emavusertib (CA-4948)

P1, N=48, Recruiting, Washington University School of Medicine | Not yet recruiting --> Recruiting

P1/2, N=366, Suspended, Curis, Inc. | Recruiting --> Suspended

P1/2, N=40, Not yet recruiting, Curis Inc.

P2, N=270, Not yet recruiting, National Cancer Institute (NCI)

P1, N=24, Active, not recruiting, Curis Inc. | -> Active, not recruiting | Phase classification: PN/A --> P1

P2, N=108, Recruiting, Curis, Inc. | Not yet recruiting --> Recruiting

P2, N=108, Not yet recruiting, Curis, Inc.

P1, N=48, Not yet recruiting, Washington University School of Medicine | Trial completion date: Dec 2031 --> Apr 2032 | Initiation date: Oct 2025 --> Feb 2026 | Trial primary completion date: Jan 2030 --> May 2030

Using an innovative collagen gel implantation model, we demonstrate that loss of MYD88 in CAFs enhances T cell infiltration and suppresses tumor growth. Combining MYD88 inhibition with immune checkpoint blockade significantly reduces tumor size and enhances antitumor immune responses, underscoring its potential as a therapeutic target in PDAC.

P1, N=48, Not yet recruiting, Washington University School of Medicine

Clinical data from the targeted small-molecule IRAK4 inhibitor emavusertib (CA-4948) were presented, including data from the TakeAim Leukemia and TakeAim Lymphoma trials of emavusertib in myeloid and lymphoid malignancies, respectively, and preliminary data from trials of emavusertib in multiple solid tumors. The meeting closed with expert discussion of the emerging profile of IRAK4 inhibition in cancers and the potential for IRAK4 inhibition to improve outcomes across both solid and liquid tumors.

Among them, HB-29 had the remarkable activity towards FLT3-WT (IC50 = 1.95 nM) and IRAK4 (IC50 = 53.72 nM), outperforming the positive control, CA-4948...Moreover, HB-29 demonstrated an acceptable bioavailability (F = 13.4 %). These findings confirm that FLT3/IRAK4 inhibitor is a promising strategy for the treatment of AML.