For research use only. Not for therapeutic Use.
Emavusertib (CA-4948) is a selective, potent and orally active IRAK4/FLT3 inhibitor. Emavusertib has an IC50 of 57 nM for IRAK4 in a FRET kinase assay. Emavusertib shows anti-tumor activity[1][2][3].
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].
Emavusertib (CA-4948) shows anti-tumor activity in animal models including tumors containing MyD88 gene mutations. Emavusertib shows antileukemic activity in mouse models of FLT3 wild-type and FLT3 mutated acute myeloid leukemia (AML)[1].
Emavusertib (25-150 mg/kg, Orally, once daily, for 14 consecutive days) induces tumor growth inhibition in mice[3].
| Catalog Number | I026812 |
| CAS Number | 1801344-14-8 |
| Synonyms | N-[5-[(3R)-3-hydroxypyrrolidin-1-yl]-2-morpholin-4-yl-[1,3]oxazolo[4,5-b]pyridin-6-yl]-2-(2-methylpyridin-4-yl)-1,3-oxazole-4-carboxamide |
| Molecular Formula | C24H25N7O5 |
| Purity | ≥95% |
| InChI | InChI=1S/C24H25N7O5/c1-14-10-15(2-4-25-14)23-27-18(13-35-23)22(33)26-17-11-19-20(28-21(17)31-5-3-16(32)12-31)29-24(36-19)30-6-8-34-9-7-30/h2,4,10-11,13,16,32H,3,5-9,12H2,1H3,(H,26,33)/t16-/m1/s1 |
| InChIKey | SJHNWSAWWOAWJH-MRXNPFEDSA-N |
| SMILES | CC1=NC=CC(=C1)C2=NC(=CO2)C(=O)NC3=CC4=C(N=C3N5CCC(C5)O)N=C(O4)N6CCOCC6 |
| Reference | [1]. Wiese MD, et al. Investigational IRAK-4 inhibitors for the treatment of rheumatoid arthritis. Expert Opin Investig Drugs. 2020 Apr 17:1-8. [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. [3]. Parrondo RD, et al. IRAK-4 inhibition: emavusertib for the treatment of lymphoid and myeloid malignancies. Front Immunol. 2023 Oct 26;14:1239082. |
