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Principaux documents

SML2855

Sigma-Aldrich

LY2603618

≥98% (HPLC)

Synonyme(s) :

(S)-1-[5-Bromo-4-methyl-2-(morpholin-2-ylmethoxy)phenyl]-3-(5-methylpyrazin-2-yl)urea, 1-[5-Bromo-4-methyl-2-(S)-(morpholin-2-ylmethoxy)phenyl]-3-(5-methylpyrazin-2-yl)urea, IC-83, LCI-1, LY 2603618, LY-2603618, Rabusertib

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About This Item

Formule empirique (notation de Hill) :
C18H22BrN5O3
Numéro CAS:
Poids moléculaire :
436.30
Numéro MDL:
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.77

Niveau de qualité

Essai

≥98% (HPLC)

Forme

powder

Couleur

white to beige

Solubilité

DMSO: 2 mg/mL, clear (warmed)

Température de stockage

2-8°C

Chaîne SMILES 

CC1=C(Br)C=C(NC(NC2=CN=C(C)C=N2)=O)C(OC[C@H]3OCCNC3)=C1

InChI

1S/C18H22BrN5O3/c1-11-5-16(27-10-13-8-20-3-4-26-13)15(6-14(11)19)23-18(25)24-17-9-21-12(2)7-22-17/h5-7,9,13,20H,3-4,8,10H2,1-2H3,(H2,22,23,24,25)/t13-/m0/s1

Clé InChI

SYYBDNPGDKKJDU-ZDUSSCGKSA-N

Actions biochimiques/physiologiques

LY2603618 (LCI-1) is a potent and selective checkpoint kinase 1 (Chk1) inhibitor (IC50 = 7 nM) that produces a cellular phenotype identical to that reported upon Chk1 depletion by RNAi. LY2603618 prevents doxorubicin-induced Chk1 autophosphorylation (IC50 = 52 nM; HeLa), allowing cells to traverse the G2/M checkpoint and proceed into mitosis with unresolved replicated chromosomes. LY2603618 renders mutant p53, but not wild-type, HT-29 colon cancer cells more sensitive to gemcitabine both in vitro and in mice in vivo.
Potent and selective checkpoint kinase 1 (Chk1) inhibitor that renders mutant p53 cancer cells more sensitive to DNA-damaging agents in vitro and in vivo.

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Point d'éclair (°F)

Not applicable

Point d'éclair (°C)

Not applicable


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Certificats d'analyse (COA)

Lot/Batch Number

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Consulter la Bibliothèque de documents

Anne M van Harten et al.
Oncogenesis, 8(7), 38-38 (2019-06-19)
Head and neck squamous cell carcinomas (HNSCCs) coincide with poor survival rates. The lack of driver oncogenes complicates the development of targeted treatments for HNSCC. Here, we follow-up on two previous genome-wide RNA and microRNA interference screens in HNSCC to
Constance King et al.
Investigational new drugs, 32(2), 213-226 (2013-10-12)
Interference with DNA damage checkpoints has been demonstrated preclinically to be a highly effective means of increasing the cytotoxicity of a number of DNA-damaging cancer therapies. Cell cycle arrest at these checkpoints protects injured cells from apoptotic cell death until
Nicole D Vincelette et al.
Scientific reports, 9(1), 3617-3617 (2019-03-07)
CPX-351 is a liposomally encapsulated 5:1 molar ratio of cytarabine and daunorubicin that recently received regulatory approval for the treatment of therapy-related acute myeloid leukemia (AML) or AML with myelodysplasia-related changes based on improved overall survival compared to standard cytarabine/daunorubicin
Characterization and preclinical development of LCI-1, a selective and potent Chk1 inhibitor in phase I clinical trials
Marshall M, Barda D, Barnard D, et al.
Molecular Cancer Therapeutics, 8, B248-B248 (2009)
Kamila Burdova et al.
The EMBO journal, 38(20), e101443-e101443 (2019-08-20)
Cyclins are central engines of cell cycle progression in conjunction with cyclin-dependent kinases (CDKs). Among the different cyclins controlling cell cycle progression, cyclin F does not partner with a CDK, but instead forms via its F-box domain an SCF (Skp1-Cul1-F-box)-type

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