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商品描述
Related Products
- VE-822
- KU 55933
- Rocilinostat (ACY-1215)
- SCR7
- (S)-Crizotinib
- JNJ-26481585
Molarity CalculatorDilution Calculator
| DiscoveryProbe™ DNA Damage/DNA Repair-related Compounds Panel |
Sample solution is provided at 25 µL, 10mM.
Click and Customize the Panelwith your own choices of compounds/size/quantities/chemical forms etc.
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| Catalog No. | Product Name | Summary | Targets | CAS Number | Smiles | |
| A4605 | KU 55933 | ATM inhibitor,potent and selective | DNA Damage/DNA Repair|ATM/ATR | 587871-26-9 | C1COCCN1C2=CC(=O)C=C(O2)C3=C4C(=CC=C3)SC5=CC=CC=C5S4 | |
| B1383 | VE-822 | ATR inhibitor | DNA Damage/DNA Repair|ATM/ATR | 1232416-25-9 | CC(C)S(=O)(=O)C1=CC=C(C=C1)C2=CN=C(C(=N2)C3=CC(=NO3)C4=CC=C(C=C4)CNC)N | |
| A8705 | SCR7 | DNA ligase IV inhibitor | DNA Damage/DNA Repair|DNA Ligases | 1533426-72-0 | S=C(NC(/N=C/C1=CC=CC=C1)=C2/N=C/C3=CC=CC=C3)NC2=O | |
| A4083 | Rocilinostat (ACY-1215) | Selective HDAC6 inhibitor | DNA Damage/DNA Repair|HDAC | 1316214-52-4 | C1=CC=C(C=C1)N(C2=CC=CC=C2)C3=NC=C(C=N3)C(=O)NCCCCCCC(=O)NO | |
| A4090 | JNJ-26481585 | Potent HDAC inhibitor | DNA Damage/DNA Repair|HDAC | 875320-29-9 | CN1C=C(C2=CC=CC=C21)CNCC3CCN(CC3)C4=NC=C(C=N4)C(=O)NO | |
| A8802 | (S)-Crizotinib | Potent MTH1 inhibitor | DNA Damage/DNA Repair|MTH1 | CC(C1=C(C=CC(=C1Cl)F)Cl)OC2=C(N=CC(=C2)C3=CN(N=C3)C4CCNCC4)N | ||
| A1945 | BIBR 1532 | Telomerase inhibitor,novel and selective | DNA Damage/DNA Repair|Telomerase | 321674-73-1 | CC(=CC(=O)NC1=CC=CC=C1C(=O)O)C2=CC3=CC=CC=C3C=C2 | |
| A3966 | Doxorubicin | Topo II inhibitor,immunosuppresive antineoplastic antibiotic | DNA Damage/DNA Repair|Topoisomerase | 23214-92-8 | CC1C(C(CC(O1)OC2CC(CC3=C(C4=C(C(=C23)O)C(=O)C5=C(C4=O)C=CC=C5OC)O)(C(=O)CO)O)N)O | |
| Download the DNA Damage/DNA Repair-related Compounds Panel - XLSXDownload the DNA Damage/DNA Repair-related Compounds Panel - SDF | ||||||
Related Biological Data
RPE cells were treated with TSA at various concentrations (0.2, 0.4, 0.8 and 1.0 μM). The protein expression levels of cyclinD1, CDK4 and CDK6, p-Rb, P21 and P27 were detected by western blot.
Related Biological Data
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" to show IC50- Cost-effective and competitive price to save your findings
- Potent, selective and cell-permeable in inhibiting or activating target molecules
- Diverse in chemical structure and route of administration (oral/i.m/i.v injection etc.)
- Detailed files describing potency, selectivity and applications etc.
- Supported by published data from top peer-reviewed journals
- Guaranteed high quality with NMR and HPLC validation
| Solubility | Soluble in DMSO | Storage | Desiccate at -20°C |
| Packaging | 96 well plate | Form | Powder |
| General tips | For obtaining a higher solubility , please warm the tube at 37°C and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20°C for several months. | ||
| Shipping Condition | Evaluation sample solution : ship with blue iceAll other available size:ship with RT , or blue ice upon request | ||
A wide range of well-characterized bioactive molecules that covers various targets related to DNA damage/DNA repair, including ATM/ATR, HDAC, and topoisomerase etc. Facilitate your research towards the insights of cancer, genome instability and immune diseases etc. Applicable in cellular assays, animal models and drug screenings etc.
1. Lord CJ, Ashworth A. The DNA damage response and cancer therapy. Nature. 2012 Jan 18;481(7381):287-94.Abstract Genomic instability is probably the combined effect of DNA damage, tumour-specific DNA repair defects, and a failure to stop or stall the cell cycle before the damaged DNA is passed on to daughter cells. A better understanding of the cellular response to DNA damage will not only inform our knowledge of cancer development but also help to refine the classification as well as the treatment of the disease.
2. Park J, Thomas S, Munster PN. Epigenetic modulation with histone deacetylaseinhibitors in combination with immunotherapy. Epigenomics. 2015;7(4):641-52.Abstract HDAC inhibitors have been approved as single agents for cutaneous and peripheral T-cell lymphoma and have shown promising activity in reversing therapy resistance in other tumor types. This review describes the current understanding on integrating HDAC inhibitors into various immunotherapeutic approaches, such as cancer vaccines, adoptive T-cell transfer and immune checkpoint inhibitors. Furthermore, it summarizes promising treatment strategies in epigenetic immune priming from clinical trials that are currently underway.
