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Merck

C3742

Sigma-Aldrich

Chk2 Inhibitor II hydrate

≥98% (HPLC)

Synonim(y):

2-(4-(4-Chlorophenoxy)phenyl)-1H-benzimidazole-5-carboxamide hydrate

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About This Item

Wzór empiryczny (zapis Hilla):
C20H14ClN3O2 · xH2O
Numer CAS:
Masa cząsteczkowa:
363.80 (anhydrous basis)
Numer MDL:
Kod UNSPSC:
12352200
Identyfikator substancji w PubChem:
NACRES:
NA.77

Próba

≥98% (HPLC)

Postać

solid

kolor

off-white to tan

rozpuszczalność

DMSO: ≥2 mg/mL (warmed)

inicjator

Johnson & Johnson

temp. przechowywania

2-8°C

ciąg SMILES

O=C(C1=CC=C2C(N=C(C3=CC=C(OC4=CC=C(Cl)C=C4)C=C3)N2)=C1)N

InChI

1S/C20H14ClN3O2/c21-14-4-8-16(9-5-14)26-15-6-1-12(2-7-15)20-23-17-10-3-13(19(22)25)11-18(17)24-20/h1-11H,(H2,22,25)(H,23,24)

Klucz InChI

UXGJAOIJSROTTN-UHFFFAOYSA-N

informacje o genach

human ... CHEK2(11200)

Działania biochem./fizjol.

Chk2 Inhibitor II is a checkpoint kinase 2 inhibitor, which controls the p53 response to DNA breaks induced by radiation, leading to apoptosis. Protection of T-cells from apoptosis implies use as an adjuvant for radiation therapy in cancer. IC50 = 15 nM; Ki = 37 nM. Chk2 Inhibitor II shows 1000-fold greater selectivity for the Chk2 serine/threonine kinase than for the Cdk1/B and CK1 kinases (for which IC50 = 12 μM and 17 μM, respectively). Chk2 Inhibitor II weakly inhibits a panel of 31 other kinases (<25% inhibition at a concentration of 10 μM and prevents apoptosis of human CD4+ and CD8+ T-cells subjected to ionizing radiation (EC50 = 3 μM and 7.6 μM, respectively).

Cechy i korzyści

This compound was developed by Johnson & Johnson. To browse the list of other pharma-developed compounds and Approved Drugs/Drug Candidates, click here.
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Kod klasy składowania

11 - Combustible Solids

Klasa zagrożenia wodnego (WGK)

WGK 3

Temperatura zapłonu (°F)

Not applicable

Temperatura zapłonu (°C)

Not applicable


Certyfikaty analizy (CoA)

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Dokumenty związane z niedawno zakupionymi produktami zostały zamieszczone w Bibliotece dokumentów.

Odwiedź Bibliotekę dokumentów

Elena Oropeza et al.
Science advances, 9(26), eadf2860-eadf2860 (2023-06-30)
Cell cycle dysregulation is prerequisite for cancer formation. However, it is unknown whether the mode of dysregulation affects disease characteristics. Here, we conduct comprehensive analyses of cell cycle checkpoint dysregulation using patient data and experimental investigations. We find that ATM
Lauren E Williamson et al.
Journal of virology, 93(8) (2019-02-08)
The human B cell response to natural filovirus infections early after recovery is poorly understood. Previous serologic studies suggest that some Ebola virus survivors exhibit delayed antibody responses with low magnitude and quality. Here, we sought to study the population
Ran Guo et al.
Antioxidants (Basel, Switzerland), 11(6) (2022-06-25)
Reactive oxygen species (ROS) act as a signaling intermediate to promote cellular adaptation to maintain homeostasis by regulating autophagy during pathophysiological stress. However, the mechanism by which ROS promotes autophagy is still largely unknown. Here, we show that the ATM/CHK2/ULK1
Wenyu Zhang et al.
Cell death and differentiation, 27(2), 482-496 (2019-06-19)
Both the stress-response protein, SIRT1, and the cell cycle checkpoint kinase, CHK2, play critical roles in aging and cancer via the modulation of cellular homeostasis and the maintenance of genomic integrity. However, the underlying mechanism linking the two pathways remains
Yi Luan et al.
Science advances, 8(51), eade1846-eade1846 (2022-12-22)
Cyclophosphamide and doxorubicin lead to premature ovarian insufficiency as an off-target effect. However, their oocyte death pathway has been debated. Here, we clarified the precise mechanism of ovarian depletion induced by cyclophosphamide and doxorubicin. Dormant oocytes instead of activated oocytes

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