catastrophe

By Targets:	Apoptosis (6) Checkpoint Kinase (Chk) (5) CXCR (2) DNA/RNA Synthesis (1) FGFR (1) Haspin Kinase (2) Proteasome (1) Survivin (1) VEGFR (1)
By Research Areas:	Cancer (11) Inflammation/Immunology (1)

Cat. No.	Product Name	Target	Research Areas	Chemical Structure

HY-P1103

CTCE-9908	CXCR	Cancer
CTCE-9908 is a potent and selective CXCR4 antagonist. CTCE-9908 induces mitotic catastrophe, cytotoxicity and inhibits migration in CXCR4-expressing ovarian cancer cells .

HY-U00177

GDP366 1 Publications Verification	Survivin	Cancer
GDP366, a dual inhibitor of survivin and Op18, induces cell growth inhibition, cellular senescence and mitotic catastrophe in human cancer cells.

HY-13737

R1530 1 Publications Verification	VEGFR FGFR Apoptosis	Cancer
R1530 is a highly potent, orally active, dual-acting mitosis/angiogenesis inhibitor, with anti-tumor and anti-angiogenic activities. R1530 is a multikinase inhibitor which binds to 31 kinases with K_d values of <500 nM. R1530 inhibits VGFR2 and FGFR1 with IC₅₀ of 10 nM and 28 nM, respectively. R1530 triggers apoptosis (mitotic catastrophe) or senescence .

HY-18174

Prexasertib Maximum Cited Publications 17 Publications Verification LY2606368	Checkpoint Kinase (Chk) Apoptosis	Cancer
Prexasertib (LY2606368) is a selective, ATP-competitive second-generation checkpoint kinase 1 (CHK1) inhibitor with a K_i of 0.9 nM and an IC₅₀ of <1 nM. Prexasertib inhibits CHK2 (IC₅₀=8 nM) and RSK1 (IC₅₀=9 nM). Prexasertib causes double-stranded DNA breakage and replication catastrophe resulting in apoptosis. Prexasertib shows potent anti-tumor activity .

HY-P1103A

CTCE-9908 TFA	CXCR	Cancer
CTCE-9908 TFA is a potent and selective CXCR4 antagonist. CTCE-9908 TFA induces mitotic catastrophe, cytotoxicity and inhibits migration in CXCR4-expressing ovarian cancer cells .

HY-18174A

Prexasertib dihydrochloride Maximum Cited Publications 17 Publications Verification LY2606368 dihydrochloride	Checkpoint Kinase (Chk) Apoptosis	Cancer
Prexasertib dihydrochloride (LY2606368 dihydrochloride) is a selective, ATP-competitive second-generation checkpoint kinase 1 (CHK1) inhibitor with a K_i of 0.9 nM and an IC₅₀ of <1 nM. Prexasertib dihydrochloride inhibits CHK2 (IC₅₀=8 nM) and RSK1 (IC₅₀=9 nM). Prexasertib dihydrochloride causes double-stranded DNA breakage and replication catastrophe resulting in apoptosis. Prexasertib dihydrochloride shows potent anti-tumor activity .

HY-18174B

Prexasertib Mesylate Hydrate LY2606368 Mesylate Hydrate; LY2940930	Checkpoint Kinase (Chk) Apoptosis	Cancer
Prexasertib Mesylate Hydrate (LY2606368 Mesylate Hydrate) is a selective, ATP-competitive second-generation checkpoint kinase 1 (CHK1) inhibitor with a K_i of 0.9 nM and an IC₅₀ of <1 nM. Prexasertib Mesylate Hydrate inhibits CHK2 (IC₅₀=8 nM) and RSK1 (IC₅₀=9 nM). Prexasertib Mesylate Hydrate causes double-stranded DNA breakage and replication catastrophe resulting in apoptosis. Prexasertib Mesylate Hydrate shows potent anti-tumor activity .

HY-18174C

Prexasertib mesylate LY2606368 mesylate	Checkpoint Kinase (Chk) DNA/RNA Synthesis Apoptosis	Cancer
Prexasertib mesylate (LY2606368 mesylate) is a selective, ATP-competitive second-generation checkpoint kinase 1 (CHK1) inhibitor with a K_i of 0.9 nM and an IC₅₀ of <1 nM. Prexasertib mesylate inhibits CHK2 (IC₅₀=8 nM) and RSK1 (IC₅₀=9 nM). Prexasertib mesylate causes double-stranded DNA breakage and replication catastrophe resulting in apoptosis. Prexasertib mesylate shows potent anti-tumor activity .

HY-18174E

Prexasertib dimesylate Maximum Cited Publications 17 Publications Verification LY2606368 dimesylate	Checkpoint Kinase (Chk) Apoptosis	Cancer
Prexasertib dimesylate (LY2606368 dimesylate) is a selective, ATP-competitive second-generation checkpoint kinase 1 (CHK1) inhibitor with a K_i 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 .

HY-124757

FiVe1	Proteasome	Inflammation/Immunology
FiVe1 is a potent vimentin (VIM; the intermediate filament and mesenchymal marker) inhibitor . FiVe1 promotes VIM disorganization and phosphorylation during metaphase, leading to mitotic catastrophe, multinucleation, and the loss of stemness.?FiVe1 selectively and irreversibly inhibits the growth of multiple FOXC2-expressing breast cancer cell lines (HMLER cells (IC₅₀:?267 nM); FOXC2-HMLER cells (IC₅₀:?447 nM). FiVe1 inhibits the migration of mesenchymally transformed cells .

HY-15217

CHR-6494 5+ Cited Publications	Haspin Kinase	Cancer
CHR-6494 is a potent inhibitor of haspin, with an IC₅₀ of 2 nM. CHR-6494 inhibits histone H3T3 phosphorylation. CHR-6494 can be used in the research of cancer .

HY-110350

CHR-6494 TFA	Haspin Kinase	Cancer
CHR-6494 TFA is a potent inhibitor of haspin, with an IC₅₀ of 2 nM. CHR-6494 TFA inhibits histone H3T3 phosphorylation. CHR-6494 TFA induces the apoptosis of cancer cells, including melanoma and breast cancer. CHR-6494 TFA can be used in the research of cancer .

Cat. No.	Product Name

HY-L020

Wnt/Hedgehog/Notch Compound Library	352 compounds
The developmental proteins Hedgehog, Notch and Wnt are key regulators of cell fate, proliferation, migration and differentiation in several tissues. Their related signaling pathways are frequently activated in tumors, and particularly in the rare subpopulation of cancer stem cells. The Wnt signaling pathway is a conserved pathway in animals. Deregulated Wnt signaling has catastrophic consequences for the developing embryo and it is now well appreciated that defective Wnt signaling is a causative factor for a number of pleiotropic human pathologies, including cancer. Hedgehog signaling pathway is linked to tumorigenesis and is aberrantly activated in a variety of cancers. The Notch signaling pathway is a highly conserved cell signaling system present in most animals. It plays an important role in cell-cell communication, and further regulates embryonic development. MCE designs a unique collection of 352 Wnt/Hedgehog/Notch signaling pathway-related small molecules. Wnt/Hedgehog/Notch Compound Library serves as a useful tool for stem cell research and anti-cancer drug screening.

Wnt/Hedgehog/Notch Compound Library

352 compounds

The developmental proteins Hedgehog, Notch and Wnt are key regulators of cell fate, proliferation, migration and differentiation in several tissues. Their related signaling pathways are frequently activated in tumors, and particularly in the rare subpopulation of cancer stem cells. The Wnt signaling pathway is a conserved pathway in animals. Deregulated Wnt signaling has catastrophic consequences for the developing embryo and it is now well appreciated that defective Wnt signaling is a causative factor for a number of pleiotropic human pathologies, including cancer. Hedgehog signaling pathway is linked to tumorigenesis and is aberrantly activated in a variety of cancers. The Notch signaling pathway is a highly conserved cell signaling system present in most animals. It plays an important role in cell-cell communication, and further regulates embryonic development.

MCE designs a unique collection of 352 Wnt/Hedgehog/Notch signaling pathway-related small molecules. Wnt/Hedgehog/Notch Compound Library serves as a useful tool for stem cell research and anti-cancer drug screening.

Cat. No.	Product Name	Target	Research Area

HY-P1103

CTCE-9908	CXCR	Cancer
CTCE-9908 is a potent and selective CXCR4 antagonist. CTCE-9908 induces mitotic catastrophe, cytotoxicity and inhibits migration in CXCR4-expressing ovarian cancer cells .

HY-P1103A

CTCE-9908 TFA	CXCR	Cancer
CTCE-9908 TFA is a potent and selective CXCR4 antagonist. CTCE-9908 TFA induces mitotic catastrophe, cytotoxicity and inhibits migration in CXCR4-expressing ovarian cancer cells .

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