006 also results in more than 40% of cells dying via apoptosis and decreases cell viability in A549 and LNCaP cells. [1] XI-006 inhibits biosynthesis of nucleic acids and proteins in L1210 cells. [2] XI-006 interacts with DNA repair to activate the DNA damage repair pathway in three species (S. cerevisiae, S. pombe and H. sapiens). [3] XI-006 acts as cytotoxic agent in the G/R-luc astrocytoma cell line with GI50 of 117 nM. [4]
StoragePowder: -20°C for 3 years | In solvent: -80°C for 1 year | Shipping with blue ice.
Solubility InformationDMSO : 55 mg/ml (196.96 mM)
Ethanol : < 1 mg/mL (insoluble or slightly soluble)
H2O : < 1 mg/mL (insoluble or slightly soluble)
KeywordsLPS | p53 | MDMX | XI006 | Inhibitor | NSC-207895 | inhibit | MDM2 | XI 006 | MDM-2/p53 | NSC207895
Inhibitors RelatedMilademetan | Alrizomadlin | Rotenone | RG7112 | DPBQ | Indole-3-carbinol | Idasanutlin | RITA | P53R3
Related Compound LibrariesAnti-Lung Cancer Compound Library | Anti-Pancreatic Cancer Compound Library | Bioactive Compound Library | Ubiquitination Compound Library | Anti-Cancer Metabolism Compound Library | Pyroptosis Compound Library | NO PAINS Compound Library | Anti-Aging Compound Library | Bioactive Compounds Library Max | Anti-Cancer Active Compound Library

Company Profile Introduction

Target Molecule Corp. (TargetMol) is a global high-tech enterprise, headquartered in Boston, MA, specializing in chemical and biological research product and service to meet the research needs of global customers. TargetMol has evolved into one of the biggest global compound library and small molecule suppliers and a customer based on 40+ countries. TargetMol offers over 80 types of compound libraries and a wide range of high-quality research chemicals including inhibitors, activator, natural compounds, peptides, inhibitory antibodies, and novel life-science kits, for laboratory and scientific use. Besides, virtual screening service is also available for customers who would like to conduct the computer-aided drug discovery.

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