Industry news, page-1828

Anthracyclines function by inducing DNA strand breaks via intercalation. Topoisomerase II poisons associate themselves within the strand breaks induced by Topoisomerase II during typical torsional reducing functions preventing topoII from resealing the strand break and DNA damage ensues. Doxorubicin is so extremely effective at inserting itself into DNA and inducing DNA strand breaks because it requires a common nucleotide sequence to intercalate into.

Anthracyclines most certainly exert their anti-cancer function via DNA damage, and speaking more specifically of Doxorubicin, it does this as well as a broad spectrum of other effects which contribute to cellular death. Plenty of work out there correlating doxorubicin efficacy to dna strand breaks, as well as work finding no correlation between Bisantrene efficacy and dna strand breaks.

Doxorubicin sales have endured multiple approved anthracyclines over the last 60-years, which are all less cardiotoxic. Dox sales aren't going anywhere, and they'll probably improve if Dox is (for the first time ever) paired with a compound that improves its effect while also providing cardioprotection.