Juq-399 Apr 2026

All data are from internal company reports; raw data have not been independently validated. | Disease | Rationale | |---------|-----------| | Myelofibrosis / Primary Myelofibrosis (PMF) | JAK2 V617F mutation drives pathological proliferation; selective JAK2 inhibition could reduce splenomegaly with fewer immunosuppressive side‑effects. | | Rheumatoid arthritis (RA) | IL‑6 signaling is JAK2‑dependent; early‑phase data suggest possible disease‑modifying activity. | | Systemic lupus erythematosus (SLE) | TYK2 plays a role in type I interferon signaling; dual JAK2/TYK2 inhibition may dampen the interferon signature. | | Acute Myeloid Leukemia (AML) with FLT3‑ITD | JAK2/TYK2 cross‑talk with FLT3 pathways; pre‑clinical synergy observed when combined with FLT3 inhibitors. |

These are indications based on target biology; no clinical trials have been announced. 6. Intellectual Property Landscape | Patent family | Priority date | Key claims | |----------------|--------------|------------| | US 2023/0189540 A1 (Juvenal) | 12 Mar 2023 | Core quinazoline scaffold; specific substituents for JAK2/TYK2 selectivity; method of use in inflammatory disease. | | WO 2024/112233 A1 (International filing) | 08 Sep 2024 | Expanded SAR covering cyclopropyl‑methyl side‑chains (including JUQ‑399) and formulation claims. | | US 2025/006789 A1 (Continuation) | 14 Jan 2025 | Crystalline forms, pro‑drug derivatives, and combination therapy with anti‑PD‑1 antibodies. | JUQ-399