NSC12

NSC12 is an orally active pan-FGF trap. NSC12 inhibits the interaction between FGF2/FGFR. NSC12 suppresses the phosphorylation of FGFR3. NSC12 reduces c-Myc levels, induces DNA damage, triggers the cleavage of Caspase 3, and promotes ROS production. NSC12 exhibits anticancer activity against lung cancer and multiple myeloma^[1][2]. In Vitro:NSC12 (0.3-10.0 μM; 48 h for LLC cells, 72 h for H520 cells) inhibits the proliferation of mouse Lewis lung carcinoma (LLC) cells and H520 lung cancer cells, with an IC₅₀ of 2.0 μM for the former and 4.1 μM for the latter^[1].
NSC12 (6 μM; 6 h) inhibits FGFR3 phosphorylation by 75% in multiple myeloma KMS-11 cells treated with 6 μM NSC12 for 6 h^[2].
NSC12 (6 μM; 6 h) inhibits FGFR phosphorylation in multiple myeloma cell lines KMS-11, OPM-2, U-266, and the Bortezomib-resistant strain KMS-11/BTZ^[2].
NSC12 (6 μM; 6 h) reduces c-Myc levels and induces DNA damage in multiple myeloma KMS-11 cells^[2]. In Vivo:NSC12 (7.5 mg/kg; i.p.; every other day) reduces multiple myeloma tumor growth by ~40% in NOD/SCID mice, inhibits FGFR signaling, and induces tumor cell death without causing measurable toxicity^[2].