PAR-2 Agonist I

Native proteinase activated receptor-2- (PAR-2) specific agonist, SLIGRL-NH₂, modified with an N-terminal furoyl group to increase its potency and resistance to metabolic degradation. Shown to activate [Ca²⁺]_i mobilization in PAR-2-expressing cells (EC₅₀ = 253 nM in HCT-15 cells) in vitro. Also induces PAR-2-mediated salivation (ED₅₀ = 30 nmol/kg, i.v.) in vivo. Exhibits no effects on PAR-2^-/- mice. Reactive towards human, rat, and mouse PAR-2.

The native PAR-2-specific agonist, SLIGRL-NH₂, is modified with an N-terminal furoyl group to increase its potency and resistance to metabolic degradation. Shown to activate [Ca²⁺]_i mobilization in PAR-2-expressing cells (EC₅₀ = 253 nM using HCT-15 cells) in vitro and induce PAR-2 mediated salivation (ED₅₀ = 30 nmol/kg, i.v.) in vivo, while exhibiting no effect on PAR-2^-/- mice. Reactive towards human, rat, and murine PAR-2.

Cell permeable: no

EC50 = 253 nM as PAR-2-specific agonist using HCT-15 cells

Primary Target
PAR-2

Product does not compete with ATP.

Reversible: no

Packaged under inert gas

Toxicity: Standard Handling (A)

2-Furoyl-Leu-Ile-Gly-Arg-Leu-NH₂

Supplied as a trifluoroacetate salt.

Following reconstitution, aliquot and freeze (-20°C). Stock solutions are stable for up to 3 months at -20°C.

Kawabata, A., et al. 2004. J. Pharmacol. Exp. Ther.309, 108.
Kawabata, A., et al. 2004. J. Pharmacol. Exp. Ther.309, 1098.
Ferrell, W.R., et al. 2003. J. Clin. Invest.111, 35.

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