Cells of interest can express the blasticidin resistance genes BSD or bsr, and can then survive treatment with the antibiotic.

[2] Blasticidin S is typically used at 2–300 micrograms per milliliter of media, depending on the type of cell being grown.

It works by inhibiting termination step of translation and peptide bond formation (to lesser extent) by the ribosome.

Both deaminases work by modifying blasticidin S directly, replacing the amine on the cytosine ring with a hydroxyl group, resulting in the inactive deaminohydroxy-blasticin S.[2][4] bsr and BSD are the most commonly used resistance genes.

In the 1950s, a drug screening program was designed in Japan to discover a new antibiotic that prevents blast disease by the fungus Magnaporthe grisea.