Gedeon Richter Plc
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György Németh has been the Neuropsychiatry Global Portfolio Director at Gedeon Richter Plc. since 2020. He is responsible for leading Gedeon Richter’s pillar of neuropsychiatry, which includes chairing global clinical research, development and strategy teams of the field; as well as managing medical-regulatory-marketing issues. He began his carrier at the Medical School of Debrecen University, Department of Neurology and Psychiatry. Later on, he worked as a fellow of Alexander von Humboldt Foundation at the University of Heidelberg, Germany. Afterwards he had different fellowships at the Karolinska Institute in Stockholm, Sweden and at New York University Medical Center in New York, USA. He continued his professional career as a clinical researcher at Knoll AG, Department of CNS R&D, where later, he took over the responsibility as Global Strategic Director for world-wide clinical and regulatory activities, launching among others two blockbuster new chemical entities. His main activities were international leader in the clinical development of drug candidates for the treatment of different neuropsychiatric indications. Between 2002 and 2020 he was the Chief Medical Officer at Gedeon Richter Plc. and was responsible for leading the Medical Division of the company. In 2021 he was promoted to become Neuropsychiatry Global Portfolio Director. One of the success stories under his clinical leadership at Gedeon Richter was that a pioneering antipsychotic (cariprazine) was approved by the FDA. In the meantime, he succeeded in verifying the efficacy of cariprazine in predominantly negative symptoms which was previously lacking therapeutic possibilities as well as in bipolar disorders and major depression. Thus, he instituted and led the clinical developments of a first-in-class drug by using broad spectrum approach. Owing to his comprehensive science operation, he is an active member of umpteen societies including Hungarian, European, and American societies. He is committed to personalized medicine. He has been the President of Hungarian Personalized Medicine Society since its foundation (2010).

Presenter of 1 Presentation

From a Pathophysiological Concept to a New Drug

Session Type
Educational
Date
Sat, 04.06.2022
Session Time
12:30 - 14:00
Room
On Demand 3
Session Icon
On Demand
Lecture Time
12:30 - 12:50

Abstract

Abstract Body

Although antipsychotics were discovered over fifty years ago, it took another decade until dopamine antagonism was demonstrated as central to their clinical effectiveness. Since accumulated evidence implicates the dopamine system in the pathophysiology of schizophrenia, all licensed first-line treatments operate primarily via antagonism of the dopamine D2 receptor.

However, dopamine D2 receptor blockade does not effectively treat negative, cognitive and affective symptoms and, in a significant proportion of patients, it does not improve positive symptoms either. Therefore, additional neurochemical targets were considered. The “revised dopamine hypothesis” proposes that positive symptoms emerge due to hyperactive dopamine transmission in mesolimbic areas, while hypoactive dopamine transmission via the mesocortical pathway in the prefrontal cortex is linked to negative, cognitive, and partly affective symptoms. In this context, the role of D3 receptors were recognised. However, there is also evidence for the involvement of other neurotransmitter systems, suggesting that dopamine signalling relies on a suite of receptors that are thought to either facilitate or inhibit neurotransmitter activity through several interconnected neural circuits.

Furthermore, there seem to be clusters of symptoms that cross the boundaries of disorders. Symptoms having similar pathophysiology at neurotransmitter level can be treated with the same drug or class of drugs. Thus, one particular drug might be effective in more than one indication.

This lecture aims to illustrate the process of a new drug development by explaining how the underlying pathophysiology on receptor level impacts clinical studies and vice versa.

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