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SML2855

Sigma-Aldrich

LY2603618

≥98% (HPLC)

Synonym(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

Empirical Formula (Hill Notation):
C18H22BrN5O3
CAS Number:
Molecular Weight:
436.30
MDL number:
UNSPSC Code:
12352200
NACRES:
NA.77

Quality Level

Assay

≥98% (HPLC)

form

powder

color

white to beige

solubility

DMSO: 2 mg/mL, clear (warmed)

storage temp.

2-8°C

SMILES string

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

InChI key

SYYBDNPGDKKJDU-ZDUSSCGKSA-N

Biochem/physiol Actions

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.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable


Certificates of Analysis (COA)

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Resistance to standard chemotherapy agents remains a major obstacle for improving treatment outcomes for acute myeloid leukemia (AML). The Bcl-2-selective inhibitor ABT-199 has demonstrated encouraging preclinical results, drug resistance remains a concern. Mcl-1 has been demonstrated to contribute to ABT-199
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Molecular Cancer Therapeutics, 8, B248-B248 (2009)
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Chondrosarcomas are malignant cartilage tumors that are relatively resistant towards conventional therapeutic approaches. Kinase inhibitors have been investigated and shown successful for several different cancer types. In this study we aimed at identifying kinase inhibitors that inhibit the survival of
Constance King et al.
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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

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