Emavusertib
Based on 7 publication(s) in Google Scholar
Emavusertib is an orally active inhibitor for IRAK4 (IC50=57 nM) and FLT3. Emavusertib inhibits NF-κB and MyD88 signaling pathways, reduces the generation of pro-inflammatory cytokines like IL-6 and IL-10, thereby exhibiting anti-inflammatory and anti-proliferative activities against cancer cells, leading to cell apoptosis. Emavusertib exhibits antitumor activity in mouse model
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- Pureté : 99.97%
- CAS No.: 1801344-14-8
- Formule: C24H25N7O5
- Masse moléculaire:491.50
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Stockage:Powder -20°C, 3 years , 4°C, 2 years ; In solvent -80°C, 1 year , -20°C, 6 months
To place orders, for customer services and technical support, please contact: MedChemExpress USA
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Activité biologique
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Chemical Information
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Solvant et solubilité
- Protocole
- Pureté et documentation
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Publications Citing Use of MedChemExpress (MCE) Emavusertib
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Customer Validation & Images
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Cell Proliferation/Viability Assay
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WB
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In Vivo Efficacy Study
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IHC
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Bio/Physico-chemical Assay
Activité biologique
Description
IC50 & Target
[1]|
IRAK4 57 nM (IC50) |
Cellular Effect
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Cell Line
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Type | Value | Description | References |
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| OCI-Ly10 | IC50 |
1.5 μM
Compound: 24; CA-4948
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Growth inhibition of human OCI-LY10 harboring mutant MYD88
Growth inhibition of human OCI-LY10 harboring mutant MYD88
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[PMID: 33335659] |
In Vitro
Emavusertib (CA-4948) is over 500-fold more selective for IRAK-4 compared to IRAK-1. Emavusertib reduces TNF-α, IL-1β, IL-6 and IL-8 release from TLR-Stimulated THP-1 Cells with an IC50 <250 nM. Emavusertib also has antiproliferative activity due to inhibition of receptor-type tyrosine-protein kinase FLT3[1].
Emavusertib exhibits >350-fold higher binding affinity for IRAK-4 than that observed for IRAKs 1, 2 and 3[3].
Emavusertib (10 μM, 72 h) decreases the percentage of proliferating cells and induces a moderate increase in the sub-G0 fraction in marginal zone lymphomas (MZL) cell lines[3].
Emavusertib (10 μM, 72 h) induces a significant increase in the apoptotic cell population of MZL cells, particularly when combined with Ibrutinib (HY-10997) compared to ibrutinib and emavusertib alone[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. Further protocols information, click here.
In Vivo
Emavusertib (25-150 mg/kg, Orally, once daily, for 14 consecutive days) induces tumor growth inhibition in mice[3].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Mice bearing OCI-LY10 tumors[3]
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Dosage:25, 50, or 150 mg/kg (once daily), 12.5, 25, or 50 mg/kg (twice daily)
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Administration:Orally, once daily or twice daily, for 14 consecutive days
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Result:Induced tumor growth inhibition. Emavusertib administered as a twice-daily divided dose was equivalent to the corresponding once-daily dose with regards to antitumor activity, i.e., 12.5 mg/kg BID versus 25 mg/kg QD.
Essai clinique
| NCT Number | Sponsor | Condition | Start Date |
Phase
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|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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CAS No. 1801344-14-8
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Appearance Solid
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Masse moléculaire 491.50
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Formule C24H25N7O5
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Color Light yellow to green yellow
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SMILES
O=C(C1=COC(C2=CC(C)=NC=C2)=N1)NC3=C(N4C[C@H](O)CC4)N=C5C(OC(N6CCOCC6)=N5)=C3
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Synonyms
CA-4948
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Livraison
Room temperature in continental US; may vary elsewhere.
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Stockage
Powder -20°C 3 years 4°C 2 years In solvent -80°C 1 year -20°C 6 months
Publications (7)
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Journal Impact Factor
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Most Recent
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Blood
2023 Sep 14;142(11):989-1007. PMID: 37172199
Emavusertib purchased from MedChemExpress. Usage Cited in: Blood. 2023 Sep 14;142(11):989-1007. [Abstract]
IC50 curves for CA-4948 (Emavusertib) (0.01-10000 nM; 24 h) and PF-06650833 in an assay measuring NF-kB activity upon TLR2 stimulation with PAM3CSK4 in THP1 NF-kB reporter cells.
Emavusertib purchased from MedChemExpress. Usage Cited in: Blood. 2023 Sep 14;142(11):989-1007. [Abstract]
Immunoblots for phospho-IRAK1, total IRAK1, IRAK2, and IRAK4 in MDSL and AML (1714) treated for 24 hours with CA-4948 (Emavusertib) (10 μM). The results showed that treatment with CA-4948 resulted in increased IRAK1 phosphorylation.
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Leukemia
Targeting of IRAK4 and GSPT1 enhances therapeutic efficacy in AML via c-Myc destabilization. [Abstract]2025 Sep;39(9):2163-2173. PMID: 40670672
Emavusertib purchased from MedChemExpress. Usage Cited in: Leukemia. 2025 Sep;39(9):2163-2173. [Abstract]
Cell viability was determined in THP1 and HL60 cells cultured with 10 µM CA-4948 (Emavusertib) or in OCI-AML3 and K562 cultured with 1 µM CA-4948 or vehicle (n = 4) for 14 days and then treated with CC-885 (n = 4).
Emavusertib purchased from MedChemExpress. Usage Cited in: Leukemia. 2025 Sep;39(9):2163-2173. [Abstract]
Immunoblots for c-MYC in the patient-derived AML samples (AML1794, AML1714) cultured with CA-4948 (Emavusertib) (10 µM) or vehicle for 14 days and then treated with CC-885 (50 nM) for 4 h.
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Cell Rep
Disruption of fibroblast MYD88 signaling promotes antitumor immunity in pancreatic ductal adenocarcinoma. [Abstract]2025 Sep 24;44(10):116347. PMID: 41004339
Emavusertib purchased from MedChemExpress. Usage Cited in: Cell Rep. 2025 Sep 24;44(10):116347. [Abstract]
Harvested tumor weights by treatment condition (n = 8 per condition).Tumor growth studies demonstrated statistically significant inhibition with both CA-4948 (Emavusertib) (50 mg/kg; oral gavage; once daily) alone and ICB alone.
Emavusertib purchased from MedChemExpress. Usage Cited in: Cell Rep. 2025 Sep 24;44(10):116347. [Abstract]
H&E and trichrome staining of tumors by treatment condition (Emavusertib (50 mg/kg; oral gavage; once daily), ect.) at 10× magnification. The scale bar represents 100 μm.
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Front Immunol
Activation of Toll-Like Receptor 7 Signaling Pathway in Primary Sjögren's Syndrome-Associated Thrombocytopenia. [Abstract]2021 Mar 9:12:637659. PMID: 33767707 -
Curr Issues Mol Biol
FLT3 and IRAK4 Inhibitor Emavusertib in Combination with BH3-Mimetics in the Treatment of Acute Myeloid Leukemia. [Abstract]2024 Mar 29;46(4):2946-2960. PMID: 38666914 -
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Solvant et solubilité
In Vitro:
DMSO : 50 mg/mL (101.73 mM; Need ultrasonic; Hygroscopic DMSO has a significant impact on the solubility of product, please use newly opened DMSO)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
In Vivo:
Select the appropriate dissolution method based on your experimental animal and administration route.
- For the following dissolution methods, please ensure to first prepare a clear stock solution using an In Vitro approach and then sequentially add co-solvents:
- To ensure reliable experimental results, the clarified stock solution can be appropriately stored based on storage conditions. As for the working solution for In Vivo experiments, it is recommended to prepare freshly and use it on the same day.
- The percentages shown for the solvents indicate their volumetric ratio in the final prepared solution. If precipitation or phase separation occurs during preparation, heat and/or sonication can be used to aid dissolution.
Add each solvent one by one: 10% DMSO 40% PEG300 5% Tween-80 45% Saline
Solubility: ≥ 2.08 mg/mL (4.23 mM); Clear solution
This protocol yields a clear solution of ≥ 2.08 mg/mL (saturation unknown).
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 400 μL PEG300, and mix evenly; then add 50 μL Tween-80 and mix evenly; then add 450 μL Saline to adjust the volume to 1 mL.
Preparation of Saline: Dissolve 0.9 g sodium chloride in ddH₂O and dilute to 100 mL to obtain a clear Saline solution.
Add each solvent one by one: 10% DMSO 90% (20% SBE-β-CD in Saline)
Solubility: 2.08 mg/mL (4.23 mM); Suspended solution; Need ultrasonic
This protocol yields a suspended solution of 2.08 mg/mL. Suspended solution can be used for oral and intraperitoneal injection.
Taking 1 mL working solution as an example, add 100 μL DMSO stock solution (20.8 mg/mL) to 900 μL 20% SBE-β-CD in Saline, and mix evenly.
Preparation of 20% SBE-β-CD in Saline (4°C, storage for one week): 2 g SBE-β-CD powder is dissolved in 10 mL Saline, completely dissolve until clear.
In Vivo Dissolution Calculator
Please enter the basic information of animal experiments:
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Recommended: Prepare an additional quantity of animals to account for potential losses during experiments.
Please enter your animal formula composition:
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%DMSO +
Recommended: Keep the proportion of DMSO in working solution below 2% if your animal is weak.
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%+
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+%Tween-80 + +
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%Saline +
The co-solvents required include: DMSO, . All of co-solvents are available by MedChemExpress (MCE). , Tween 80. All of co-solvents are available by MedChemExpress (MCE).
Working solution concentration: 0.22 mg/mL
Method for preparing stock solution: mg drug dissolved in μL DMSO. Stock solution concentration: mg/mL.
1. Take μL DMSO stock solution;
2. Add μL .
μL , mix evenly;
3. Then add μL Tween 80, mix evenly;
4. Then add μL
Please ensure that the stock solution in the first step is dissolved to a clear state, and add co-solvents in sequence. You can use ultrasonic heating (ultrasonic cleaner, recommended frequency 20-40 kHz), vortexing, etc. to assist dissolution.
Protocole
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Apoptosis
Apoptosis, also called programmed cell death, is generally characterized by distinct morphological characteristics.
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TUNEL staining for apoptotic DNA fragmentation
TUNEL staining detects DNA strand breaks by using terminal deoxynucleotidyl transferase to add labeled nucleotides to exposed 3′-OH DNA termini, generating either microscopic staining in fixed cells or tissue sections, or fluorescence/cytometric signal in cell suspensions. TUNEL positivity reflects DNA fragmentation but should not be interpreted alone as definitive apoptosis, because TUNEL can also label necrotic, autolytic, mechanically damaged, or DNA-repair-associated DNA breaks.
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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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LPS-Induced Endotoxemia/Systemic Inflammation
Lipopolysaccharide (LPS)-induced endotoxemia is a widely used in vivo model of acute systemic inflammation in which LPS, a Gram-negative bacterial endotoxin, activates innate immune signaling primarily through TLR4, leading to rapid and transient induction of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β in circulation and tissues. This cytokine surge is commonly used as a measurable readout of systemic inflammatory activation and immune dysregulation, and is typically assessed within hours after intraperitoneal LPS administration in mouse models of endotoxemia. The model captures key features of systemic inflammatory response syndrome, including cytokine release, immune cell activation, and downstream tissue responses, and has been used to evaluate anti-inflammatory interventions such as cytokine modulation, lipid mediators, and immune cell-targeting therapies.
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Annexin V plus membrane-impermeant dye apoptosis staining
Annexin V-based apoptosis assays rely on the detection of phosphatidylserine (PS) externalization from the inner leaflet of the plasma membrane to the outer leaflet, an early biochemical hallmark of apoptosis. Fluorescently labeled Annexin V binds PS in a calcium-dependent manner, enabling identification of early apoptotic cells by flow cytometry or fluorescence microscopy. When combined with a membrane-impermeant DNA-binding dye (e. g. , propidium iodide), this approach allows discrimination between viable (Annexin V−/dye−), early apoptotic (Annexin V+/dye−), and late apoptotic or necrotic (Annexin V+/dye+) cell populations by assessing membrane integrity and PS exposure.
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Apoptosis Solutions
Apoptosis is a regulated, generally non-lytic cell-death pathway that removes unwanted, damaged, infected, or abnormal cells through coordinated morphological changes, caspase activation, DNA fragmentation, and membrane remodeling. The intrinsic apoptosis pathway is controlled mainly by mitochondrial outer membrane permeabilization, BCL-2 family proteins, cytochrome c release, apoptosome formation, caspase-9 activation, and downstream executioner caspase-3/7 activation. The extrinsic apoptosis pathway is initiated by death receptors such as Fas, TNFR, and TRAIL receptors, which recruit adaptor proteins and activate caspase-8 before engaging executioner caspases or mitochondrial amplification through BID cleavage. Apoptosis is linked to many phenotypes, including cancer cell killing, tissue homeostasis, immune regulation, neurodegeneration, infection response, and treatment-induced cytotoxicity; unresolved questions include how apoptosis interacts with necroptosis, pyroptosis, ferroptos
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Research Protocol for Inflammation-related Diseases
The NLRP3 inflammasome is a cytosolic innate immune signaling platform that integrates priming signals and danger-signal activation to promote caspase-1 activation, maturation of IL-1β and IL-18, and gasdermin D-mediated pyroptotic cell death. The core experimental logic is to determine whether inflammatory disease phenotypes are driven by increased NLRP3 expression, ASC-containing inflammasome assembly, caspase-1 cleavage, GSDMD cleavage, and extracellular release of IL-1β/IL-18 rather than by nonspecific cell injury alone. The pathway is strongly linked to inflammation-related disease phenotypes because monosodium urate crystals activate NALP3/NLRP3 inflammasome signaling in gout-like crystal inflammation, cholesterol crystals activate NLRP3 inflammasomes in atherogenesis models, and DSS-induced intestinal inflammation has been reported to involve NLRP3 inflammasome activity. However, experimental colitis studies also show context-dependent protective effects of NLRP3 inflammasome co
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Subcutaneous Cell-Line-Derived Xenograft
Subcutaneous cell-line-derived xenograft (CDX) models are established by implanting cultured human cancer cell lines into immunodeficient mice, where the injected cells form localized tumors that can be monitored in vivo as a measure of tumorigenic potential, growth kinetics, and treatment response. These models are widely used in oncology research because they allow reproducible tumor formation and enable comparative assessment of tumor growth between different cell lines or genetic manipulations in a controlled in vivo microenvironment. Subcutaneous implantation of cancer cells in immunodeficient mice is a standard approach for evaluating tumor growth behavior and therapeutic response across multiple cancer types, including prostate, esophageal, pancreatic, and colon cancer models.
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Cell Viability Determination by MTT Colorimetric Assay
The following protocol uses the MTT colorimetric assay as a classic literature-established method for assessing cell viability/metabolic activity in cultured mammalian cells. MTT[3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide] is reduced by metabolically active cells to a colored formazan product; the amount of formazan is quantified spectrophotometrically and provides an indirect measure of metabolically active viable cells. Importantly, MTT reduction reflects cellular oxidoreductase/metabolic activity rather than an absolute direct count of living cells, so changes in cellular metabolism can alter the signal independently of cell number.
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How to Choose the Right Model Animal
Choosing the right model animal is a validity-driven decision in which the species, strain, sex, age, genetic background, disease-induction method, outcome measures, and welfare burden must match the scientific question rather than laboratory tradition or convenience. A model should be selected by judging face validity, construct validity, and predictive validity: whether it resembles the human phenotype, whether it reproduces relevant mechanisms, and whether results are likely to predict human biology or treatment response. Animal studies often fail to translate because of species differences, weak disease resemblance, poor experimental design, inadequate reporting, publication bias, and underuse of randomization, blinding, and sample-size justification. Unresolved questions include how to rank competing models objectively, how much human-disease complexity must be reproduced for a given objective, and when non-animal systems such as organoids, ex vivo tissue, or computational models
Pureté et documentation
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Fiche technique (277 KB)
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SDS (393 KB)
- English - EN (393 KB)
- Français - FR (393 KB)
- Deutsch - DE (393 KB)
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- Español - ES (393 KB)
- Swedish - SV (393 KB)
- Italian - IT (393 KB)
- Korean - KR (393 KB)
- Portuguese - PT (393 KB)
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Instruction de manipulation (2659 KB)
Références
[1]. Wiese MD, et al. Investigational IRAK-4 inhibitors for the treatment of rheumatoid arthritis. Expert Opin Investig Drugs. 2020 Apr 17:1-8. [Content Brief]
[2]. Guidetti F, et al. Targeting IRAK4 with Emavusertib in Lymphoma Models with Secondary Resistance to PI3K and BTK Inhibitors. J Clin Med. 2023 Jan 4;12(2):399. [Content Brief]
[3]. Parrondo RD, et al. IRAK-4 inhibition: emavusertib for the treatment of lymphoid and myeloid malignancies. Front Immunol. 2023 Oct 26;14:1239082. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| DMSO | 1 mM | 2.0346 mL | 10.1729 mL | 20.3459 mL | 50.8647 mL |
| 5 mM | 0.4069 mL | 2.0346 mL | 4.0692 mL | 10.1729 mL | |
| 10 mM | 0.2035 mL | 1.0173 mL | 2.0346 mL | 5.0865 mL | |
| 15 mM | 0.1356 mL | 0.6782 mL | 1.3564 mL | 3.3910 mL | |
| 20 mM | 0.1017 mL | 0.5086 mL | 1.0173 mL | 2.5432 mL | |
| 25 mM | 0.0814 mL | 0.4069 mL | 0.8138 mL | 2.0346 mL | |
| 30 mM | 0.0678 mL | 0.3391 mL | 0.6782 mL | 1.6955 mL | |
| 40 mM | 0.0509 mL | 0.2543 mL | 0.5086 mL | 1.2716 mL | |
| 50 mM | 0.0407 mL | 0.2035 mL | 0.4069 mL | 1.0173 mL | |
| 60 mM | 0.0339 mL | 0.1695 mL | 0.3391 mL | 0.8477 mL | |
| 80 mM | 0.0254 mL | 0.1272 mL | 0.2543 mL | 0.6358 mL | |
| 100 mM | 0.0203 mL | 0.1017 mL | 0.2035 mL | 0.5086 mL |
Emavusertib Related Classifications
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