Gabby Dower

• Group leader managing direct reports and matrixed resources to support the Immunology early discovery portfolio, leveraging each individual’s strength and expertise. • Led a biology team evaluating multiple targets in autoimmune diseases; brought targets to Go/No-go decision points • Project leader for a lead optimization program, working closely with multidisciplinary colleagues to define and implement project strategy • Lead the biology on a project with protein degrader (PROTACs) as modality; • Identified and assembled a Key Opinion Leader panel to provide input on an early target validation. • Coached and mentored junior PhD scientists to help them design experiments, prioritize their efforts, and become more efficient and independent in the industry setting

• Experience working in different groups including early discovery, epithelial biology, and translational biomarkers in the Inflammation and Immunology department • Group leader, set strategy and goals for newly formed group, managed direct reports to establish and characterize 2D and 3D intestinal in-vitro disease systems in-house, and built infrastructure around a new disease area • Inflammation & Immunology Lead in a multi-year collaboration with DRAPER to establish intestinal gut-on-a-chip system to validate IBD targets and better predict efficacy. • Identified, evaluated, and established a collaboration with a CRO to investigate microbiome in healthy and IBD samples. • Biology Lead for late stage IBD program; coordinated and managed efforts working closely with pharmacologists, chemists and DMPK colleagues to understand compound MOA in preparation for FIH. • Biology Lead for an early exploratory project in kidney fibrosis; managed activities within Pfizer and with external academic collaborators to validate target and establish cell-based functional screen assays. • Led translational biomarker plan for multiple programs in the early preclinical portfolio. • Worked with CROs and academics to source clinical samples (blood and tissues) from various inflammatory and fibrotic diseases (IBD, Lupus, CKD) to support translational biomarker discovery and target validation for multiple programs.

Supervisor: Jeremy S. Duffield • Responsible for designing and performing in vivo and in vitro experiments to study the role of macrophage activation in regeneration and fibrosis. 1) Screened tissue and identified candidate genes for therapy targeting. 2) Generated recombinant protein and evaluated for efficacy in sterile inflammation models. 3) Characterized various inflammatory signaling pathways during kidney injury. • Developed and characterized a new transgenic mouse model of selective ablation of pericytes that enabled to study the role of these cells during homeostasis and fibrosis. • Collaborate effectively within the department and with other institutions. • Supervised and trained students and technicians.

Supervisor: Joseph V. Bonventre, MD, Ph.D. • Generated and validated a new transgenic mouse model to specifically target renal epithelial cells by using cre/lox and diphtheria toxin approach. • Characterized the role of epithelial cell injury in kidney repair and fibrosis. • Designed and performed in vivo experiments using various models of kidney injury to test efficacy of novel therapeutics in treating the disease. • Collaborated with other professors within the department to test fibrinogen peptides as new candidates for acute kidney injury therapy.

Supervisor: Niels Olsen Saraiva Camara, MD, Ph.D. Thesis: The role of B1 bradykinin receptor in experimental models of direct and indirect acute lung injury. • Studied and defined the role of B1 bradykinin receptor in inflammatory experimental models of kidney and lung injury, using transgenic mice and antagonists. • Characterized acute lung injury in vivo induced by LPS or secondary to kidney ischemia and reperfusion injury.

Supervisor: Alvaro Pacheco-Silva, MD, Ph.D. • Investigated pioglitazone as a candidate drug to attenuate nephrotoxicity in rats caused by long-term treatment with cyclosporine.