Disease relevance of CP99994

• This eosinophilia was not altered by pretreatment with the NK1 receptor antagonist CP99994 [1].

High impact information on CP99994

• Mobilization of the receptor by SP was blocked by the NK(1)-receptor antagonist CP99994 [2].
• The affinity and potency of NKR agonists and the NK(1)R antagonists CP99994 and RP67580 (NK(1)R-selective) and ZD6021 (NK1/2R) were assessed in vitro by monitoring [(3)H]-SarMet SP binding and substance P-evoked mobilization of intracellular Ca(2+) [3].
• Responses to SP were inhibited by the NK-2 receptor antagonist SR48968, but not by NK-1 antagonist CP99994, indicating the involvement of NK-2 rather than NK-1 receptors [4].
• Pretreatment of sensitized guinea-pigs with the NK1 receptor antagonists CP99994 (4 mg kg(-1), i.p.), SR140333 (1 mg kg(-1), s.c.) or CP96345 (15 mg kg(-1), i.p.) before antigen challenge, prevented M2 receptor dysfunction [1].
• The dipeptide potently antagonizes bronchoconstriction provoked by exogenous substance P in the guinea-pig and acts longer than the non-peptide antagonist CP99994, when administered as aerosol [5].

Anatomical context of CP99994

• NK-1 antagonist CP99994 inhibits stress-induced mast cell degranulation in rats [6].

Gene context of CP99994

• The inhibitory effect of SP on ATP action was blocked by CP99994, indicating that the SP receptors are of the neurokinin-1 type [7].

Analytical, diagnostic and therapeutic context of CP99994

• METHODS: NK(1)-receptor immunoreactivity was examined by confocal microscopy in tissue incubated with or without 10(-7) mol/L substance P (SP), 10(-7) mol/L SP plus 10(-6) mol/L NK(1) receptor antagonist (CP99994), or with fluorescent cyanine 3.18 (Cy3) SP [2].

References