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MW 384.5 Da, Purity >=98%. Potent RIP3 kinase inhibitor (IC₅₀ = 20.8 nM). It binds to the ATP binding pocket of RIP3 and inhibits ATP binding to prevent RIP3 enzymatic activity in vitro. . It inhibits TNF-induced necroptosis but does not inhibit TNF-induced apoptosis, indicating that HS-1371 has a specific inhibitory effect on RIP3-mediated necroptosis via the suppression of RIP3 kinase activity.

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Key facts

CAS number
2158197-70-5
Purity
>= 98%
Form
Solid
Molecular weight
384.5 Da
Molecular formula
C24H24N4O
PubChem identifier
134817449
Nature
Synthetic

Alternative names

Recommended products

MW 384.5 Da, Purity >=98%. Potent RIP3 kinase inhibitor (IC₅₀ = 20.8 nM). It binds to the ATP binding pocket of RIP3 and inhibits ATP binding to prevent RIP3 enzymatic activity in vitro. . It inhibits TNF-induced necroptosis but does not inhibit TNF-induced apoptosis, indicating that HS-1371 has a specific inhibitory effect on RIP3-mediated necroptosis via the suppression of RIP3 kinase activity.

Key facts

Purity
>= 98%
PubChem identifier
134817449
Solubility

>10 mg/ml DMSO.

Biochemical name
7-(1-(Piperidin-4-yl)-1h-pyrazol-4-yl)-4-(p-tolyloxy)quinoline
Biological description

Potent RIP3 kinase inhibitor (IC₅₀ = 20.8 nM). It binds to the ATP binding pocket of RIP3 and inhibits ATP binding to prevent RIP3 enzymatic activity in vitro. . It inhibits TNF-induced necroptosis but does not inhibit TNF-induced apoptosis, indicating that HS-1371 has a specific inhibitory effect on RIP3-mediated necroptosis via the suppression of RIP3 kinase activity.

Canonical SMILES
CC1=CC=C(C=C1)OC2=C3C=CC(=CC3=NC=C2)C4=CN(N=C4)C5CCNCC5
InChI
InChI=1S/C24H24N4O/c1-17-2-5-21(6-3-17)29-24-10-13-26-23-14-18(4-7-22(23)24)19-15-27-28(16-19)20-8-11-25-12-9-20/h2-7,10,13-16,20,25H,8-9,11-12H2,1H3
InChIKey
VPVLPCIBKVWFDT-UHFFFAOYSA-N
IUPAC name
4-(4-methylphenoxy)-7-(1-piperidin-4-ylpyrazol-4-yl)quinoline

Storage

Shipped at conditions
Blue Ice
Appropriate long-term storage conditions
-20°C

Notes

This product is manufactured by BioVision, an Abcam company and was previously called B2430 HS-1371. B2430-5 is the same size as the 5 mg size of ab287049.

Supplementary info

This supplementary information is collated from multiple sources and compiled automatically.
Activity summary

ALK (Anaplastic Lymphoma Kinase) LTK (Leukocyte Tyrosine Kinase) VEGF Receptor 2 (Vascular Endothelial Growth Factor Receptor 2) FGFR1 (Fibroblast Growth Factor Receptor 1) Met (c-Met) TIE2 Activin A Receptor Type IB (ALK-4) H-ERG (Human Ether-a-go-go-Related Gene) and SMEK2 are of high importance in various cellular processes. These targets have different alternative names and vary in molecular masses. For example ALK is a receptor tyrosine kinase with a prominent role in neuronal tissue while H-ERG a potassium ion channel primarily contributes to the cardiac tissue. Each target plays important roles in specific signaling pathways and is expressed throughout different tissues impacting diverse cellular functions.

Biological function summary

These targets operate within intricate cellular networks that include signal transduction and ion channel regulation. ALK MET and VEGF Receptor 2 partake in receptor-mediated pathways that guide cell proliferation and angiogenesis while H-ERG controls cardiac repolarization by mediating potassium flow. The SMEK2 protein is part of a protein phosphatase complex influencing various signal transduction pathways. These molecular players interact with cellular machinery to regulate development response to environmental stimuli and maintenance of cellular homeostasis.

Pathways

ALK MET and VEGF Receptor 2 are fundamental in the PI3K-AKT and MAPK signaling pathways influencing cell growth and survival. These proteins often interact with other kinases to transmit extracellular signals into proper cellular responses. MET also integrates within crosstalk of the HGF signaling pathway collaborating with partners like beta-catenin. These pathways illustrate the dynamic role of these targets in cellular signaling linking them to other key proteins and metabolites.

Associated diseases and disorders

Abnormalities in ALK MET and FGFR1 are associated with cancer while H-ERG dysfunction often leads to cardiac arrhythmias like Long QT syndrome. ALK fusions and mutations trigger tumorigenesis in various cancers including lung cancer where it interacts with EGFR and KRAS mutations. Meanwhile aberrations in H-ERG contribute to lethal cardiac conditions such as Torsades de Pointes through its involvement with ion channel proteins. Understanding these targets aids in addressing disease pathogenesis and guiding therapeutic development.

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