CBP501 Affinity Peptide is a Chk kinase inhibitor that can abrogate G2 arrest induced by DNA-damaging agents. CBP501 Affinity Peptide can be used in cancer research[1].
PF 477736 is a potent, selective ATP-competitive inhibitor of Chk1, with a Ki of 0.49 nM, 100-fold selectivity versus Chk2 (Ki, 47 nM).
AZD-7762 is a potent ATP-competitive checkpoint kinase (Chk) inhibitor in with an IC50 of 5 nM for Chk1.
CCT245737 is a orally active and seletive Chk1 inhibitor, with an IC50 of 1.3 nM。
VRX0466617, a selective Chk2 inhibitor, inhibits the phosphorylation of Chk2 Ser 19 and Ser33-35. VRX0466617 can be used in the study of cancer[1].
MRT00033659 is a potent broad-spectrum kinase inhibitor of CK1 (IC50=0.9 µM for CK1δ) and CHK1 (IC50=0.23 µM). MRT00033659, a pyrazolo-pyridine analogue, induces p53 pathway activation and E2F-1 destabilisation[1].
Chk1-IN-5 is a potent checkpoint kinase 1 (Chk1) inhibitor. Chk1-IN-5 inhibits Chk1 phosphorylation and inhibits tumor growth in colon cancer xenograft model[1].
A potent and highly selective Chk2 inhibitor with IC50 of 0.14 nM; displays greater than 100 uM for Chk1 in vitro.
LY2880070 is an orally active CHK1 inhibitor. LY2880070 can be used as an anticancer agent for combination with DNA damaging agents[1].
Chk1-IN-6 is a potent, selective, and orally bioavailable CHK1 inhibitor candidate.
GNE-900 is a an ATP-competitive, selective, and orally active ChK1 inhibitor with IC50s of 0.0011, 1.5 µM for ChKl, ChK2, respectively. GNE-900 abrogates the G2-M checkpoint, enhances DNA damage, and induces Apoptosis. gemcitabine (HY-17026) and GNE-900 administration shows anti-tumor activity[1].
LY2603618 is a potent and selective inhibitor of Chk1 with an IC50 of 7 nM.
GDC-0575 dihydrochloride is an orally bioavailable CHK1 inhibitor, with an IC50 of 1.2 nM, and has antitumor activity.
SCH900776 is a potent, selective and oral inhibitor of checkpoint kinase1 (Chk1) with an IC50 of 3 nM. It shows 50- and 500-fold selectivity over CDK2 andChk2, respectively.
Chktide is a substrate for CHK1 and CHK2. Chktide can be used in kinase assays[1][2].
GDC-0575 (ARRY-575, RG7741) is a highly-selective oral small-molecule Chk1 inhibitor with an IC50 of 1.2 nM.
Prexasertib Mesylate Hydrate (LY2606368 Mesylate Hydrate) is a potent, selective, ATP competitive CHK1 and CHK2 inhibitor, with a Ki of 0.9 nM for CHK1 and IC50s of <1 nM, 8 nM for CHK1 and CHK2, respectively. Prexasertib Mesylate Hydrate inhibits HT-29 CHK1 autophosphorylation (S296) and HT-29 CHK2 autophosphorylation (S516). Prexasertib Mesylate Hydrate shows potent anti-tumor activity, significantly abrogates the G2/M checkpoint in p53 deficient HeLa cells with an EC50 of 9 nM[1].
CCT244747 is a potent, orally bioavailable and highly selective CHK1 inhibitor, with an IC50 of 7.7 nM; CCT244747 also abrogates G2 checkpoint with an IC50 of 29 nM.
Prexasertib dihydrochloride (LY2606368 dihydrochloride) is a potent and selective ATP competitive inhibitor of the Chk1 protein kinase, with IC50s of <1 nM and 8 nM for CHK1 and CHK2, respectively, and a Ki of 0.9 nM against purified CHK1.
CCT241533 hydrochloride is a potent and selective CHK2 inhibitor with an IC50 of 3 nM and a Ki of 1.16 nM.
Prexasertib dimesylate (LY2606368 dimesylate) is a selective, ATP-competitive second-generation checkpoint kinase 1 (CHK1) inhibitor with a Ki of 0.9 nM and an IC50 of <1 nM. Prexasertib dimesylate inhibits CHK2 (IC50=8 nM) and RSK1 (IC50=9 nM). Prexasertib dimesylate causes double-stranded DNA breakage and replication catastrophe resulting in apoptosis. Prexasertib dimesylate shows potent anti-tumor activity[1][2].
CHK1-IN-3 is a Checkpoint Kinase 1 (CHK1) inhibitor with an IC50 of 0.4 nM[1].
BML-277 is a selective checkpoint kinase 2 (Chk2) inhibitor with an IC50 of 15 nM.
CHIR-124 is a potent and selective Chk1 inhibitor with IC50 of 0.3 nM, and also potently targets PDGFR and FLT3 with IC50s of 6.6 nM and 5.8 nM.
GDC-0425 (RG-7602) is an orally available, highly selective small molecule ChK1 inhibitor. GDC-0425 can be used for the research of various malignancies[1][2].
Prexasertib (LY2606368) is a potent, selective and ATP-competitive checkpoint kinase 1 (Chk1) inhibitor, with an IC50 and a Ki of <1 nM and 0.9 nM, respectively.
AZD-7762 hydrochloride is a potent ATP-competitive checkpoint kinase (Chk) inhibitor in with an IC50 of 5 nM for Chk1.
A potent and selective (up to 263-fold) inhibitor of breast cancer cells with GI50 of 0.5 uM (MCF-7), via activation the aryl hydrocarbon receptor (AhR) pathway; inhibits other cell lines derived from other tumour types with GI50 of 3.2-46 uM (lung, colon, ovary, neuronal, glial, prostate, and pancreas); potently inhibits the growth of T47D, ZR-75-1, MCF-7, SKBR3, and MDA-MB-468 breast cancer cells with GI50 of 0.16-0.38 uM, induces cell cycle arrest checkpoint activation and DNA damage; binds to the AhR, induces translocation to the nucleus, activates the XRE, induces CYP1 activity, culminating in cell cycle arrest, checkpoint activation, DNA damage and cell death.
Monalizumab is a first-in-class immune checkpoint inhibitor targeting Natural Killer Group 2A (NKG2A). Monalizumab, a humanized anti-NKG2A blocking mAb, increases IFN-γ production, thereby promoting NK cell effector functions. Monalizumab can be used for the research of head and neck squamous cell carcinoma (HNSCC)[1][2].
CHK1-IN-7 (Compound 10c) is a potent human CHK1 inhibitor. CHK1-IN-7 shows no single agent effect, potentiates the antiproliferative effect of Gemcitabine HY-17026 in both prostate and breast cancer cell lines. CHK1-IN-7 can be used for the research of cancer[1].