132746-60-2
Chemical Structure
CP-96,345
- CAS No.: 132746-60-2
- Formula:C28H32N2O
- Molecular Weight:412.57
IUPAC Name: (2S,3S)-2-benzhydryl-N-(2-methoxybenzyl)quinuclidin-3-amine
InChIKey: FLNYLINBEZROPL-NSOVKSMOSA-N
SMILES: COC1=C(C=CC=C1)CN[C@@H]2[C@@H](N3CCC2CC3)C(C4=CC=CC=C4)C5=CC=CC=C5
Biological Activity: CP-96,345 is a non-peptide selective NK-1 receptor antagonist (Ki = 0.31 nM). CP-96,345 inhibits cell rolling, adhesion, and plasma extravasation, and inhibits degranulation and pancreatic MPO activity. CP-96,345 attenuates neurogenic inflammation, edema, and adhesion molecule expression. CP-96,345 attenuates static contraction- and muscle stretch-evoked pressor reflexes through blockade of NK-1 receptors in the dorsal horn. CP-96,345 impairs post-ischemic recovery of LVDevP, HR, and CF in isolated hearts and increases reperfusion fibrillation. CP-96,345 can be used for research on chronic colitis, myocardial ischemia-reperfusion injury, smoke inhalation and burn injury, acute pancreatitis, oxazolone colitis, and neurogenic inflammation[1][2][3][4][5][6][7][8][9].
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CP-96,345 | 99.9% | CP-96,345 is a non-peptide selective NK-1 receptor antagonist (Ki = 0.31 nM). CP-96,345 inhibits cell rolling, adhesion, and plasma extravasation, and inhibits degranulation and pancreatic MPO activity. CP-96,345 attenuates neurogenic inflammation, edema, and adhesion molecule expression. CP-96,345 attenuates static contraction- and muscle stretch-evoked pressor reflexes through blockade of NK-1 receptors in the dorsal horn. CP-96,345 impairs post-ischemic recovery of LVDevP, HR, and CF in isolated hearts and increases reperfusion fibrillation. CP-96,345 can be used for research on chronic colitis, myocardial ischemia-reperfusion injury, smoke inhalation and burn injury, acute pancreatitis, oxazolone colitis, and neurogenic inflammation. | ||||||||||||||||||||
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References
- [1]. Gad M, et al. Blockage of the neurokinin 1 receptor and capsaicin-induced ablation of the enteric afferent nerves protect SCID mice against T-cell-induced chronic colitis. Inflammatory bowel diseases. 2009 Aug;15(8):1174-82.
- [2]. Wilson LB, et al. Segmental effect of spinal NK-1 receptor blockade on the pressor reflex. American Journal of Physiology-Heart and Circulatory Physiology. 1998 Sep 1;275(3):H789-96.
- [3]. Ustinova EE, et al. Neuropeptide depletion impairs postischemic recovery of the isolated rat heart: role of substance P. Cardiovascular research. 1995 Jul;30(1):55-63.
- [4]. Jacob S, et al. Substance P antagonist CP-96345 blocks lung vascular leakage and inflammation more effectively than its stereoisomer CP-96344 in a mouse model of smoke inhalation and burn injury. Toxicology mechanisms and methods. 2010 May;20(4):197-203.
- [5]. Lau HY, et al. Effect of CP-96,345 on the expression of adhesion molecules in acute pancreatitis in mice. American journal of physiology. Gastrointestinal and liver physiology. 2007 May;292(5):G1283-92.
- [6]. Rubino A, et al. Endothelium-dependent relaxant effect of neurokinins on rabbit aorta is mediated by the NK1 receptor. European journal of pharmacology. 1992 Mar 03;212(2-3):237-40.
- [7]. Engel MA, et al. Opposite effects of substance P and calcitonin gene-related peptide in oxazolone colitis. Digestive and liver disease : official journal of the Italian Society of Gastroenterology and the Italian Association for the Study of the Liver. 2012 Jan;44(1):24-9.
- [8]. Castagliuolo I, et al. Neurotensin is a proinflammatory neuropeptide in colonic inflammation. The Journal of clinical investigation. 1999 Mar;103(6):843-9.
- [9]. Baluk P, et al. NK1 receptors mediate leukocyte adhesion in neurogenic inflammation in the rat trachea. Am J Physiol. 1995 Feb;268(2 Pt 1):L263-9.
