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To determine the pharmacological impact of SP600125 on zebrafish development, we incubated embryos in various concentrations of SP600125 from 18\u2009h postfertilization (hpf) to 48\u2009hpf. Embryos treated with 1.25\u2009\u00b5<jats:sc>m<\/jats:sc> appeared with occasional pericardium edema. Treatment with 12.5\u2009\u00b5<jats:sc>m<\/jats:sc> resulted in complete mortality by 120\u2009hpf, preventing an assessment of physiological defects. Embryos treated with 5\u2009\u00b5<jats:sc>m<\/jats:sc> exhibited slowed overall growth, a delay in hatching and numerous morphological defects such as pericardium edema, yolk sac edema, swim bladder deflation, bent vertebrae and eye and jaw malformations. Whole\u2010mount immunohistochemical studies using an anti\u2010acetylated <jats:italic>\u03b2<\/jats:italic>\u2010tubulin antibody confirmed developmental defects in the nervous system. Within the retina, fish treated with 1.25\u2009\u00b5<jats:sc>m<\/jats:sc> showed a mild reduction of immunoreactivity. Immunoreactivity in the retina was further reduced in fish treated with 5\u2009\u00b5<jats:sc>m<\/jats:sc> of SP600125. In these fish, eyes and olfactory organs were half the size compared with other groups. Multiple lenses were observed in 67% of these fish. A second experiment with a shorter exposure period of SP600125 (6\u2009h) presented significantly fewer morphological defects. The treatment led to a delay in hatching, and increased incidences of swim bladder deflation and pericardium edema with increasing concentrations. In summary, SP600125 caused developmental abnormalities during zebrafish organogenesis starting at 1.25\u2009\u00b5<jats:sc>m<\/jats:sc> and the defects were exacerbated with increasing concentrations. Our study suggests that SP600125 at 1.25\u2009\u00b5<jats:sc>m<\/jats:sc> and beyond has devastating consequences for zebrafish development. 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