LSD1 Inhibition May Modulate Response to Nucleoside Analogue Therapies
- Perspective-style article proposing that pharmacological inhibition of the epigenetic enzyme LSD1 (KDM1A) can modulate cellular sensitivity to nucleoside analogue therapeutics.
- Synthesizes evidence across myeloid malignancies and viral infections, two disease areas where nucleoside analogues are already established treatments.
- Argues LSD1-driven chromatin and transcriptional changes may underlie altered drug response, positioning LSD1 inhibitors as potential combination partners to enhance nucleoside analogue efficacy across both fields.
💡 Points
What grabs me is that clinical-stage LSD1 chemotypes already exist (bomedemstat, seclidemstat, and friends) — if the chromatin argument holds up, repurposing into combo trials is cheap and fast. But this is a Perspective stitching two literatures together, not new data; before I'd trust a DDI-manageable combo across both AML and antivirals, I want real mechanistic proof that LSD1 inhibition actually changes nucleoside analogue uptake/incorporation, not just correlation.