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However, under the conditions we examined, the activities of AsGGT1 and AsGGT3 to deglutamylate -glutamyl- S -allyl-L-cysteine sulfoxide were too weak to perform further enzymatic characterization

For example, interleukin (IL)-6/STAT3 signaling is aberrantly activated in many CSCs, promoting self-renewal, immune evasion, and resistance to therapy, 63,64 whereas NF-B signaling supports CSC survival by sustaining inflammation-associated transcriptional programs

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The primary pharmacokinetic difference between the routes is therefore kinetic rather than total exposure: IM produces sharper, faster peaks while SubQ produces slower, more sustained plasma profiles