chk2

Baricitinib (INCB028050) is a JAK1 and JAK2 inhibitor (IC50=5.9 5.7 nM) with selective and oral activity. Baricitinib has potential anti-inflammatory, immunomodulatory and anti-tumor activity.

Prexasertib (LY2606368) is an inhibitor of checkpoint kinase 1 (chk1) with potential antineoplastic activity.

CCT241533 is an effective and selective ATP competitive inhibitor of CHK2 (Ki: 1.16 nM; IC50: 3 nM).

SCH900776 (MK-8776) is an agent targeting cell cycle checkpoint kinase 1 (Chk1) with potential radiosensitization and chemosensitization activities.

AZD-7762, an effective and specific inhibitor of Chk1(IC50=5 nM), is equally potent against Chk2 and less potent against CAM, Yes, Fyn, Lyn, Hck and Lck.

CCT241533 hydrochloride is an effective and selective ATP competitive inhibitor of CHK2 (Ki: 1.16 nM; IC50: 3 nM).

PF 477736 (PF-736,PF-00477736) is a specifc, effective and ATP-competitive Chk1 inhibitor (Ki: 0.49 nM ) and also inhibits FGFR3, Aurora-A, VEGFR2, Flt3, Fms (CSF1R), Ret and Yes.

4-Demethyldeoxypodophyllotoxin, an aryl tetrahydronaphthalenyl lignan analog from the roots of Podophyllum peltatum, has anticancer activity and modulates the Chk-2 signaling pathway in MCF-7 breast cancer cells.

Chk2-IN-2 (compound 2) serves as a selective CHK2 inhibitor, showing promise for anticancer applications [1].

ANI-7 is an activator of the aryl hydrocarbon receptor (AhR) pathway, inhibiting the growth of various cancer cells and selectively inhibiting the growth of MCF-7 breast cancer cells (GI50: 0.56 μM).

CHK-IN-1 is a dual inhibitor of CHK1 and CHK2 with antiproliferative activity.

Rabusertib (IC-83) is an inhibitor of the cell cycle checkpoint kinase 1 (chk1) with potential chemopotentiating activity. Rabusertib has been used in trials studying the treatment of Cancer, Solid Tumors, Advanced Cancer, Pancreatic Neoplasms, and Non-Small Cell Lung Cancer.

BML-277 (C 3742) is a selective checkpoint kinase 2 (Chk2) inhibitor.

PHA-767491 (CAY10572) is a potent ATP-competitive dual Cdc7 CDK9 inhibitor with IC50 of 10 nM and 34 nM, respectively.

CCT245737 is an orally active, selective Chk1 inhibitor with an IC50 of 1.3 nM, and is >1,000-fold selective over CHK2 and CDK1.

GNE-900 is an ATP-competitive ChK1 inhibitor with selective and oral activity.GNE-900 inhibits ChKl and ChK2 with IC50 values of 0.0011 and 1.5 µM, respectively.GNE-900 enhances DNA damage and induces apoptosis. GNE-900 has antitumor activity.

NSC 109555 is a selective, reversible, ATP-competitive Chk2 inhibitor (IC50 = 0.2 μM) that displays no effect on a range of other kinases including Chk1 (IC50 > 10 μM). Inhibits histone H1 phosphorylation (IC50 = 0.24 μM) and attenuates mitochondrial ATP synthesis. Exhibits antiproliferative activity in a number of leukemias in vivo.

VER-00158411 is a checkpoint kinase 1 and CHK2 inhibitor [IC50: 4.4 nM and 4.5 nM, respectively].

Potent Chk2 inhibitor (IC50 = 3 nM). Shows >63-fold selectivity for Chk1 over Chk2 and a panel of 84 other kinases. Inhibits Chk2 activation in response to etoposide-induced DNA damage in HT29 cells. Blocks ionizing radiation-induced apoptosis of mouse thymocytes. Caldwell et al (2011) Structure-based design of potent and selective 2-(quinazolin-2-yl)phenol inhibitors of checkpoint kinase 2. J.Med.Chem. 54 580 PMID:21186793

Prexasertib dihydrochloride (LY2606368) is an ATP-competitive CHK1 inhibitor (Ki: 0.9 nmol L). in the cell-free assay, its IC50 values are 8 nM and 9 nM for CHK2 and RSK, respectively.

SC-203885 is a checkpoint kinase 2 inhibitor.

PHA-767491 hydrochloride (CAY-10572 hydrochloride) is an effective ATP-competitive dual Cdc7 CDK9 inhibitor (IC50: 10 34 nM). It has ~20-fold selectivity against GSK3-β and CDK1 2, 50-fold selectivity against CDK5 and MK2, 100-fold selectivity against CHK2 and PLK1.

Chk2 inhibitor,ATP-competitive

Prexasertib is a potent and selective Chk1/Chk2 inhibitor. Prexasertib increases the effectiveness of conventional therapy in B-/T- cell progenitor acute lymphoblastic leukemia. LY2606368 causes replication catastrophe and antitumor effects through CHK1-d