[1][2] The toxin causes the disease in humans by gaining entry into the cell cytoplasm and inhibiting protein synthesis.

It catalyzes the ADP ribosylation of the unusual amino acid diphthamide in eEF-2 by transferring the ADP-ribosyl group from NAD+.

The steps involved in generating toxicity are as follows:[citation needed] Diphtheria toxin is extraordinarily potent.

In 1890, Emil Adolf von Behring developed an anti-toxin based on the blood of horses immunized with attenuated bacteria.

[11] In 1951, Freeman found that the toxin gene was not encoded on the bacterial chromosome, but by a lysogenic phage (corynephage β)[2] infecting all toxigenic strains.