The Effect of Novel, Small-Molecule Drugs as Agonists or Antagonists on G-Protein Coupled Receptors

Session Number

A03

Advisor(s)

Brittany Hopkins, Northwestern University
Richard Miller, Northwestern University

Location

A-121

Start Date

28-4-2016 9:50 AM

End Date

28-4-2016 10:15 AM

Abstract

G-Protein Coupled Receptors are seven-transmembrane receptors known to be the target receptors of onethird of all prescribed medicines, which demonstrates their importance in the pharmaceutical and pharmacological context. When activated, these receptors signal through stereotyped intracellular signaling pathways, demonstrating the ligands’ effects. We used the Tango assay which relies on a modified beta-arrestin recruitment signaling pathway, ours specifically targeting the dopamine (D2) receptor to activate this pathway. In the five-day assay, we primarily completed the fourth day, consisting of injecting novel, small-molecule drugs designed to interact with the CXCR4 receptor on HTLA cells. The assay allows for downstream signaling of luciferase transcription, which indicates the efficacy of the drug as either a D2 agonist or antagonist. We injected quinpirole, a D2 selective agonist, onto the cells as a control for other injected drugs for the agonist screen. For the antagonist screen, we injected quinpirole in combination with other drugs to determine those drugs’ effects in blocking quinpirole activity. Preliminary results suggest that the majority of tested drugs do not act as agonists nor antagonists for the D2 receptor. These results are not unexpected as the drugs were designed to target the CXCR4 receptor, showing their clinical possibilities. However, the observed specificity of the drugs for the CXCR4 receptor compared to the D2 receptor are encouraging.


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Apr 28th, 9:50 AM Apr 28th, 10:15 AM

The Effect of Novel, Small-Molecule Drugs as Agonists or Antagonists on G-Protein Coupled Receptors

A-121

G-Protein Coupled Receptors are seven-transmembrane receptors known to be the target receptors of onethird of all prescribed medicines, which demonstrates their importance in the pharmaceutical and pharmacological context. When activated, these receptors signal through stereotyped intracellular signaling pathways, demonstrating the ligands’ effects. We used the Tango assay which relies on a modified beta-arrestin recruitment signaling pathway, ours specifically targeting the dopamine (D2) receptor to activate this pathway. In the five-day assay, we primarily completed the fourth day, consisting of injecting novel, small-molecule drugs designed to interact with the CXCR4 receptor on HTLA cells. The assay allows for downstream signaling of luciferase transcription, which indicates the efficacy of the drug as either a D2 agonist or antagonist. We injected quinpirole, a D2 selective agonist, onto the cells as a control for other injected drugs for the agonist screen. For the antagonist screen, we injected quinpirole in combination with other drugs to determine those drugs’ effects in blocking quinpirole activity. Preliminary results suggest that the majority of tested drugs do not act as agonists nor antagonists for the D2 receptor. These results are not unexpected as the drugs were designed to target the CXCR4 receptor, showing their clinical possibilities. However, the observed specificity of the drugs for the CXCR4 receptor compared to the D2 receptor are encouraging.