Fig. 4: The molecular mechanism of the SSTR subtype selectivity by paltusotine over octreotide.
From: Prospect of acromegaly therapy: molecular mechanism of clinical drugs octreotide and paltusotine
a Gi signaling of SSTR1–5 activated by paltusotine. Data represent mean ± SEM from three independent experiments. b Sequence alignment of the residues around the paltusotine binding pocket in SSTR2 with sequences of other SSTR subtypes. c, d The effects of the residue substitution of N1032.64V or T19445.51H in SSTR2 (c) and V1012.64N or H19245.51T in SSTR3 (d) on the paltusotine-induced cAMP inhibition. Data represent mean ± SEM from three independent experiments.
