NCI-65828 sodium

ABWT; Tg(fli1a:EGFP) transgenic line (embryos, developmental stage-dependent treatment initiation)^[1]

80 µM

immersion; continuous; 17 hours (10 hpf to 27 hpf); 26 hours (10 hpf to 36 hpf); 9 hours (18 hpf to 27 hpf); 54 hours (18 hpf to 72 hpf)

Reduced number of islet+ motor neuron and Rohon-Beard sensory neuron nuclei in the spinal cord trunk when treated from 10 hpf to 27 hpf.
Shortened CaP primary motor axons (anterior axons: 68.3 µm; posterior axons: 45.8 µm) with aberrant medial branching and distal tip looping when treated from 10 hpf to 27 hpf.
Caused severe inter-somitic vessel (ISV) growth retardation, with most failing to progress past the midline, and reduced branching when treated from 10 hpf to 27 hpf.
Restored CaP axon lengths to control levels but retained abnormal distal branching when treated from 10 hpf to 36 hpf.
Enabled ISVs to grow to control-comparable lengths with reduced truncations when treated from 10 hpf to 36 hpf.
Induced moderate CaP axon shortening and aberrant medial branching, less severe than 10 hpf initiation, when treated from 18 hpf to 27 hpf.
Caused mild ISV growth retardation with shorter lengths than controls when treated from 18 hpf to 27 hpf.
Produced normal CaP, RoP, and MiP primary motor axon positioning and projection angle, but longer RoP axons (249.7 µm) with increased posterior branching, and increased length and branching of secondary motor neuron axons when treated from 18 hpf to 72 hpf.
Enabled ISVs to recover to control-comparable lengths with rare truncations but reduced branching when treated from 18 hpf to 72 hpf.
Induced abnormal swimming behavior (pectoral fin-only movement, no sinusoidal lateral muscle movements) and mild dorsal curvature by 72 hpf.