Pre-Conference Workshop Day


*All workshop timings below are displayed in EDT. For PDT, please download the full program here*

Our workshops are streamed so you are able to attend 3 out of 6 workshops. You can choose A or B, followed by C or D, followed by E or F. Do you want to attend all of our workshops? Check out our group booking discounts so your colleagues can join you!

8:30 am Online Registration & Virtual Coffee Networking

Workshop A

Workshop B

9.00am Expanding Novel Approaches Towards RAS Drug Discovery with Degradation Strategies

Ubiquitylation and degradation of RAS is one of the key mechanisms for covalent and PROTAC RAS drugs. As ubiquitylation masks target protein epitope, monitoring degradation ubiquitylation and degradation of RAS need to be explored with new methods. Navigating through clinical and preclinical, it is important to consider the use of covalent and non-covalent RAS inhibitors and their mechanisms. Similarly, evaluating the value of biochemical, cellular and imaging methods will aid effective drug discovery.

Topics to be covered:

  • Discuss and highlight why RAS proteins are so undruggable
  • Explore the possibility of drugging different RAS isoforms with a universal inhibitor?
  • Describe the structure and ubiquitous nature of GTP binding properties that makes it difficult to target
  • Consider how ubiquitylation and de ubiquitylation plays a big role in stability of RAS
  • Discover the most efficient methods to monitor ubiquitylation of RAS proteins

Tauseef Butt
Chief Executive Officer


9.00am Exploring Allosteric Modulation of RAS: Utilizing Recent Data to Rethink RAS Experimentation

Our understanding how RAS proteins interact with GTP and downstream kinases has become more solid thanks to new structural biology and theoretical chemistry data. At the same time, basic assumptions about RAS/GPT and RAS/ kinase binding dynamics are under re evaluation. In the workshop we will look to discuss these fundamentals and how those effect on drug design and even clinical experiment. Through this updated detailed understanding of the structural modulation it is possible we can advance RAS-targeted therapies.

Topics to be covered:

  • RAS-GTP and RAS-kinase recognition mechanisms
  • Based on recent findings, should we rethink conduction of experiments and interpretation of RAS data?

Antti Poso
Professor of Drug Design
University of Eastern Finland & University Hospital Tübingen

11:00 am Morning Break & Virtual Speed Networking

Workshop C

Workshop D

11.30am Navigating the Future Potential of Combination Strategies: Combining Inhibitors Inside & Outside the RAS Pathway

As combination strategies become more abundant in our labs and increasingly important to targeted RAS, still our knowledge is limited. It is important to discuss how to best use combination strategies to optimize therapies for patients with RAS-driven cancers. This workshop will facilitate discussion around both combining inhibitors within the RAS pathway and targets outside the RAS pathway and how to select optimal combinations of RAS pathway inhibitor. It will also cover the potential of biomarkers to select of the right combination to overcome RAS inhibitor failure.

Topics to be covered:

  • What combination strategies make sense within the RAS pathway, and why?
  • What combinations may be required outside the canonical RAS-signalling pathway?
  • How can we select patients or  combinations for RASdriven cancers up front
  • How can we select or predict the best combination at progression or failure of RAS inhibitors?

Jan Smith
Vice President Biology
Revolution Medicines

Ryan Corcoran
Associate Professor of Medicine
Harvard Medical School

11.30am Mechanisms of Resistance: Identifying Effective Tools & Techniques to Accelerate Anti-RAS Drug Development

Approximately 30% of all cancers present with mutations in one of the RAS genes, making the RAS family the most prevalent oncogenic driver in human cancer. Targeted therapies against oncogenic drivers have led to dramatic responses clinical responses.  Unfortunately, these responses are often short-lived due to the acquisition of drug resistance through a variety of genetic and non-genetic mechanisms. In order to maximize the success of Ras targeted therapies, it will be important to gain an early understanding of the mechanisms driving resistance to inhibitors with diverse MOAs. With this in mind, it is important to delve into the most effective tools and techniques to study these resistance mechanisms.  Understanding such mechanisms may enhance patient selection and combination strategies and accelerate anti-RAS drug discovery and development.

Topics to be covered:

  • Review our current understanding of resistance mechanisms to anti-Ras therapies
  • Explore available and potential tools to study mechanism of resistance
  • Discuss best approaches to resistance modelling

Erica Jackson
Senior Director

Marie Evangelista
Project Team Leader

1:30 pm Lunch & Virtual Networking

Workshop E

Workshop F

2.00pm Enhancing Applicability, Specificity & Effectivity: Leveraging the Potential of a Protein Aggregation Based Platform to Transform RAS Drug Discovery

Whilst RAS proteins remain promising targets for anticancer therapies, the inability to effectively target such proteins remains a salient challenge for the RAS community. With the protein-aggregation based platform, effective and selective targeting of RAS proteins becomes more achievable. Through harnessing this new technology, we can overcome challenges surrounding discovery of RAStargeted therapies and effectively drug the “undruggable”

Topics to be covered:

  • Outline the technology and potential of the protein aggregation platform
  • Aelin’s platform as an alternative in the space of PROTAC’s (Proteolysis Targeting Chimeric’s)

Alexander Scheer
Chief Scientific Officer
Aelin Therapeutics

2.00pm Exploring How RASopathy Syndromic Disorders Will Help Target the RAS Pathway

This workshop will introduce the ‘RASopathies’, a group of neurodevelopmental genetic syndromes caused by germline mutations in genes encoding members of the RASMAPK signaling pathway. Amongst the 20 different genes implicated in RASopathy syndromes most mutations result in activation of RAS signaling. Discussions will consider how knowledge of RAS mutant cancers and cancer therapeutics can inform treatment of RASopathies, as well as how cancer biology may benefit from understanding the role of RAS signaling in human development revealed by study of the RASopathies.

Topics to be covered:

  • What are the RASopathy syndromes, how do they manifest, and how prevalent are they?
  • How do RASopathy mutations compare with RAS cancer mutations?
  • What can RASopathy variants teach us about RAS signalling biology, mechanisms of action and new target opportunities?
  • What preclinical models of RASopathies exist; and what have early/small clinical trials told us?
  • What clinical endpoints are amenable to measuring in individuals with RASopathies?

Beth Stronach
Board Member & Parent Advocate
RASopathies Network