The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
Chemical Compound Review

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

Welcome! If you are familiar with the subject of this article, you can contribute to this open access knowledge base by deleting incorrect information, restructuring or completely rewriting any text. Read more.

Disease relevance of LF 16-0687


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


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].


  1. 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]
  2. 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]
  3. 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]
  4. 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]
  5. 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]
  6. 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]
  7. 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]
  8. 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]
WikiGenes - Universities