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However, there was a significant growth inhibitory effect of semaglutide alone, which could be clinically significant to decrease the growth of cells refractory to standard-of-care AR-targeted therapy (Figure 4A)

Additionally, in mice with a point mutation of PAR2 at Arg 38 to Glu (PAR2-R38E mice), PAR2 was rendered insensitive to activation at the canonical cleavage site by bacterial and endogenous trypsin-like proteases (21, 22, 30, 31)

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