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Brussels, Belgium

UCB is a multinational biopharmaceutical manufacturing company headquartered in Brussels, Belgium. Every 3 years, the company presents the UCB Award under the patronage of the Queen Elisabeth Medical Foundation to promote neuroscience research. The winner of this award is selected by an independent scientific committee. Wikipedia.

Diaz A.,UCB Pharma
Expert review of neurotherapeutics | Year: 2012

Seizures and chronic kidney disease are both common and often coexist. Treating seizures in patients with renal failure, including those on dialysis, is a challenge that is frequently encountered, especially in the inpatient setting. For the newer antiepileptic drugs, there are limited data available, so an understanding of how each drug is affected by kidney disease and dialysis is critical in order to make rational choices qualitatively (which drug) and quantitatively (dosing). Generally, newer (second-generation) antiepileptic drugs are associated with fewer systemic side effects and drug-drug interactions, so they tend to be preferred in this population. The landscape of antiepileptic drugs is constantly evolving, with new compounds being released on a regular basis. Thus, several new agents have become available since the last review of this topic (in 2006) and these are the ones discussed here. Most require dosage adjustment according to the degree of renal failure, and most require extra doses after dialysis. Source

Cawello W.,UCB Pharma
Clinical Pharmacokinetics | Year: 2015

Lacosamide—a third-generation antiepileptic drug available in multiple formulations—was first approved in 2008 as adjunctive therapy for partial-onset seizures (POS) in adults. In 2014, lacosamide was approved as monotherapy for POS by the US Food and Drug Administration (FDA). A loading dose administration was approved in 2013 by the European Medicines Agency and in 2014 by the FDA. Unlike traditional sodium channel blockers affecting fast inactivation, lacosamide selectively enhances sodium channel slow inactivation. This mechanism of action results in stabilization of hyperexcitable neuronal membranes, inhibition of neuronal firing and reduction in long-term channel availability without affecting physiological function. Lacosamide is rapidly absorbed, with maximum plasma concentrations reached 0.5–4 h after intake. Oral bioavailability is high (100 %) for a dose up to 800 mg. Bioavailability is irrespective of food intake. Variability in pharmacokinetic parameters is low (coefficients of variation almost all <20 %). The pharmacokinetic profile of lacosamide is consistent in healthy subjects and across different patient populations studied. Lacosamide elimination from plasma occurs with a terminal half-life of approximately 13 h in young subjects and 14–16 h in elderly subjects; this difference does not impact the dose regimen. Lacosamide produces a pharmacodynamic effect that is closely correlated with its plasma concentration. The pharmacokinetic and pharmacodynamic relationship for reduction of seizure frequency can be described by a maximum effect (Emax) model. Lacosamide does not induce or inhibit cytochrome P450 enzymes or known drug transporter systems, has low protein binding of less than 15 % and, because it has multiple elimination pathways, it has no clinically relevant interactions with commonly prescribed medications. © 2015, Springer International Publishing Switzerland. Source

UCB Pharma | Date: 2015-03-31

The present invention is directed to a pharmaceutical composition comprising a Compound (a) of a class of peptide Compounds and at least one further Compound (b) for the prevention, alleviation or/and treatment of epileptic seizures.

The present invention provides a recombinant gram-negative bacterial cell, characterized in that the cell comprises a recombinant polynucleotide encoding DsbC and has reduced Tsp protein activity compared to a wild-type cell.

UCB Pharma | Date: 2015-08-17

A recombinant gram-negative bacterial cell comprising one or more of the following mutated protease genes: a) a mutated Tsp gene, wherein the mutated Tsp gene encodes a Tsp protein having reduced protease activity or is a knockout mutated Tsp gene; b) a mutated ptr gene, wherein the mutated ptr gene encodes a Protease III protein having reduced protease activity or is a knockout mutated ptr gene; and c) a mutated DegP gene encoding a DegP protein having chaperone activity and reduced protease activity; wherein the cell is isogenic to a wild-type bacterial cell except for the mutated Tsp gene and/or mutated ptr gene and/or mutated DegP gene and optionally a polynucleotide sequence encoding a protein of interest.

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