CXCL12 and pituitary gland adenoma: The synthesized derivatives were evaluated for their ability to inhibit proliferation, migration, and CXCL12-dependent ERK1/2 MAP kinase phosphorylation/activation in GH4C1 cells of the rat pituitary adenoma cell line; although all compounds were able to antagonize the effects of CXCL12, with varying potency and efficacy, parazoanthine-B (Figure 20) was identified as the most potent CXCR4 antagonist, with an IC50 value of 9.3 nM.