Comparison

Mirin European Partner

Item no. HY-19959-25mg
Manufacturer MedChem Express
CASRN 1198097-97-0
Amount 25 mg
Quantity options 100 mg 10 mM/1 mL 10 mg 200 mg 25 mg 50 mg 5 mg
Category
Type Inhibitors
Specific against other
Purity 99.63
Citations [1]Rozier L, et al. The MRN-CtIP pathway is required for metaphase chromosome alignment. Mol Cell. 2013 Mar 28;49(6):1097-107.|[2]Lee JH, et al. Ataxia telangiectasia-mutated (ATM) kinase activity is regulated by ATP-driven conformational changes in the Mre11/Rad50/Nbs1 (MRN) complex. J Biol Chem. 2013 May 3;288(18):12840-51.|[3]Garner KM, et al. Corrected structure of Mirin, a small-molecule inhibitor of the Mre11-Rad50-Nbs1 complex. Nat Chem Biol. 2009 Mar;5(3):129-30.|[4]Aude Dupré, et al. A forward chemical genetic screen reveals an inhibitor of the Mre11-Rad50-Nbs1 complex. Nat Chem Biol. 2008 Feb;4(2):119-25.|[5]Adel Alblihy, et al. Selective Killing of BRCA2-Deficient Ovarian Cancer Cells via MRE11 Blockade. Int J Mol Sci. 2023 Jun 30;24(13):10966.
Smiles O=C1N=C(S/C1=C\C2=CC=C(C=C2)O)N
ECLASS 10.1 32160490
ECLASS 11.0 32160490
UNSPSC 12000000
Shipping Condition Room temperature
Available
Manufacturer - Type
Reference compound
Manufacturer - Applications
Cancer-programmed cell death
Manufacturer - Targets
Apoptosis; ATM/ATR
Shipping Temperature
Room Temperature
Storage Conditions
-20°C, 3 years; 4°C, 2 years (Powder)
Molecular Weight
220.25
Product Description
Mirin is a potent Mre11-Rad50-Nbs1 (MRN) complex inhibitor. Mirin prevents MRN-dependent activation of ATM (IC50=12 μM) without affecting ATM protein kinase activity, and it inhibits Mre11-associated exonuclease activity. Mirin abolishes the G2/M checkpoint and homology-dependent repair in mammalian cells. Mirin prevents ATM activation in response to DNA double-strand breaks (DSBs) and blocks homology-directed repair (HDR) in mammalian cells[1][2].
Manufacturer - Research Area
Cancer
Solubility
DMSO: ≥ 31 mg/mL
Manufacturer - Pathway
Apoptosis; Cell Cycle/DNA Damage; PI3K/Akt/mTOR
Clinical information
No Development Reported

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