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May 19, 2011British Journal of Pharmacology161 citationsOpen Access

In vitroandin vivocharacterization of PF‐04418948, a novel, potent and selective prostaglandin EP2receptor antagonist

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KFKJ af ForsellesJRJames RootTCTracey L. Clarke

Key Result

PF-04418948 is a potent and selective EP2 receptor antagonist that inhibited PGE2-induced increases in cAMP with a functional KB of 1.8 nM and attenuated butaprost-induced cutaneous blood flow in rats.

Structured PICO

P
Population
Cell-based systems expressing human EP2 receptors, native tissue preparations from human, dog, and mouse, and in vivo rat models
I
Intervention
PF-04418948 (a novel prostaglandin EP2 receptor antagonist)
O
Outcome
Functional antagonist potency (inhibition of PGE2-induced increase in cAMP, tissue relaxation/contraction shifts, and cutaneous blood flow response)surrogate

PF-04418948 is an orally active, potent, and selective EP2 receptor antagonist that serves as a useful pharmacological tool for studying EP2 receptor function.

Main Result

Effect estimate: KB 1.8 nM

Abstract

BACKGROUND AND PURPOSE: Studies of the role of the prostaglandin EP (2) receptor) have been limited by the availability of potent and selective antagonist tools. Here we describe the in vitro/in vivo pharmacological characterization of a novel EP (2) receptor antagonist, PF-04418948 (1- (4-fluorobenzoyl) -3- (6-methoxy-2-naphthyl) oxymethyl azetidine-3-carboxylic acid). EXPERIMENTAL APPROACH: Functional antagonist potency was assessed in cell-based systems expressing human EP (2) receptors and native tissue preparations from human, dog and mouse. The selectivity of PF-04418948 was assessed against related receptors and a panel of GPCRs, ion channels and enzymes. The ability of PF-04418948 to pharmacologically block EP (2) receptor function in vivo was tested in rats. KEY RESULTS: PF-04418948 inhibited prostaglandin E (2) (PGE (2) ) -induced increase in cAMP in cells expressing EP (2) receptors with a functional K (B) value of 1. 8 nM. In human myometrium, PF-04418948 produced a parallel, rightward shift of the butaprost-induced inhibition of the contractions induced by electrical field stimulation with an apparent K (B) of 5. 4 nM. In dog bronchiole and mouse trachea, PF-04418948 produced parallel rightward shifts of the PGE (2) -induced relaxation curve with a K (B) of 2. 5 nM and an apparent K (B) of 1. 3 nM respectively. Reversal of the PGE (2) -induced relaxation in the mouse trachea by PF-04418948 produced an IC (50) value of 2. 7 nM. Given orally, PF-04418948 attenuated the butaprost-induced cutaneous blood flow response in rats. PF-04418948 was selective for EP (2) receptors over homologous and unrelated receptors, enzymes and channels. CONCLUSIONS AND IMPLICATIONS: PF-04418948 is an orally active, potent and selective surmountable EP (2) receptor antagonist that should aid further elaboration of EP (2) receptor function.

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Cite This Study

Forselles et al. (2011) studied Pharmacological characterization of EP2 receptor antagonist. PF-04418948 was evaluated on Inhibition of PGE2-induced increase in cAMP in cells expressing EP2 receptors (KB 1.8 nM). PF-04418948 is a potent and selective EP2 receptor antagonist that inhibited PGE2-induced increases in cAMP with a functional KB of 1.8 nM and attenuated butaprost-induced cutaneous blood flow in rats.

synapsesocial.com/papers/6a167ebe51b6ba61365d46a8https://doi.org/10.1111/j.1476-5381.2011.01495.x
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