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Mirin

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].

Product Specifications

CAS Number

[1198097-97-0]

UNSPSC

12352005

Hazard Statement

H302, H315, H319, H335

Target

Apoptosis; ATM/ATR

Type

Reference compound

Related Pathways

Apoptosis; Cell Cycle/DNA Damage; PI3K/Akt/mTOR

Applications

Cancer-programmed cell death

Field of Research

Cancer

Assay Protocol

https://www.medchemexpress.com/Mirin.html

Purity

99.63

Solubility

DMSO : ≥ 31 mg/mL

Smiles

O=C1N=C(S/C1=C\C2=CC=C(C=C2)O)N

Molecular Formula

C10H8N2O2S

Molecular Weight

220.25

Precautions

H302, H315, H319, H335

References & 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.

Shipping Conditions

Room Temperature

Storage Conditions

-20°C, 3 years; 4°C, 2 years (Powder)

Scientific Category

Reference compound1

Clinical Information

No Development Reported

Available Sizes

Curated Selection

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