Andrew Ho

I am thrilled to step into role of Head of R&D Projects at AIM, leading an ambitious initiative bridging biotechnology to healthcare. Current project focuses on the development of Smart Microsystems and high-throughput methodologies for the evaluation of drugs and biomarkers in the treatment and understanding of congenital muscle diseases. My goal is not only to advance scientific knowledge but also to create significant impacts on patient diagnosis and treatment prediction. By integrating advanced technology with biomedical research, we aim to accelerate the development of effective therapies and enhance the quality of life for those affected by these challenging conditions.

▪ Guided the design and optimization of preclinical studies using in vitro and in vivo models to evaluate the efficacy of small molecule inhibitors, by collaborating with CROs and overseeing data control and analysis. ▪ Worked closely with teams specializing in pharmacokinetics, drug modeling, and biodistribution studies, ensuring efficient collaboration. ▪ Played a significant role in the drug development process (PK, toxicity, etc.) by contributing expertise and insights, enhancing the overall success of the projects. ▪ Analyzed multi-omic dataset to obtain insights for mechanism of action, efficacy validation and biomarker discovery.

At Université Paris Cité, my work focuses on rare congenital muscle diseases, aiming to advance the understanding and treatment of these disorders. My projects involve the analysis of patient genomic data to identify disease-specific signatures, and the translation of preclinical findings to establish reliable biomarkers for disease progression and therapeutic efficacy. I have developed liquid biopsy assays and strategies for drug lead development, streamlining the process of identifying and validating potential therapeutic targets. Leveraging cutting-edge tools and techniques, I have established high-throughput readouts to assess muscle bioenergetics, endoplasmic reticulum (ER) stress, and mitochondrial dysfunction, enabling the detection of subtle changes in cellular pathways and disease-specific signatures. My interdisciplinary approach combines molecular biology, genomics, bioinformatics and data science to improve our understanding of rare congenital muscle diseases and develop novel therapeutic strategies.

In this small startup company, I have been closely involved in various aspects of drug efficacy validation, including the design and refinement of preclinical studies using in vitro and in vivo models to evaluate the efficacy of small molecule inhibitors. My responsibilities extended to conducting data control and analysis to ensure accurate and reliable results. Actively participating in the development of drug testing strategies, data interpretation, and regulatory compliance, I played a crucial role in the company's growth and progress. Furthermore, I designed and executed experiments to validate specific indicators, contributing to a comprehensive understanding of drug performance, mechanism of action, and potential in the rapidly evolving industry landscape.

At Stanford University, I held the position of Senior Scientist, where my work primarily focused on neuromuscular and muscle inflammatory biology, particularly in relation to Duchenne muscular dystrophy and sarcopenia. I guided multiple research projects and supervised students in their academic pursuits, leveraging innovative biotechnologies and multidisciplinary approaches. One of the major accomplishments was the implementation of single-cell time-lapse imaging and bioluminescent in vivo imaging that are critical for validating therapeutic target leads. Leveraging on machine learning algorithms, we establish methods which allow us to understand how target lead alters muscle cell fate, which played a significant part in advancing our understanding of muscle biology. These achievements led to high-impact publications, competitive awards, and patents, contributing to the overall success of the research team.

This thesis investigates the mechanisms of caspase activation and apoptosis, relevant to oncobiology and development. It demonstrates that caspase activation can occur independently through either Apaf1-induced dimerization or Smac/Diablo-mediated IAP sequestration, with the dependency on Apaf1 dictated by IAP activity. Furthermore, the study uncovers a compensatory Rb and p53-independent apoptosis pathway, which has significant implications for cancer therapy, where p53 and Rb are commonly mutated, rendering them insensitive to conventional drug treatments. The study also shows that pRb inactivation partially disrupts myoblast differentiation, and while p130 deletion doesn't affect apoptosis or endoreduplication, it transiently restores Troponin-T expression. These findings advance our understanding of cell death regulation, myogenesis, and cancer research, paving the way for novel therapeutic strategies.