Biochemical mechanism: Originally characterized as a non-nucleotide-competitive and reversible ARF6-selective inhibitor (IC50 = 1.4 μM without GEF and 2.4 μM with 100 nM ARNO or BRAG2/GEP100) that targets ARF6 GEF-binding region, NAV-2729 prevents GEF-dependent ARF1 & ARF6 activity (% inhibition of BRAG2Sec7PH-stimulated GTPase activity/[NAV-2729] = 50% Δ17Arf1/10 μM and 15% Δ13Arf6/25 μM) with higher potency against BRAG2- than ARNO-dependent ARF1 activity (64% vs. 20% Δ17Arf1 inhibition at 25 μM in the presence of respective GEF sec7 domain). NAV-2729 treatment effectively inhibits G-alpha-q downstream signaling pathways and anchorage-independent colony growth of Mel92.1 & Mel202 melanoma cells in vitro (10 μM) as well as uveal melanoma tumor establishment in Mel202 xenograft mice in vivo (30 mg/kg/day i.p.). product description： Grassofermata is an inhibitor of fatty acid transport.1 It inhibits C1-BODIPY-C12 uptake in HepG2, Caco-2, C2C12, and INS-1E cells (IC50s = 8.1-10.6 μM).1 Grassofermata prevents palmitate-mediated lipid accumulation and cell death in HepG2 cells and primary hepatocytes. In vivo, grassofermata (300 mg/kg) decreases absorption of 13C-oleate in mice.