It was said many years ago that the reason Imetelstat failed in solid tumor studies was because (in addition to requiring multiple cell divisions), the effect on telomere shortening “escaped” with the help of alternative mechanisms for telomere maintenance (ALT). Here’s a look at a sequential telomerase inhibitor followed by an agent (already on the market) that has ALT effects in preclinical work in lymphoma:
https://mdpi-res.com/d_attachment/biome ... 1663550578
Another potential combination with possible far reaching consequences
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