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Tesofensine isn't technically a peptide - it's a small molecule drug that acts as a triple monoamine reuptake inhibitor affecting dopamine, norepinephrine, and serotonin simultaneously

144,156,157 C9orf72 mutation, the leading genetic cause of ALS and FTD, disrupts microglial autophagy and triggers sustained activation of NLRP3 inflammasome and nuclear factor-B (NF-B) signaling in human-induced pluripotent stem cell-derived microglia-like cells (hiPSC-MG)

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[7] Tesamorelin and sermorelin represent two different engineering answers to the same problem how to turn that endogenous signaling peptide into something usable in research or clinical settings