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CHEMBL333994 (FK-480) Sale

(Synonyms: FK-480) 目录号 : GC30674

CHEMBL333994 (FK-480) 是一种有效的口服有效的胆囊收缩素 A (CCK-A) 拮抗剂,IC50 为 0.67 nM。

CHEMBL333994 (FK-480) Chemical Structure

Cas No.:167820-10-2

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产品描述

CHEMBL333994 is a potent and orally effective Cholecystokinin A (CCK-A) antagonist, with an IC50 of 0.67 nM.

[1]. Satoh Y, et al. Studies on a novel, potent and orally effective cholecystokinin A antagonist, FK-480. Synthesis and structure-activity relationships of FK-480 and related compounds. Chem Pharm Bull (Tokyo). 1994 Oct;42(10):2071-83.

Chemical Properties

Cas No. 167820-10-2 SDF
别名 FK-480
Canonical SMILES O=C(C(N1)=CC2=C1C=CC=C2)N[C@H]3C(N4C5=C(CC4)C=CC=C5C(C6=CC=CC=C6F)=N3)=O
分子式 C26H19FN4O2 分子量 438.45
溶解度 Soluble in DMSO 储存条件 Store at -20°C
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Research Update

Studies on a novel, potent and orally effective cholecystokinin A antagonist, FK-480. Synthesis and structure-activity relationships of FK-480 and related compounds

We prepared various novel tricyclic 1,4-benzodiazepine derivatives as cholecystokinin (CCK) A antagonists, which were evaluated preliminarily for inhibition of 125I-CCK-8 binding to rat pancreatic membranes in vitro and inhibiting effect on CCK-8-induced inhibition of charcoal meal gastric emptying in mice. On the basis of structure-activity relationship (SAR) studies, as well as the stability and availability of the starting materials of those compounds, (S)-N-[1-(2-fluorophenyl)-3,4,6,7-tetrahydro-4-oxo- pyrrolo[3,2,1-jk][1,4]benzodiazepin-3-yl]- 1H-indole-2-carboxamide (9f, FK-480) was selected as a candidate compound for further evaluation. The absolute configuration of the precursor of FK-480, (3S)-amino-1,4-benzodiazepine derivative ((S)-8a, R1 = F) was determined by an X-ray crystallographic study of its ureido derivative with (S)-alpha-methylbenzyl isocyanate. FK-480 is now undergoing clinical studies for the treatment of chronic pancreatitis.

Effect of a new cholecystokinin antagonist (FK 480) on gene expression of cholecystokinin and secretin in rat intestine

The effects of a new cholecystokinin (CCK) antagonist (FK 480; 0.1 mg/kg per day given by intragastric administration to rats for 3 days) on the expression of the CCK and secretin genes, plasma CCK immunoreactivity, and CCK content in the intestinal mucosa were examined. FK 480 increased the level of CCK mRNA in the intestine to 1.7 times the level in control rats, but did not affect the level of secretin mRNA. It did not increase plasma CCK immunoreactivity or CCK content in the intestinal mucosa. These results suggest that the ingested FK 480 directly increased CCK mRNA level in the intestine and produced a dissociation between the synthesis and release of CCK.

The pre-synaptic blocker toosendanin does not inhibit secretion in exocrine cells

Aim: Toosendanin is a pre-synaptic blocker at the neuromuscular junction and its inhibitory effect is divided into an initial facilitative/stimulatory phase followed by a prolonged inhibitory phase. The present study investigated whether the subsequent inhibitory phase was due to exhaustion of the secretory machinery as a result of extensive stimulation during the initial facilitative phase. More specifically, this paper examined whether toosendanin could directly inhibit the secretory machinery in exocrine cells.
Methods: Rat pancreatic acinar cells were isolated by collagenase digestion. Secretion was assessed by measuring the amount of amylase released into the extracellular medium as a percentage of the total present in the cells before stimulation. Cholecystokinin (CCK)-induced increases in intracellular calcium in single cells were measured with fura-2 microfluorometry.
Results: Effects of toosendanin on CCK-induced amylase secretion and calcium oscillations were investigated. Toosendanin of 87-870 microM had no effect on 10 pM-100 nM CCK-stimulated amylase secretion, nor did 8.7-870 microM toosendanin inhibit 5 pM CCK-induced calcium oscillations. In contrast, 10 nM CCK(1) receptor antagonist FK 480 completely blocked 5 pM CCK-induced calcium oscillations.
Conclusion: The pre-synaptic "blocker" toosendanin is a selective activator of the voltage-dependent calcium channels, but does not interfere with the secretory machinery itself.

CK-independent increases in pancreatic secretion induced by dietary protein in chronic BPJ-diverted rats

Previously, we demonstrated that, in rats with chronic bile-pancreatic juice (BPJ) diversion, pancreatic enzyme secretion was increased after feeding animals a 25% casein fat-free diet. We determined whether cholecystokinin (CCK) or the cholinergic pathway is associated with the response of pancreatic secretion after protein ingestion in the diverted rats, using a potent CCK antagonist, MK-329 or FK-480, and a cholinergic blocker, atropine. Secretion rates of chymotrypsin and trypsin in the fasting state were very high 7 days after a BPJ diversion, and the hypersecretion of the proteases was markedly reduced with an injection of MK-329, FK-480, or atropine and was further reduced by combined injection of FK-480 and atropine. The lowered secretion of the proteases in CCK-antagonized rats was increased after oral feeding of a protein diet and after a duodenal instillation of some protein sources, especially hydrolysate of guanidinated casein (HGC). The CCK-independent increases by HGC instillation are completely depressed by atropine. In rats treated with only atropine, the lowered secretion tended to be increased by a duodenal instillation of HGC. Increases in secretion after an administration of the protein source in CCK-antagonized rats were not affected by bestatin, an inhibitor of brush-border peptidases. We conclude that the stimulatory effects of dietary protein on the pancreatic enzyme secretion partially do not depend on CCK in chronic BPJ-diverted rats and that the CCK-independent increase is atropine sensitive.

Selective activation by photodynamic action of cholecystokinin receptor in the freshly isolated rat pancreatic acini

1 Sulphonated aluminium phthalocyanine (SALPC) photodynamic action induces amylase secretion and permanent calcium oscillation in rat pancreatic acinar cells, because of the activation of phospholipase C or signalling proteins upstream. The aim of the present study was to investigate the involvement of muscarinic acetylcholine and cholecystokinin (CCK) receptors. 2 Muscarinic receptor antagonist atropine (10 micro M) blocked amylase secretion induced by bethanechol (100 micro M), and CCK(1) receptor antagonist (S)-N-[1-(2-fluorophenyl)-3,4,6,7-tetrahydor-4-oxo-pyrrolo-[3,2,1-jk][1,4] benzodiazepine-3yl]-1H-indole-2-carboxamide (FK480) (1 micro M) blocked amylase secretion induced by CCK (100 pM). 3 Amylase secretion induced by SALPC photodynamic action was not inhibited when atropine and FK480 were present during photodynamic action. However, addition of FK480 1 micro M after initiation of photodynamic action inhibited photodynamic amylase secretion. Bethanechol (10, 100 micro M) added after photodynamic action resulted in a full secretory response. 4 Atropine (10 nM) abolished calcium oscillation induced by bethanechol (5 micro M), and FK480 (10 nM) blocked calcium oscillation induced by CCK (10 pM). 5 Atropine up to 10 micro M was without effect on Ca(2+) oscillation triggered by photodynamic action, but these oscillations were abolished by FK480 (10 nM). FK480 (10 nM) had no effect on calcium oscillations induced by bethanechol (5 micro M). Bethanechol 5 micro M, added after FK480 blockade of photodynamic calcium oscillation, still triggered regular calcium oscillation. 6 It is concluded that SALPC photodynamic action selectively and permanently activates CCK receptor in rat pancreatic acini. Such permanent and selective modulation of signalling proteins has important implications for the treatment of pancreatitis, prion diseases, and neurodegenerative disorders.