FC131

FC131 is a CXCR4 antagonist that inhibits AKT kinase activity in AML OCI-AML3 cells. D-ArgFC131, a derivative of FC131, inhibits the phosphorylation of downstream ERK1/2 and Akt, induces caspase-3 pathway-mediated apoptosis, and causes cell cycle arrest. FC131 exerts cytotoxic effects in cancer cells such as AML cells. FC131 is applicable for cancer-related research^[1][2][3]. In Vitro:FC131 (0.5-4.0 μM; 48 h) combined with Panobinostat (HY-10224) synergistically induces apoptosis in human AML OCI-AML3 cells, and the corresponding combination index value is less than 1.0^[1].
FC131 (2 μM plus 50 nM Panobinostat; 48 h) induces significantly higher lethality in primary human AML cells than in normal human CD34⁺ bone marrow progenitor cells^[1].
FC131 (1 μM; 24 h) partially inhibits AKT kinase activity in human AML OCI-AML3 cells, and combined treatment with 50 nM Panobinostat enhances this AKT kinase inhibitory effect without altering the Panobinostat-mediated reduction in the levels of CXCR4, GRK3 and downstream signaling proteins^[1].
FC131 (100 nM; 6 h) inhibits the activity of the GH promoter in GH3 rat pituitary tumor cells, reducing luciferase activity to 0.3-fold that of the control group^[2].
FC131 (10-100 nM; 6 days) slightly inhibits the proliferation of GH3 rat pituitary tumor cells^[2].
FC131 (1 nM-100 μM; 10 min pre-incubation, 90 min co-incubation with CXCL12) potently inhibits CXCL12-mediated IP accumulation in COS-7 cells expressing wild-type CXCR4, with an IC₅₀ of 0.40 μM; the H113A, D171N and D262N mutations significantly reduce its potency, while the W94A and D97A mutations enhance its potency^[3].
FC131 (1 nM-100 μM; 3 h) binds to wild-type CXCR4 expressed in COS-7 cells, with an IC₅₀ of 0.76 μM; the H113A, Y116A, D171N and D262N mutations significantly reduce its binding affinity, the H281A, D187A and E288A mutations moderately reduce its binding affinity, while the W94A and D97A mutations increase its binding affinity^[3].