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Chemical Compound Review:

AC1NSM1F (2S)-N-[3-[[4-(aminomethyl) phenyl]carbonyl...

Synonyms:

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Disease relevance of LF 16-0687

Pretreatment with 10 microg/kg/min LF 16-0687 decreased brain swelling significantly to 6.4 +/- 1.3% (p < 0.05) [1].
The extent of edema was significantly reduced when LF 16-0687 Ms was given 1 h (-45%), 2 h (-52%), and 4 h (-63%) but not 10 h (-24%) after CHT [2].
The neuroprotective effect of LF 16-0687 Ms, a B(2) receptor antagonist, has been described when given prior to induction of transient focal cerebral ischemia in rat, but there are no data regarding the consequence of a treatment when given after injury [3].
4. Post-treatment with LF 16-0687 Ms (1.5 mg kg(-1)) significantly decreased brain edema (-28%), BBB disruption (-60%) and neutrophil accumulation (-65%) induced by ischemia [3].
The potent non-peptide B2 receptor (R) antagonist, Anatibant mesylate (Ms) (LF 16-0687 Ms), reduces brain edema and improves neurological function recovery in various focal and diffuse models of traumatic brain injury in rodents [4].

High impact information on LF 16-0687

In addition, the inducible NO synthase (iNOS) mRNA level increased markedly, and this was reduced by LF 16-0687 Ms. Taken together, these data support a detrimental role of B2R in the development of the neurological deficit and of the inflammatory secondary damage resulting from diffuse traumatic brain injury [5].
Therefore, in a murine model of transient middle cerebral artery occlusion (MCAO), we evaluated the effect of LF 16-0687 Ms given prior to and/or after the onset of ischemia on neurological deficit, infarct volume and inflammatory responses including cerebral edema, blood-brain barrier (BBB) disruption and neutrophil accumulation [3].
Treatment with LF 16-0687 Ms and B(2)R gene deletion decreased the accumulation of neutrophils at 24 h after CHT (50% and 36%, respectively) [5].
In a rat model of focal cerebral ischemia, blockade of B2 receptors before initiation of ischemia with the B2 receptor antagonist, LF 16-0687 Ms, afforded substantial neuroprotection [6].
In competition binding studies using [3H]bradykinin (BK), LF 16-0687 bound to the human, rat and guinea-pig recombinant B2 receptor expressed in CHO cells giving K(i) values of 0.67 nM, 1.74 nM and 1.37 nM, respectively [7].

Chemical compound and disease context of LF 16-0687

CONCLUSION: Ethanol does not affect the improvement of NSS and the decrease of cerebral edema seen with LF 16-0687 Ms after CHT, but does reverse the ability of LF 16-0687 Ms to minimize the increase of PGE(2) release [8].

Anatomical context of LF 16-0687

Subcutaneous administration of LF 16-0687 at 1.1 micromol/kg to rats markedly reduced BK-induced edema of the stomach (- 69%), duodenum (-65%) and pancreas (-56%) [7].

Analytical, diagnostic and therapeutic context of LF 16-0687

In order to assess the potential clinical value of this approach, we evaluated the effect of LF 16-0687 Ms given at reperfusion following focal cerebral ischemia on local cerebral blood flow (LCBF), neurological outcome, and infarct size [6].
A continuous intravenous infusion of LF 16-0687 antagonized in a dose-dependent manner and with a rapid onset of action BK-induced hypotensive response [7].

References

Role of bradykinin B2 receptors in the formation of vasogenic brain edema in rats. Plesnila, N., Schulz, J., Stoffel, M., Eriskat, J., Pruneau, D., Baethmann, A. J. Neurotrauma (2001) [Pubmed]
LF 16-0687 Ms, a bradykinin B2 receptor antagonist, reduces brain edema and improves long-term neurological function recovery after closed head trauma in rats. Kaplanski, J., Pruneau, D., Asa, I., Artru, A.A., Azez, A., Ivashkova, Y., Rudich, Z., Shapira, Y. J. Neurotrauma (2002) [Pubmed]
LF 16-0687 Ms, a bradykinin B2 receptor antagonist, reduces ischemic brain injury in a murine model of transient focal cerebral ischemia. Ding-Zhou, L., Margaill, I., Palmier, B., Pruneau, D., Plotkine, M., Marchand-Verrecchia, C. Br. J. Pharmacol. (2003) [Pubmed]
Autoradiographic analysis of mouse brain kinin B1 and B2 receptors after closed head trauma and ability of Anatibant mesylate to cross the blood-brain barrier. Ongali, B., Hellal, F., Rodi, D., Plotkine, M., Marchand-Verrecchia, C., Pruneau, D., Couture, R. J. Neurotrauma (2006) [Pubmed]
Detrimental role of bradykinin B2 receptor in a murine model of diffuse brain injury. Hellal, F., Pruneau, D., Palmier, B., Faye, P., Croci, N., Plotkine, M., Marchand-Verrecchia, C. J. Neurotrauma (2003) [Pubmed]
Neuroprotective effects of a postischemic treatment with a bradykinin B2 receptor antagonist in a rat model of temporary focal cerebral ischemia. Lumenta, D.B., Plesnila, N., Kläsner, B., Baethmann, A., Pruneau, D., Schmid-Elsaesser, R., Zausinger, S. Brain Res. (2006) [Pubmed]
Pharmacological profile of LF 16-0687, a new potent non-peptide bradykinin B2 receptor antagonist. Pruneau, D., Paquet, J.L., Luccarini, J.M., Defrêne, E., Fouchet, C., Franck, R.M., Loillier, B., Robert, C., Bélichard, P., Duclos, H., Cremers, B., Dodey, P. Immunopharmacology (1999) [Pubmed]
LF 16-0687 Ms, a new bradykinin B2 receptor antagonist, improves neurologic outcome but not brain tissue prostaglandin E2 release in a rat model of closed head trauma combined with ethanol intoxication. Asa, I., Ivashkova, Y., Artru, A.A., Lifshitz, M., Gavrilov, V., Azab, A.N., Kapuler, V., Alouchin, A., Rachinsky, M., Pruneau, D., Shapira, Y., Kaplanski, J. The Journal of trauma. (2003) [Pubmed]

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