Schedule

Presentation 1

Time: 12:00 - 12:30

Title: The End of Medicine as we know it: From Chronic Disease to Mechanism-Based Cure

Speaker: Harald H.H.W. Schmidt

Abstract: For complex diseases, most drugs are highly ineffective, and the success rate of drug discovery is in a constant decline. Whilst low quality, reproducibility issues, and translational irrelevance of most basic and preclinical research have contributed to this, the current organ-centricity of medicine and the one disease-one target-one drug dogma obstruct innovation most profoundly. Systems and network medicine and their therapeutic arm, network pharmacology, revolutionize how we define, diagnose, treat and ideally cure diseases. Descriptive disease phenotypes are replaced by endotypes defined by causal, multi-target signaling modules that also explain respective comorbidities.
These modules are however distinct from classical pathways, which we now recognize to be not more than highly curated mind maps of signaling events. Modules more often than not contain several fragments of several different canonical pathways. Precise and effective therapeutic intervention depends on precise inclusion and exclusion of module members and is subsequently achieved by synergistic multi-compound network pharmacology, ideally through drug repurposing, obviating the need for drug discovery, and speeding up the clinical translation. Network pharmacology is, however, not to be confused with current combination therapies with multiple non-synergistic drugs targeting non-causal proteins that rather treat symptoms but do not cure disease.

Presentation 2

Time: 12:30 - 13:00

Title: Mechanistic Disease Endotypes: Module Construction and Validation.

Speaker: Cristian Nogales

Abstract: There are hardly any diseases that we understand molecularly, and current disease definitions are mostly organ- and symptom-based. Thus, we treat disease symptoms chronically with low precision. Only in rare, typically monogenic diseases, the causal mechanism is known.
However, in complex diseases, the pathomechanism is most likely a dysfunctional signalling module rather than a single gene or protein. Here we explore diseasome-based clusters and find disease modules as novel disease definitions or endotypes. Theranostic strategies designed around these disease modules will increase the precision of pharmacological interventions, hopefully curing patients.