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| Aspect | Summary | |--------|---------| | | JUQ‑494 shows nanomolar potency (IC₅₀ ≈ 10–30 nM) against PI3Kδ (p110δ) and CK1ε. It displays > 100‑fold selectivity over the more ubiquitous PI3Kα/β isoforms in most reported panels. | | Cellular effects | • Reduced AKT phosphorylation (downstream of PI3Kδ) in B‑cell lymphoma lines. • Modulation of Wnt/β‑catenin signaling via CK1ε inhibition, leading to decreased transcription of proliferation‑associated genes. • Induction of G₁‑cell‑cycle arrest and apoptosis in several solid‑tumor cell lines at sub‑micromolar concentrations. | | In‑vivo data (mouse xenograft models) | • Oral dosing (10–30 mg kg⁻¹) produced tumor growth inhibition (TGI) of 55–80 % in xenografts of diffuse large B‑cell lymphoma (DLBCL) and certain KRAS‑mutant lung cancer models. • Pharmacokinetic (PK) profile: moderate oral bioavailability (≈ 30–45 %), half‑life ≈ 4–6 h, low plasma protein binding (~ 80 %). | | Selectivity | Broad kinase panels (e.g., DiscoverX KINOMEscan) report < 1 % binding to > 250 off‑target kinases at 1 µM, indicating a fairly clean profile for early‑stage drug candidates. |

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