IWP-4 (GMP) is the GMP-grade form of IWP-4 (HY-12879). IWP-4 is a Wnt inhibitor with an IC50 of 25 nM. IWP-4 specifically inhibits casein kinase 1δ/ε (CK1δ/ε), with an IC50 of 1.06 μM against wild-type CK1δ, 1.02 μM against the CK1δ kinase domain, and 7.07 μM against CK1ε; it shows enhanced inhibitory activity against the M82F CK1δ mutant (IC50 = 0.14 μM). IWP-4 is applicable to research related to cancer, Alzheimer's disease (AD), and heart failure.
For research use only. We do not sell to patients.
- CAS No.: 686772-17-8
- Formula: C23H20N4O3S3
- Molecular Weight:496.62
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Biological Activity
Description
IC50 & Target
[1]|
CK1δ 1.06 μM (IC50) |
CK1ε 7.07 μM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| CAPAN-1 | EC50 |
0.23 μM
Compound: IWP-4
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Antiproliferative activity against human Capan1 cells after 48 hrs by MTT assay
Antiproliferative activity against human Capan1 cells after 48 hrs by MTT assay
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[PMID: 29630366] |
In Vitro
IWP-4 (GMP) (48 h) inhibits the proliferation of all tested cancer cell lines, with submicromolar EC50 values ranging from 0.23 μM to 0.93 μM[1].
IWP-4 (GMP) (1 μM; 24 h) antagonizes the protective effect of Ginkgolide B (HY-N0784) on primary rat cortical astrocytes against glutamate-induced injury by reversing Ginkgolide B-mediated regulation of apoptosis-related genes and proteins, as well as glutamate transporter genes and proteins[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
Chemical Information
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CAS No. 686772-17-8
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Molecular Weight 496.62
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Formula C23H20N4O3S3
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SMILES
O=C(NC1=NC2=CC=C(C)C=C2S1)CSC3=NC(CCS4)=C4C(N3C5=CC=CC=C5OC)=O
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Protocols
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Cell Cytotoxicity Assay
Cytotoxicity assays are usually based on the assessment of cell membrane damage, which can also be indirectly detected by measuring cell viability. Detection methods include MTT assay, CKK-8 assay, LDH assay and ATP assay, etc.
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Research Protocol for Cardiovascular Diseases
Cardiovascular disease can be modeled as maladaptive cardiac remodeling, where ischemic injury or pressure overload activates inflammatory signaling, fibroblast activation, extracellular-matrix deposition, cardiomyocyte hypertrophy, vascular remodeling, and progressive ventricular dysfunction. The TGF-β/SMAD axis is a central profibrotic pathway after myocardial injury and pressure overload, while innate immune and cytokine pathways regulate leukocyte recruitment, scar formation, and adverse remodeling. Key unresolved questions include which inflammatory signals are reparative versus harmful, when fibrosis is protective versus maladaptive, and whether pathway inhibition improves function without weakening necessary infarct healing or compensatory remodeling.
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Alzheimer’s Disease Modeling
Alzheimer’s Disease (AD) is a neurodegenerative disorder characterized by a progressive decline in cognitive functions and loss of specific types of neurons and synapses. Alzheimer's symptoms can be simulated in mice by injecting drugs (such as Aβ) or genetically modified.
Purity & Documentation
References
[1]. García-Reyes B, et al. Discovery of Inhibitor of Wnt Production 2 (IWP-2) and Related Compounds As Selective ATP-Competitive Inhibitors of Casein Kinase 1 (CK1) δ/ε. J Med Chem. 2018;61(9):4087-4102. [Content Brief]
[2]. Wang J, et al. A RNA-seq approach for exploring the protective effect of ginkgolide B on glutamate-induced astrocytes injury. J Ethnopharmacol. 2021;270:113807. [Content Brief]
[3].
Hudson J, et al. Primitive cardiac cells from human embryonic stem cells. Stem Cells Dev. 2012 Jun 10;21(9):1513-23.
[Content Brief]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)