Miaa-376 -

| Model | Dose & Route | Tumor Growth Inhibition (TGI) | Survival Benefit | Key Observations | |-------|--------------|-------------------------------|------------------|------------------| | | 30 mg/kg PO daily (14 d) | 68 % (p < 0.001) | Median OS ↑ 3.2 wk vs. control | ↓ Ki‑67, ↑ cleaved caspase‑3 | | B16‑F10 (murine melanoma, syngeneic) | 25 mg/kg PO BID + anti‑PD‑1 (10 mg/kg i.p.) | 85 % (p < 0.0001) | 100 % long‑term survivors (≥ 90 d) | ↑ CD8⁺ T‑cell infiltration (CD45⁺CD8⁺) | | Patient‑Derived Xenograft (PDX) #23 (NRAS‑mutant) | 40 mg/kg PO QD | 55 % (p = 0.004) | Trend ↑ (not statistically powered) | Down‑regulation of EMT markers (Vimentin) | | Pharmacokinetics (mouse) | 30 mg/kg PO | Cmax ≈ 5 µM; t½ ≈ 7 h; AUC₀‑∞ ≈ 30 µM·h | — | Good oral bioavailability (~45 %). |

Finally, "MIAA-376" might stem from a . For example: MIAA-376

The future significance of MIAA-376 will depend on its actual nature and the context in which it is being researched or developed. If it pertains to a medical treatment, the path forward would involve clinical trials and regulatory approvals. For a technological innovation, it would entail further development, testing, and commercialization. | Model | Dose & Route | Tumor

MIAA-376 may have therapeutic potential in various types of cancer, including: For example: The future significance of MIAA-376 will