Emavusertib hydrochloride
Based on 7 publication(s) in Google Scholar
Emavusertib hydrochloride (CA-4948 tosylate) is the hydrochloride salt form of Emavusertib (HY-135317). Emavusertib hydrochloride is an orally active inhibitor for IRAK4 (IC50=57 nM) and FLT3. Emavusertib hydrochloride 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 hydrochloride exhibits antitumor activity in mouse model.
For research use only. We do not sell to patients.
- CAS No.: 2376399-42-5
- Formula: C24H26ClN7O5
- Molecular Weight:527.96
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
Publications Citing Use of MedChemExpress (MCE) Emavusertib hydrochloride
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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
Biological Activity
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IRAK4 57 nM (IC50) |
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.
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.
Chemical Information
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CAS No. 2376399-42-5
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Molecular Weight 527.96
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Formula C24H26ClN7O5
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SMILES
O=C(C1=COC(C2=CC=NC(C)=C2)=N1)NC3=C(N4CC[C@H](C4)O)N=C5C(OC(N6CCOCC6)=N5)=C3.Cl
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Synonyms
CA-4948 hydrochloride
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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.
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 hydrochloride 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 hydrochloride 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 hydrochloride 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 hydrochloride 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 hydrochloride 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 hydrochloride 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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Purity & Documentation
References
[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]
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)