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BIM 189

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BIM 189 is a bombesin antagonist that reduces bombesin-induced satiety.

Category
Peptide Inhibitors
Catalog number
BAT-010326
CAS number
142062-55-3
Molecular Formula
C56H73ClN14O10
Molecular Weight
1137.73
BIM 189
IUPAC Name
(2S)-N-[(2S)-1-[[(2S)-1-[[(2S)-1-[[2-[[(2S)-1-[[(2S)-1-[[(2S)-1-amino-3-(4-chlorophenyl)-1-oxopropan-2-yl]amino]-4-methyl-1-oxopentan-2-yl]amino]-3-(1H-imidazol-5-yl)-1-oxopropan-2-yl]amino]-2-oxoethyl]amino]-3-methyl-1-oxobutan-2-yl]amino]-1-oxopropan-2-yl]amino]-3-(1H-indol-3-yl)-1-oxopropan-2-yl]-2-[[(2R)-2-amino-3-phenylpropanoyl]amino]pentanediamide
Synonyms
[D-Phe6,Leu13,Cpa14]bombesin-(6-14)NH2
Appearance
White Lyophilized Solid
Purity
>96%
Density
1.309 g/cm3
Boiling Point
1600.4°C at 760 mmHg
Sequence
FQWAVGHLX(Modifications: X = Phe-4-Cl)
Storage
Store at -20°C
InChI
InChI=1S/C56H73ClN14O10/c1-30(2)21-43(54(79)68-42(49(60)74)23-34-15-17-36(57)18-16-34)69-55(80)45(25-37-27-61-29-64-37)66-47(73)28-63-56(81)48(31(3)4)71-50(75)32(5)65-53(78)44(24-35-26-62-40-14-10-9-13-38(35)40)70-52(77)41(19-20-46(59)72)67-51(76)39(58)22-33-11-7-6-8-12-33/h6-18,26-27,29-32,39,41-45,48,62H,19-25,28,58H2,1-5H3,(H2,59,72)(H2,60,74)(H,61,64)(H,63,81)(H,65,78)(H,66,73)(H,67,76)(H,68,79)(H,69,80)(H,70,77)(H,71,75)/t32-,39+,41-,42-,43-,44-,45-,48-/m0/s1
InChI Key
XJWMPWLZAVKSPK-UYBYNCNQSA-N
Canonical SMILES
CC(C)CC(C(=O)NC(CC1=CC=C(C=C1)Cl)C(=O)N)NC(=O)C(CC2=CN=CN2)NC(=O)CNC(=O)C(C(C)C)NC(=O)C(C)NC(=O)C(CC3=CNC4=CC=CC=C43)NC(=O)C(CCC(=O)N)NC(=O)C(CC5=CC=CC=C5)N
1. Effects of neonatal blockade of bombesin (BN) receptors with [D-Phe6, phi Leu13-Cpa14]BN(6-14) on adult behavior and sensitivity to BN
Z Merali, H D Piggins, T W Moody Peptides . 1993 Jul-Aug;14(4):845-8. doi: 10.1016/0196-9781(93)90123-x.
Long-term consequences of neonatal blockade of bombesin (BN) receptors were examined in the present study. Rat pups were injected twice daily with [D-Phe6, phi Leu13-Cpa14]BN(6-14), a BN receptor antagonist, at either high (10 mg/kg; HD group) or low (5 mg/kg; LD group) doses from postnatal day 1 through 8. Their behavioral responses to a variety of conditions were compared to those of rats neonatally injected with saline (SAL group) or animals handled but not injected during infancy (UNT group). Adult HD rats entered and spent more time on the open arms of the elevated plus maze than LD, SAL, or UNT animals. Under the conditions of a water deprivation schedule, neither central nor peripheral injections of BN differentiated the neonatally pretreated groups as determined by measures of grooming, feeding, and drinking behaviors. These results indicate that at the dosage regimen employed, neonatal injections of [D-Phe6, phi Leu13-Cpa14]BN(6-14) had little effect on adult sensitivity to BN, but that such treatments could alter activity on the elevated plus maze through as yet unknown mechanisms.
2. Effects of bombesin, of a new bombesin agonist (BIM187) and a new antagonist (BIM189) on food intake in rats, in relation to cholecystokinin
A Le Gall, A Basdevant, G Bonhomme, B Guy-Grand, B Laferrère, F Leroy Eur J Pharmacol . 1992 Apr 29;215(1):23-8. doi: 10.1016/0014-2999(92)90603-2.
To study the mechanism by which bombesin induces satiety, we studied the effect of two new peptides, BIM187, a bombesin agonist, and BIM189, a bombesin antagonist, on food intake in rats fed 6 h a day. BIM187 at 4 micrograms/kg, significantly reduced food intake at 30 min, but did not change the total 6-h food intake. BIM189 (10 mg/kg), had no effect on food intake when administered alone, even at high doses (20 mg/kg). BIM189 selectively reduced bombesin-induced satiety but had no effect on satiety induced by BIM187. To examine the extent to which the satiety effect of bombesin or related peptides depends on the release of cholecystokinin (CCK), we studied the ability of CCK antagonists, BIM18216 and L364718, to reduce satiety induced by bombesin and BIM187. Neither BIM18216 nor L364718 alone had an effect on the 30-min food intake. They were not able to reverse the effect of bombesin on food intake. In our model, bombesin seems to act on satiety by a mechanism independent of CCK.
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