SML3054
CHIR124
≥98% (HPLC)
别名:
4-[((3S)-1-Azabicyclo[2.2.2]oct-3-yl)amino]-3-(1H-benzimidazol-2-yl)-6-chloroquinolin-2(1H)-one, 4-[(3S)-1-Azabicyclo[2.2.2]oct-3-ylamino]-3-(1H-benzimidazol-2-yl)-6-chloro-2(1H)-quinolinone, CHIR 124, CHIR-124, f 4-[((3S)-
quinuclidin-3-yl)amino]-3-benzimidazol-2-yl-6-chloro-hydroquinolin-2- one
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关于此项目
经验公式（希尔记法）:
C23H22ClN5O
化学文摘社编号:
分子量:
419.91
UNSPSC Code:
12352200
NACRES:
NA.77
MDL number:
InChI
1S/C23H22ClN5O/c24-14-5-6-16-15(11-14)21(25-19-12-29-9-7-13(19)8-10-29)20(23(30)28-16)22-26-17-3-1-2-4-18(17)27-22/h1-6,11,13,19H,7-10,12H2,(H,26,27)(H2,25,28,30)/t19-/m1/s1
SMILES string
O=C1NC2=CC=C(Cl)C=C2C(N[C@@H]3CN4CCC3CC4)=C1C5=NC6=C(C=CC=C6)N5
InChI key
MOVBBVMDHIRCTG-LJQANCHMSA-N
assay
≥98% (HPLC)
form
powder
color
white to beige
solubility
DMSO: 2 mg/mL, clear
storage temp.
2-8°C
Quality Level
Biochem/physiol Actions
CHIR124 is a potent and selective inhibitor of checkpoint kinase 1 (Chk1)( IC50 = 0.3 nM) that produces G2-M abrogation which induces chemosensitisation. It also inhibits PDGFR and FLT3 (IC50 = 6.6 nM and 5.8 nM respectively). CHIR-124 inhibits Pgp activity in multidrug-resistant cell lines KB-V1 and A2780-Pac-Res.
potent and selective inhibitor of checkpoint kinase 1 (Chk1)
存储类别
11 - Combustible Solids
wgk
WGK 3
flash_point_f
Not applicable
flash_point_c
Not applicable
法规信息
新产品
此项目有
Archie N Tse et al.
Clinical cancer research : an official journal of the American Association for Cancer Research, 13(2 Pt 1), 591-602 (2007-01-27)
Chk1 kinase is a critical regulator of both S and G(2)-M phase cell cycle checkpoints in response to DNA damage. This study aimed to evaluate the biochemical, cellular, and antitumor effects of a novel Chk1 inhibitor, CHIR124. CHIR-124 was evaluated
Rida Zahra et al.
PloS one, 15(6), e0233993-e0233993 (2020-06-03)
Multidrug resistance (MDR) to chemotherapeutic drugs remains one of the major impediments to the treatment of cancer. Discovery and development of drugs that can prevent and reverse the acquisition of multidrug resistance constitute a foremost challenge in cancer therapeutics. In
Siang-Boon Koh et al.
Cancer research, 78(11), 3054-3066 (2018-05-08)
Combination of cytotoxic therapy with emerging DNA damage response inhibitors (DDRi) has been limited by tolerability issues. However, the goal of most combination trials has been to administer DDRi with standard-of-care doses of chemotherapy. We hypothesized that mechanism-guided treatment scheduling
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